SEMIOLOGY OF THE DIGESTIVE APPARATUS.
The group of diseases which affect the digestive apparatus is one of the most important in bovine pathology, because almost all animals of the bovine species are bred with the object of utilising to the full their powers of digestion and assimilation.
Whether we consider adult fat animals, calves intended for slaughter or milch cows, the object sought is always the same—i.e., to secure the greatest possible economic return through the medium of the digestive functions.
Even although in working oxen there is no tendency to overfeeding, the animals remain none the less predisposed to diseases of the digestive apparatus; the meal times are often too short, and rumination has to be performed under the yoke or during work—in a word, under unfavourable physiological conditions.
Semiology. To ensure correct diagnosis it is necessary here, perhaps more than in any other department of pathology, to be capable of grasping the symptoms or syndromes and signs afforded by the different parts of the digestive apparatus; to know how to co-ordinate and group them so as logically to deduce the final synthesis, the diagnosis. The diagnosis proving correct, the prognosis becomes easy, and this is the chief object from the economic standpoint. The practitioner who undertakes treatment knows how to deal with the case, and the owner likewise knows what he undertakes to do.
Although this classification may appear arbitrary, we shall consider successively diseases of the mouth, of the pharynx, œsophagus, stomach, intestines, etc., firstly describing the symptoms characterising these diseases. At the same time we should state that many symptoms are common to a large number of diseases and in themselves have absolutely nothing characteristic. They are simply sign-posts capable of showing the way.
Mouth. External examination reveals the condition of the muzzle, the lips and their commissures, and the surroundings of the buccal opening, and detects the existence of any desquamation, rents, eruptions, ulcerations, etc., which may be present.
In quiet animals the practitioner can examine the cavity of the mouth single-handed, but in troublesome animals it becomes necessary to have an assistant, who seizes the muzzle with one hand and the tongue with the other, or who simply fixes the animal’s head. In exceptional cases it will be necessary to secure the patient to a post, tree, or wall. The mere attempt at examination will show whether there is trismus or absolute freedom of movement in the jaws.
Fig. 57.—Examination of the mouth.
By introducing the fingers between the commissures and applying them to the bars or to the free portion of the tongue, the practitioner will be able approximately to estimate the local and general temperature. The sensations experienced will also inform him of the degree of moisture or dryness of the mouth and of its sensibility.
On separating the jaws, he will note the odour exhaled and its possible abnormalities—its acid, sourish, fœtid, or putrid character. He will directly observe any anæmia or hyperæmia of the mucous membrane, from the inner surface of the lips and cheeks up to the soft palate, although owing to the thickness of the buccal epithelium it is not always easy to estimate anæmia or hyperæmia in the ox. The surface of the tongue should also be examined, and a note made whether it appear dry, pasty, dusty, sooty, etc., though these appearances are occasionally apt to lead one astray. The observer should also inquire regarding want of appetite, depraved or exaggerated appetite, etc.
Even the manner in which the animal picks up its food will serve to direct his attention to the development, or possible existence, of some disease of the mouth, although want of appetite is not always characteristic of a lesion in the pharynx or œsophagus, but sometimes of a lesion in its neighbourhood, like hypertrophy of the retro-pharyngeal or bronchial lymphatic glands.
This examination will also detect the existence on the lips of wounds, cuts, injuries or specific eruptions (aphtha, tuberculous ulcerations, the ulcerations of gangrenous coryza, etc.) on the gums indications of gingivitis, periostitis, mercurial poisoning, actinomycosis of the maxilla, and ulcerations of all kinds; on the tongue, of wounds, of simple or specific inflammatory eruptions (aphtha, the ulcerations of actinomycosis, tuberculosis, gangrenous coryza, etc.), as well as the swellings due to superficial or deep-seated glossitis. By the same method of examination, though with somewhat more difficulty, one can detect abnormal mobility, irregularity of development, caries, etc., of the teeth, the condition of the excretory ducts of the salivary glands, the state of the hard and soft palate, and the existence of fissures, vegetations, polypi and tumours.
Fig. 58.—Examination of the mouth.
Salivary glands. The salivary glands, particularly the parotid and submaxillary, should be examined by direct inspection and palpation.
Direct inspection reveals the existence of swellings, deformity of parts, increase in salivation, or ptyalism, which sometimes occur in conjunction with foot-and-mouth disease, actinomycosis, acute stomatitis and mercurial poisoning, as well as increase in size of the salivary ducts.
Palpation reveals the degree of sensibility of the parts, the existence of œdema, induration, cysts, and, more frequently, distension of the salivary ducts as well as the presence of calculi, tumours, the direction of fistulæ, etc.
Difficulties may occur, particularly when the submaxillary and parotid glands are affected; but methodical and complete examination will usually enable one to differentiate the conditions.
Pharynx. The pharynx may be examined externally by inspection and palpation, and internally by direct digital palpation. Inspection reveals possible deformities of the region of the gullet, palpation the condition of the tissues as well as abnormal sensibility and infiltration. Internally, digital examination must be cautiously conducted, and after a strong gag has been securely inserted in the mouth. Under such conditions it is without danger. The hand being inserted exactly in the median line will detect obstructions which may already have been partly identified by external palpation, as well as the existence of inflammation with or without the formation of false membranes, and of ulcerations, polypi, etc.
Œsophagus. In consequence of its anatomical formation, situation and course, the œsophagus may be divided into two distinct parts—viz., the cervical, which can be examined from the outside, and the thoracic, which cannot so be examined.
The cervical part may be examined by inspection, by palpation from one side, or by palpation with both hands and from both sides.
Fig. 59.—Examination of the pharynx.
Inspection leads to the detection of changes in the shape of the œsophagus and of the jugular furrow. In fat subjects, however, it is of little value. As the position and the course of the œsophagus are known, unilateral palpation, or, better still, bilateral palpation, employing both hands, is of very much greater service. These methods reveal the presence of swellings, infiltrations, changes in shape and sensibility, the presence of foreign bodies, the existence of dilatations or contractions of the tube, etc.
Auscultation and percussion, though recommended by some practitioners, are not of much service.
Inability to swallow, due to change in the œsophagus, is also detected by inspection. Its existence suggests a number of possible conditions, such as fissure or ulceration of the œsophagus, compression in the mediastinal region as a result of tuberculous or other disease, contraction or dilatation of the œsophagus, etc. Furthermore, inspection will betray the existence of dilatation of the tube, to which vomiting and regurgitation of food are sometimes due.
Internal exploration is the only method of detecting changes in the thoracic portion, and may also be utilised to locate lesions in the cervical region. It is practised by passing a sound of small calibre or any flexible cylindrical object, such as a cart rope, etc. The patient must be fixed with the head extended on the neck and a proper gag or speculum introduced into the mouth. Exploration assists us in recognising the existence of inflammation of the œsophagus, true or false contraction, dilatation and the presence of obstructions.
In animals of the bovine species all these lesions—viz., inflammation of the œsophagus, fissuring and ulceration, obstructions, compressions, dilatations and contractions of the tube—although not very frequent, are nevertheless from time to time encountered.
Stomach. Exploration of the stomach or of the different gastric compartments presupposes an exact knowledge of the respective positions of the different reservoirs. Topographical anatomy shows that the rumen is situated in the left flank, and that it occupies the whole of the left abdominal region from the diaphragm to the pelvic cavity. As a consequence, it may be explored from the region of the twelfth rib; it is inclined slightly from above downwards, and from left to right, its extreme right border extending as far as, or a little beyond, the white line.
The reticulum, the smallest of the four reservoirs, is situated in the sub-ensiform region at right angles to the median plane of the body. On the left it touches the rumen and the diaphragm; on the right side it is in contact in front with the diaphragm, above with the omasum, and to the right and towards the rear with the abomasum. The omasum is situated above the reticulum and conical right portion of the rumen; in front it touches the liver, and towards the back and left the rumen. The abomasum is situated obliquely in the right hypochondriac region, its anterior surface resting on the lower wall of the abdomen towards the middle and right side of the body, its pyloric portion extending upwards, behind the right hypochondriac region.
Rumen. The rumen can be examined by inspection, palpation, percussion, and auscultation. The use of the œsophageal sound and of the trocar and canula is also of value in diagnosis.
Inspection affords information of a varying character, according to the moment when it is practised, even in a condition of health. It only extends to the condition of the flank before or after a meal, etc., emptiness of the rumen being accompanied by hollowness of the flank, and distension, following an abundant meal, by fulness in this region.
When digestion is not proceeding normally, the flank may be distended unduly by gaseous accumulations or by the presence of solid food. In abdominal and mediastinal tuberculosis and in gastro-enteritis there may be simple tension or slight dilatation. When indigestion or enteritis is entering on a favourable stage, the flank may appear hollow, and in cases of chronic diarrhœa it may appear retracted.
Fig. 60.—Position of the thoracic and abdominal viscera of the left side. A, posterior aorta; P, paunch or rumen; Id, line of insertion of the diaphragm; C, heart and pericardium; Pd, anterior lobe of right lung; Pg, left lung; D, diaphragm; Rg, left kidney.
Digital examination or palpation may be practised over the entire region of the flank. It shows whether the rumen is full or empty, reveals the consistence of the contained food in cases of chronic indigestion, the sensibility of the walls, and the rate and order of the muscular contractions. Direct or indirect percussion may be carried out on a horizontal line from the twelfth rib as far back as the flank, and vertically from the lumbar vertebræ to the white line. In health one discovers in young animals an upper zone of normal resonance due to gas, a zone of semi-dulness and an inferior zone of absolute dulness, due to the liquids in the rumen. The spleen, which is attached to the supero-anterior surface of the left side of the rumen, does not seriously restrict the area open to percussion.
In pathological conditions percussion from above downwards may produce a tympanitic sound, due to gaseous indigestion or a clear sound throughout the greater portion of the vertical diameter suggestive of acute gastro-enteritis with the formation of gas in the rumen, or of adhesive peritonitis preventing the rumen from collapsing. Indigestion due to excess of solid food, on the contrary, is characterised by a dull sound throughout the entire region from above downwards. Percussion along a horizontal line permits of the delimitation of certain zones which vary a great deal in area, according to the case.
Auscultation is more instructive than percussion. Like percussion, it may be practised throughout the entire depth of the abdomen, from the transverse processes of the lumbar vertebræ as far as the white line, and in a horizontal direction from the eleventh rib to the region of the flank.
Auscultation of the upper zone enables one to detect sounds of deglutition, gurgling sounds (glou-glou), and a sound resembling falling water, due to the movement of solids or liquids in the rumen and reticulum. The sounds heard vary in different cases, and depend on the state of repletion or of emptiness of the rumen.
Auscultation of the middle zone reveals:
Firstly, a very special crepitation sound, which may be compared to the deflagration of a handful of salt thrown on burning coal. It is believed to result from the bursting of bubbles in the contents of the rumen under the action of normal digestion.
Secondly, a churning sound produced by the rhythmic peristaltic contractions of the rumen, by which the substances ingested are very intimately mixed. By applying the ear over the flank region or by palpation the rhythmic contractions of the rumen, two per minute in most cases, can readily be perceived.
In practice examination of the rumen is confined to these four methods.
Puncture. From an exclusively scientific point of view, exploration of the rumen also comprises analysis of the gas collected through puncture and analysis of the liquids removed by aspiration (first stages of gastric digestion). Normally, these gases, in the order of their abundance in the mixture, consist of the following: Carbonic acid, carburetted hydrogen and nitrogen.
In disease, and in most cases of abnormal fermentation, the carburetted hydrogen is greatly in excess of the carbonic acid. In chronic gastro-enteritis, ammonium sulphide and other offensive gases are found in addition.
Chemical analysis. In the rumen the ingested food is macerated in an alkaline liquid at a temperature of 100° to 101° Fahr. (the alkalinity is due to the saliva). This process markedly modifies the composition of the ingested matter. Nevertheless, the upper portion in contact with the gas sometimes presents a slightly acid reaction, probably due to carbonic acid. The sugary and fatty materials contained in the food respectively undergo lactic and butyric fermentation. Only a small quantity of the starch, however, is transferred into sugar. In the calf, and in very young animals, the reaction of the rumen is acid throughout the entire period of sucking. In disease, when rumination has long been suspended and chronic loss of appetite or gastro-enteritis exists, the reaction is generally acid. The sugars, gums, and soluble salts of forage, roots, etc., are dissolved in the rumen, but fatty materials undergo no modification.
The reticulum, which is the smallest of the gastric compartments, is situated in the sub-ensiform and retrodiaphragmatic regions, extending right and left of the middle line to a nearly equal distance. Above and to the left it communicates freely with the rumen, to the right with the omasum.
In practice it can only be examined in two ways: inspection and palpation.
By inspection changes in the configuration of the ensiform region may sometimes be detected. Such changes are rare, and must be distinguished from congenital deformity. They sometimes accompany inflammation of the reticulum produced by a foreign body, when the lower abdominal wall is directly perforated by such body.
In cases of inflammation of the reticulum due to foreign bodies, abscess formation, perforation, etc., it is possible to detect œdematous infiltration, abnormal sensibility, fluctuation and increased heat, etc., by manipulating the parts with the fingers or the clenched fist.
If the evidence pointing to the presence of a foreign body in the reticulum is considered sufficient, gastrotomy may be performed and the interior of the viscus examined with the hand, but although the operation is possible it is very rarely practised.
Omasum. The omasum occupies, so to speak, a position inverse to that of the reticulum, lying deep down on the right side, behind the diaphragm, under the hypochondrium, and above the abomasum and reticulum.
It is the only gastric compartment which cannot be examined, although when impacted it may be felt on the right side.
Abomasum. The abomasum is lodged in the lower part of the right flank under the circle of the hypochondrium. It extends obliquely from below, upwards from the sub-ensiform to the sublumbar region. The smaller curvature is turned towards the rumen on the left side; the larger curvature is in contact with the abdominal wall. In spite of what has so often been stated by those who have never seen it, the abomasum can be examined and is accessible along the circle of the hypochondrium.
In adults useful information can rarely be obtained by inspection; but in sucking calves the abomasum, if distended by indigestion, gastro-enteritis, etc., sometimes appears prominently in the right abdominal region. Palpation with the fingers or with the fist will detect exaggerated sensibility, irritation, inflammation, or distension.
Percussion and auscultation furnish no very precise information. The information obtained by the above-described examination of the stomach is in practice amplified by a search for certain symptoms which are usually easy to detect. They comprise:
(a) Suppression or irregularity of rumination. This very important symptom suggests the degree of gravity of the digestive disturbance, and to some extent the gravity of the general condition. Suppressed rumination is a common symptom in many diseases, some of which are purely digestive, though all are not. It is, however, a grave sign in most cases.
(b) Eructation, which is usually frequent, may be regarded as normal provided the exhaled gas preserves the fresh odour of grass or of the food swallowed, like brewers’ grains, turnips, etc. Sometimes the gas is sour, acid, fœtid, or putrid, all of which conditions indicate disease.
(c) Yawning is not common. It becomes frequent and attracts attention in certain abnormal conditions; in others, again, it may be completely suppressed.
(d) Nausea and vomiting are rare. Vomiting is commoner in calves, and results from inability to digest the milk, or simply to over-distension of the abomasum. The matter vomited by adults usually consists of partly masticated food, and is derived from the rumen; while the contents of the abomasum are occasionally rejected, in which case the material is of pulpy consistence and has an acid smell.
(e) Digestive disturbance is sometimes accompanied by various modifications in the breathing, such as immobilisation of the hypochondriac region and of the diaphragm; abnormal sensibility and reflex coughing on palpation, and, in inflammation of the reticulum due to foreign bodies, costal respiration.
Fig. 61.—Position of the abdominal viscera, seen from below. Gi, large intestine; V.c.g., left pouch of the rumen; E, E, epiploon (line of insertion); P, paunch or rumen; Ax, xiphoid appendix of the sternum; R, reticulum; C, abomasum; V.c.d., right pouch of the rumen; Ig, small intestine.
It is by methodically observing, grouping, and classifying the symptoms presented that one is enabled to detect the links connecting them.
Intestine. The intestinal mass is contained in the right half of the abdomen above the compartment of the stomach. The large intestine occupies the upper zone, corresponding externally with the hollow of the flank from the thirteenth rib to the haunch. The small intestine occupies the middle zone from the thirteenth rib to the entrance to the pelvis and the stifle region; the inferior zone is occupied by the rumen and abomasum, and in pregnant females by the gravid uterus.
Notwithstanding these indications it is somewhat difficult to examine the mass of the large intestine, separated as it is from the abdominal wall by the U-shaped inflection of the duodenal loop, of which the deep retrograde branch is in contact with the terminal portion of the floating colon.
Inspection of the right flank furnishes no information of value in diseases of the intestine, nor is auscultation of much service beyond enabling one to detect the frequency, diminution, or absence of borborygmus. Palpation alone is really of service. Practised gently and superficially with the tips of the fingers it detects abnormal sensibility in acute cases of enteritis; when with more energy, palpation reveals whether the bowel be full or empty, provided that the muscular resistance be not too marked.
Colic. In colic the clinical signs, their varieties, and the lesions which give rise to them are of much more importance. When it results from intestinal congestion à frigore (due, for example, to the ingestion of cold water), colic is usually violent, sudden, and of relatively short duration. In other cases it is violent and prolonged for several hours, a whole day, or even two days, and may be followed by coma and suppressed peristalsis; it then indicates invagination, volvulus, or strangulation. Sometimes, on the contrary, it remains dull and is slow and continued (acute gastro-enteritis, hæmorrhagic gastro-enteritis, etc.).
Finally, colic of the latter character may, in addition, be accompanied by icterus, in cases of retention of bile, biliary calculi, hepatitis, etc.
Anus. Examination of the anus is easy. Simple inspection reveals its presence or absence, and consequently the existence of congenital rectal atresia, which is somewhat common in calves and colts. Digital exploration is, however, sometimes useful, for in occasional cases an anus may exist, which externally appears normal, but terminates in a sac, the rectum being closed by a membranous partition.
Nothing is easier to recognise than tenesmus; it occurs in cases of profuse diarrhœa, diarrhœa of calves, and dysentery in newly-born animals.
Fig. 62.—Position of the thoracic and abdominal viscera as seen from the right side. ID, insertion of the diaphragm; V, gall bladder; C, abomasum; I, small intestine; D, duodenum; GC1—GC2, large intestine (colon); Co, cæcum; Pc, point of the cæcum; CF, floating colon (first part); P, pancreas; R, right kidney; F, liver; Di, diaphragm (line of projection towards the front); Pd, right lung.
Rectal exploration. Exploration of the rectum is a last and most valuable means of confirming the diagnosis in all visceral diseases of the pelvis and abdomen. To utilise this method to the full, the rectal pouch should first be thoroughly emptied by the free use of enemata, the subsequent examination being made with great care. The animal’s hind legs being secured, the operator smears his hand and forearm with some fatty substance, and, forming the fingers into a cone, introduces them with gentle pressure through the anus, the palm of the hand being turned downwards. Passing the hand gently along the rectum, the operator will be able to distinguish the conical posterior pouches of the rumen, the loop of the duodenum, the mass of convolutions of the small intestines and of the colon, etc. Next, he will examine the vagina, uterus, bladder, ureters, kidneys, aorta, and the pelvic and sublumbar lymphatic glands. He may be able to recognise distension of the rumen with food, twists of the intestine, herniæ, mesenteric or diaphragmatic invagination or volvulus of the bowel, etc.
In other cases he may be able to discover lesions of the kidney, of the uterus, of the broad uterine ligaments, of the ovaries, or of vessels.
In all cases it is desirable to make a methodical and complete examination, whatever the primary object may have been. Such an examination may be carried out as follows: The operator having introduced his hand into the rectum, begins by examining the state of the pelvic organs, the rectum, base of the vagina, the body and horns of the uterus, the bladder and the lymphatic glands and ligaments of the pelvis.
By laying the hand flat in the rectum and pressing gently downwards the anterior border of the pubis may be felt, somewhat more deeply placed. The rectum is then thrust slightly to the right, and the ascending branch of the right ilium, as high as the sacro-iliac articulation, and the lower surface of the sacrum, are directly examined; lastly, the hand is directed towards the left, gliding down the left ilium, and returning to the point of departure. In this way the state of the pelvic floor, of the arteries, veins, and lymphatic glands, etc., the degree of mobility, tension, or fulness of the uterus, as well as the condition of the broad ligaments, are all ascertained.
Still more deeply placed, and at the extreme limit to which the arm can be introduced, will be found some or all of the above-mentioned organs—viz., the small intestine, large intestine, kidney, etc.
Defæcation: Examination of the fæcal material. The character of the fæces is very important in certain diseases; e.g., diarrhœa assumes a varying importance, according as the discharges are of an alimentary, serous, mucous, or sanguinolent type, and are slight, temporary, intense, profuse, or continued. In other cases defæcation is slow, becomes difficult, and various degrees of constipation exist. Defæcation may be completely suppressed, as in invagination or strangulation of the intestines; on the other hand, one may observe diarrhœa, dysentery (microbic or sporozoic diarrhœa), and intestinal hæmorrhage. The last named may be of varying degrees of acuteness, from the passage of simple drops or streaks of blood, distributed over almost normal excreta, to the passage of unchanged blood in liquid jets or in clots.
Macroscopic examination. Macroscopic examination takes cognisance, firstly, of the quantity (40 to 80 lbs.), consistence (firmness or softness), colour (olive green, blackish green, greyish black, sooty, or tarry) and odour (normal, fœtid, putrid, etc.) of the fæces.
Sometimes the excreta are moulded and covered with glairy mucus, or contain such abnormal products as undigested food (a sign of chronic diarrhœa), false membranes, false membranes due to pseudo-membranous enteritis, fibrinous clots, or parasites like liver flukes, tæniæ and strongyles.
Microscopic examination. Microscopic and bacteriological examination is sometimes useful; and even when macroscopic examination has revealed nothing, it is possible to detect the presence of the eggs of parasites like flukes, strongyles, hooked worms, etc., the presence of sporozoa (as in intestinal coccidiosis) and of specific microbes, as in the diarrhœa of calves, etc.
It is only by the synthesis of methodically collected signs that one finally succeeds in exactly diagnosing the numerous diseases which may affect the intestine: intestinal congestion, invagination, volvulus, intestinal strangulation (mesenteric or diaphragmatic herniæ, etc.), atresia of the anus, acute or hæmorrhagic enteritis, or intestinal helminthiasis.
Liver. The liver is situated in the right sublumbar region. It is fixed behind the diaphragm and under the hypochondriac region, and extends from the ninth to the thirteenth rib. It can be examined by palpation through the last intercostal spaces and behind the thirteenth rib. In health it is difficult to pass the fingers sufficiently under the hypochondriac circle to reach the liver; but in case of morbid hypertrophy it extends more or less beyond the last rib, and palpation between the last ribs sometimes reveals abnormal sensibility.
Percussion better than palpation enables one to delimit the space occupied by the liver, particularly towards the back, where there is no interposed layer of lung. Percussion is especially useful in detecting hypertrophy due to cancer, tuberculosis, echinococcosis of the liver, etc., or hepatic atrophy. In isolated cases icterus may exist, confirming the conclusions otherwise arrived at.
Pancreas. The pancreas is situated rather deeply in the right sublumbar region, below the kidney, behind the liver, above the floating colon, and within the duodenal loop. It is therefore very difficult to examine; moreover, the diseases which affect it are still little understood.
The point most prominently brought forward by this demonstration of the topographical anatomy and semiology of the digestive apparatus is the difficulty of accurately diagnosing digestive diseases in the ox when one confines oneself to a superficial examination. To have any chance of arriving at an exact diagnosis, methodical and thorough examination is indispensable. Given this condition, accurate diagnosis becomes possible, despite all difficulties.
CHAPTER I.
DISEASES OF THE MOUTH.
STOMATITIS.
Definition. By stomatitis we mean inflammation of the buccal mucous membrane. Stomatitis may be simple—i.e., due to accidental causes, to varying local forms of irritation, or to wounds; or, on the contrary, it may be specific, of infectious origin, like the stomatitis of foot-and-mouth disease, gangrenous coryza, cattle plague, etc.; or, finally, it may be of toxic origin, like the stomatitis of mercurial poisoning.
Here we shall only study the simple forms of stomatitis, the gangrenous stomatitis of calves, and mercurial stomatitis. The others will be noticed in speaking of the diseases of which they form one of the symptoms.
SIMPLE STOMATITIS.
Causation. Simple stomatitis of bovine animals is often due to feeding with rough forage, or forage containing prickly or spiny plants, like thistles, sea holly, eryngo, etc. Sometimes it follows prolonged irritation by rough teeth, premolars or stumps, or accompanies the shedding of the temporary molars. Ingestion of irritant plants like nettles, certain specimens of the orders Labiatæ and Umbelliferæ, leaves covered with vesicant insects, cabbage and turnip leaves infested with aphides, oil beetles, etc., or the swallowing of hot liquids, may also, though more rarely, produce it. Finally, in grave diseases of the digestive apparatus, the buccal mucous membrane may secondarily become affected.
Symptoms. The primary symptoms are usually represented by ptyalism and a certain difficulty in grasping food. In other cases the mucous membrane appears slightly dry for some time before salivation sets in. On introducing the fingers into the animal’s mouth some elevation of temperature may be noted, and on direct inspection the non-pigmented regions are seen to be abnormally vascular, a fact which has earned for this form of stomatitis the names of “erythematous” and “erysipelatous stomatitis.”
If the stomatitis is due to local multiple irritation, such as results from spines and prickles in the food, the abnormal vascular appearance is confined to the neighbourhood of the abrasions or punctures, and the affected regions are of very varying size. In some cases, principally as a consequence of trifling local irritation and of burns of the first and second degree, blisters of varying size may develop and break, leaving behind ulcerations, which, however, always heal rapidly. The aphthous non-contagious stomatitis mentioned by certain authors seems most probably to pertain to this class.
Diagnosis. The diagnosis is usually easy, and a little attention to the accompanying symptoms is sufficient to avoid confusion with the various forms of symptomatic stomatitis.
The prognosis is favourable.
Treatment is based on removal of the determining cause, if this can be recognised, withdrawal of rough forage, removal of sharp points on the teeth, extraction of stumps, etc. As a rule, recovery follows rapidly. It can be hastened by washing out the mouth directly, or by means of a syringe, with water containing honey, vinegar, decoctions of brier twigs, oak bark, barley or rice. This treatment is completed by supplying nourishing gruel and food demanding little mastication.
CATARRHAL STOMATITIS IN SHEEP.
“The more delicate buccal mucosa in these animals would render them more subject to inflammations, but this is more than counterbalanced by the mode of prehension of aliments, not by the tongue, but by the delicately-sensitive lips, and further by the daintiness and care with which these animals select their food. The treatment would not differ materially from that prescribed for the ox.” (Law’s “Veterinary Medicine,” Vol. II. p. 15.)
[The treatment referred to consists of simple astringent and antiseptic washes, borax given in the drinking water, or mixed with honey or treacle and smeared occasionally on the tongue. Washes of sodii hyposulphis or sulphis, or even weak solution of carbolic acid, may be used after the irritant cause has been removed. Vinegar or diluted mineral acids may be used alternately with decoctions of blackberry bark or other vegetable astringents. When there are symptoms of gastric disorder a laxative, followed by vegetable bitters and other tonics, may be prescribed. Foreign bodies—thorns, wire, etc.—fixed in the tongue, cheek, or palate should be searched for and removed at the first examination of the patient.]
NECROSING STOMATITIS IN CALVES.
Definition. This name is applied to a special stomatitis, which in very young animals produces superficial necrosis of more or less extensive areas of the buccal mucous membrane, and sometimes of subjacent parts.
The disease, although somewhat rare in France, has been mentioned by Lafosse and well studied by Damman and Lenglen.
Causation. Its cause is still imperfectly understood. Some regard it as a consequence of insufficient nourishment, of disturbance resulting from dentition, of general exhaustion, and of bad hygienic conditions. These explanations are scarcely sufficient, however, and at the present time there is a tendency to regard it as a complication of primary grave, debilitating diseases, like the diarrhœa of calves, omphalitis, omphalo-phlebitis, etc. Moussu has never seen it apart from omphalitis, and he considers the lesions due to the action of the bacillus of necrosis. Infection occurs through the umbilicus becoming soiled by contact with the litter.
The early symptoms consist in loss of appetite, congestion of the mucous membranes, and salivation. Early examination of the buccal cavity reveals the presence everywhere, except on the palate, of whitish-grey or yellowish patches, whose aspect is markedly in contrast with that of neighbouring parts. These are fragments of the mucous membrane undergoing necrosis. They are numerous, are surrounded by a narrow inflamed zone, and may be from ½ inch to 1 inch in diameter.
Necrosis advances rapidly, and extends throughout the thickness of the mucous membrane; the slough soon becomes delimited and separates. The odour of the mouth is then absolutely fœtid, and the saliva appears streaked with pus and blood.
The ulcerations exhibit a livid base, and show no tendency to heal. Necrosis extends in depth, and affects the muscles, tendons, and even the periosteum and the bones. The teeth are frequently loosened.
Grave complications, such as pharyngitis, broncho-pneumonia, infectious enteritis, and septicæmia soon appear, and the animals are carried off by septic infection and intoxication in a few days—at the longest in a week.
Diagnosis. The diagnosis is only difficult at first; and, at a later stage, the only mistake possible is that of confounding the condition with a very grave attack of aphthous stomatitis. Local sanitary conditions are sufficient to secure the avoidance of this error.
Prognosis. The prognosis is extremely grave; the disease usually results in death; recovery is exceptional. Very luckily the disease seems to become rare in direct proportion as the hygienic conditions of cattle breeding and keeping are improved.
Treatment. Curative treatment always appears to be ineffectual when a grave primary disease has already enfeebled the animal before necrosing stomatitis appears. In those cases where the stomatitis constitutes the primary condition, attempts should be made as far as possible to cleanse the wounds. The buccal cavity should be thoroughly washed out, and the wounds then cauterised with solution of carbolic acid of 6 per cent. strength, nitric acid of 10 per cent. strength, hydrochloric acid of 7 to 8 per cent. strength, or chromic acid of 20 per cent. strength.
This local cauterisation is performed with a tampon of cotton wool fixed to a handle; for necessarily it is impossible to apply any dressing whatever of a permanent nature. The cauterisations may be repeated twice a day. The stump of the umbilical cord should never be forgotten, for it sometimes contains a mass of necrotic tissue the size of a man’s thumb. It should be thoroughly cleansed and the wound plugged with a mixture of iodoform and boric acid.
This treatment will not avail unless the functions are stimulated by rich food that can be easily masticated and digested, and by giving milk of good quality, or boiled milk, eggs, meat-powder, cooked beans, etc. Aromatic infusions and hay tea containing coffee and small quantities of alcohol or tincture of quinine are also of service.
MYCOTIC STOMATITIS IN CALVES.
Thrush. Muguet.
“This is a form of stomatitis manifested by a raised white patch on the mucous membrane and determined by the presence of the Oidium albicans (Saccharomyces albicans), a cryptogam discovered by Berg in 1842 in thrush in children. It is closely allied to the mucor, and attacks only the young and feeble. The white crust consists of epithelial cells intermingled with an abundance of the white mycelium and oval spores of the fungus. Andry in his artificial cultures found that it was pearly white when grown on gelatine, dirty white on potato, and snow white on carrot.”
Symptoms. “Buccal mucosa, red, congested and tender, shows here and there white curdy looking elevations, or red erosions caused by the detachment of such masses. These bear a strong resemblance to the crusts seen on this mucosa in rinderpest, but are easily distinguished by the absence of the attendant fever, and by the discovery, under the microscope, of the specific microphyte. The eruption may extend to the pharynx and œsophagus and interfere fatally with deglutition, but usually it merely renders sucking painful and is not serious.”
Treatment. Cleanse and disinfect the sheds, “and invigorate the young animals by sunshine, free air and exercise. Locally ... borax, which arrests the growth of the parasite, whether in artificial cultures or in the mouth. The powder may be rubbed into the sores, or it may be mixed with ... molasses and used as an electuary. As substitutes boric acid, salol, thymol, potash chlorate, or Condy’s fluid may be used.” (Law’s “Veterinary Medicine,” Vol. II. p. 36.)
ULCERATIVE STOMATITIS IN SHEEP.
The name of ulcerative stomatitis of sheep has been given to a disease which is characterised by the appearance of a pultaceous deposit on the surface of the buccal mucous membrane and later by the development of ulcerations and of vegetative growths.
Causation. The cause is imperfectly understood. In certain years the disease appears to attack lambs at the time of weaning, but it may also affect flocks of animals as old as fifteen or eighteen months, two years, or even more. It is contagious, and may extend to one-half or two-thirds of the entire number in the flock. Full-grown and old animals appear to be immune.
It was formerly thought, à priori, and in consequence of the character of the buccal deposit, that the disease was identical with thrush, and that the lesions were produced by Oidium albicans. Neumann in 1885 declared, however, that he could not find the fungus in question in scrapings from the mucous membrane.
Moussu had similar negative results in the experiments he made during 1894, when he examined both young and old animals belonging to flocks in the departments of Berry and of La Brie.
In addition it has been suggested that the disease affects badly cared-for and badly fed lambs, and subjects suffering from “watery cachexia.” This seems correct in many cases, and Moussu has seen ulcerative stomatitis decimate flocks which had previously been attacked with intestinal helminthiasis and verminous broncho-pneumonia; but, on the other hand, in the environs of Melun he saw it in animals which had previously been quite free of disease and were kept under perfect hygienic conditions.
The conditions in which animals are reared, the use of common drinking ponds, and the method of supplying flocks with food, are the chief causes of the distribution of the disease.
Symptoms. The symptoms consist in loss of appetite, or rather in difficulty in grasping and masticating food, wasting, a certain degree of dulness, and salivation. Somewhat later one often sees appear on the free margin of the upper and lower lips an eruption of small vesico-pustules, which quickly become covered with yellowish-brown crusts and bleed on the slightest touch. The lips swell, become sensitive and painful, so that examination of the cavity of the mouth should be made with care. The mucous membrane is then seen to present a very varying number of greyish-white or greyish-brown points, each of which is due to the destruction of the epithelium and to the production of a pultaceous deposit, which can very readily be removed, leaving uncovered superficial ulcerations, which bleed if very lightly touched. These ulcerations are of irregular shape, and are distributed most freely over the gums, the internal surface of the lips and cheeks. The palate and tongue are only invaded in the last stages. Still later one notes, instead of these ulcerations and as a consequence of abnormalities in the process of repair, reddish-violet turgid vegetations varying in size from that of a millet seed to that of a pepper-corn or even of a small mulberry.
The total duration of the disease varies with its degree of intensity. In favourable cases it may not exceed eight to ten days; in grave cases it continues for fifteen to twenty days. Recovery is usual when the subjects are vigorous and well-nourished lambs, or well-kept sheep, previously free of disease. On the other hand, Moussu has noted a mortality of 15 to 20 per cent. in thin animals of bad bodily condition and already depressed by verminous broncho-pneumonia and intestinal helminthiasis. When the attack is about to prove fatal, complications such as gastro-enteritis, resulting from septic infection or intoxication, and accompanied by fœtid diarrhœa, often make their appearance.
Diagnosis. The diagnosis presents no difficulty, the characteristics of this stomatitis being entirely different from those of the aphthous form. The claws are never affected, and there is no lameness.
Prognosis. In this connection the practitioner will do wisely to avoid committing himself, and to closely study the conditions under which the disease has developed. In all cases the appearance of fœtid diarrhœa must be regarded as of very unfavourable augury.
Treatment. The first precaution to take consists in separating all the healthy animals in the flock, and placing them in a non-contaminated spot.
The diseased are then treated one by one; each day the buccal cavity is washed out with boiled water or with a solution of borax or boric acid. After each washing the ulcerations should be touched with tincture of iodine or with some other rather active antiseptic solution. Finally it might be useful, and would be of value, to add to the gruel or water a small quantity of common salt and of salicylate of soda at the rate of 15 grains to the pint.
GENERAL CATARRHAL STOMATITIS IN SWINE.
Causes. “Swine suffer from simple stomatitis when exposed to thermal, mechanical, or chemical irritants. Such irritants comprise food that is too hot, or is hard and fibrous, or which contains spikes and awns, capable of entering and irritating gland ducts or sores, or food which is fermented or putrid, food or medicine of an irritant character. The habit of catching and holding swine with a running noose over the upper jaw, and the forcing of the jaws apart with a piece of wood in search of the Cysticercus cellulosa are further causes. In several specific infectious diseases inflammation of the mucous membrane, with eruption or erosion, is not uncommon. This aphthous fever is marked by vesicular eruption, muguet by epithelial proliferation and desquamation, hog cholera and swine plague by circumscribed spots of necrosis and erosion. Patches of false membrane are not unknown, and local anthrax, tubercle, and actinomycosis are to be met with. Inflammation may start from decaying teeth.”
“Symptoms resemble those in other animals, refusal of food, or a disposition to eat sparingly, to select soft or liquid aliments, to swallow hard materials half chewed, or to drop them, to champ the jaws, and to seek cold water. Accumulation of froth around the lips is often seen, and the mouth is red, angry, dry, and hot, and exhales a bad odour.”
“Treatment does not differ materially from that adopted in other animals: Cooling, astringent, antiseptic lotions, honey and vinegar, and in case of spongy or eroded mucosa, tincture of myrrh daily or oftener. Soft feeding, gruels, pulped roots, ... and clean water should be constantly within reach. In case of ... indigestion a laxative, followed by vegetable tonics, will be in order.” (Law’s “Veterinary Medicine,” Vol. II. p. 17.)
ULCERATIVE STOMATITIS IN SWINE.
“This is the scorbutus of Friedberger and Fröhner, the glossanthrax of Benion.”
Causes. “It has been attributed to insufficient or irritant food, to damp, close pens, and to chronic debilitating diseases, and all these act as predisposing causes. In gastritis and in infectious fevers like hog cholera, swine plague, and rouget (hog erysipelas) the spots of congestion and petechiæ on the buccal mucous membrane may become the starting points for ulcerative inflammations. These conditions appear, however, to be supplemented by infection from bacteria present in the mouth or introduced in food and water, and, as in the case of other domestic animals, the most successful treatment partakes largely of disinfectant applications.”
Symptoms. “Loss of appetite, grinding of the teeth, champing of the jaws, the formation of froth round the lips, fœtor of the breath, redness of the gums and tongue, and the formation of vesicles, or white patches, which fall off, leaving red, angry sores. These may extend, forming deep unhealthy ulcers, with increasing salivation and fœtor. As the disease advances the initial dulness and prostration become more profound, and debility and emaciation advance rapidly. Unless there is early improvement an infective pharyngitis or enteritis sets in, manifestly determined by the swallowing of virulent matters from the mouth, and swelling, redness, and tenderness of the throat, or colics and offensive black diarrhœa, hasten a fatal issue. Rachitis may be a prominent complication, as it seems in some instances to be a predisposing cause.”
Treatment. “Isolate the healthy from the diseased, and apply disinfection to all exposed articles and places. Employ local antiseptics as in other animals. Sulphuric or hydrochloric acids, in fifty times their volume of water, or tincture of iron, chlorate of potash, or chloride of ammonia, or borax have been used successfully. Bitters and aromatics have also been strongly recommended.” (Law’s “Veterinary Medicine,” Vol. II. p. 29.)
MERCURIAL STOMATITIS.
This form of stomatitis possesses certain distinguishing characters, and develops after severe or trifling mercurial poisoning.
Causation. Sheep sometimes suffer from mercurial poisoning as a result of the use of baths containing corrosive sublimate or mercurial ointment for acariasis or other cutaneous parasitism. Animals of the bovine species seem predisposed to the disease as a consequence of their special sensitiveness to the action of mercury, which is not shared by other species.
Mercurial poisoning may occur accidentally, but is usually the result of some attempt at treatment. Any preparation containing mercury or mercurial salts may produce it. In domesticated animals it most frequently results from the action of the ordinary mercurial blister or mercurial ointment of the pharmacopœia, or again of calomel. Sometimes it follows the use of mercurial salts in uterine douches, or in lotions used to wash out large abscess cavities or wounds.
The application of blisters or of anti-parasitic dressings, or infriction with grey ointment over extensive surfaces, favours this intoxication. It may result from direct local intra-cutaneous absorption, from vapour given off by mercurial applications obtaining entrance into the body through the broncho-pulmonary and digestive tracts, from vapour given off by metallic mercury (as in ships’ holds), or from ingestion of mercurial compounds licked off the skin, as certainly occurs. Hitherto in all discussions, even the most recent, on the mechanism of poisoning, partisans of different views do not appear to have given sufficient attention to these now clearly proved facts. The conclusion to be drawn is that in animals of the bovine species mercurial preparations ought to be used with caution, and that even under such conditions stomatitis may appear. Finally, it should be remembered that all lesions of the kidney indicated by albuminuria and other signs, and all lesions of the liver, favour poisoning by checking or preventing the elimination of mercury by the kidney, or by interfering with its transformation in the hepatic cells.
Nature. Regarding the essential nature of stomatitis, it would appear (according to the work carried out in 1890 by Gallipe on mercurial stomatitis in man), that we should regard it as a septic stomatitis, and not as a primary toxic stomatitis. The mercury absorbed by the body not only produces salivation, but a very important change in the chemical composition of the saliva. The vitality and toxicity of the saprophytic microbes normally present in the buccal cavity appear greatly to increase, and although only the most trifling erosions may exist in the mucous membrane, true intra-mucous inoculation takes place, and forms the point of origin for septic stomatitis.
It has been found that it is not even necessary to have lesions in the buccal mucous membrane; in fact, this is the weak point in the theory emitted. Nor is a modification in the chemical composition of the saliva sufficient; for when a mixture of iodine and the iodides, for example, is being given, the saliva is chemically modified, and yet stomatitis, properly so-called, does not occur.
What seems most probable is that mercurial stomatitis is a toxi-infectious stomatitis, in the development of which mercury acts primarily by its toxic effect on the salivary glands, whose secretion it modifies, and on the buccal epithelium, the renewal of which it checks. Infection of the mucous membrane is thereby favoured, even in the absence of any previous lesion, and stomatitis develops.
Symptoms. The symptoms consist in abundant salivation with discharge from the mouth, suggesting the existence of foot-and-mouth disease. In grave cases the saliva appears streaked with blood, even from the beginning. The buccal cavity exhales an intense fœtid odour which, during the following days, becomes more marked; the mucous membrane is pale in colour, and coated with a greyish exudate. The mouth is hot and sensitive, the gums are swollen, reddish-violet in colour, and painful. Alveolar periostitis soon sets in, the teeth become loose, and mastication is rendered impossible, especially as the inflammation causes the tongue to swell and lose its mobility. These symptoms are unaccompanied by fever.
In the last stage ulcerations and local necroses appear on the gums, on the inner surface of the lips and cheeks, and around the commissures of the lips. The patients are almost unable to feed, rapidly lose flesh, become anæmic, and die from septic infection. The temperature is often below normal.
A toxi-infectious gastro-enteritis, with fœtid, blood-stained diarrhœa, is grafted on the primary stomatitis. Complications in connection with the respiratory, circulatory, and urinary apparatus appear, and the patients die in a condition of absolute exhaustion.
Naturally this termination is not inevitable; trifling cases of poisoning, and even grave forms, when properly treated, may, and should, recover.
Diagnosis. The diagnosis is mainly based on the history, except in cases of accidental and unsuspected poisoning.
Prognosis. The prognosis is grave, for even when the disease does not prove fatal the animals remain anæmic and exhausted for long periods.
Treatment should principally be directed towards combatting the local complications. When poisoning is due to external applications of mercury or its salts the skin should be washed with soap and water, and afterwards dressed with a soluble sulphide, which renders the mercury insoluble. The mouth should frequently be rinsed with boiled water, with decoctions of barley or marsh-mallow, with a 30 per cent. solution of boric acid or alum, or with a 1 to 2 per cent. solution of salicylic acid.
Fully grown cattle receive daily doses of 1¼ to 2 drams of chlorate of potash internally. This drug appears to owe its favourable action to the fact that it is partly eliminated by the salivary glands. Lastly, with the idea (which may, perhaps, be illusory) of minimising and checking the bad effects of the mercury introduced into the body, certain practitioners have recommended the administration of eggs, flowers of sulphur (2½ to 5 drams), sulphate of iron (1¼ to 2½ drams), and of iodide of potassium (1¼ to 2½ drams), drugs which are alleged to form insoluble compounds with mercury.
GLOSSITIS.
The term “glossitis” is applied to all inflammations of the tongue, whether superficial or deep seated. These inflammations may result from trifling causes, in which case they are termed “simple, acute, or chronic glossites”; or, on the other hand, from well-recognised causes, like tuberculosis or actinomycosis, in which case they receive the name of “specific glossites.” Here only ordinary glossites are investigated, the others being more particularly described in chapters specially reserved for the description of the primary diseases of which these form symptoms.
SUPERFICIAL GLOSSITIS.
This condition is characterised by lesions in the mucous membrane or in the immediately subjacent tissues, deeper seated structures not being involved.
The causes are similar to those of simple stomatitis, and as in animals of the bovine species the tongue is the principal and almost the only organ of prehension, it is particularly exposed to the chance of injury.
As mechanical injury done by rough fodder first makes its effects felt on the tongue, superficial glossitis is often due to the action of sharp or prickly plants like furze, wrestharrow, thistles, sea holly, etc. The glumes, awns, and spikelets on certain plants play a similar part.
Caustic medicinal draughts, hot drinks, and sharp points on the molar teeth may also produce the disease without the rest of the buccal mucous membrane being involved.
Symptoms. These are extremely simple. There is, first of all, some difficulty in grasping the food and some diminution of appetite, which, however, is more apparent than real, the digestive organs acting well. The second symptom consists in moderate salivation without special characters.
The local symptoms alone are characteristic. The mucous membrane covering the tongue appears red, swollen, locally inflamed, and painful. The inflamed areas are usually located on the free part near the frænum or opposite the molar teeth.
Thorns, foreign bodies, awns or spikelets of rough grasses can often be seen implanted in the tongue, and if the disease has existed for a short time, little ulcerations may not improbably be discovered.
Diagnosis. The characteristics of this superficial glossitis are sufficiently marked to allow of easy diagnosis, and to prevent it being confused with the lesions of actinomycosis or tuberculosis or with the extensive desquamation which accompanies foot-and-mouth disease.
Prognosis. The prognosis is never grave. Recovery occurs in six to eight days, provided the primary cause be removed.
Treatment consists in avoiding the use of rough food, in removing foreign bodies implanted in the mucous membrane or in rasping rough and irregular teeth. For the rest, as in stomatitis, mere attention to cleanliness suffices. The mouth is washed out with boiled water, boric acid solution, mixtures of vinegar and water, or with water containing a small percentage of alcohol.
ACUTE DEEP-SEATED GLOSSITIS.
This disease has also been termed parenchymatous and interstitial glossitis, because all the deep-seated tissues, including the muscles and connective tissue layers are involved in the inflammation.
Causes. The disease may be due to a neglected attack of superficial glossitis, to some grave microbic infection, or to excoriation and ulceration of the mucous membrane. Very often it is of traumatic origin, and is due to violent traction on the tongue by herdsmen or others when administering draughts of their own composition. This traction causes rupture of the muscle and slight interstitial hæmorrhage.
The symptoms develop somewhat rapidly. Whilst at first the animal shows difficulty in grasping food, it is soon totally incapable of doing so. The tongue loses its mobility, is no longer protruded from the mouth, and swallowing becomes so painful that salivation sets in. On direct examination the tongue is found swollen, thickened, immobile, painful, and occupying the whole of the oral cavity, sometimes projecting beyond the region of the incisors, and preventing the mouth being closed. Inflammation may become so intense that the point of the tongue hangs out of the mouth. It becomes blackish, bleeding, swollen, and excoriated by contact with foreign bodies or simply with the row of incisor teeth. The saliva becomes fœtid, blood-stained and purulent, and contains large quantities of broken down epithelial cells. It is not uncommon to note more or less extensive necrosis.
Diagnosis. The diagnosis of this form of glossitis presents no difficulty, for if under certain conditions it may resemble, for example, the glossitis of actinomycosis, it differs essentially from that disease by its rapidity of development, by its complications, and also by the absence of the specific ray fungus.
Prognosis. The prognosis is grave, not only on account of the possible complications, but also because the animals are unable to feed and therefore lose flesh with very great rapidity.
Treatment. The first steps in treatment are in the nature of local disinfection, in order to prevent general infection. The mouth therefore should be washed out five or six times per day with boiled water, followed by antiseptic injections until improvement commences. Solutions of boric acid or borax (3 per cent.), chlorate of potassium (2 to 3 per cent.), or salicylic acid (3 to 4 per cent.), are useful, but the free employment of 1, 2, or 3 per cent. solutions of chloral is even preferable.
With the idea of protecting the organ from external injury, Lafosse formerly suggested the use of a suspensory bandage for the tongue, fixed to the base of the horns by small bandages. Guittard recommends scarification of the free part, and the application of a support perforated at the bottom to allow the blood, saliva, pus, etc., to escape. In spite of careful attention the disease may last from two to three weeks.
CHRONIC GLOSSITIS.
This form of disease has also been termed “sclerosing glossitis” and “non-actinomycotic wooden tongue,” because it is anatomically characterised by induration of the tissues, and because apparently it resembles true “wooden tongue,” with which it was confused until within the last few years. Imminger in 1888 and Pflug in 1891 described two forms. The first, termed “superficial sclerosing glossitis,” is said to be the more frequent, and most commonly affects young animals suffering from irregularities in dentition. It seems due to a superficial acute glossitis assuming a chronic form. The submucous connective tissue in time undergoes hyperplastic changes, so that the tongue at first becomes swollen and afterwards absolutely rigid. One never finds ulcerations or actinomyces.
Diagnosis. A close examination will always enable the case to be diagnosed at the first visit, or under any circumstances after a short time.
The prognosis is very grave, because the animal has the greatest difficulty in grasping and masticating food, or may even be unable to do so. Patients lose flesh very rapidly, and end by dying of hunger.
Treatment is of little service. The administration of iodine, the only drug which appears indicated, has proved of very questionable value. Economically, it is better to slaughter the animal.
The second variety is rare, and has been termed “deep-seated sclerosing glossitis.” It is simply a chronic form of ordinary deep-seated glossitis. The layers of connective tissue separating the muscles are represented by very hard, inelastic vertical partitions. As a consequence, the whole tongue becomes indurated and more or less completely immobile. In this condition, again, there is neither ulceration nor actinomyces.
Diagnosis. The diagnosis necessitates a careful examination. In the living animal it is very difficult to establish a distinction between this and the preceding form, though after death the task becomes much easier.
The prognosis is grave, complete restoration of the parts being impossible.
The treatment differs in no respect from that given in the preceding instance. It is of little value.
Imminger and Pflug have also described a deep-seated nodular sclerosing glossitis, characterised anatomically by the existence in the depth of the tongue of fibrous nodules, varying in size between a small nut and a fowl’s egg. The tongue is only slightly increased in size.
This disease may perhaps be due to actinomycosis.
CHAPTER II.
DISEASES OF THE SALIVARY GLANDS, TONSILS AND PHARYNX.
PAROTIDITIS (PAROTITIS).
The term “parotiditis” indicates an inflammatory condition of the parotid gland. Of this disease several forms exist. The disease is termed simple when due to accidental causes or infections, specific when resulting from some special disease germ like the ray fungus. Anatomically, these diseases consist in inflammation of the glandular parenchyma and connective tissue stroma which surrounds the acini.
ACUTE PAROTIDITIS.
Causation. The causes of acute parotiditis are varied. Mechanical violence or contusions (due to collisions with fixed bodies, horn thrusts, or blows from the ox-goad) may produce it, the glandular parenchyma and connective tissue separating the acini or the peri-glandular tissue being torn, crushed, lacerated, and often also directly infected in consequence of the injury. Ascending infection through the medium of the salivary ducts represents a second possible cause of the disease.
Finally, parotiditis may, in some cases, constitute only a localisation of a general disease. It seems a fact that in rare circumstances parotiditis may assume an epizootic character, and attack a large number of animals in a particular stable or in neighbouring stables; and if, under these circumstances, we are unable to blame the food (which has not been done), we are forced to admit the influence of infection and contagion.
Symptoms. Whatever the cause, the symptoms are generally well marked. In many cases the first indication of the disease is apparent or real want of appetite, always complicated with difficulty in swallowing, and often accompanied by trifling fever.
Salivation, resulting from irritation of the gland and inability to swallow, becomes abundant, and at once draws attention to the buccal cavity and adjacent parts. Inspection of the patient then reveals the existence in the parotid region of a diffuse swelling, which on palpation is found to be hot and painful, and to occupy the whole of the parotid region between the lower jaw and the upper extremity of the neck. The lesion is usually unilateral, but occasionally bilateral.
Parotiditis may terminate in resolution, suppuration, or necrosis. The suppuration may either be simply subcutaneous and extra-glandular, or may involve a portion of the salivary gland and of the parotid lymphatic gland in addition.
Necrosis is exceptional, though Moussu saw double and total gangrene of both parotids, complicated with septicæmia, in the animal, of which a sketch is given herewith.
Fig. 63.—Acute parotiditis.
If the disease is due to violent injury by a foreign body, traces of a wound may be found, but it is often useless to search for these, even when the parts have been pricked with a sharp goad. When the inflammation has resulted from ascending infection of the salivary ducts, exaggerated sensibility may sometimes be detected throughout the whole length of Stenon’s duct, particularly at the point where the duct crosses the jaw. There is always marked difficulty in moving the head, particularly towards the side, and sometimes in a vertical plane. The head is extended on the neck, and is held stiffly in such a way as to suggest the possibility of tetanus. Some observers have described as an important symptom marked swelling of the orifice of Stenon’s duct. It is certainly difficult to detect, and furthermore is of no great significance.
Diagnosis. Although diagnosis is easy, it is a difficult matter to detect the point of origin of the disease. The salivation and difficulty in swallowing might seem to suggest pharyngitis, a condition which sometimes exists simultaneously. The distinction between this disease and the forms of chronic parotiditis, or tumour formation in the parotid (due to actinomycosis, lymphadenoma, melanoma), is also easy, on account of the slow development of the last-named conditions. The only condition liable to be confused with that under consideration is abscess of the subparotid gland.
Prognosis. The gravity of the disease varies greatly. When inflammation is slight, resolution usually occurs in eight to fifteen days. The onset of suppuration is announced by renewal of the fever, by more marked swelling, which becomes localised at a given point, and by the existence of deep or superficial fluctuation. Care, however, is required to detect the last named.
Necrosis may occur suddenly when the infecting organism is specially virulent, and may affect one-third, one-half, or the whole of the gland. The prognosis then becomes extremely grave, and if diagnosis has not been prompt and treatment energetic, death may follow in a short time from septic infection.
Treatment. Unless some well-marked sign foreshadows a complication, treatment should be directed to ensuring resolution. Bleeding has been recommended; its good effects, however, are open to doubt, though one cannot entirely forbid it. All practitioners agree in recognising the value of vesicant applications. The affected parts may be freely dressed with an ointment containing 2 per cent. each of pulverised tartar emetic and bichromate of potash, with the ordinary cantharides blister, or even with a weak mercurial blister, provided that the animals can be prevented from licking the wound.
Some practitioners prefer vesicants prepared with cantharides and croton oil. Whatever be the vesicant chosen, it is best after three or four days to apply emollients of slightly antiseptic character, such as ointments containing camphor, boric acid, salol, etc. When abscess formation is recognised the abscess should be opened as early as possible. Some precautions are necessary to avoid injuring important nerves and vessels; in dealing with a deep-seated abscess it is necessary to use the knife for dividing the skin alone, to seek the abscess by blunt dissection with the finger or with round-pointed scissors, and to open it with a similar instrument. The cavity should then be freely washed out with a warm antiseptic solution—3 per cent. carbolic solution, or 1 per cent. iodine solution, etc. If necessary a drain composed of iodoform gauze can be inserted, or a counter-opening made.
In the case of partial necrosis, all the necrotic tissue must be carefully removed, injury to vessels, which would favour septicæmic infection, being avoided. Afterwards free antiseptic irrigation should be employed several times per day.
In necrosis of the entire parotid extirpation may seem indicated; but the greatest prudence is demanded, for the operation is extremely serious and delicate.
CHRONIC PAROTIDITIS—PAROTID FISTULA.
When a case of acute parotiditis is not treated, and does not end in suppuration, it is usually succeeded by chronic inflammation and fibrous induration of the gland. Any obstruction of Stenon’s duct, whatever the originating cause (foreign bodies like wheat awns, oat grains, calculi, etc.) stops the flow of saliva throughout the excretory apparatus, and produces over the entire parotid region a doughy swelling, which might seem to indicate the existence of indolent parotiditis. The collections of liquid thus produced have improperly been termed “salivary abscesses.” If ascending infection fails to occur, or if infection is unimportant and does not lead to suppuration, a relatively painless chronic parotiditis develops, and in this case movements of the head and mastication and deglutition alone are impeded.
The salivary ducts, however, may become so distended that the main superficial collecting duct undergoes softening, and the skin covering it becomes ulcerated, just as would occur had a true abscess formed. Under such circumstances the skin soon yields and a salivary fistula is established.
The symptoms consist in swelling or induration of the gland, interference with movement of the head and with mastication; the whole developing slowly without pain or fever.
The distinction of this condition from actinomycosis of the parotid may sometimes present some difficulty until a fistula develops.
The prognosis is grave, because there is no hope of normal conditions being restored.
Treatment. Treatment often proves unsuccessful. Should the condition have resulted from an obstruction, it is first necessary to attempt the removal of such obstruction, whether it be a foreign body or calculus, and so to re-establish the normal channel for the saliva. Local stimulation may be tried, though in cases of fistula without much hope of success. Smart blistering of the parts surrounding the opening and firing in points have been recommended; but rather than persist in prolonged treatment of doubtful value, it is often better to prepare the animals for slaughter.
INFLAMMATION OF THE SUBMAXILLARY SALIVARY GLAND.
Inflammation of the submaxillary gland is rare in the ox. As in the horse, it is usually caused by the penetration of foreign bodies, such as glumes or awns of grain, fragments of straw, thorns, etc., into Wharton’s duct.
The difficulty in grasping food and the restricted movement of the tongue are the first symptoms to attract attention. On examination, the region of the “barbs,” usually on one side, appears injected, swollen, inflamed, and sensitive.
The submaxillary space is effaced by the swelling of Wharton’s duct; the corresponding submaxillary gland is doughy and painful on pressure. The symptoms rarely become more threatening than this.
The diagnosis presents no difficulty.
The prognosis is favourable.
Treatment consists primarily in removing the obstruction from the duct. Steady pressure from behind, forwards along the course of the duct, may sometimes cause the foreign body to be ejected into the mouth, along with a jet of offensive saliva. The distended and inflamed duct soon becomes emptied, and all the symptoms rapidly diminish. In other cases, when the obstructing body is firmly fixed in position, it is necessary to open the duct within the mouth by a stroke of the bistoury.
TONSILITIS IN PIGS.
“Acute and chronic forms are seen. The former has the general causes and symptoms of pharyngitis—fever, dulness, a disposition to lie with head extended and buried in litter, drooping ears, watery eyes, indifferent appetite, painful deglutition, and sometimes vomiting. Mouth red and hot, breath fœtid, tonsils swollen, their alveoli filled with muco-purulent matter or with fœtid cheese-like masses. Cough at first dry and hard, later loose and gurgling.
In chronic form there is general swelling of the tonsils with distension of follicles by above-mentioned putty-like masses, which are often calcareous. These are due to the proliferation of microbes, which find in these alveoli a most favourable field for their propagation. The affection usually ends in recovery, but may go on to grave local ulceration and general infection.
Treatment. Astringent antiseptics to buccal mucous membrane. Electuaries of honey or treacle and borax, sal ammoniac, chlorate or permanganate of potash and externally stimulating embrocations to the skin of the throat. In some cases solutions of iron chloride or tincture of iodine may be used with advantage and as a wash for the mouth and fauces. Attend to general health. If constipated give Glauber’s salt or jalap, ... and elimination through the kidneys must be sought through the use of nitrate of potash or other diuretic.” (Law’s “Veterinary Medicine,” Vol. II. p. 46.)
PHARYNGITIS.
Inflammation of the mucous membrane of the pharynx is less frequent in the ox than in the horse, a fact probably due to its less sensitive character in the ox and to differences in the methods of working oxen.
Causation. The causes are numerous and varied; and although local microbic infection undoubtedly plays the most effective part in the development of the disease, it is none the less certain that external influences are of considerable importance. For this reason chills, sudden variations in temperature, sudden arrest of perspiration, and currents of cold air have always been invoked as causes. Cruzel thinks that the ingestion of ice-cold water in winter is sufficient to produce acute pharyngitis. The action of rough forage may of itself explain the development of pharyngitis in animals constantly kept indoors under excellent hygienic conditions. In such cases the disease may be regarded as of traumatic origin. Furthermore, it is necessary to mention direct injuries of the mucous membrane caused by clumsy examination, awkwardness in passing the probang, and attempts on the animal’s part to swallow sharp foreign bodies, which scratch, tear, lacerate, or penetrate the mucous membrane and become fixed in it.
Finally, another series of causes, and not the least important, remains to be considered—viz., the forced administration of irritant substances like ammonia, tincture of iodine, oil of turpentine, very hot liquids, etc.
To sum up, the four great series of causes consist in direct irritation, intra-pharyngeal wounds, variations in temperature, or primary or secondary microbic infections.
The symptoms are characteristic. They consist in loss of appetite, difficulty in swallowing, consequent on the condition of the pharynx, and fever, which is often marked from the first. Pharyngeal dysphagia can easily be distinguished from that due to injury of the œsophagus, inasmuch as it occurs on the first attempt to swallow.
Urged on by hunger, the animal grasps food, which it chews and attempts to swallow, but immediately allows it to fall back into the manger, or ejects it by a painful coughing effort. In the case of liquids, even of lukewarm drinks, the same accident occurs, the food or liquid being returned by the nostrils. Slight salivation results from this difficulty in swallowing. The animal’s attitude is similar to that in parotiditis. The head is held stiffly, extended on the neck, in order to avoid compressing the region of the pharynx, and can only be moved slowly and with much pain. There is no apparent swelling of the parotid region, but on manipulating or pressing on the gullet the animal sometimes manifests the very acute tenderness of the parts by coughing and endeavouring to thrust away or to kick the examiner. Finally, examination of the mouth sometimes shows reddening and excessive sensibility of the soft palate and of the pillars of the fauces.
These symptoms often assume a more alarming character, or are complicated by others; in fact, the condition very rarely stops at pharyngitis, but is usually accompanied by inflammation of the larynx, of the soft palate, and of the naso-pharynx. The whole throat is then inflamed; the nose and sometimes the eyes discharge, and there is difficulty in swallowing, interference with respiration or noisy respiration, and intense fever.
Diagnosis. The diagnosis presents no difficulty, the symptoms mentioned being easy to identify, whether the condition be simply inflammation of the pharynx or be of a more extensive character. Nevertheless, cases occur where the symptoms are alarming, but in which one might hesitate between the diagnosis of ordinary acute sore throat and the sore throat which ushers in gangrenous coryza. A definite expression of opinion must then be deferred to a later date; for one cannot be absolutely certain whether or not the other signs of gangrenous coryza will appear.
When there is only difficulty in swallowing one might à priori suspect traumatic injury of the mucous membrane, with or without the presence of a foreign body. It is also necessary to bear in mind the possibility of difficulty in swallowing being occasioned by reflex irritation without local lesions, originating in enlargement of the retro-pharyngeal lymphatic glands as a consequence of tuberculosis or other disease.
The prognosis is favourable; even without treatment acute pharyngitis usually tends to recovery in eight to twelve days, and rarely becomes complicated. Nevertheless, some reserve ought to be exhibited in cases of pharyngitis due to the action of rough forage, the removal of the cause being here indispensable to any improvement. Similarly in cases of pharyngitis due to foreign bodies having penetrated the mucous membrane, which are chiefly characterised by inability to swallow, the disease may continue for a very much longer time than above indicated, unless the foreign body is discovered and removed. Inflammation is limited to a zone surrounding the point of implantation. It extends more deeply with movements of the foreign body, and may end in the formation of an abscess. Of this variety is Hopsomer’s remarkable case, in which a darning-needle finally obtained exit through the submaxillary space, in which it had caused the formation of an abscess.
Treatment. The treatment is the same whether we are dealing with a simple acute pharyngitis or with a more widely distributed inflammation. It consists in smartly stimulating the region of the throat with mustard, cantharides oil, or ointment, or with an ointment containing 2 per cent. of tartar emetic and of bichromate of potash, and then covering the parts with a flannel hood. This mode of treatment seems preferable to that recommended by German authors—viz., the application of cold compresses to the throat, the administration of cold gargles, etc. Moderate bleeding, to the extent of two or three quarts, has the great advantage, as in all similar cases, of lowering the temperature.
This treatment may, if necessary, be completed by the internal administration of 3 to 5 drams of Kerme’s mineral (oxysulphuret of antimony) in electuary, according to the animal’s size. Medicated inhalations diminish local irritation, render swelling less painful, and facilitate the separation of false membranes and the discharge of adherent mucous secretions.
The ordinary food should be replaced by cooked roots, lukewarm drinks and gruels, all rough fodder being prohibited.
If difficulty in swallowing alone continues, the operator should examine the mucous membrane of the pharyngeal cavity with the hand, in order to discover and remove any foreign body which may have become implanted there.
PSEUDO-MEMBRANOUS PHARYNGITIS IN CATTLE.
In addition to the above acute forms of pharyngitis, a pseudo-membranous, croupal, or pseudo-diphtheritic pharyngitis has been described in the ox. It is due to polymicrobic infection, and is characterised by the formation of false membranes on the pharyngeal mucous membrane. The condition seems to be a pharyngitis of exceptional intensity, varying markedly from the classic type and being most nearly related to severe sore throat, laryngitis, gangrenous coryza, etc.
It rarely attacks aged cattle, but is readily transmissible to calves and young stock. Cadéac failed to inoculate it on guinea-pigs and rabbits. Damman succeeded with sheep and with rabbits, the latter dying in twenty-four hours after inoculation with hæmorrhage at the seat of puncture. Löffler hypodermically infected mice and produced extensive infiltration of the abdominal walls, and often of the peritoneum, surface of the liver, kidneys and intestine, on which formed a thick yellowish exudate containing the organism.
Causes. Löffler found filaments of a long delicate bacillus about half the thickness of the bacillus of malignant œdema. The bacillus did not grow in nutrient gelatine or in sheep’s blood serum, but readily grew in blood serum of the calf. Cadéac gives as predisposing causes: sudden chills, rapid alterations of temperature, inhalation of irritant vapours, suppression of cutaneous secretion, swallowing irritant liquids, and injuries.
Symptoms. The nasal membrane is reddened, thickened and covered in patches with false membrane, causing snuffling and wheezing breathing. The throat is tender and swollen, cough is frequent, gurgling, and followed by expulsion of false membrane, muco-pus and some blood. Shreds of false membrane adhere to the nose and lips. Other symptoms are: fever, accelerated pulse, dark mucous membranes, haggard countenance, mouth open, hanging tongue, stringy salivation, and constipation or diarrhœa.
The disease runs a rapid course, and death may occur in twenty-four hours. Recovery may be equally rapid, but often convalescence is protracted.
Lesions. Intense congestion of mucosæ of nose, mouth, pharynx, larynx, and bronchi, with here and there patches of false membrane, which may be soft or tough, according to the duration of the attack. The deep surface of the false membranes is blood-stained; and, according to Preitsch, false membranes sometimes occur in the œsophagus, rumen, and omasum, which in consequence may show patches of ulceration.
Treatment (as for the horse). This includes poultices, counter-irritants, laxatives, febrifuges, alkalies and antiseptics. Inhalations of medicated vapour, warm water to which has been added some antiseptic—carbolic, lysol, creolin, camphor, sulphurous acid; or for calves, iodoform, oil of turpentine, calcium sulphide, silver nitrate, coal tar. To detach the false membranes ipecacuanha and potash chlorate, or soda sulphate, or magnesia sulphate may be tried. Papayin and pepsin have been suggested as appropriate remedies. Anyodnes—digitalis, belladonna, morphia and aconite—may be useful. Tracheotomy is indicated as a last resort.
PSEUDO-MEMBRANOUS PHARYNGITIS IN SHEEP.
Roche-Lubin states that this is common in flocks as a result of moving the sheep in dusty enclosures. The dust is supposed to excite the intense croupous inflammation of the mucous membrane. The disease has been noticed in spring in young lambs shortly after weaning. Damman states that he transmitted the disease to the sheep from the exudate of the calf.
Symptoms. Frothy salivation with constant movements of the jaws, viscid nasal discharge, difficult deglutition, panting, snuffling breathing, throat swollen and very tender, frequent cough, discharge of exudate. The head and neck are extended, the eyes dull, appetite is lost, the mucous membranes are red or cyanotic, and the animal appears weak and listless. As respiration becomes more difficult the mouth is held open, the tongue is protruded, and with each cough shreds of false membrane are expelled. Death from suffocation is not uncommon.
The lesions are not different from those seen in the calf.
The treatment is similar to that for the calf. Tepid drinks containing hydrochloric acid, or sulphate of soda (1 lb. to 50 sheep) in the drinking water, has been recommended. Fumigation with sulphurous acid or chlorine may be tried. Small numbers may be treated by swabbing the throat with solution of sodii hyposulphis or weak caustics and antiseptics.
In young and in adult pigs pseudo-membranous pharyngitis is often only a manifestation of pneumo-enteritis. It therefore calls for no special description at this point. No exact investigation of the organisms which produce these forms of pharyngitis with false membrane formation has been made in veterinary surgery. We only know that these diseases are not true diphtheria due to “Klebs’ bacillus.” Treatment should be very energetic from the commencement, but otherwise it differs in no respect from that ordinarily adopted.
Tonics and stimulants, like alcohol, wine, coffee, etc., are indicated.
[The following account of the disease is summarised from Law’s “Veterinary Medicine,” Vol. II.]
“Pseudo-membranous pharyngitis has long been recognised as a contagious disease of swine, attacking especially swine kept in herds or in close, insanitary pens. Young pigs are more liable to attack than older animals, perhaps, owing to the older animals having suffered the disease in early life.
Modern observation shows that pharyngitis with false membranes is common in swine plague, and the present tendency is to refer all such cases to that category. It is, however, altogether probable that the occurrence of local irritation, with the addition of an irritant or septic microbe altogether distinct from that of swine plague or hog cholera, gives rise at times to this exudative angina. Certain it is that septic poisoning with the food is not at all uncommon in the hog, in the absence of these infectious diseases.
Symptoms are those of sore throat, with much prostration, a croaking cough, yellow discharge from nose and mouth, and marked muscular weakness. The tongue, tonsils and soft palate are red, swollen, and studded with patches of false membrane. The identification of swine plague may be made by the history of the outbreak, the number of animals affected, the tendency to pulmonary inflammation, the enlarged lymph glands, the presence of the non-motile bacillus, which does not generate gas in saccharine media, and which readily kills rabbits and pigs with pure cultures of the germ.
Treatment. Isolation, cleansing and disinfection. Locally antiseptics and generally a febrifuge regimen will be advisable.”
PHARYNGEAL POLYPI.
The term “pharyngeal polypi” includes tumours of varying character, which affect the polypus form, and occur with considerable frequency in the bovine species. Many of these polypi are simply actinomycotic growths springing from the pillars of the fauces, from the upper parts of the palate or from its posterior surface. Less frequently they arise from the lateral walls or the free surface of the hard palate.
Symptoms. The symptoms are so characteristic that the diagnosis rarely presents much difficulty. They may shortly be described as indicative of repeated obstruction in the pharyngeal, œsophageal or laryngeal region. At the moment of deglutition, the polypus is thrust towards and obstructs the œsophageal orifice.
Reflex stimuli are thus excited, which prevent deglutition; an attack of coughing occurs, and food mixed with saliva is ejected from the mouth and nostrils. The attack of coughing displaces the polypus either in a forward or lateral direction, and swallowing then again becomes possible, until by changing its position the growth produces fresh signs of obstruction.
In other cases the polypus may only be of such small size as to impede the food passing through the pharynx on its way into the œsophagus or to cause difficulty in respiration by partially blocking the pharyngeal portion of the nasal cavities. In such cases deglutition is only checked and rendered slower.
Or again, the pedicle of the polypus may be sufficiently long to allow the growth at certain moments to fall in front of the laryngeal opening. Respiration is then painful, difficult and noisy. Unless the growth is displaced during the subsequent attack of coughing, asphyxia may appear imminent, or may even occur unless assistance is afforded.
Guided by these symptoms, the operator will explore the pharynx manually, and thus discover the position and size of the tumour. Tumours of the naso-pharynx produce very similar symptoms.
The prognosis is based on the information obtained by manually exploring the pharynx. It is relatively favourable if the polypus has a well-marked neck, but is very grave if the tumour is largely sessile and cannot be removed.
Treatment. Medical treatment appears useless except in cases of polypi due to the presence of actinomyces. The administration of iodine and iodide of potassium, in large doses, may then lead to resorption; but extirpation is often preferable.
In other cases extirpation is the only rational treatment. The operation necessitates the performance of provisional tracheotomy in order to avoid risk of asphyxia. The growth may be directly removed through the buccal cavity without incision, provided that it prove possible to pass the chain of an écraseur around the pedicle; or through the buccal cavity, with incision, after vertically or obliquely dividing the soft palate; or, lastly, through the larynx, after performing median laryngotomy, thus obtaining access to the pharynx.
Only the first method of intervention is to be recommended; the last two are more delicate. They necessitate after-treatment, and when the patients are in a condition for slaughter it is frequently preferable to send them to the butcher. The essential point is not to act without a full knowledge of the causes.
CHAPTER III.
DISEASES OF THE ŒSOPHAGUS.
Fig. 64.—Schema illustrating anatomy of the œsophagus: a strong external layer of muscle, intermediate cellulo-elastic layer, inner layer of mucous membrane lying in folds and capable of great dilatation.
The œsophageal tube is of very simple anatomical construction, and performs an equally simple physiological function; nevertheless, in the ox it is liable to a large number of diseased conditions. These conditions may affect only a circumscribed area of the mucous membrane or the entire extent of the tube. Again, both the muscular and mucous tissues may be affected, as in inflammation of the œsophagus accompanied or followed by contraction, and in the formation of œsophageal abscesses and tumours; or the muscular tissue alone may be affected, as in cases of dilatation. Even where no lesion is apparent the normal rhythm of deglutition may be interfered with, either by the presence of a foreign body (obstruction) or by spasm of the muscular layers (œsophagismus) or by compression due to tissues surrounding the œsophagus (false contractions).
We shall successively study the different forms of œsophagitis, contraction, and dilatation, together with their complications; then obstructions, ruptures of the œsophagus, œsophagismus, and false contractions.
ŒSOPHAGITIS.
Inflammation of the œsophagus may be due to many different causes, and may occur in one of three different degrees of severity. It may be either superficial, i.e., limited to the epithelial layer of the mucous membrane; or deep, affecting the entire thickness of the mucous membrane (epithelium, corium, and œsophageal glands); or, finally, it may attack both the mucous and muscular layers. German authors recognise various divisions, such as erythematous, catarrhal, follicular, and phlegmonous œsophagitis. In reality these are not always different forms, but simply successive stages in the evolution of a single morbid condition. Here we shall only study the ordinary forms of œsophagitis, leaving on one side those which occur symptomatically during foot-and-mouth disease, cattle plague, gangrenous coryza, actinomycosis, etc.
Causation. The causes of œsophagitis may be divided into three groups of different character:—(a) Rough fodder (clover containing wrestharrow, thistles, thorns, furze, or splinters of wood, etc.) must be placed in the first rank, for its repeated action abrades and irritates the mucous membrane to such an extent as finally to produce inflammation. This inflammation usually remains superficial and of moderate intensity; its occurrence can be anticipated during years of scarcity, when the animals feed on rough and irritating material like fern, broom, heather, furze, etc.
(b) Hot drinks, whether in the nature of beverages or medicinal draughts, are a frequent cause of œsophagitis if administered by careless or inexperienced persons. The mucous membrane is scalded over a varying area and with different degrees of severity, or is destroyed by the chemical action of such drugs as ammonia, dilute acids, iodine solution, etc.
(c) Rough or clumsy manipulation in withdrawing or displacing foreign bodies, or merely passing the probang, produces that variety of œsophagitis termed traumatic. In clumsy hands œsophageal sounds or catheters may abrade or even tear the mucous membrane and subjacent tissues.
Symptoms. These vary to some extent, according to the intensity of the inflammatory phenomena. If the lesions are superficial and only implicate the epithelium, as in catarrhal œsophagitis, the symptoms often pass unnoticed, and only produce difficulty in swallowing. When inflammation has involved the entire thickness of the mucous membrane the immediate consequence is loss of appetite due to pain during swallowing. After the bolus of food has been masticated, and has passed into the pharynx, the animal stretches out its head and neck and seems to be making efforts to force it down the œsophageal canal. The progress of the bolus is slow and clearly difficult.
In œsophagitis due to scalding the blisters are soon broken by the passage of food, the corium is exposed, and the animal has equal difficulty in swallowing either solids or liquids. The reflex action provoked by the passage of the food over these lesions may be so violent that the ingesta never arrive at the stomach, but are violently rejected by a sudden and unexpected antiperistaltic contraction. Even saliva is returned. Moreover, in these cases the history is generally clear, and the animal is feverish or greatly depressed. These objective symptoms are very significant, and when, in addition, an abnormal and exceptional degree of sensibility is detected at some point by palpation, they unmistakably indicate the existence of œsophagitis.
The irregularity in deglutition, and therefore also in rumination, sometimes excites moderate tympanites without any very apparent cause. Should the condition still appear doubtful the œsophageal sound may be passed, but with great care. It generally aggravates the pain and produces intense antiperistaltic movements, which the practitioner should not attempt to overcome.
Complications. If œsophagitis is moderate, recovery is the rule. The symptoms of pain gradually diminish.
When, on the contrary, inflammation is very intense, as in certain cases of traumatic œsophagitis, the injured spot may become infected and suppuration follow. The existing fever then persists or becomes more marked; the animal is extremely depressed; respiration may be difficult and accelerated, and appetite is entirely lost.
If the œsophageal abscess remains submucous the diagnosis is difficult, but it is often problematical, even when the abscess develops in the cervical region. The jugular furrow (usually on the left side) becomes the seat of a severe diffuse inflammatory swelling, the course of which clearly indicates the development of the symptoms. In exceptional cases fluctuation may be detected.
If from the first the abscess develops around the œsophagus or in the course of suppuration comes to occupy this position, swelling in the jugular furrows is more apparent and easier to detect, and in this case fluctuation may be localised. When the lesions are within the thorax no tangible symptoms can be detected. Death may occur in a few days, when an abscess in the lower cervical region breaks into the anterior mediastinum, or when an abscess in the thoracic region opens into the pleural cavity. In œsophagitis produced by scalding and from swallowing hot or caustic liquids the mucous membrane, and sometimes the muscular tissue, is destroyed, and ulcerations and cicatrices result, or the œsophagus may even be perforated, with rapidly fatal results; even when recovery occurs, cicatrices form and cause very grave contraction.
Diagnosis. The diagnosis is generally easy, provided that the symptoms noted are methodically analysed and the history of the case is taken into consideration.
Prognosis is favourable in ordinary cases. On the other hand, it may be very grave when general symptoms become marked, when the vital functions are disturbed and a deep-seated abscess appears to be forming.
Lesions. In the first degree the lesions are confined to inflammation and desquamation of the epithelium; in the second, to inflammation of the corium and of the mucous membrane; in the third, to infiltration of the submucous layers and of the muscular and periœsophageal tissues. Sloughing and perforation follow the administration of caustic liquids.
Treatment. As the direct application of medicines to the inflamed mucous membrane can only be of a momentary character, treatment is confined to administering emollient, anodyne, and slightly astringent drinks, the action of which is assisted by feeding with milk, farinaceous or mucilaginous foods. Under these circumstances recovery occurs in ten to fifteen days. The application of stimulant or blistering ointments along the jugular furrow may have a good effect.
When the general condition of the patient becomes aggravated, and the formation of an abscess appears certain, it is best to recommend slaughter. In the case of a submucous abscess the passage of the probang may, however, predispose or cause the abscess to open into the œsophagus, and thus lead rapidly to recovery, but this is exceptional. The “pointing” of the abscess and its opening towards the jugular furrow may be followed by temporary improvement, but at a later stage is followed by fistula formation, or by contraction of the œsophagus itself. From an economic standpoint it is better to slaughter.
STRICTURE OF THE ŒSOPHAGUS.
Under normal conditions the cavity or lumen of the œsophageal tube is, so to speak, imaginary: the walls of the tube lie flatly together, and the mucous membrane is in folds. During the act of swallowing the tube becomes dilated to a degree varying with the size of the bolus of food, and again retracts as soon as deglutition is effected. Whenever the dilatability of the tube is markedly diminished by changes in its walls, and, in a much higher degree, when this dilatability has disappeared, true stricture exists. In the former case small boluses of food and liquids alone succeed in passing the stricture; in the latter, liquids alone can pass.
Causation. Strictures are never primary. They result from intense attacks of œsophagitis, ending in sclerosis of the mucous coat, extensive ulceration consequent on scalding, or interstitial inflammation affecting the muscular coats, which then become thickened or sclerosed.
Internal injuries due to attempts to withdraw or propel foreign bodies along the œsophagus may also cause strictures.
Lesions. In simple strictures the lesions are confined to the development in the depths of the mucous membrane and in the muscular layers of inflammatory tissue, which becomes denser with lapse of time. This alters the character of the walls and the structure of the tissues, and causes them to lose their elasticity. After extensive ulceration the tissue of the cicatrix contracts and hardens to a very varying degree.
Symptoms. The apparent symptoms are very clearly marked; the appetite is good, and the animal masticates as usual, but in the act of deglutition is seen to extend the head on the neck, and to make efforts to swallow, which prove unavailing when the contraction is too marked. A reflex antiperistaltic movement often causes the substances ingested to be at once rejected. These violent efforts, however, in time provoke dilatation above the stricture. A quantity of food accumulates in this dilatation, and the symptom so characteristic of œsophageal stricture then appears—viz., regular regurgitation. The second constant symptom associated with compression or obstruction of the œsophagus is tympanites after feeding, however trifling may be the amount swallowed. Rumination is suspended, and even eructation of gas is difficult. Finally, the characteristic sign of stricture is noted on passing the probang, which reveals the existence of the condition, indicates its position, and suggests its degree of development.
Fig. 65.—Schema of recent and old-standing contraction of the œsophagus. R, simple contraction; D, secondary dilatation.
Diagnosis. Strictures only develop progressively and slowly, a fact which enables them to be differentiated from œsophagitis. It is more difficult to differentiate them from dilatations, because the stricture always ends by becoming complicated with dilatation; but this distinction is of little practical importance, the consequences being identical.
Prognosis. The prognosis is very grave, and there is no economic reason for attempting treatment except in special cases; the indications are in the direction of slaughter.
From the economic standpoint there is no treatment. Basing their actions on human practice, the Germans have recommended progressive dilatation of the lumen of the œsophagus by passing a series of catheters of gradually increasing size. What, however, is justifiable in human medicine, where the only object is to keep the patient alive at any cost, may be highly objectionable in veterinary practice; and in the present instance this is the case. Except in very rare instances, which the practitioner alone can appreciate, dilatation is contra-indicated, and the owner’s interest lies in slaughtering the animal before it has lost much condition.
DILATATION OF THE ŒSOPHAGUS.
Dilatations are more frequent than strictures. Their mode of origin is easily understood. When the muscular tissue has lost its tonicity and contractile power at a given point, or when, as a consequence of any form of inflammation, it has begun to undergo atrophy, the mucous membrane becomes herniated, because its circumference is not supported regularly during deglutition. The ectasia, which at first is of small size, becomes more marked in consequence of the tendency that exists for the food to accumulate in the dilated region. Dilatation is thus set up.
Fig. 66.—Schema of œsophageal stricture (the muscular layer above the stricture has undergone atrophy; the mucous membrane is dilated).
Localised attacks of œsophagitis, accidental injuries and fissuring of the œsophageal muscular tissue, produced by clumsy efforts to displace foreign bodies with the probang, are the principal causes of dilatation. When the probang is imprudently or clumsily manipulated, it may press excessively at any point where the œsophagus makes a slight bend, and thus split the contracted muscular coat without injuring the lax mucous membrane.
Œsophageal contractions, as we have seen, may form the point of origin of dilatations, but in this case the dilatations are more regular in form, and affect the entire circumference of the tube. The muscular tissue is still everywhere normal, and becomes dilated in consequence of equally-applied eccentric pressure.
Symptoms. When the dilatation develops slowly and progressively, as a consequence of muscular atrophy, the symptoms remain unnoticed for a long time, and the owner only begins to be anxious when the animal loses condition, or when the driver or cowman detects masses of half-chewed food mixed with the saliva in the manger.
Certain signs are pathognomonic; others may be regarded as of secondary importance. By carefully watching an animal which is feeding the following symptoms may be noted: As a general rule hunger is very marked, and the animal chews its food and swallows the first few mouthfuls in a perfectly normal way. Three, five, eight, or even ten mouthfuls may be swallowed; then the animal suddenly stops, appears a little anxious, extends its head and neck, an antiperistaltic contraction occurs, and one or two masses of food are rejected and fall into the manger. The discomfort being thus momentarily relieved, the animal, which is dying of hunger, although faced with food which it is unable to swallow, returns to its meal, swallows one, two, or three boluses of food, regurgitation again occurs, and the whole process is repeated.
What is going on under these circumstances is easy to explain.
At the commencement of the meal the dilatation is usually empty, or nearly empty. A mouthful of food is swallowed. It descends the œsophagus until it arrives at the diverticulum, into which it partially or wholly passes, the peristaltic wave of contraction ceasing at this point. The second mouthful follows with the same result, then a third, a fourth, etc. The diverticulum soon becomes filled to repletion, and no more food can enter it. The food therefore accumulates in the upper portion of the œsophageal tube until the latter becomes nearly filled; but as this tube, provided its innervation is intact, is intolerant of the presence of any foreign body, and as efforts to swallow prove fruitless, a sudden antiperistaltic wave of contraction occurs, with the result that all the material contained in the tube above the dilatation is ejected into the mouth, whence it falls into the manger. The same result follows any further attempts to swallow during a particular feeding time. From this it will be seen that the animal can ingest at a given time only as much as the dilatation will contain.
In the intervals between meal times and under the action of the saliva and warmth, the food collected in the dilatation becomes softened, breaks down, and slowly moves onward towards the rumen. When the next feeding time arrives the dilatation is almost empty, and the same set of symptoms recurs.
If, instead of forage, the animal begins by taking gruel or very fluid material, deglutition appears normal, or at least fairly easy; but if drinking is deferred until after taking hard food, it becomes almost impossible, because the passage is obstructed. These symptoms are, so to speak, pathognomonic. Under any circumstances they are so significant that error in diagnosis is unlikely.
By careful examination œsophageal regurgitation can very easily be distinguished from true vomiting; the character of the rejected material shows that it has not come from the stomach, while the boluses of food preserve their cylindrical form, and are still saturated with saliva.
Some secondary signs also deserve to be mentioned, such as the animal’s anxiety and restlessness whilst its neighbours are feeding, the existence of trifling and intermittent tympanites due to suppressed eructation, suppression or irregularity of rumination, constipation, etc. At a later stage there is rapid wasting and disordered appetite, and finally the patients die slowly of hunger, whatever efforts are made to feed them.
When the seat of dilatation is in the cervical portion of the œsophagus, there are other symptoms which leave no doubt as to the condition. When empty the pouch cannot be detected; but during a meal the accumulation of food causes it to assume the appearance of a doughy, diffuse, indolent swelling, which alters the outline of the jugular furrow, yields to pressure, and sometimes produces respiratory disturbance by pressing on the trachea, the pneumo-gastric and inferior laryngeal nerves, etc.
When the dilatation is intra-thoracic and the above-described symptoms have been observed, the dilated spot can only be detected and localised by using the probang. The greatest possible prudence, however, is required in manipulating the instrument, in order to avoid rupturing the thin walls of the dilated portion.
The diagnosis is not always easy; when food is regurgitated, and one finds by auscultation that the sound usually produced by the passage of solids or liquids into the rumen is absent, there need be no hesitation in diagnosing either a dilatation or a stricture. The clinical consequences being the same, the possible error would be of little importance.
Prognosis. The animal’s life is rarely in immediate danger, but from the economic point of view the prognosis is extremely grave, and it is in the owner’s interest to slaughter the animal as soon as possible in order to avoid loss. Even in cases of dilatation in the cervical region, surgical interference is not advisable.
Treatment. As foreshadowed by what has been said, there is no rational economic treatment. When the dilatation is in the cervical region, one might in exceptional cases attempt to restore the regular calibre of the œsophagus by removing an elliptical portion of mucous membrane, and bringing the muscular tissue together with sutures; that is to say, when the rupture or fissuring of the muscular coat has been accidental. But as one is usually unable to remove the primary cause, to which the change in the muscular tissue is essentially due, the dilatation would recur without the operation having conferred any benefit.
When an exact diagnosis has been made, the only useful indication is to confine the animal to very fluid food, which will not obstruct the œsophagus. Ordinary forage should be withheld.
ŒSOPHAGEAL OBSTRUCTIONS.
In this chapter we shall only consider such obstructions as occur in consequence of the animal having attempted to swallow without sufficiently chewing objects which become arrested in the œsophagus.
Obstruction is termed “total” or “partial,” according as the obstructing body fills the entire calibre of the œsophagus at the point of obstruction, or only occupies a part of the space. Partial obstructions produced by beet and turnip tops, etc., are usually but momentary; liquids and saliva are still able to pass between the obstruction and the walls of the tube, and as soon as the arrested food becomes a little softened it is displaced and the œsophagus again becomes patent.
Causation. The circumstances under which this accident occurs are extremely easy to understand. Obstructions are produced by apples, potatoes, turnips, carrots, cabbage-stalks, beetroots, etc., which, whether sliced or not, are swallowed gluttonously. Not having been sufficiently comminuted, and being of larger size than the œsophagus can readily accommodate, they become arrested at some point between the commencement of the œsophagus or a few inches behind the pharynx, or just in front of the point of entry of the gullet into the stomach. The latter is the commonest position, though not infrequently the obstruction occurs in the intra-thoracic portion.
It may occur in the stable, but is commoner in animals which, having broken loose, have entered orchards, gardens or potato or turnip fields and attempted to swallow apples, cabbages, potatoes, etc., found there.
In sheep, obstruction of the œsophagus is due to similar causes, but in their case the above-mentioned objects are replaced by small wild apples, turnip shells, Jerusalem artichokes, horse-chestnuts, carrots, etc.
The symptoms may be divided into general and local.
General symptoms. As soon as the foreign body becomes fixed in position, the animal begins to make exceptional efforts to swallow. The head is extended on the neck, and the œsophagus and the muscles surrounding the trachea are violently contracted. These efforts proving fruitless, feeding is necessarily stopped, and the animal at once appears slightly anxious.
Very soon afterwards salivation sets in, saliva being continuously secreted. If the obstruction is total, the saliva cannot be swallowed, and is either returned in quantities by antiperistaltic movements or escapes in frothy filaments from the mouth.
Tympanites is not long in appearing. It is progressive, and results both from arrest of eructation and from continued fermentation in the rumen. It may eventually come to a standstill, or may continue and threaten to produce asphyxia.
Local symptoms. The local symptoms are difficult to appreciate, except in cases of cervical obstruction. Sometimes the foreign body produces a local swelling, which changes the outline of the jugular furrow, most frequently on the left side. In many cases it can only be detected by manipulating the parts between the trachea and the lower surface of the cervical vertebræ. When the obstruction is within the thorax, the probang alone can detect its position.
Diagnosis. The diagnosis is usually easy. The history and the observed symptoms are often very clear, and the suddenness with which the obstruction has made its appearance prevent the condition from being confused with dilatation or stricture.
The prognosis is very variable. It is often easy to remove the obstacle; in other cases intervention is difficult, and death may occur rapidly.
Treatment is confined to one essential point—removal of the obstruction. The chief difficulty lies in choosing the mode of intervention. Moreover, success depends on several factors, which, in the order of their importance, are as follows: the size of the obstructing body; the time which has elapsed since the accident occurred; the bodily condition of the animal—i.e., whether it be fat or thin—and the extent to which tympanites has developed.
The first thing to do (and in favourable cases all that is required) is to puncture the rumen and leave the canula for some time in position. The onward progress of the foreign body, especially when the obstruction is in the intra-thoracic portion of the tube, is often impeded by the tympanites, which tends to thrust the object towards the pharynx, or at least to fix it in position. In consequence of a sudden change in the conditions of pressure the foreign body may move and pass into the rumen; all danger is then at an end.
Even though the obstruction does not immediately cease, puncture of the rumen, by removing the danger of asphyxia, allows one at least to wait for several hours, sometimes until next day, during which time the object may pass into the rumen without further extraneous assistance. The other methods may be grouped into four series:
I. External taxis. This is directed towards loosening the foreign body and thrusting it towards the pharynx and buccal cavity. It can only be used against obstructions in the cervical region. Two methods, although very ancient, are still practised.
(a) The first is carried out in the following way: the animal is fixed to a post or tree so that it cannot struggle, its head being drawn up as high as possible. The operator stands on the left side, with his back turned towards the patient’s head, his left hand is pressed into the right jugular furrow, his right hand is placed on the left jugular furrow immediately below the foreign body. By using the fingers the foreign body is moved, and is progressively thrust towards the pharynx, in spite of the animal’s efforts to swallow. In carrying out this manipulation it is absolutely indispensable not to let slip the obstructing body for a single instant, otherwise the peristaltic action will immediately return it to its former place. When it has been raised as far as the pharynx, an assistant passes his hand into the back of the mouth, as indicated in a former chapter, seizes the object and withdraws it; or, instead, the assistant takes over the operator’s duties, while the latter himself extracts the foreign body.
(b) In the second method the animal is fixed in a different position, the head being held about 10 to 12 inches from the ground, with the neck lowered and inclined towards the earth. As in this position the œsophagus is longitudinally relaxed, and can be dilated to its fullest extent transversely, the difficulty of displacing the obstacle should be very much less. In this case the operator always stands on the left side of the neck, but with his back towards the animal’s body. The right arm is passed around the neck and the right hand pressed into the right jugular furrow, the left hand being similarly engaged in the left jugular furrow. The method of employing the fingers is identical, or instead of the fingers the thumbs may be used.
Fig. 67.—Œsophageal sounds. Probangs.
When the obstructing object has been lifted as far as the pharynx it has a tendency to fall out of the mouth, and if it fail to do so it can be fixed in position and removed as in the preceding case.
II. Extraction. These methods are applicable to cases where the foreign body has become fixed in the cervical region, but more especially to obstructions in the intra-thoracic part of the œsophagus. In the majority of cases they are dangerous, and may lead to pinching, rupture, or perforation of the œsophageal mucous membrane. They should therefore be regarded as exceptional measures. Theoretically, the instruments described are perfect, but practically they do not secure the results anticipated, because one can never prevent displacement, wrinkling, and involution of the œsophageal mucous membrane.
The forceps probang has the drawback of seldom grasping smooth foreign bodies with sufficient firmness to permit of their extraction.
The corkscrew sound exposes one to the great danger of completely piercing the œsophagus, because it has to be managed blindly, and because one never knows at what depth the corkscrew portion should be protruded in order to obtain a proper hold of a foreign body.
III. Passage of the probang. When taxis fails or is inapplicable, we are forced to attempt thrusting the foreign body onwards. The method is much safer than the preceding, but, nevertheless, demands great tact, prudence, and gentleness. Suitable œsophageal sounds are made with cupped extremities, though in cases of emergency an instrument can often be successfully improvised from a cane, whip handle, or flexible stick, about 4½ to 5 feet in length, securely wrapped at one end with cloth or tow and freely coated with some greasy material such as lard, vaseline, or oil.
The end of the sound having arrived in contact with the obstacle, the operator exercises moderate but permanent pressure. The obstacle may not move immediately, because of spasm of the œsophagus, which grasps it. It is therefore necessary to wait and to take advantage of a moment when the resistance is less, and even then the obstacle may not move.
Rough manipulation with improvised sounds may tear, fissure, or perforate the muscular and mucous coats, producing the gravest consequences.
IV. Crushing. The crushing of an obstruction in the cervical region was long ago suggested, and is still greatly commended by empirics and farriers. It is performed by means of a little mallet and a piece of board. The method is barbarous, and exposes the animal to such grave complications as crushing of the œsophageal walls, followed by necrosis, laceration of the connective tissue, and interstitial hæmorrhage, injuries of the superficial or deep-seated jugulars, of the carotid artery, pneumo-gastric nerve, etc. It should never be practised, even although attempts have been made to improve it by replacing the mallet and board by specially formed forceps intended for crushing potatoes or roots. Only in the rare cases where one is certain that the foreign body consists of a very ripe fruit could crushing be justified, and in this case there is no need to have recourse to special instruments, for the hands alone suffice.
Injection of alkaloids. The practitioner occasionally finds himself in the embarrassing position of having vainly tried all the above methods. Before adopting the last resource, viz., œsophagotomy, it is then worth while to test the action of certain alkaloids, injected subcutaneously, after having punctured the rumen.
We know that pilocarpine and eserine stimulate secretion and the action of the bowels. Injected under the skin they cause frequent swallowing efforts, and intense peristalsis extending throughout the length of the digestive tract. Doses of 1½ to 2 grains of pilocarpine and 1 to 1½ grains of eserine, according to the size of the animal, sometimes produce excellent results, and rapidly remove obstructions.
Apomorphine, the effects of which are, so to speak, inverse, because they tend to produce anti-peristalsis and vomiting, may be tried in doses of 2 or 3 grains.
Œsophagotomy. The last resource is œsophagotomy, which, however, is only applicable in cases of obstruction of the cervical portion of the œsophagus. It should be performed as described in the section hereafter on operative manipulation. (See also Möller and Dollar’s “Regional Surgery,” p. 166.)
The point selected is necessarily governed by the position of the obstacle. There is no need to enter into full details. We may remark that it is not always necessary to perform the complete operation, and the third and fourth stages can sometimes be avoided by substituting for them attempts to break down the foreign body by submucous manipulation. The œsophagus, having been exposed and isolated, is punctured with a straight tenotome immediately below the obstacle. A curved tenotome is then introduced, and the root, potato, or fruit divided. As a rule, a little pressure from the outside then causes one or other of the fragments to move onwards and deglutition becomes normal.
Attempts have also been made to divide the obstructing body directly without previous incision and without isolating the œsophagus. It is much more difficult, for the least movement of the patient changes the relationships of the superposed layers and introduces obstacles to the manipulation of the blunt-pointed tenotome which is employed. More success often attends attempts to puncture the object with a fine trocar.
RUPTURES AND PERFORATIONS OF THE ŒSOPHAGUS.
Causation. Wounds of the œsophagus caused by external violence are rare, or at least secondary; lacerations produced from within, on the contrary, as a result of clumsy manipulation are relatively frequent. They may extend throughout the length of the tube, but in a far greater number of cases are found near the entrance to the stomach at the point where the œsophagus turns towards the left.
The passage of the œsophageal sound or probang is apt to exaggerate this curvature, and if pushed violently the instrument may produce first a flexure, then a partial rupture or even a perforation of the tube.
In other cases a rough, irregular, infected foreign body may when swallowed penetrate the wall and cause inflammation, necrosis and perforation of the œsophagus.
The symptoms are always very grave, and of rapid development. They consist in local œdematous swelling, sero-sanguineous infiltration at the entrance to the chest, in the pretracheal region and along the jugular furrows.
The pneumo-gastric and inferior laryngeal nerves being compressed, dyspnœa results. If the œsophagus is perforated in the thoracic cavity septic pleurisy at once sets in.
Diagnosis. The diagnosis is easy, provided the history point to perforation of the œsophagus.
The prognosis is fatal whenever the perforation is within the thorax. It is sometimes possible to intervene in cases of perforation in the cervical region, but from the economic standpoint such intervention is of little value.
CHAPTER IV.
DEPRAVED APPETITE—PICA—THE LICKING HABIT.
Depraved appetite, causing animals to swallow bodies which cannot properly be described as food, is frequent. The condition is commonest in adult animals of the bovine species, in calves and in lambs. The consequences are sometimes very serious, so that although depraved appetite does not represent a well-defined morbid entity, it is important to be in a position to remedy it.
Depraved appetite does not appear under the same conditions in young and in old animals. In adults it often results from faulty feeding, or from some wasting disease which develops insidiously, or remains unrecognised; in young animals it is the result of insufficient nourishment.
Roloff & Röll hold that pica is the first symptom of osteomalacia (which see).
DEPRAVED APPETITE IN THE OX.
Causation. In the bovine species depraved appetite occurs in adult, debilitated animals, which are often, though not always, suffering from some well-marked digestive disturbance.
The frequency of this symptom, and the peculiarities in its occurrence, have caused it to be referred to a large number of different causes, among which may be mentioned bad hygiene, chronic gastro-enteritis, tuberculosis, osseous cachexia, pasteurellosis, gestation, etc.
It is very certain that the peculiarity in the appetite is, above all, the result of incomplete and irrational alimentation. The animal has certain special requirements, to meet which the food must be of suitable composition. If these alimentary and digestive conditions are not fulfilled, depraved appetite may occur, even in animals which appear well nourished. Certain authors refer the appearance of this condition to want of certain soda salts in the daily ration, and, in support of this opinion, they point to the frequency of the disease in mountainous regions where the geological formation is chiefly granite, as in the Black Forest. Alluvial soils are supposed not to produce it. It certainly seems more common on soils lacking in certain constituents or exhausted by repeatedly growing certain crops. Nevertheless, in France it might be urged that pica occurs equally on all kinds of soil, and a German author, Lemke, ascribes this perversion of nutrition to the want of phosphorus. Haubner and Siedamgrotsky attribute it to a nervous disorder. All causes which exhaust the organism, especially all chronic diseases of digestive origin, may induce aberration of appetite.
Permanent stabling, confinement, absence of sunlight, want of exercise and pure air contribute to the general debility which predisposes to attack. Dry seasons, by reducing the supply of food, have a similar effect.
In tuberculosis and in pasteurellosis, it is the general organic decline which produces these puzzling changes in appetite. Similarly the influence of gestation depends on the superadded demands on the organism caused by the development of the fœtus.
Symptoms. The symptoms may be divided into two phases.
In the first phase, the animals still preserve their appetite, but whenever they have an opportunity they eat earth, sand, manure, litter saturated with urine, plaster, etc. They lick the walls, the boarding, the mangers and the trees, and they chew and swallow linen spread out to dry.
This phase may continue for a very long time, three to four months or more, provided no acute complication results from the eating of such foreign material. There is no fever, but the appetite, although well preserved, is often capricious, and the ordinary food is eaten slowly.
In the second phase, which frequently marks the development of complications produced by the passage, contact, or prolonged sojourn of various materials in the digestive tract, fever appears, little marked as a rule, but continuous in character.
The appetite is diminished. The animal wastes; the secretion of milk diminishes, and signs of chronic gastro-enteritis may be noted. The perversion of appetite still continues; rags, decomposing or filthy materials, pieces of old shoes, etc., are eaten, and it is not surprising that such substances should have an unfavourable effect on the mucous membrane of the digestive tract.
The wasting process slowly leads to marked emaciation, and after an interval of from six months to a year, or even two years, the patients die in a state of complete exhaustion. The lesions found on post-mortem examination are those of various diseases capable of producing depraved appetite or simply lesions of chronic gastro-enteritis.
Diagnosis. The diagnosis presents no difficulty. The important point is to discover whether or not there exists some previously unrecognised primary disease.
Prognosis. The prognosis of this condition is grave, because depraved appetite is frequently only a symptom of some incurable disorder, or because the changes in the digestive mucous membrane are already too far advanced to permit of much improvement.
The lesions comprise: general emaciation, presence of a yellow serum in the fatty tissue, muscles pale and flabby, catarrh of the mucous membrane of the stomach and bowel. The blood seems less in quantity and coagulates feebly or not at all.
Treatment. The treatment should be directed against the primary cause, if such exists (osseous cachexia, pasteurellosis, gestation, etc.).
In other cases a change in management and in feeding, and the administration of food rich in mineral salts like chlorides, carbonates, and phosphates of lime, soda or potash, produces the best possible results. The leguminous foods, sainfoin, clover and lucern, are to be recommended. The animal, if formerly stabled, should be turned out and its living conditions entirely altered.
It is often useful to place a block of rock-salt in the manger; when hyperacidity of the stomach is suspected lime water, chalk, or magnesia should be given. Where digestion is weak or slow HCl, pepsin and vegetable bitters are indicated. Nevertheless, one sees cases which refuse to yield to any of the ordinary methods. In treating these, Lemke has recommended the subcutaneous injection of chloride of apomorphine, a drug which may be regarded as a true specific. The doses vary between 1½ and 3 grains, and an injection is given once a week for three weeks in succession. After this the tendency to pica is said to disappear and the general condition to improve. The treatment must be repeated every three months in countries where depraved appetite appears general and permanent.
It is difficult to understand by what mechanism this drug produces the effects attributed to it, but those who have employed it speak very highly of its action.
We may add that in addition to the different modes of treatment, it is not infrequently necessary to hastily perform gastrotomy in order to avoid fatal consequences, which would otherwise follow indulgence in this habit. When an animal has swallowed a considerable quantity of linen, for example (and Moussu has seen cases in which many pounds weight had been devoured), immediate intervention is required to avoid intestinal obstruction. Furthermore, when the history is quite clear gastrotomy allows the entire mass of foreign bodies, ingested at different times, to be removed.
DEPRAVED APPETITE IN CALVES AND LAMBS.
Causation. Depraved appetite is commonest in calves and lambs when the animals are insufficiently nourished, or when the mothers are suffering from chronic debilitating diseases and are therefore yielding milk poor in fat and in mineral constituents. In a few rare cases it is impossible to discover what causes the young animals to devour these foreign materials. Even fully-grown sheep, when shut up together in winter, acquire the habit of chewing each other’s wool, sometimes to the extent of virtually depilating their fellows and accumulating wool balls in their stomachs.
Symptoms. Calves have a tendency to lick themselves or their neighbours, and thus little by little collect a varying quantity of hair which they swallow. When this habit of licking is little marked the quantity of hair ingested may not be dangerous; but in the contrary case the hair (which cannot be digested) accumulates and is permanently retained in the abomasum. It soon becomes converted into masses, cemented together with mucus, and forms round balls, to which the name of œgagrophiles has been given. If these œgagrophiles, or hair balls, are of small size, they prove of trifling importance; but too frequently they attain considerable dimensions and obstruct the pylorus or the intestine. The young calves then refuse all nourishment, and die in twenty-four to forty-eight hours in a state of complete exhaustion or after a series of epileptiform attacks.
In lambs the complications due to depraved appetite develop in a similar way, but the wool swallowed is obtained from the mothers. The lambs first suck the locks of wool, then tear them off and swallow them. So long as these peculiarities of appetite are little marked no bad results follow; but if the shepherd is careless, and fails to note the condition of his young flock sufficiently early, accidents occur.
The wool is not so easily converted into balls as is hair, but it soon accumulates in the pyloric region or in the intestine, and forms obstructing masses. The little patients lose appetite and lie down in corners, where they are found dead after twenty-four to forty-eight hours. The masses of wool or of hair are rarely passed with the excrement; more frequently they are vomited, but this again is exceptional; usually they become arrested at the entrance to the pylorus. The lambs show colic, tympanites of the abomasum, and attempts at vomiting, though unfortunately these are often overlooked. The quantity of wool found in the abomasum and intestine on post-mortem examination may be considerable, in relation to the size of the digestive compartments. Death results from intestinal obstruction, exactly as in the case of calves.
These aberrations of appetite in lambs have been considered as due to the want of sufficient mineral salts in the mother’s milk; and it has been stated that the lambs practise this habit because of the laxative result of the fat contained in the wool swallowed. The explanation seems very logical, though it is by no means perfectly proved. It is certain that this habit becomes particularly common after years in which forage has been scarce and among flocks in bad bodily condition. The force of example also plays a certain part, and animals probably imitate one another, and so acquire the disease. This explains the importance of early segregation.
Diagnosis. The diagnosis of depraved appetite, pica, or the licking habit presents no difficulty; but it can only be arrived at by the cowman or shepherd, for the symptoms can only be detected by continued watching.
The diagnosis of pyloric or intestinal obstruction is very difficult in the absence of information. It becomes easy after the first post-mortem examination has been made.
Prognosis. The prognosis is grave. In calves, obstruction of the bowel by hair balls inevitably causes death, and in sucking lambs the mortality may be high: as much as 15 per cent. to 20 per cent. according to the observations of several observers. The mortality occurs about the age of six weeks to two months, whilst the licking habit may begin towards the end of the second week.
Treatment. Prophylaxis demands that the mothers (whether cows or ewes) be well fed. An excellent precaution consists in adding to the food a sufficient quantity of salt and of phosphate of lime (2 drams to 2½ drams of each). This treatment of the mothers is necessary as soon as the tendency to licking becomes manifest.
In calves the best method of avoiding fatal results is to prevent the young animals licking one another; and the method now usually practised on well-managed farms consists in applying a simple muzzle of wicker work immediately after each meal.
In lambs treatment is more difficult. As soon as the shepherd sees any tendency to depraved appetite the lambs should only be left with their mothers whilst being suckled. The flock should be exercised in the open, and ordinary salt should be placed at a number of points on the ground occupied by the animals.
COLIC IN THE OX.
COLIC DUE TO INGESTION OF COLD WATER. CONGESTIVE COLIC.
Causation. Congestive colic occurs in the stable, in animals which have been doing heavy work, and, returning in a heated condition, drink large quantities of cold water. It is commoner when animals have not eaten for a considerable time, and when, therefore, the stomach is nearly empty. Under these circumstances chill of the digestive viscera is direct and immediate.
Symptoms. This form of colic occurs suddenly, soon after the water has been swallowed, and is characterised by violent pain. At first the animals show uneasiness, stamp, and continually move about striking themselves in the flank with the feet or horns, swishing the tail, etc. They refuse food, lie down and rise frequently, and paw the ground.
As a general rule this form of colic lasts from half an hour to one hour, and terminates in recovery. In some rare cases where death occurred Cruzel found on post-mortem examination congestion of the abomasum, and, in a few, congestion of the small intestine, with or without rupture.
The diagnosis is easy, on account of the suddenness of onset, rapid development and history of the disease, discovered on questioning the owner or herdsman.
The prognosis is not grave. This form of colic generally cures itself. Nevertheless precautions are required against possible complications, such as intestinal hæmorrhage and invagination.
The necessary preventive measures are self-evident. Animals returning from work should not be allowed to drink freely of cold water, but should first receive a little food and afterwards water at the temperature of the atmosphere.
When colic has set in, the patient can be walked about. If pain persists, the region of the abdomen may be dressed with oil of turpentine, mustard, or similar counter-irritants. The application of warm clothing is also useful. Finally, in grave cases, a moderate quantity (three, four, or five quarts) of blood may be withdrawn from the jugular. The administration of stimulants like wine, alcohol, etc., is also indicated.
COLIC DUE TO INVAGINATION.
Invagination consists in the passage of one portion of the intestine into the next-following portion. When once the condition has been set up it tends to become aggravated, the invaginated part being drawn further and further forwards. Invaginations therefore may vary in length between a few inches and sixteen to twenty inches.
Law states (Vol. II. p. 347) that in cattle and swine invagination of the large colon is almost impossible owing to the relation of the bowel with the layers of the mesentery. The anatomical arrangement is opposed to the formation of invagination, yet this accident is not uncommon in cattle and swine. The small intestine can be invaginated into the cæcum or into itself. The cæcum may become invaginated, or it may pass into the colon or rectum.
Cartwright, Veterinarian (1829), reports a case of invagination in a bull calf, and Youatt gives particulars of a similar case which was followed by sloughing and discharge per anum of the intussuscepted portion of bowel. (See also Möller and Dollar’s “Regional Surgery,” p. 328.)
Causation. This variety of colic is due to a number of somewhat obscure causes. In a general sense we may say that anything which increases intestinal peristalsis increases the risk of invagination. The accident may follow intestinal congestion, but is most frequent in animals suffering from intestinal worms, or in animals used for heavy work. Under the influence of violent tractive efforts the peristaltic movements are stimulated, and the intestine being in an oblique position on a plane inclined backwards, the contracted portion may slip into the dilated section behind it.
Fig. 68.—Invagination of the intestine in an ox (the constricting portion has been incised longitudinally).
Invagination may also occur without any apparent cause, even in animals standing in the stable.
Symptoms. The attack always occurs suddenly, develops rapidly, and is of an extremely grave character.
Colic comes on while the animal is working, moving about, or resting, according to circumstances, and at first resembles that due to congestion. It afterwards becomes very violent; the animals paw, stamp, show great uneasiness, throw themselves violently down, and rise suddenly, only to again lie down as before. The face expresses anxiety, suffering and depression; the tail is often kept lifted, and efforts are continually made to defæcate, mucus being passed. By passing the hand into the rectum the invagination may occasionally be discovered.
Colic persists with great intensity for ten to twelve hours, interrupted only by rare periods of calm. At the end of this time, however, it may suddenly disappear, and the animal may fall into a semi-comatose state. This indicates the onset of necrosis in the invaginated section, the painful reflexes no longer being transmitted to the sympathetic system. The disappearance of colic is sometimes regarded as a sign of improvement, but this improvement is illusory. From this time onwards the animals stand stolidly, obstinately refusing both food and drink. If they lie down, it is with great care. Palpation of the right side of the abdomen is painful, and the animal actively resents it. One of the most important and constant signs at this stage is the absence of defæcation, due to obstruction of the intestine, which is occluded. The animals may survive for ten, twelve, or even fifteen days (see also Möller and Dollar’s “Regional Surgery,” loc. cit.). The invaginated, necrosed portion may even be passed with the fæces, and recovery may occur, the continuity of the intestinal tube being secured by the adhesion of the serous surfaces; but such spontaneous recoveries are exceptional. Usually after a few days death results from peritonitis.
Occasionally, trifling invaginations may become reduced spontaneously, Diarrhœa, with the passage of blood-stained material is then seen for a time, a sign which alone at this stage would justify the diagnosis of invagination.
Diagnosis. The intensity of the colic and the absence of defæcation for several days afterwards, justifies the diagnosis of invagination. Purgatives then remain without effect. In addition, rectal exploration offers a valuable means of diagnosis. The last portions of the intestine are found absolutely empty, and the arm when withdrawn is found to be covered with viscous blood-stained mucus, resulting from the sero-sanguinolent exudate, due to compression of the blood-vessels.
In cases of this kind accompanied by the above-mentioned symptoms abdominal exploration by the rectum should always be practised, but it rarely gives exact information. The hand, when passed towards the right flank, may sometimes reach the invaginated part, which conveys the impression of a cylindrical swelling. The invagination, however, can rarely be reached. If the operator is successful, he will find that as he displaces this cylindrical mass or attempts to grasp it, the animal shows signs of exaggerated sensitiveness.
The prognosis is of exceptional gravity. Apart from the rare cases where the invaginated portion becomes necrotic and is eliminated, death is inevitable. Unless an operation is performed, septic peritonitis may develop about the fifth or sixth day.
Treatment. The only treatment consists in surgical intervention. Some practitioners have recommended giving large doses of purgatives with the idea of causing changes in the neighbourhood of the invaginated part; but such treatment presents little chance of success. The same is true of the administration of large doses of olive oil, either in the form of draught or of enema.
Siebert attempted reduction by generating CO2 from soda bicarbonate dissolved in water and diluted HCl, injected successively per rectum. In time fæces and CO2 escaped, and the patient recovered. Siebert claims to have cured by this method a cow with invagination of five days’ duration; but the effect of his treatment may be doubted, as afterwards a portion of bowel was found in the cow’s dung.
When diagnosis is certain, the only treatment that can be recommended consists in performing laparotomy followed by enterotomy. One cannot, however, operate in all cases, nor do all cases offer the same chances of success. If the invagination is situated in the first portion of the small intestine, and is hidden beneath the circle of the hypochondrium, intervention is out of the question, but if it has been detected by rectal exploration in the last portion of the intestine, operation may prove successful. Only in cases of the latter description should it be attempted.
Laparotomy is performed in the right flank according to the usual method (see Möller and Dollar’s “Regional Surgery,” p. 313). After opening the peritoneal cavity, the invaginated loop of intestine must be sought. It is not always easy to discover amongst the mass of intestines present, but can be recognised by its hardness and by the congestion of neighbouring parts. After withdrawing it through the abdominal opening, the operator may then proceed by one of several methods.
(1.) Some authors recommend grasping the two ends, drawing them apart, and thus reducing the invagination. The actual manœuvre is not difficult, but even when unattended by accident or tearing of the intestine it is by no means always followed by recovery. Although the intestine may not appear gangrenous externally, necrosis often occurs eventually.
This method should only be practised during the first twenty-four hours after the appearance of colic, and even then one must always bear in mind the possible consequences just mentioned, and the chances of rapidly fatal septic peritonitis.
(2.) The second method consists in removing the invaginated portion of intestine. It is best to apply bichromatised catgut or silk ligatures to all the arteries which pass from the mesentery into the loop to be removed; after which the loop itself may be simply divided an inch or two above and below the invagination, in order to be quite certain that one is operating on healthy tissue, the divided ends being held meanwhile by an assistant. The intestine is afterwards sutured with a fine needle and bichromatised catgut or boiled silk. The form of suture will be found described in Dollar’s “Operative Technique.” It may be valuable to test the efficacy of decalcified bone tubes for uniting the ends of the intestine.
The operation is long, delicate and difficult, and it is imperative not to infect the abdominal cavity during its performance. To prevent this the liquid and solid materials present in the bowel may be thrust upwards and downwards away from the diseased part before the section is made; and in this way the wound and the operator’s hands are preserved from infection. The intestine should be kept closed during the application of sutures by means of flat clamps cautiously applied. In their absence the ends may be held by an assistant, whose hands should previously have been carefully disinfected.
(3.) In cases where the serous coats of the two portions of bowel constituting the invagination are to some extent adherent, another operation of a less perilous character may be performed. This consists in liberating the invaginated part by means of longitudinal incision, without previously disengaging the parts, and without resection. The invaginated (external) portion of intestine is divided longitudinally; the gangrenous part immediately becomes visible, and may be removed. The operator has then only to suture the longitudinal wound, an operation which is much easier and demands much less time than any circular intestinal suture whatever. These operations must not be attempted except in response to the express wish of the owner, who should be fully informed of the dangers to which they expose the animal; for after the second day of invagination local peritonitis has often developed and one is then operating on injured or infected tissues, in itself a very unfavourable modifying condition. The current formula that “the operation was very successful” is not accepted in veterinary practice when the patient dies three or four days afterwards. From the economic standpoint it is better to slaughter animals of any value, for unless secondary peritonitis has occurred, and the animal is not feverish, the meat is fit for consumption. “Volvulus,” or twist of the intestine, is said to be almost unknown in cattle, though Reichert records a case of volvulus of the ileum.
COLIC AS A RESULT OF STRANGULATION.
The symptoms of this colic differ very little from those of the preceding with which they are often confused. But in regard to its causation the condition is essentially different.
Causation. Strangulation of the intestine in the ox may be produced in several different ways: by the passage of a loop of intestine through a tear in the epiploon, through the diaphragm, mesentery, broad ligament of the uterus, the serous layer surrounding the spermatic cord, etc., or by strangulation of an intestinal loop by fibrous bands resulting from chronic peritonitis, etc. Of these various causes, the three principal may here be described:—
(1.) Tearing of the mesentery. As a result of mechanical violence the epiploon or mesentery becomes fissured, and the peristaltic movements cause a loop of intestine to pass through and become fixed in the fissure. If the opening is narrow, as is usually the case, the base of the intestinal loop, riding on the lower lip of the slit, becomes constricted by the margins of the opening through which it has passed.
Fig. 69.—Schema of hernial strangulation.
(2.) In pelvic hernia a loop of intestine passes between the spermatic cord and the walls of the pelvis. The fissure in this case is in the serous fold which supports the large testicular arteries and the vas deferens. The fold is often ruptured during castration, especially during the practice of “bistournage,” in consequence of traction exercised on the cord.
(3.) Pseudo-ligaments and fibrous bands due to chronic peritonitis.—In local, subacute or chronic peritonitis false membranes may become organised, forming fibrous cords or folds connecting the parieto-visceral or inter-visceral surfaces. If by accident a loop of intestine insinuates itself beneath one of these fibrous bands, the passage of digestive material is first impeded and then stopped. The intestine becomes engorged, and symptoms of strangulation soon follow.
The symptoms appear suddenly, and are similar to those of invagination. They consist of very acute colic, which disappears after ten to twelve hours.
The peristaltic movements drive the semi-digested food, whether liquid or gaseous, towards the lower (strangulated) end, from which it cannot escape. It therefore distends the herniated loop and sets up intestinal engorgement. This constitutes the first stage of strangulation, and is accompanied by severe disturbance in the local circulation. The mucous membrane of the intestine becomes swollen and infiltrated, so that it alone soon fills the entire neck of the hernia. Necrosis of the loop of intestine is then only a matter of time.
The diagnosis of colic by strangulation is difficult. The condition cannot often be recognised at an early stage, and may easily and excusably be confused with invagination. Only in rare cases will rectal and abdominal examination enable one to detect a pelvic or mesenteric hernia.
The prognosis is even graver than in cases of invagination. Intestinal hernia progresses very rapidly, necrosis soon sets in, and is followed by fatal consequences if the condition be not relieved.
The treatment is exclusively surgical. As a general rule, whenever colic is recognised as resulting from strangulated hernia, it is immediately necessary to perform laparotomy in the right flank, and after having discovered the cause of strangulation, to divide the mesentery, epiploon, serous fold supporting the testicular cord, or accidental fibrous bands, so as to free the herniated loop and avoid necrosis. If necrosis already exist, the intestine may be resected, exactly as in invagination.
DISEASES OF THE STOMACH.
In ruminants diseases of the gastric compartments are numerous, and, although they have been recognised since the earliest times, much remains to be discovered concerning at least some of them. This fact results from the imperfect state of our knowledge concerning the essential phenomena of gastric digestion in ruminants. Digestion really consists of a number of different acts—some mechanical or neuro-motor, some chemical; in addition to which must be reckoned the phenomena of sensation, concerning which patients cannot give any information.
The mechanical phenomena, consisting in the constant movement of ingested material through the different compartments, rumination, eructation, evacuation towards the intestine, etc., are well known to us; and a careful examination of diseased animals enables us to estimate the importance of changes in them.
On the other hand, the chemical phenomena are little understood. It has hitherto been considered that the rumen, reticulum, and omasum are only simple diverticula, with mechanical functions, and that the abomasum is the reservoir in which the chemical changes take place. Another view, which is perhaps not altogether justified, presupposes that the chemical transformation of the food in the abomasum takes place as in other animals, and in particular as in man, in whom the chemistry of gastric digestion has been the object of extremely careful research by certain French and other pathologists. We do not believe (for reasons too long to be explained here) that the gastric digestion of ruminants, or even of herbivora in general, can be identified with that of omnivora.
The nature of the food being totally different, the chemical reactions in the stomach and intestines are also different; in proof of which we need only cite the single fact that ptyalin is absent from the saliva. Straw and oats are not digested in the same way as a mutton cutlet.
But even supposing that the broad outlines of physiological action are the same, nothing has hitherto been discovered in veterinary surgery respecting possible variations in the chemical processes taking place in the stomach during different gastric diseases; and it appears not improbable that in this direction causes might be discovered which veterinary practitioners have hitherto sought elsewhere. Excess or insufficiency of hydrochloric acid, and variations in the quantity of the organic acids, play so important a part in the theory of gastric pathology in man, that it is scarcely surprising to find similar ideas recurring in the pathology of domestic animals. The correctness of these views remains to be proved; and without wishing actually to classify dyspeptic conditions as in man, we may assert that diseases described under other names stand in direct relation to variations in the gastric secretion or to disturbance of gastric movements—e.g., simple chronic tympanites, which, without a doubt, is often a neuro-motor dyspepsia.
The classification we shall adopt in studying the diseases of the gastric compartments is, therefore, extremely simple. In the first series we shall consider sudden, accidental, and temporary forms of indigestion, and in the second series, acute or chronic forms of gastric inflammation.
INDIGESTION.
GASEOUS INDIGESTION.
Gaseous indigestion, also described as indigestion of the rumen, is characterised by the rapid accumulation of gases (chiefly carbon dioxide, carbon monoxide, and marsh gas), due to fermentation in the upper part of the rumen. It is common in oxen and sheep, and has received the names of mephitic indigestion, acute tympanites, meteorism, etc. It occurs during or immediately after feeding.
Causation. Numerous causes have been invoked to explain the sudden occurrence of gaseous indigestion.
The most important is the particular condition of the animal at the moment when it has been attacked. For if external influences alone were responsible, there is no reason why all the animals of a given herd or flock, or of a particular stable, which are under similar conditions as regards feeding, etc., should not be affected in the same way.
That the external causes cited (cold, excessive heat, stormy weather, etc.) may affect different animals differently and unfavourably is beyond doubt. But the temporary morbid condition of the animal itself is the essential condition to the development of indigestion.
In all probability the animal has in every case been more or less unwell, except in those attacks of indigestion resulting from progressive poisoning during the course of a meal, such as occur when toxic plants like belladonna, veratrine, colchicum, poppies, tobacco, hemlock, etc., have been eaten. In such temporary abnormal states movement of the rumen is partly abolished, or at least is markedly retarded, and, as a consequence of vaso-motor disturbance, the mucous membrane is probably not so abundantly covered with mucus nor so freely irrigated with secretion, as usual. Under these conditions, if the animal, which may appear perfectly well, is allowed to partake of soft, wet, fermentescible food, gaseous indigestion is very likely to develop.
Cultivated grasses, like lucern, sainfoin, clover, and especially grasses grown on artificially manured fields, are regarded as particularly liable to cause gaseous indigestion. This conclusion seems justified by experience, particularly by the fact that young shoots or young, tender after-growths are very liable to fermentation.
This exaggerated tendency to fermentation of tender grasses has even been held exclusively responsible for indigestion, and the cessation of peristalsis in the rumen has been considered a secondary phenomenon, due to distension.
Whether atony of the rumen be the primary condition and abnormal fermentation secondary or inversely, whether fermentation be primary and atony secondary, is not of importance; for either view may be adopted without altering the results, and without the theory being invalidated by the objection that other animals subjected to similar influences had not contracted the condition.
We have already drawn attention to the importance of the condition of the animal’s health for the time being. Digestive peristalsis being diminished, eructation, admixture of food in the rumen, and its onward movement being impeded, fermentation proceeds rapidly. As a consequence the rumen becomes distended, and, cause and effect changing places, the distension in its turn arrests peristalsis, which had previously only been checked.
Local chills, produced by ingestion of food covered with rime, hoarfrost, or simply with dew, may favour gaseous indigestion; such conditions retard or suspend the peristaltic movements by direct local action, and probably by producing vaso-motor disturbance of the mucous membrane. In very rare cases chill has an undeniable influence, either by provoking general vaso-motor disturbance, which reacts on the secretions, or neuro-motor trouble. Gaseous indigestion is not uncommon in animals living on dry winter food, which have been moved from their ordinary quarters and sent on railway journeys or to fairs, etc. As a general rule this form of indigestion is commonest in spring, when the transition from dry winter food to grass, etc., has not been carefully effected. It is also frequent during stormy weather in full summer. Marked barometric changes seem to have an influence on the general health, and particularly on the nervous system, thus favouring organic fermentations.
Symptoms. The earlier symptoms of indigestion escape observation, but they soon begin to develop rapidly, and are then very easy to follow. They always exhibit the same characters, developing, however, with more or less rapidity in different cases. Soon after they commence feeding animals appear to experience special discomfort, which causes those at grass to stop grazing; even when stabled they stop feeding. From this time they show eructation, repeated yawning, restlessness, and some anxiety.
In a quarter of an hour, or less, the left flank begins to project, both laterally and vertically, so that eventually the walls of that part of the abdomen may project above the transverse processes of the lumbar vertebræ. The right flank also becomes swollen, as a consequence of the intestine being thrust out of position. The animal very rapidly shows general disturbance; the nostrils are dilated, the mucous membranes congested, respiration becomes rapid, and asphyxia threatens. The respiration soon becomes panting, for the distended rumen paralyses the diaphragm and compresses the lungs. To ease respiration the animals open the mouth, extend the neck, and stand with the front limbs spread apart; but this fails to prevent dyspnœa becoming more intense and asphyxia imminent.
The heart beats more rapidly, the superficial veins appear swollen, and the mucous membranes cyanotic. The rhythmic contractions of the rumen can no longer be detected by manual examination of the left flank; and on auscultation one neither hears the liquid nor the rolling sound, but only exaggerated crepitation. Finally, there is marked tympanitic resonance on percussion.
In cases of very grave tympanites the gaseous pressure in the interior of the rumen appears to stop the crepitation sound. The animals soon become unable to walk or even to move, suddenly fall to the ground, and die rapidly from asphyxia.
The rapidity with which gaseous indigestion develops varies greatly. Sheep and oxen may die from tympanites, within an hour or even half an hour of their arrival in the field; but more frequently the symptoms develop slowly, only becoming alarming after some hours and continuing for twelve or even twenty-four hours without causing death.
As a rule, the gas is voided by a series of eructations which empty the rumen, and recovery follows; but when distension is extreme eructation cannot occur, and gaseous indigestion then ends in asphyxia and death.
Lesions. It might be imagined that this form of indigestion would only appear when the rumen contains a large quantity of food; but, in point of fact, the rumen often contains very little.
On post-mortem examination the rumen is found to contain an enormous quantity of gas, which, when collected and submitted to analysis, reveals approximately the following composition:—Carbonic acid, 74 per cent.; carburetted hydrogen, 24 per cent.; sulphuretted hydrogen, 2 per cent.; nitrogen, traces. The composition of this mixture varies within certain limits, according to its origin; but carbonic acid always predominates.
Lungwitz, after elaborate experiments with different foods kept in closed vessels at the body temperature and with similar agents fed for days as an exclusive aliment to oxen provided with a fistula of the rumen for purposes of collection, found carbonic dioxide the predominating gas in all cases, though the proportion varied with the nature of the food.
Marsh gas varied from 16 to 39 per cent., being especially abundant in cases of abstinence. Hydrogen sulphide was found only in traces. Oxygen and nitrogen were present in small amount, and were attributed to air swallowed with the food. In fermentation the oxygen may be completely consumed.
The abdominal organs, particularly the intestine, are congested, as a result of impediment to the venous circulation. The thoracic organs exhibit the lesions of asphyxia.
Pathogeny. Death is due to carbonic acid poisoning, brought about in two different ways—viz., progressive asphyxia, caused by inability to inflate the lungs, and absorption of carbonic acid gas from the rumen; by virtue of the laws of diffusion, part of the gas contained in the rumen passes into the blood.
The diagnosis is always very easy, and even farm servants may recognise the condition.
The prognosis varies, according to the rapidity with which the disease develops. In rapid cases, where the condition is fully established in thirty minutes to one hour, asphyxia may be threatened from the beginning; but in others, e.g., when the attack follows consumption of dry food, tympanites may develop slowly, only attaining its maximum intensity after a considerable lapse of time. In general one may say that tympanites is grave in proportion to the rapidity with which the gas is generated.
Treatment. From the prophylactic point of view, it is necessary to avoid suddenly changing animals from dry to green food; the transition should be effected by giving mixtures of dry and green food.
Curative treatment comprises a large number of methods.
The latest, and one of the most practical, consists in massage of the left flank. The open hand is applied to the left flank and sharply pressed directly downwards, care being taken not to injure the parts. This manipulation excites reflex action, awakens the dormant contractility of the rumen, and leads to restoration of peristaltic movement. The gases pass into the omasum and abomasum, or in many cases make their way into the œsophagus. The sudden impulses sometimes cause food to be returned into the mouth, eructation recommences, and the gas accumulated in the rumen is partially and progressively evacuated. This manipulation is often practised in breeding districts, particularly in the case of sheep, in which the disease occurs with the same characters. The shepherd fixes the animal between his legs, and, thrusting the extended fingers of either hand into the flanks, makes sudden, sharp movements, which again set up eructation and get rid of the excess of gas.
In Germany cold douches are often applied to the flanks. These excite vaso-motor action and reflex peristaltic movements, which result in eructations and in the evacuation of the rumen. But this is not a very practical method, and necessitates arrangements which seldom exist on sheep farms.
The action of massage may be completed by administering stimulants like wine, alcohol, or infusions of such aromatic plants as cummin, fennel, peppermint, camomile, etc. These act first of all mechanically, by clearing the terminal portion of the œsophagus. Furthermore, they stimulate the mucous membrane of the rumen, causing reflex peristaltic contractions, and, as a consequence, circulation of the partly digested food; finally, the majority of them arrest fermentation.
With the latter object, ether and assafœtida are also given. The use of these drugs, however, entails disadvantages, and if the animal has finally to be slaughtered renders the flesh unfit for consumption.
The giving of absorbents is probably most widely practised. The ammonia which many of them contain absorbs carbonic acid, thereby diminishing the pressure of gas contained in the rumen, and therefore the distension of the first gastric reservoirs. Unfortunately this action is only temporary, and if the drug is given in too concentrated a form, the mucous membrane of the mouth, of the œsophagus, and sometimes even of the rumen and reticulum, may be irritated and inflamed, producing lesions of stomatitis, pharyngitis, œsophagitis, contraction of the œsophagus, etc., which after recovery from the acute condition may gravely affect the animal’s general health. A further drawback is that the flesh rapidly acquires an ammoniacal odour.
Perhaps the best internal treatment consists in administering purgatives such as hyposulphite or sulphate of soda or sulphate of magnesia, in doses of 10 to 20 ounces, according to the animal’s size, or, in the case of pregnant animals, in small frequently repeated doses. These check fermentation, and so arrest the evolution of gas, whilst by their purgative properties they excite contraction of the gastric reservoirs and cause eructation.
None of these methods of treatment, therefore, should be used exclusively, but all may be utilised as auxiliaries to mechanical or surgical measures, and all should be preceded by the use of the probang and puncture of the rumen.
The first of these operations, the technique of which scarcely requires description, is often of little value; for the solids and liquid contents of the rumen being permeated with gases, rise as a fermenting mass into the upper portions of the rumen, and continually obstruct the open end of the catheter, so that very little gas escapes.
Puncture of the rumen is much more effective and easier to perform. The owner himself often operates with an ordinary pocket knife, sometimes introducing a couple of fingers or a short length of elder-wood tube into the wound thus produced.
The incision should be made at one stroke, for any hesitation may cause the wall of the abdomen to recede from the rumen, which lies immediately below. Should gas escape under the skin, emphysema, which often extends to the loins and along the quarters, may be produced, and may be followed by diffuse subcutaneous suppuration, resulting from pyogenic germs entering the subcutaneous tissue.
Large quantities of gas escape from the puncture, sometimes with such force as to drive out the canula. The flow of gas then ceases. In other cases the tube becomes blocked; because, as the pressure within the rumen diminishes, the gases dissolved or mixed with the partially digested food are freed, and the whole contents of the rumen become converted into an aerated, bubbling mass. Liquid or semi-liquid materials may be ejected to some distance, or may pass between the skin and the muscles, or between the walls of the rumen and the abdomen, producing various complications, like necrosis, abscess formation, etc. Such accidents can be avoided by exercising firm pressure with the fingers on the tissues surrounding the canula.
Even when the rumen has resumed its normal size recovery is not certain, and may not occur for several hours, or even several days, afterwards. The patients should therefore be kept under observation for some time, and it is usually best to leave the canula in place for one or two days, and to put the animal on low diet.
Necrosis of aponeurotic tissues, fistula formation, and local peritonitis only occur if the instrument is dirty or is introduced in a wrong direction.
IMPACTION OF THE RUMEN. INDIGESTION AS A RESULT OF OVER-EATING.
In this condition the rumen is over-distended with food. The symptoms are principally due to abnormal fermentation, the peristaltic action of the rumen being in abeyance, and the food failing to pass towards the omasum and abomasum. Rumination is generally suppressed.
The disease usually follows change of diet. When the diet has long been restricted, as occurs during years of bad harvests, and animals are afterwards set at liberty in rich pastures, they eat greedily, distend the rumen with large quantities of green fodder, and set up all the necessary conditions for this form of indigestion. Similar results follow when gluttonous animals are freely supplied with rich food. Working oxen also suffer if withdrawn from work and fed with roots, beetroot refuse, brewers’ grains, or other manufacturing residue for the purpose of fattening. These materials can only be absorbed in moderate quantity, and the large amount of water, etc., they contain is apt to disturb the animal’s digestive powers, while owing to its fine state of division such food cannot be returned to the mouth for secondary mastication, and rumination therefore remains incomplete: the food accumulates in the rumen, distending and eventually paralysing it. This is a common result of feeding on semi-liquid pulp, which in order to be ruminated should be mixed with rough forage.
Insufficiency of drinking water is another and more frequent cause, especially during the winter, because the ox-herd or cowman is often too lazy to give a regular and sufficient supply unless water is laid on in the stable itself. The dry food becomes compacted into a mass, which cannot be returned to the mouth for rumination. Moreover, less saliva is then secreted, and Colin has shown that rumination is impossible when the parotid ducts are ligatured.
Symptoms. As may readily be imagined, the symptoms vary, according to the quantity and digestibility of the food swallowed. In the first place the appetite falls off: animals suffering from commencing indigestion only take part of their food; later on appetite ceases, and with it rumination. Trifling colic sets in, resembling that due to congestion, and is indicated by unrest, switching of the tail, lifting of the hind legs, slight groaning, moving from side to side, and lying down and rising at short intervals. The animals seem oblivious of their surroundings, anxious, and at times semi-comatose.
When the case has been neglected for several days the animal may masticate without having any food in the mouth, and may attempt to eructate and to regurgitate food; but such attempts always fail. It then absolutely refuses food, and animals which have eaten large quantities of green forage may show tympanites. If called in at this period of the disease the veterinary surgeon finds nothing positive except signs referable to the digestive apparatus. By methodically examining the digestive tract, and in particular the stomachs, one discovers during palpation of the left flank that the rumen is distended. This is characteristic. By deep palpation it is even possible to detect marked resistance and a certain characteristic firmness resulting from accumulation of food. The percussion sounds over this region are dull, and pressure causes pain, as though the rumen and peritoneum were inflamed. When the open hand is laid flat on the rumen and thrust downwards, no peristaltic movement can be discovered. Finally, on auscultation the normal sounds, including crepitation, fermentation, and rolling sounds are all absent.
There are no well-marked general symptoms. Respiration and circulation are hardly accelerated, nor is the artery particularly tense.
Course and Termination. The course of the disease varies, and the condition may be divided into two forms, acute and chronic. The first develops in a single day, and may cause death by the same mechanism as acute tympanites—i.e., asphyxia or carbonic acid poisoning; the other continues for five, ten, or even twenty or thirty days, according to the promptitude with which treatment is undertaken.
In protracted cases, however, the indigestion itself ceases to be as important as the complications. Sometimes spontaneous recovery occurs, the food passing away towards the intestine, or even being vomited, though the latter conclusion is rare. Recovery may also follow from treatment. If the disease is neglected it may become complicated with gastro-enteritis.
The diagnosis is not very difficult. Indigestion resulting from impaction is distinguished from acute tympanites by its less rapid course and by the less marked distension of the rumen (in this case due to solid food), and from acute gastro-enteritis by the varying degree of fever which accompanies the latter condition.
Prognosis. The prognosis is always grave, even in cases of acute indigestion resulting from eating green food.
In this case gaseous indigestion occurs as a complication, and necessitates immediate intervention. The other forms may rapidly yield to proper treatment, or, in spite of every care, may give rise to prolonged complications.
Lesions. On post-mortem examination of animals which have died of complicated forms of the disease, we find certain lesions peculiar to gaseous indigestion associated with impaction of the rumen.
If death has followed the consumption of root pulps, we see signs of poisoning. As a consequence of prolonged stagnation of food in the rumen, there follows an exaggerated organic fermentation, whose products are absorbed through the stomach or intestine and pass into the circulation.
These various fermentations, which may be of the lactic, butyric, and even putrid order, produce changes in the mucous membrane of the rumen; wide tracts of the epithelium may be shed, exposing the corium, and producing enormous ulcerations, which in certain cases implicate the entire inner surface of the rumen.
The treatment must be varied, according to the cause, symptoms, and immediate complications. When the disease is of an acute type, such as that produced by over-gorging with lucern and green food, it is best to proceed as in gaseous indigestion, i.e., to puncture the rumen and give frequent large doses of purgatives until the stomach and bowels have been freely unloaded. The animals should then be kept for some days on small quantities of easily digested food, and should be allowed lukewarm, mucilaginous drinks.
When tympanites and impaction occur simultaneously, immediate surgical intervention becomes necessary, and gastrotomy may then be performed by a very simple method.
Two loops of cord are passed around the abdomen, one behind the hypochondriac circle, the other in front of the angle of the haunch. Assistants placed on the right side draw these loops tight, so as to immobilise the left flank. A bistoury is then thrust directly through the walls of the abdomen and rumen. As a consequence of the pressure exercised by the ropes, if not of the pressure of gas itself, the food material contained in the rumen is often expelled in a powerful stream. As the superposed tissues cannot very readily change their mutual relations, the author of this suggestion claims that there is little danger either of infectious materials passing into the subcutaneous connective tissue, or of peritonitis; but this rude treatment can only be resorted to in cases of extreme urgency, and it appears by no means without danger.
Injections of 10 to 15 centigrammes of pilocarpine and 5 to 10 centigrammes of eserine are also useful.
When impaction of the rumen assumes a less acute form, moderate doses of purgatives may be given and repeated daily, or twice a day, until the peristaltic action of the rumen is restored and resumes its normal rhythm. In certain cases, however, recovery is only apparent. The food in contact with the walls of the rumen breaks down, and passes away into the abomasum and intestine, while appetite returns. The animals then resume feeding, and some days afterwards show all their former symptoms. Low diet should therefore always be continued for some time.
In spite of treatment, or in consequence of treatment being too long delayed, no improvement may follow. The ingested food is not expelled. Putrid fermentation results, auto-intoxication sets in, and the temperature rises to 40° or 41° C. Unless gastrotomy is performed death is then certain.
This operation should be undertaken whenever the fever rises to 40° C., and two-thirds of the contents of the rumen removed. The rumen should not be completely emptied, as there is danger of collapse of its walls. Complications in the region of the wound can be avoided by drainage.
If the operation succeeds, the patients must be placed on very low diet or on milk for some days, and should be given lukewarm farinaceous drinks, and a little hay of good quality to excite rumination. In old milch cows this operation is seldom followed by a satisfactory recovery. Apart from the loss of milk, the animal loses condition, refuses to feed, and gradually succumbs to exhaustion.
IMPACTION OF THE OMASUM (THIRD STOMACH).
Definition. “A form of indigestion, of which the prominent feature is the drying and impaction of the ingesta between the folds of the third stomach. It may seem to be a primary disease, but in very many cases it occurs as a result of some acute febrile or inflammatory affection.” (Law’s “Veterinary Medicine,” Vol. II. p. 123.)
Synonyms. Dry murrain, clew-bound, fardel-bound, stomach staggers, grass staggers, vertigo, chronic dyspepsia, chronic indigestion.
Causes. Torpidity of the omasum, suppression of salivary secretion, with absence of “waves of liquid floating the finely divided food from the mouth or rumen to third stomach, are prime conditions of desiccation of the contents.” The third stomach, like the first and second, has no provision for liquid secretion, and depends for its supply on constant flushing by swallowed fluids. Therefore, if feeding and rumination are arrested and salivary secretion is suppressed, and if movements of the rumen and resulting overflow into the third stomach are checked, the ingesta of the third stomach, compressed between its folds, becomes drained of liquid and converted into a powder or dry mass. All febrile and inflammatory affections tend to this end, and more or less drying, with impaction of the contents of the omasum, is a constant feature in such cases. But in the majority of cases this condition is to be looked on as a secondary or subsidiary affection, and the real disease must be sought elsewhere.
The explanation of the susceptibility of the third stomach in constitutional troubles has been sought in the source of its innervation. Electric stimulation of the vagus rouses the movements of the first and second stomachs, but not those of the third. Action of the third stomach is excited by stimulation of the spinal cord, and of the sympathetic nervous branches going to the ganglionic cells in the walls of the omasum (Colin and Ellenberger). Its nerve supply coming from a different source, derangement of its function may occur independently of antecedent disorder of the first or second, and its motor supply coming from a source so closely related to the vaso-motor centres, perhaps affords some explanation of the connection of disorders of the omasum with febrile and inflammatory diseases.
Food is an important cause. Impaction of the omasum is a winter disease—the time of dry feeding. Dry, fibrous, innutritious fodder, and scarcity of water contribute to its production. It attacks cattle in spring or autumn on pastures in which fresh grass grows among the dead, dried, or withered stems of a previous growth. It occurs when stock are fed on corn or corn stalks (maize stalks) affected with smut or ergot, or on cereals or grasses similarly damaged, and in both cases especially when the water supply is deficient or restricted.
Sheep and goats, which habitually drink little, suffer less than do cattle, which drink freely.
Other causes. Fermented foods, microbian ferments and their products, which tend to induce torpidity of the omasum, fever, and lessened secretion of saliva, with diminished supply of liquid from mouth or rumen.
Pericarditis, by causing vascular stasis in the omasum, may induce torpor and impaction.
Lead poisoning paralyses action and favours impaction. Finely divided food stuffs—meal and bran—eaten greedily, may pass in quantity directly into the omasum and induce impaction. “The most acute and fatal forms occur in connection with a sudden change from dry to rich, luscious, green food in spring, the unwonted stimulus giving rise to general irritation of the whole gastric mucosa, with disordered and impaired function of all four stomachs, but especially of the third. Such cases are usually congestive and inflammatory, and the suspension of the gastric movements is a grand cause of impaction. In such cases, too, the brain or spinal cord, or both, are seriously involved, and the early death is preceded by torpor, paralysis, violent delirium or convulsions, following largely the type of acute lead poisoning.” (Law, loc. cit.)
The symptoms depend on the degree of impaction, and vary from simple, irregular, or suspended rumination to severe gastric and nervous disorder. The less acute cases are marked by failure to re-establish regular rumination or partial convalescence from fever or inflammation. The fever subsides, but the appetite remains capricious, the muzzle dry, eyes dull, spirits low, and breathing accelerated; the condition is sometimes accompanied by moaning. Slight tympanites may appear, and the contents of the rumen may feel solid, the mouth hot, clammy, and fœtid. The bowels are constipated, the fæces small in quantity, hard, covered with mucus or blood-streaked, and containing particles of undigested food; in other cases diarrhœa may set in, to be followed later by constipation. Alternations of constipation and diarrhœa may be repeated again and again. Exploration by pressure of the closed hand over the omasum will give an impression of solid resistance. There may be slight shivering, the ears and limbs are cold, the hair is erect in patches, dry and lustreless.
In cases occurring independently of previous disease, diarrhœa may be the first symptom observed, the malady being preceded by local irritation and congestion; but this soon gives place to constipation or diarrhœa and the symptoms above mentioned. The animal is found lying apart on its left side, with its nose in its right flank, the pulse and breathing quickened, the eyes congested; expiration is accompanied by a grunt. The patient walks with its back arched and dragging its limbs. The appetite may continue, but only in an impaired and irregular form, and as rumination ceases grinding of the teeth becomes common. The secretion of milk is diminished or arrested, emaciation advances day by day. Fœtid eructation may be a marked symptom. This form may last from ten to fourteen days, and merge finally into paralysis of the hind limbs, drowsiness and stupor, or delirium and convulsions.
“In more acute cases (from sudden access of green food, change of water, or ingestion of irritant plants), the affection partakes more or less of the nature of congestion or inflammation of the viscus (omasitis), and may run a rapidly fatal course” (Law, loc. cit.). The animal is seen apart from the herd in a characteristic recumbent position, the eyes are red and glassy, the eyelids semi-closed, the patient shows much drowsiness and stupor, but when raised may still feed in a sleepy, listless manner. The bowels are loose or confined, the pulse and breathing accelerated, the right hypochondrium is firm and tender, and the sound of fermentation absent or subdued over the omasum. Soon nervous disorder appears, the eyes glare wildly, the animal seeks relief in motion—sometimes in a straight line, sometimes to one side—and being blind and unconscious of obstacles, may fall into pits or ditches, knock against trees, fences, gates, or buildings, and continue pushing against resisting objects, breaking its horns or teeth; and otherwise sustaining injury through violent muscular contractions.
Course. Chronic cases may continue indefinitely, with symptoms of poor health, impaired digestion, and gradual loss of condition. After death the omasum may contain dried food which the animal consumed several months before the attack.
In cases ending in early recovery there occurs abundant diarrhœa, “the fæces are mixed with flattened, dark, solid, and polished masses, the impacted ingesta from the omasum. Tympany subsides; movement in rumen and omasum and rumbling in bowels can be heard. Appetite returns.” (Law.)
Diagnosis. The condition of the pulse and respiration, and the grunting with expiration may lead to confusion with pneumonia.
At first there is no fever, tenderness is confined to the right flank; there is an absence of pulmonary crepitation, of pleural effusion, and of movement in the rumen and omasum. Signs of gastric and intestinal disorder can be detected.
Lesions. The omasum is gorged—it may be twice its normal size—solid, resistant, almost stony. The spaces between the leaves are packed with dried food, which, when removed, carries a layer of epithelium from the mucous membrane. (This (layer on contents) is not inconsistent with health.)
The rumen contains ingesta packed in masses, more or less offensive from putrefaction.
The abomasum is empty of food, but contains much mucus. Its mucous membrane is congested.
The small intestine is red in places, empty and collapsed.
The larger intestine contains a quantity of dry, glistening pellets, and much mucus.
Treatment follows the lines of impaction of rumen, though the response is usually less certain, and always slower. Flax-seed tea, several bucketfuls per day, will often succeed.
Epsom and common salts, with sol. ammoniæ, excite thirst; liquids should be supplied freely.
In obstinate cases, and in absence of gastric or cerebral congestion, 20 croton beans, or 20 drops of croton oil, may be added to the purgative. Nux vomica stimulates the nervous supply. Enemata may be given freely.
Other remedies, stimulating contractility and secretion, are: Eserine, 1½ grains; veratrine, 1 grain; barium chloride, 10 to 15 grains; or pilocarpin, 3 grains, hypodermically.
The patient may be days or even a week without alvine discharge and recover.
If fever and symptoms of gastric congestion appear, a blister may be applied to the right side over the omasum.
Nervous symptoms, such as dilated pupils, blindness, congested mucous membrane, hot horns and ears, drowsiness or excitement, are combated by applying cold water or ice to poll, etc.
When free action of the bowels is restored, laxative diet, roots (pulped), green food, plenty of common salt, and free access to drinking water should be prescribed.
During convalescence a course of tonics, including nux vomica, is advisable to help in restoring normal gastric functions.
ABOMASAL INDIGESTION.
Primary indigestion in the abomasum appears to be rare in adults, for until the present time no one has given a sufficiently characteristic description of this disease to enable it readily to be recognised. On the other hand, it is to be presumed, although final proof has certainly not been furnished, that in cases of gaseous indigestion, or of impaction of the rumen, the abomasum, whose physiological action is predominant, must simultaneously suffer.
Primary abomasal indigestion, on the contrary, is common in young animals before weaning, so that the condition has been given the name of “milk indigestion.” It could not very well be otherwise, for the abomasum is the only one of the gastric divisions which in ruminants is active during the first few weeks of life. At this period it is larger than the other gastric reservoirs; and the rumen, the reticulum, and the omasum do not undergo great development till weaning begins.
Causation. Milk indigestion attacks young animals, under varying conditions.
In animals suckled by the mother the disease rarely occurs, but yet when the mothers are good milkers, like the Flemish, Norman, Jersey, and Holland breeds, and when there is too long an interval between the feeds, calves, which are naturally greedy, and in addition are hungry, are apt to take too large a quantity of milk—in fact, they often gorge to the fullest possible extent. Owing to its over-distended state the abomasum either fails to secrete sufficient of the rennet ferment necessary for coagulating the milk or secretes an insufficiently active ferment. The first stage of digestion remains incomplete, giving rise to so-called “milk indigestion.”
When the cows are employed in ploughing, etc., or in drawing carts, not only are the calves fed at long intervals, but the milk is not always of proper chemical composition even in the udder. As a result of work, fatigue, over-exertion and irregular feeding, the cow’s yield of milk for the time is less digestible than the normal supply, or may even prove irritant to the calf’s stomach. Milk indigestion is thus set up.
When the cows are fed on factory waste, like beetroot-pulp or brewers’ grains, toxic or irritant products may even find their way into the milk, which then irritates the little creature’s abomasum and produces gastric indigestion. Just as in the production of congenital alcoholism in man, the young animal is then ingesting, unknown to those responsible for its well-being, chemical substances which produce various pathological changes.
But milk indigestion is commonest of all in calves fed by hand. The food usually given is a mixture of milk from the previous night, and skim milk or even butter milk. It contains lactic ferments and various microbes, some capable of producing toxic principles.
When swallowed and brought directly in contact with the mucous membrane these cause abomasal indigestion.
Symptoms. Soon after feeding, the little animal appears dull and somnolent, and shows moderate abdominal pain, suggesting trifling colic.
This stage is soon followed by nausea; the breathing and the heart’s action become rapid, vomiting efforts are made, and finally milk, in the form of firm or partially softened curds, depending on the time which has elapsed since the last feed was taken, are vomited. The quantity ejected varies. Pressure over the right side of the abdomen produces pain, and tympanites of the abomasum may sometimes be detected on percussion.
The sensitiveness and gaseous inflation are confined to the middle and lower zone of the hypochondrium. Soon after vomiting the animal begins to improve. The patient seems brighter, relief is very marked, and in some cases proves permanent; but more frequently a certain degree of depression persists, the mouth emits a sourish odour, and for a time the appetite remains poor. This temporary irritation of the abomasum has a tendency to become permanent; or even to extend to the intestine, in which the conditions appear more favourable to the development of microorganisms than do those in the stomach. Indigestion then becomes complicated with diarrhœic enteritis.
The diagnosis presents no difficulty.
The prognosis is not serious, provided that the young animals are carefully attended to; but such complications as diarrhœic enteritis may become very grave if neglected.
The treatment. To prevent recurrences:
(1) The periods of feeding should be regulated;
(2) The cows should not be worked, or should be worked as little as possible;
(3) Mixed milk, or milk which has already undergone lactic or other fermentation, should be avoided.
If the calves must be reared by hand, the mixed milk should at least be boiled or relatively pasteurised by heating to 70° or 80° C., and the buckets used for feeding should be kept scrupulously clean. These precautions become absolutely necessary when diarrhœa exists amongst the calves. Curative treatment consists in placing the animals on low diet for two or three days after the attack of indigestion, or in giving them boiled milk diluted with from one-half to two-thirds of boiled water.
The addition of a mild saline purgative like sulphate of soda, in doses of one-half to three-quarters of an ounce, usually ensures a cure. Infusions of lime-tree flowers, peppermint, camomile, etc., may advantageously be used to replace boiled water in diluting the first foods.
ACUTE GASTRIC INDIGESTION IN SWINE.
The causes comprise putrid food, swill, spoilt turnips, potatoes, apples, succulent vegetables, frozen food, and the admixture of caustic alkaline powders (used in washing table dishes) with the swill. Indigestible matters—hoof, horn, hair, bristles, tree bark, etc.—when not rejected by vomiting, cause gastritis and indigestion. Lastly, medicinal substances and poisons, paint and lead, sometimes produce the disease.
Among the symptoms may be mentioned dulness, arching of the back, standing with the feet brought together, erection of the bristles, hiding under the litter, grunting, uneasiness, shifting from place to place, tenseness of the abdominal wall, borborygmus; these may be followed by diarrhœa and recovery. Speedier relief is afforded by copious vomiting of irritant matters.
The treatment should commence with the free administration of emetics. To combat alkaline poisoning vinegar may be given, followed by a laxative. Prophylaxis calls for greater care in feeding.
CHAPTER V.
ACUTE INFLAMMATION OF THE GASTRIC COMPARTMENTS.
RUMENITIS—RETICULITIS—GASTRITIS.
Causation. Acute primary inflammation of the first gastric reservoirs, viz., the rumen and reticulum, is not common. It sometimes accompanies such infectious disorders as foot-and-mouth disease, gangrenous coryza, etc., but then constitutes an added phenomenon which should be studied along with the original disease itself. Rumenitis or reticulitis may however follow the ingestion of irritant foods or plants, of very hot liquids, and more frequently still of unskilfully compounded medicines. In such cases the mucous membrane is directly attacked, and pathological congestion, infiltration, and desquamation may follow, or even vesicles and ulcerations may rapidly be formed.
Symptoms. Inflammation of the rumen or reticulum is announced by loss of appetite, suspension of rumination or of regular peristalsis, slight tympanites, and particularly by excessive sensitiveness to palpation. This sensitiveness is general, but is more specially marked in the left lower third of the abdominal cavity, and in the retro-ensiform region which corresponds to the position of the reticulum. Moderate fever is present.
These symptoms, which indicate the gravity and intensity of the inflammation, may persist, become aggravated, provoke vomiting from the rumen, and leave as a legacy motor dyspepsia, or even more serious consequences. On the other hand, they may progressively diminish and disappear for good.
Lesions. The lesions comprise hyperæmia of the walls of the rumen and of the mucous membrane, extensive local exfoliation of epithelium, and sometimes true ulceration of the mucous membrane.
Diagnosis. The diagnosis is based on the exceptional sensitiveness of the gastric compartments on palpation, and also on the history, provided reliable information can be obtained.
Prognosis. The prognosis should be reserved, because it is never possible to foretell whether acute lesions may not give place to chronic disease, which, though apparently unimportant, may terminate in grave consequences.
Treatment. Owing to their local action demulcent drinks and teas are indicated. Cooked food is useful, because it makes little demand on the digestive powers; steamed hay and farinaceous substances are given, both on account of their nutritious qualities and of the slight local irritation they cause when swallowed.
Lukewarm drinks and saline laxatives, such as the sulphate of soda, and carbonate of soda or Carlsbad salt in small doses of 1½ to 2 ounces, seem most useful in combatting the reflex atony of the digestive compartments.
Inflammation of the omasum, like that of the rumen and reticulum, occurs as a secondary phenomenon in conditions like rinderpest, Texas fever, foot-and-mouth disease, anthrax, and gangrenous coryza (malignant catarrh); but primary inflammation is much rarer even than that of the rumen and of the reticulum.
This is accounted for by the deep position of the omasum, which is thus sheltered from external violence, early contact with irritant foods and from the effect of chills, etc. It can only become inflamed by the prolonged action of irritant food and drink, which have already produced lesions in the rumen and reticulum; or as a consequence of the prolonged stagnation of dry food in cases where animals have been deprived of water.
Under these conditions inflammation of the omasum develops slowly, and from the clinical point of view is identical with what was formerly known as obstruction of the omasum. Obstruction or impaction is probably much rarer than has been stated, in so far at least as it constitutes a primary condition, for in the great majority of cases it is consecutive to impaction, inflammation of the rumen, or inflammation of the abomasum. Obstruction of the omasum, which was formerly invoked in all doubtful and ill-defined cases of digestive disturbance, seldom occurs as an isolated disease.
It has been suggested that the omasum, being supplied with nerves solely by the sympathetic system, and provided with a relatively weak muscular coat, was more susceptible than the other reservoirs to the reaction of abdominal reflexes, and therefore more subject to inflammation, indigestion and obstruction. We do not hold that view, because, as a result of its general situation and the position of its orifices of communication, this compartment is easily able to expel its contents so long as they are liquid. Its function appears chiefly to be to complete the trituration of food after rumination.
We do not consider that inflammation of the omasum never occurs, for we are well aware of the contrary, and that the inflammation assumes a subacute course and is accompanied by stasis of the semi-digested food between the mucous leaves which partly fill the cavity. We simply wish to emphasise the view that the condition is not a primary and isolated inflammation.
Symptoms. The symptoms are always vague and very difficult clearly to define.
Inflammation of the omasum is indicated by relative loss of appetite, marked thirst, general atony, and diffuse and vague sensitiveness in the inferior half of the right hypochondrium (zone of the asternal ribs). There are no pathognomonic symptoms.
Obstruction has also been described as accompanied by loss of appetite, constipation, the passage of black, coated, fœtid and sometimes blood-streaked fæces, symptoms of chronic tympanites with fœtid eructations and sometimes vomiting. These sometimes accompany hydrochloric acid dyspepsia, a form of chronic gastritis, and, from our standpoint, the stagnation of food in the omasum is only secondary. We therefore interpret the facts in quite a different manner, and believe that only by a rational and physiological interpretation of the symptoms observed can one diagnose the condition.
Diagnosis. The diagnosis of inflammation of the omasum can only be made by a process of exclusion; and although we are admittedly dealing with a condition secondary to disturbance of the rumen and reticulum, or on the other hand consecutive to inflammatory states or to modifications in the secretion of the abomasum (dyspepsia), the diagnosis does not present insuperable difficulties.
The prognosis is only grave when the primary acute or chronic conditions of the other gastric compartments are serious.
The lesions comprise abnormal vascularity of the mucous membrane and desquamation, and even gangrene, of the leaves. The partially digested food is not passed on, becomes dry and hard, and in time aggravates the local condition.
The treatment does not essentially differ from that of other gastric inflammations. The object to be attained is to evacuate as completely as possible, not only the omasum, but all the gastric reservoirs, for which purpose one may freely administer demulcent drinks—linseed gruel, bran mashes and lukewarm liquids containing laxatives. At first such alkaloids as arecolin and pilocarpine may be subcutaneously injected to ensure energetic and speedy evacuation.
Later on slightly stimulant aromatic infusions, like infusions of sage, peppermint, hyssop, thyme, etc., stimulate the functions of the stomach and hasten the return of normal conditions.
ACUTE GASTRITIS.
The term “acute gastritis,” sometimes “gastro-enteritis,” is used in bovine pathology to indicate inflammation of the abomasum. If this inflammation is confined to the superficial epithelial layers it is defined as superficial catarrh of the abomasum; if, on the contrary, it extends to the deep epithelium of the gastric glands and to the mucous corium, it is termed deep-seated gastritis.
Clinically it is impossible to make these distinctions. We simply recognise degrees of gravity, and only in this way can one diagnose acute gastritis, phlegmonous gastritis, ulcerative gastritis, etc.
Causation. The abomasum frequently becomes inflamed as a consequence of irritant foods, apart altogether from lesions of the rumen or reticulum, the mucous membrane lining the abomasum being so much more delicate than that of either of the two first compartments.
Irritant plants, parasites, acid drinks, very cold water, certain acid or toxic industrial residues like mouldy brewers’ grains, fermented vegetable pulp, decomposed beet, etc., and mouldy or spoilt forage of any kind may all produce acute gastritis.
Intense feeding—i.e., feeding with farinaceous materials, with large quantities of beans, roots, peas, given regularly—may also cause gastritis by overtaxing the functions of the organ. Frozen or fermented roots and sudden changes in feeding produce similar results. Chills have also been blamed, but it is probable that they only act as favouring causes.
Symptoms. It is necessary to consider these very carefully in order to arrive at a correct diagnosis.
Inflammation of the abomasum is attended with moderate fever, diminution in appetite, irregularity in rumination and some tension of the rumen, without, however, true tympanites.
At first the bowels are constipated, but in time fœtid diarrhœa sets in. Examination of the digestive apparatus on the left side and in the right posterior abdominal region reveals nothing abnormal, but pressure over the lower portion of the abdomen and along the cartilages of the right hypochondriac region produces, on the contrary, well-marked pain. This region corresponds to the position of the abomasum.
The conjunctiva appears reddish yellow, as in most visceral inflammations.
Some authors have described attacks of extreme excitement, but these are no more pathognomonic than is grinding of the teeth, which is a constant symptom, or the metallic sound noted on auscultation of the rumen. This sound occurs in all cases of inertia of the rumen, and indicates distension and emptiness of the viscus (acute peritonitis, chronic adhesive peritonitis, inflammation of the reticulum as a consequence of the presence of foreign bodies).
Dull colic and groaning are not uncommon. Finally, Thierry and others have all mentioned an alliaceous smell of the eructations as pathognomonic.
Acute gastritis develops regularly in ten to fifteen days, after which the symptoms diminish and disappear, giving place to normal health. In grave cases, despite proper treatment, acute gastritis more frequently ends in a chronic condition, finally leading to gastric atrophy, and the insufficient secretion of hydrochloric acid, with all the consequences of these conditions. The glands of the stomach degenerate; the secretion becomes abnormal and dyspepsia is set up.
Diagnosis. The diagnosis is rather difficult, for the condition is very apt to be confused with primary dyspepsia, or with inflammation of the gastric compartments. It might also be mistaken for acute enteritis of the first part of the small intestine; but as gastritis is very often complicated with duodenitis, such a mistake is without serious consequences.
Prognosis. The prognosis is grave, not because death is a frequent termination, but because the disease very often leads to chronic incurable lesions.
The lesions consist of congestion of the vascular network of the mucous and sub-epithelial coats, serous infiltration of the corium and submucous connective layers, desquamation, and later in excessive proliferation of the epithelium.
When the inflammation is deep seated the epithelium of the gastric glands becomes swollen and cloudy, and undergoes a kind of atrophic degeneration. In very grave cases, petechiæ, superficial capillary hæmorrhages, and slight ulceration may be noted. The mucous folds are always thickened and infiltrated.
Treatment. In cases of gastritis or acute gastro-duodenitis moderate bleeding (three to four quarts) and local stimulation were formerly recommended. This practice certainly has its advantages, provided it is not pushed to excess. Sinapisms give good results, but as they must be left in position for a considerable time, it is often better to apply vesicants over the lower right hypochondriac region. At first purgatives are useful, because they unload the digestive tract, arrest the organic fermentation which results from stagnation in the movement of food along the alimentary tract, and diminish the tendency to intoxications or infections.
At a later stage small doses of laxatives and bicarbonate of soda should be given daily, the diet being of an emollient character, and consisting of milk, starchy or farinaceous foods, and small quantities of good hay.
Linseed, bran, cooked grain, decoctions of pellitory, barley and various cereals may also be administered with advantage.
CATARRHAL GASTRITIS IN SWINE.
Definition. Inflammation of the gastric mucosa, with muco-purulent discharge.
The causes comprise irritants, fermented or putrid swill, decomposed food, excess of brine, alkalies (washings from table dishes, hotels, etc.), gastric parasites.
The condition occurs also in hog cholera, swine plague, rouget, etc.
The chief symptoms are: Inappetence, vomiting, uneasiness, colic, constipation or diarrhœa, fever, stiffness, tense and tender abdomen, arched back, frequent grunting, limpness of the tail. Sudden vomiting may bring about a rapid recovery.
Treatment calls for a complete change of food, which may include freshly cooked roots, linseed or meal, butter milk, boiled milk, etc.
As an emetic 30 grains of ipecacuanha may be given. Constipation can be relieved by a dose of calomel or jalap. If diarrhœa is persistent small doses of grey powder should be given, and to combat the irritation of the gastric mucous membrane bismuth subnitrate is also useful.
The piggery should be cleansed and disinfected, and the litter frequently changed.
ULCERATIVE GASTRITIS.
Ulcerative gastritis (ulcer of the abomasum) is recognised after death, but hitherto it has been impossible to so clearly identify the symptoms as to permit of diagnosis during the animal’s life. It has been found after death in adults and in calves (Ostertag).
Causation and Pathogeny. The cause of gastric ulceration is decidedly obscure, though we know that certain forms occur during infectious diseases like cattle plague, foot-and-mouth disease, gangrenous coryza, and as a consequence of certain direct local infections; other forms result from the administration of drugs; and finally some are of secretory origin.
In human medicine at the present day there is a tendency to refer the development of round ulcer and ulcerative gastritis to the secretion of an excess of hydrochloric acid. Probably the same cause may be at work in domestic animals, but the proof has not yet been given.
With regard to the pathogeny, the theories of embolism or of thrombosis of capillary vessels find favour with few authorities at the present day. Yet these explanations are logical enough, for if we prevent physiological irrigation of any given part, it is possible to conceive that ulcer formation may follow from auto-digestion, i.e., from the simple action of the gastric juice on a surface which is no longer protected.
The theory of microbic origin has been advanced; but although it may be accepted in relation to the intestine, where the most varied organisms abound, it is scarcely so applicable to the stomach, in which acidity is always very marked and must exercise a very energetic antiseptic action. In sucking calves, however, this theory appears the most plausible.
It is quite certain that ulceration may result from the unwise use of drugs, like tartar emetic or arsenious acid, especially if these be administered for long periods; but such ulceration always occurs at the same points, viz., at the deepest portion of the rumen, reticulum, or abomasum.
On the other hand, ulceration due to secretory disturbance occurs at different points, and the figure opposite shows that the mucous folds themselves may be injured and perforated.
Lesions. Ulceration of the abomasum varies in severity. The case referred to showed excavated ulcers from the site of which a portion or the whole of the epithelium and glandular layer had been shed; true round ulcers, which had destroyed the entire depth of the mucous membrane and had produced chronic inflammation and sclerosis of the muscular layer; and finally perforations resembling cleanly punched-out holes.
The Symptoms are those of a mild form of ordinary acute gastritis, without marked fever, and without special injection of the conjunctiva. The appetite is diminished and irregular, but more as a consequence of excessive reflex sensibility of the injured organ than from absence of hunger. This excessive reflex sensibility of the abomasum causes relative or absolute gastric intolerance, so that only a small amount of the food ingested passes towards the intestine.
Absolute intolerance on the part of the abomasum may even occur, as in a case described by Moussu in 1895, which produced a very special form of impaction of the rumen, absolutely different from primary impaction.
Intolerance of the abomasum for food already ingested and ruminated may extend to the omasum. Peristalsis of the rumen then ceases, and slight tympanites occurs. The most characteristic condition is the existence of obstinate constipation. If ulceration takes place without producing any important vascular lesion, which, however, is rare, the fæces are hard and coated, but without other peculiarity; if, however (and this appears to be the rule), local hæmorrhage occurs, the extravasated blood is modified by the gastric and intestinal juices, and the fæces appear of a black, tarry colour. This coloration is very significant, and differs from that produced by the bile. It occurs only in gastric hæmorrhage, and at intervals.
Diagnosis. The diagnosis of gastric ulcer is difficult, and can only be arrived at with confidence when the above-mentioned coloration of the fæces can be detected.
Prognosis. From an economic standpoint the prognosis is grave. The patient may recover; the ulcers may heal, but cicatrisation is always prolonged, and as, on the other hand, the glandular apparatus of the abomasum is generally more or less injured, complete recovery is impossible.
Fig. 70.—Ulcerative gastritis. 1, Typical round ulcer; 2 and 3, ulcers perforating folds of the abomasum; 4, 5, and 6, old-standing ulcers with sclerosis of the walls of the abomasum and adhesive perigastritis.
Treatment should be directed towards checking hæmorrhage, diminishing intolerance to food, and assisting the healing of the lesions. These objects are facilitated by prolonged complete rest in the stable, by injecting ergotine, or, ·7 per cent. saline solution, at the time when the hæmorrhage occurs, and, if possible, by placing the animals on milk diet or on emollient food, like gruels, emollient infusions, barley, milk, cooked roots, etc.
Stimulation over the region of the abomasum is also of value. At a later stage, when the acute symptoms have diminished, Carlsbad salts, in doses of 1 to 2 ounces per day, can be given. Bicarbonate of soda is also of considerable value.
CHRONIC TYMPANITES.
Chronic Indigestion—Obstruction of the Abomasum—Chronic Gastritis—Dyspepsia.
Among pathological conditions of the stomach in ruminants a certain number are clinically marked by one constant symptom, viz., chronic tympanites, a fact which was formerly recognised as indicative of chronic indigestion.
It is evident that such titles have only the significance accorded them, and the term chronic indigestion used only to mean that gastric digestion was badly performed, and that the condition was more or less permanent. It being granted, on the other hand, that the term indigestion is used to characterise temporary conditions during which digestion is suspended, and produces immediate disturbance, it would appear that the term gastric dyspepsia is more exact and more in conformity with the present state of our knowledge of general physiology. In studying this question it is clear a number of facts still require explanation, for, as has been previously indicated, we know almost nothing concerning the variations in the chemical phenomena of gastric digestion under different morbid conditions; nevertheless, the dominant fact, the imperfect or irregular digestion, is easily appreciable. Future discoveries will no doubt enable us more exactly to differentiate several dyspeptic conditions due to chemical or mechanical causes and with or without anatomical lesions. At present it is sufficient to indicate the limits of inquiry.
Causation. The symptom of chronic tympanites accompanies a great number of very different conditions—some due to disease of the digestive tract itself, others to general diseases or lesions of neighbouring parts. In the latter cases the tympanites is only indicative of secondary dyspepsia; in the former, on the other hand, the dyspepsia is primary.
Secondary dyspepsia occurs very commonly during tuberculosis, diseases of the liver, subacute or chronic peritonitis, gestation, lesions of the mediastinum, etc., etc.
(a) Secretory or Chemical Dyspepsia. In primary dyspepsia it is impossible to discover any lesion sufficient to explain the disturbance. Chronic tympanites, for instance, follows prolonged consumption of rough or bad food (in years when forage has been scarce or winter food has been lacking), and too short a supply of water for weeks in succession. It also occurs as a consequence of acute inflammation of one or other of the gastric compartments—rumenitis, reticulitis, gastritis. Sometimes it assumes an insidious, slow, progressive form, without any apparent cause whatever.
In these various conditions, the mucous membrane of the gastric compartments suffers from the deferred results of the bad feeding or want of water. Its secretory powers and anatomical structure becoming modified, it is no longer able regularly to elaborate the juices necessary for digestion, and chronic indigestion, imperfect digestion, or dyspepsia result. Similar results follow acute inflammation of the omasum, reticulum, or rumen. Integral repair becomes impossible. Anatomical injury is done, disturbance of secretion follows, and dyspepsia is a necessary consequence.
(b) Motor Dyspepsia. Finally, it would appear that general bad health, abstinence and exhausting work, may produce a form of dyspepsia, unconnected with secretory disturbance, but resulting from mechanical disturbance due to general enfeeblement and to atony of the muscular walls of the gastric compartments. The rumen ceases to perform its work of mixing the food, the reticulum also acts badly, and the abomasum receives imperfectly prepared material. The result is what might be described as motor dyspepsia, in opposition to those forms which are of chemical origin.
The condition may vary in degree, peristalsis being diminished (one contraction every two or three minutes instead of two per minute), or being simply intermittent and occurring only for a few hours during the day, or finally being altogether suppressed. Suppression is never absolute, but atony may be so marked that the mixing of the food is very imperfectly performed.
Symptoms. The most constant symptom present in all dyspeptic conditions is chronic tympanites, indicated by a certain degree of tension or by permanent dilatation of the rumen.
Rumination is impeded and irregular, the distended rumen loses its power of contraction, and no longer causes eructation nor passes gas into the intestine. It becomes progressively inert, whether the inertia be primary and occur suddenly, as a result of some particular condition of the sympathetic system (motor dyspepsia), or secondary and of slow development in consequence of disturbance in the gastric secretions and of abnormal organic fermentation (secretory dyspepsia).
This symptom of tympanites is always accompanied by irregularity, diminution, and frequently also by depravity of appetite.
Wasting occurs, but to a very varying degree, according to the nature of the primary condition and the method of feeding.
These general symptoms are accompanied either by constipation or by diarrhœa; and as stagnation of food leads to fermentation, which always forms products differing from those of normal digestion—toxic materials in fact—a chronic auto-intoxication results, which in its turn, if not remedied, becomes a cause of irritation, and aggravates the bad general condition.
In many cases fever is absent, except during the final complications, in animals in the last stages of wasting; but some signs always exist on which the diagnosis may be founded.
The most frequent clinical type of these dyspeptic conditions is motor dyspepsia, consisting in relative atony of the rumen without disturbance in the secretion of the gastric mucous membranes. Luckily, this is the most easily curable form, and is only marked by distension, dulness and constipation.
Dyspeptic diseases of secretory origin are little understood. Their essential causes have been badly described, and their clinical symptoms are ill-recognised.
We cannot prove whether the forms said to be due in man to excess of hydrochloric acid and insufficiency of hydrochloric acid really occur or are well defined in domestic animals: nor are we better informed as to the exact part played by the organic acid of fermentation (lactic, butyric, acetic acid, etc.); but the most complete investigations which have yet been made justify our supposing there is some parallel.
Moussu described primary ulcerative gastritis in 1895; and as this form is almost certainly associated with excess of pepsin, the occurrence of an excess of hydrochloric acid also seems possible, the more so as the symptoms noted resemble the general symptoms of that condition—preservation of appetite and of the motor power of the rumen, accumulation of food in the rumen as a consequence of reflex intolerance of the abomasum, constipation, and vomiting.
In addition to these two morbid conditions, a third occurs with some frequency. It is characterised by chronic tympanites, alimentary diarrhœa (the food being badly digested), and progressive wasting. This condition seems due to an insufficiency of hydrochloric acid, brought about by chronic gastritis, the epithelial cells of the mucous membrane appearing incapable of producing sufficient hydrochloric acid for digestion.
Diagnosis. In the present state of our knowledge regarding digestion in ruminants the precise diagnosis of these pathological conditions must always remain difficult; but it is indisputable that with the above grouping of symptoms we are more likely to succeed than by confining ourselves to the diagnosis formerly common, viz., that of chronic tympanites or chronic indigestion.
The difference between primary and secondary dyspepsia should always be borne in mind, and careful examination will often reveal the special condition which has served as the point of departure for gastric disturbance. Thus generalised tuberculosis, or tuberculosis of the liver or mediastinum, should always be sought for, and the possible existence of such conditions of the liver as echinococcosis, cancer of the bile ducts, tumours, etc., and diseases of the kidneys should be borne in mind. The influence of gestation, which so frequently causes gastric disturbance complicated with albuminuria, should never be overlooked, and in these secondary forms of dyspepsia the determining cause, and not the objective symptoms should receive chief attention.
Prognosis. The prognosis of secondary forms of dyspepsia varies with the gravity of the primary disease. The prognosis of primary dyspeptic conditions varies greatly, and that state in which hydrochloric acid is too sparingly secreted is certainly the gravest.
Lesions. The lesions have not been carefully studied, but it is probable that in many cases they might afford a key to the symptoms noted. Like all mucous lesions, they are difficult to demonstrate histologically. Infiltration and thickening of the mucous corium and submucous layers have been described. Such lesions indicate nothing; but in some cases new growths have been found in the gastric compartments or contractions about the pyloric orifice, the essential importance of which cannot be doubted.
Treatment. If our knowledge is still insufficient to enable us precisely to diagnose what we have termed “gastric dyspepsia,” or what is still currently described as “chronic dyspepsia,” the difficulty is even greater when attempting to lay down lines of treatment, because of the lack of known facts and the want of a base for reasoning. Thus we find, without being able to explain why, that some prescribe tartar emetic, others rapid and energetic purgatives, others, again, laxatives; whilst German authors, apparently without any justification, recommend oil of turpentine. It seems to us, however, that one might do better than this and attempt to lay down some rational indications for treatment.
(a) In cases characterised only by chronic tympanites, without diarrhœa, without manifest constipation (motor dyspepsia), and without any other apparent organic disturbance, drugs calculated to stimulate peristalsis of the rumen seem indicated. The most promising comprise ipecacuanha in doses of 1 to 2 drams per day, tincture of nux vomica in similar doses, powdered nux vomica in doses of 45 to 75 grains, and laxatives like Carlsbad salts in doses of 8 to 10 drams.
Little by little peristalsis returns, becomes regular, and the chronic tympanites disappears for good. This is frequently the case during gestation, when the condition simply consists in motor dyspepsia without anæmia.
(b) If, on the contrary, chronic tympanites is accompanied by constipation, and the fæces are hard or, as is usually the case, covered with mucus, suggesting the probability of excess of hydrochloric acid, salines are indicated—not to the point of producing purgation, which would not lead to any lasting improvement, but still as laxatives, continued daily for ten, fifteen, or twenty days, or, if necessary, even longer.
Carlsbad salts in doses of 8 to 10 drams, or one-ounce doses of sulphate of sodium associated with 2½ drams of bicarbonate of potash after each meal, are to be recommended in preference to bicarbonate of soda alone, because they act on the secretions, on the muscular system, and also on the liver.
(c) Finally, when chronic tympanites is accompanied by diarrhœa, a condition which usually indicates insufficient secretion of hydrochloric acid, the administration of that acid tends to arrest or check organic fermentation and to facilitate digestion in the abomasum by supplementing the diminished physiological secretion. The dosage is an important point. At first small quantities should be given, 2½ drams per day, divided into two doses and freely diluted in the drinking water; but this amount may, if necessary, afterwards be doubled or trebled. The drinking water is not rendered irritant by these doses, for it is admitted, and Moussu has confirmed the fact by analysis, that the quantity of HCl in the gastric juice may rise as high as ·2 to ·3 per cent. Chloride of sodium, the excito-secretory action of which on the gastric mucous membrane is well known, may be given for long periods in doses of 1 to 1½ ounces per day.
In these various chemico-pathological states the food should receive the closest attention. The forage, which should be good, may be supplemented by the addition of cooked roots, demulcent drinks, and, if possible, milk.
GASTRIC DISTURBANCE DUE TO FOREIGN BODIES.
These morbid conditions are extremely complex, but the facts that they are due only to one cause, and that they possess certain symptoms in common, permit of a certain grouping. It would obviously be illogical to speak of traumatic indigestion of the rumen, reticulum, and abomasum, as has been done in more than one book on this subject; for the gastric disturbances described below should be considered as complications, and not as diseases.
Causation. In young animals foreign bodies may be composed of hairs, wool, bristles, cotton, and clover hairs.
Hair balls are common in the rumen, and are sometimes met with in the fourth stomach. They cause irritation, indigestion, sometimes pyloric obstruction, dilatation, and eventually death.
Wool balls in lambs, bristle balls in young pigs, cause much gastric irritation. Cotton balls occur in lambs fed on cotton-seed cake; the fibre constitutes a foreign body. The hairs of clover leaves may form a ball in the abomasum of lambs.
Under the influence of depraved appetite animals of the bovine species consume, apart from their regular food, the most varying substances, such as linen, fragments of wood, nails, stones, gravel, sand, etc. Moreover, forage, even when of good quality, often contains foreign bodies like nails and pins (when the fields are near factories), sewing or knitting needles (when the animals are looked after by women), fragments of iron wire derived from bales of compressed forage, etc., etc. The ingestion of such objects is followed by various consequences, which may be studied in three divisions, in the first of which the foreign object is soft in character, in the second is blunt at one extremity and pointed at the other, and in the third is pointed at both ends.
(1.) Soft objects. The movements of the rumen, the warmth and the action of the digestive fluids, may cause soft objects to be broken up; the disturbance they produce is then insignificant.
Of such substances, however, some are quite incapable of digestion (clothing, sacks, linen, etc.), and may produce obstructions; others are both indigestible and heavy (gravel and sand), and may fall into the depressions of the compartments, where they remain, or, if passed into the reticulum, may become arrested in the deepest lying part. They then produce atony of the muscular coats, slowing of peristaltic movements, diminution in the frequency of eructation, and, as an additional consequence, chronic tympanites, sometimes visible at the flank.
The symptoms are vague and common to a number of the digestive diseases already described. The animals masticate without having anything in the mouth; rumination becomes irregular or is altogether suppressed, but this is not characteristic, being a symptom common to many visceral diseases.
Later, as a result of auto-infection, diarrhœa sets in; under the influence of abnormal fermentation in the gastric compartments the eructations become fœtid; the animals fall into a condition of marasmus. Death usually results after a varying time—when large quantities of foreign substances have been ingested, in twenty to thirty days.
The diagnosis chiefly rests on the history, and can only be of a confident character when one knows what quantity and what kind of foreign body has been swallowed.
The prognosis is grave, because the animal usually dies of progressive exhaustion.
Treatment. There is only one rational form of treatment—viz., gastrotomy, followed by examination of the rumen and reticulum and removal of the foreign body. Before undertaking operation the surgeon should be fully informed as to the cause and the probable results to be expected.
(2.) Foreign bodies with one pointed extremity. These usually consist of large-headed nails, or fragments of iron wire rolled up at one end, which have been swallowed during primary mastication along with forage.
When ingested, they may become implanted at any point in the gastric apparatus without necessarily penetrating deeply. When fixed across the division of the reticulum, they cause slowing of its physiological action. Should they penetrate the wall either of the reticulum or of the rumen, they may attack on the right the liver, or on the left the diaphragm or spleen, producing suppurating hepatitis, splenitis, or respiratory disturbance. The hypochondriac region then appears sensitive. The muscular portion of the diaphragm is partly paralysed, and costal respiration set up, while frequent coughing of reflex origin is provoked by irritation of the pneumo-gastric and diaphragmatic nerves, and may give rise to suspicion of some thoracic disease, from which, however, it is distinguished by the absence of discharge, expectoration, and pulmonary symptoms.
Finally, if implanted in the lower wall or sides of the rumen or reticulum, foreign bodies may carry with them infectious agents and set up localised or generalised peritonitis.
Early diagnosis is a matter of great difficulty, as it can only rest on the diaphragmatic disturbance or on the symptoms of peritonitis.
Lesions. Small-sized sharp bodies cause lesions of trifling extent, which in most cases are only indicated by retardation of movement of the gastric compartments, between which and the diaphragm, and between the diaphragm and the posterior portions of the lung, various adhesions are set up. In such cases the peripheral inflammation ends by producing a fibrous sleeve, which prevents the pleural cavity becoming infected. Other cases show patches of adhesive peritonitis or signs of generalised peritonitis, the real cause of which often evades discovery during life.
Treatment. Gastrotomy is the sole means of effecting a cure, but we are forced to admit that it only gives good results when the operator knows what he is trying to find. Without this information he acts in the dark, is obliged to abandon himself to chance, and although luck sometimes favours him, it more often leaves him in the lurch.
(3.) Foreign bodies pointed at both ends. Bodies like needles, pins, straight fragments of iron wire, knitting needles and broken hairpins, become implanted in the gastric walls and travel in the most diverse directions, in obedience to the varied movements of the organ injured. They produce results similar to those just described. Most frequently they fall into the lower part of the gastric compartments, pass near the ensiform cartilage, between the pleura and the triangularis sterni into the thickness of this muscle, or into the mediastinum, and there produce either an abscess in the region of the ensiform cartilage, an abscess of the thoracic wall, or a collection of pus in the subpericardial or subpleural region (pseudo-pericarditis). They may even reach the pericardium, causing pericarditis, and sometimes, when adhesions are set up between the heart and pericardial sac, carditis.
By deviating to the right or left, the foreign body may produce pleurisy or even pneumonia. If it moves towards the right, it involves the liver and produces suppurative hepatitis; if to the left, suppurative splenitis. Travelling in a downward direction, it encounters the abdominal wall, and after producing an abscess may be eliminated; passing backwards, it falls into the peritoneum, and may lead to peritonitis. In those exceptional cases in which foreign bodies reach the abomasum they generally become implanted towards the greater curvature, producing in the abdominal wall an abscess which breaks externally, and through which the foreign body is discharged; gastric fistula is then a common sequel.
The symptoms vary, according to the complications. The earliest comprise digestive disturbance, which coincides with the passage of the sharp object through the rumen or reticulum, and depends on whether such passage produces local peritonitis and pain, rendering movement of these compartments impossible. Later, when the diaphragm has been penetrated, respiratory disturbance occurs, and is succeeded by apparent improvement, which in its turn may be followed by the occurrence of pericarditis, pleurisy, or abscess formation.
In other cases where suppurative hepatitis or splenitis, or even peritonitis may be present, the symptoms are extremely vague and very difficult to refer to their real cause.
Diagnosis is difficult, unless the owner is able to supply exact information that at some previous time the animal had swallowed such and such an object.
The prognosis is grave, though cases occur where a foreign body is tolerated, and may for a long time be retained without producing accidents.
Treatment. Gastrotomy should not be performed unless the operator is possessed of very precise information. In such case the rumen and reticulum should be emptied and the foreign body sought for and removed.
When the symptoms strongly point to the presence of a foreign body exploratory gastrotomy may be performed, but the operator will do well to employ the operation only as a last resort.
Many complications, like septic peritonitis, hepatitis, and splenitis, are practically hopeless; but others show a tendency to recovery. This is the case when abscesses form in the thoracic or abdominal wall, or beneath the pleura or pericardium. The entire difficulty consists in diagnosis, for when once this is clearly defined intervention is fully justified. As, however, the surgical measures vary in every case, the exact course to be adopted must be left to the initiative of the surgeon.
TUMOURS OF THE GASTRIC COMPARTMENTS.
Papillomata result from hypertrophy of normal papillæ; they resemble those of the pharynx and œsophagus. The growth may attain the size of a fist. It often resembles a cauliflower in appearance. When very large, such growths may cause obstruction. A very striking illustration of a papilloma of the mucous membrane is given on p. 180 of Möller and Dollar’s “Regional Surgery.”
Sarcoma has been noted by Paule, Kitt, and Schütz as forming in the subserous tissue of the omasum, and later bulging out as a wounded swelling of irregular size.
Actinomycosis of the abomasum has been reported by Professor Axe.
CHAPTER VI.
ENTERITIS.
Enteritis consists in inflammation of the intestine, or, more precisely, in inflammation of the intestinal mucous membrane. All the constituent portions of the intestinal tube may be affected (duodenum, jejeunum, ileum, colon, cæcum); but clinical distinctions and localisation of inflammation in the various parts are very difficult in the domesticated animals, and at present it is impossible to describe with any accuracy the differences between duodenitis, enteritis of the jejeunum and ileum, colitis or typhlitis. Without doubt certain symptoms suggest that some regions are more affected than others; but clinically we are only able to distinguish between acute and chronic enteritis. Acute enteritis may assume different forms, according to its intensity, rapidity of development, and lesions, so that it is possible to distinguish between such conditions as simple acute enteritis and hæmorrhagic enteritis.
Chronic enteritis, an abstraction founded on our knowledge of such specific forms of enteritis as are due to tuberculosis, distomatosis, helminthiasis, etc., usually assumes the diarrhœic form.
ACUTE ENTERITIS.
As acute enteritis, whether localised in one portion of the intestine or involving the whole intestinal tube, is produced by varying causes, and assumes very varying degrees of intensity, its clinical symptoms are equally diverse.
Causation. The various forms of enteritis result from two great series of causes: infections and intoxications. Normally the intestine contains an extremely large number of different microbes, which may prove of service so long as circulation, secretion, and peristalsis continue normal; but as soon as any perturbation occurs, either in the blood supply or in the movement of the bowel, normal secretion is impeded; abnormal organic fermentation commences, producing irritant principles or toxins which at once set up local irritation, or, being absorbed, produce that complex of symptoms which we recognise as enteritis, intoxication of intestinal origin, or even infection.
Bearing in mind these facts, we are better able to understand the part played by cold, by damaged fodder, by intense, stimulating feeding, or sudden changes in the food, as well as by the action of drastic purgatives, which modify beyond physiological limits the condition of the glands, or even cause local desquamation of epithelium.
Toxic substances or plants act similarly by modifying either the circulatory, secretory, or motor systems.
Symptoms. The first appreciable external symptoms appear to result from fever—loss of appetite, suspension of rumination, dryness of the muzzle and of the mouth, earthy-red colour of the conjunctival mucous membrane, etc.
On manipulating the left flank one notes neither tympanites nor sensitiveness—in a word, there is no indication of functional disturbance of the rumen.
On the right side, on the contrary, palpation causes the animal to resist and to show signs of pain. According as this sensitiveness is more marked in the middle or upper region or towards the hypochondriac circle, we infer that the inflammation is most acute in the large or small intestine, either in the middle portions or, again, in the most anterior portion. The temperature always rises at the commencement, attaining 103° to 104° Fahr. (39·5° or 40° C.), but rarely a higher point, a fact which negatives the idea of a rapidly progressive infectious disease. Slight colic appears, and is accompanied by constipation; the fæces are covered with mucus, or false membranes, or are completely enclosed in fibrinous tubes. After four or five days the fæces change in character. Constipation gives place to a liquid, blackish, very fœtid diarrhœa. Finally the mouth exhales a stercoraceous odour, resulting from fœtid eructation.
The passage of flat or tubular false membranes continues for a certain time.
When false membranes constitute the chief symptom, the condition is termed “pseudo-membranous, croupal, or diphtheritic enteritis.” This form is only a variety of acute enteritis, but is grave, because complications due to hæmorrhage or infection are very liable to occur.
In certain cases movement causes groaning. In the slighter forms the patient may recover spontaneously. If fed with easily digested materials, the symptoms diminish in intensity. Towards the eighth day the fæces become normal, appetite and rumination reappear, and the secretion of milk which had fallen off rises to its normal amount. Resolution has occurred.
More frequently, either because the animals have less power of resistance or because decomposition is taking place more actively in the intestine, or, again, because intoxication is setting in, the disease becomes aggravated. Constipation is more marked, and the fæces passed are in small masses, covered with layers of epithelium, or sometimes streaked with blood. In other cases the diarrhœa becomes exaggerated and assumes a mucous or sero-mucous character; the temperature rises, and death results from exhaustion and infection, microorganisms passing from the lumen of the intestine through its walls and invading the general circulation.
Lesions. To study the lesions to advantage the autopsy must be performed as soon as possible after death.
In slight cases they consist of trifling generalised congestion of the intestinal mucous membrane. The points most affected show infiltration of the submucous coat, and sometimes of the muscular coat; the wall of the intestine is double its normal thickness, but the thickening never equals that seen in cases of rapidly fatal intestinal congestion.
At a more advanced stage the mucous membrane clearly is inflamed, its surface is covered with a fibrous exudate, and the glandular and epithelial cells proliferate, assume the embryonic form, and produce the new tissue which one recognises under the form of false membranes.
The false membranes are generally but slightly adherent, and are readily expelled.
In other cases, however, they adhere firmly, and when detached by the friction caused by movement of semi-digested food through the bowel, produce rupture of capillary vessels; this explains the presence of blood streaks in the fæces.
The diagnosis is relatively easy, especially at the onset, on account of the special character of the fæces and the sensitiveness of the right flank.
The prognosis is seldom grave. If the enteritis is taken at the beginning, recovery is usual; but if the animal has been ill for eight or ten days and is exhausted, and if fever and diarrhœa are intense, the prognosis should be guarded.
The treatment is that of all acute inflammatory diseases. Mustard plasters may be applied to the chest and abdomen and left in position for some hours, or may be repeated. Some practitioners prefer hot blankets or dry friction, or, again, rubbing with essence of turpentine, but this substance should be spread over large surfaces, in order to prevent injury to the skin. Bleeding is only justifiable in plethoric animals, and should never be exhaustive.
To relieve the digestive symptoms purgatives are at first given, even though diarrhœa is marked from the onset; for purgatives still constitute the best intestinal antiseptics, because they get rid of the intestinal contents and microbes. The diet should be carefully selected, and may consist of gruel, mucilaginous materials, linseed tea, cooked roots, etc.
Of drugs, sulphate of sodium in doses of 10 to 15 ounces is probably the best. It can gradually be replaced by 2 to 3 drachm doses of bicarbonate of soda or of ordinary salt per day. Laudanum, camphor, and bismuth relieve persistent colic and diarrhœa. Pilocarpine, veratrine and eserine, though recommended by some authors, present no advantage in our opinion. The first two of these substances certainly cause purgation, but the action is quite temporary. The last induces violent contraction of the striped muscular tissue, and may produce grave lesions or invagination when the bowel is diseased, thickened or infiltrated.
HÆMORRHAGIC ENTERITIS.
This form of enteritis derives its name from the dominant symptom, which consists in the passage of unaltered or clotted blood in the fæces. In the former case the blood is bright in colour, as if it came directly from an open vessel. In the second it is coagulated, and assumes the form of fibrinous clots, which seem to result from the superposition, in the intestinal tract of their constituent elements, viz., serum, blood corpuscles, and fibrin.
Causation. Hæmorrhagic enteritis is rarely seen except during the hottest days of summer, and in young animals which have previously shown nothing abnormal. The high temperature seems to favour its appearance, but is always supplemented by another cause, viz., the ingestion of irritant food, particularly of weeds and toxic plants or herbage of bad quality; amongst such may be mentioned dog’s mercury, and plants of the order Papaveraceæ, Euphorbiaceæ, etc. Otherwise the often rapid manner in which the disease develops indicates toxic enteritis.
In other cases, more benign in appearance, but quite as grave in reality, blood is passed continually, and the disease assumes a chronic form. It is then of parasitic origin, and is due to intestinal psorospermosis.
Symptoms. The primary symptoms are similar to those of acute enteritis, and consist of fever, dryness of the muzzle and of the mouth, colic and constipation. This is soon followed by loose motions containing blood or blood clots, according as the hæmorrhage occurs at a greater or less distance from the rectum. The fæces are then ejected violently to a considerable distance, on account of the exaggerated intestinal peristalsis.
The disease may produce death in twenty-four hours, though usually the end is deferred for several days, or, in cases due to sporozoa, for a considerably longer time. In these cases there is some chance of recovery, provided that treatment be prompt.
The diagnosis is very easy.
The prognosis is in all cases grave.
The lesions are ill-recognised. The animals die rapidly, and if not immediately examined show no characteristic lesions. The changes to be looked for consist in intense congestion or ulceration of the intestine, or even in ulceration of arterioles and of arteries of considerable size.
In parasitic enteritis one finds localised inflammation and, in the epithelial interstices, sporozoa, which cause the rupture of blood-vessels.
Treatment. It is necessary to act energetically from the outset, and to arrest hæmorrhage by acting on the intestine, on the vascular system, and on the skin. Mustard plasters or other external stimulant applications are therefore indicated. Internally, small doses of astringents like tannin, preparations of opium, 25 per cent. solution of sulphuric acid in alcohol, etc., are given to produce constriction of the vessels, though they seldom arrest the discharge of blood for long. In most cases it is necessary to have recourse to subcutaneous injections of ergotine, in doses of 5 to 10 grains in young animals, and 15 to 45 grains in adults. The dose may be given in two parts to prevent an unduly severe action. The smooth fibres of the small vessels are thus directly excited, and hæmorrhage ceases in consequence of clotting in the contracted vessels.
One may give for the same purpose injections of arseniate of strychnine, which has the advantage of sustaining the tone of the heart and preventing syncope. The dose should not exceed 1·5 grains in large animals.
Finally, a stimulating diet containing milk, alcohol, soup, cooked vegetables, and small quantities of vegetable pulp is useful.
With early treatment animals sometimes recover in a few hours.
Intravenous or subcutaneous injections of physiological salt solution (2 drachms of sodium chloride in one quart of water) may prove of value when hæmorrhage has been abundant and vascular pressure is low.
CHRONIC ENTERITIS (CHRONIC DIARRHŒA).
Chronic diarrhœa is common in byres. It appears suddenly, often fails to attract attention, and assumes the form of simple diarrhœa, a fact which accounts for it frequently being described as chronic diarrhœa, dysentery, etc.
Causation and pathogeny. This form of diarrhœa occurs sporadically throughout France, and under exceptional circumstances may permanently attack a number of animals in a given place.
The immediate cause is not known, but without doubt the disease is of microbic origin. Like Lignières, Moussu at one time believed that this disease was very probably identical with that known in Argentina under the names of diarrhœa, entéqué, or bovine pasteurellosis. The hypothesis has not been verified, and Lignières’ treatment, said by him to have succeeded in Argentina, always failed in Moussu’s hand.
Fig. 71.—Appearance of a patient suffering from advanced chronic diarrhœa.
The only point which seems admissible is that this disease, which Moussu considered to have analogies with chronic sporadic dysentery in man, is due to one or several organisms, which develop in the intestine and produce toxins, causing diarrhœa, without, however, marked inflammation of the intestinal mucous membrane.
Symptoms. The onset is often overlooked. The diarrhœa gradually increases without appearing to be very serious; but it persists in varying degrees of intensity. The patients do not appear to suffer, and do not lose their appetite or spirits, but in time the diarrhœa becomes exhausting; they waste, and after some months become excessively thin and poor.
Intestinal peristalsis becomes exaggerated without the existence of colic or tympanites. The evacuations are frequent, and little by little the abdomen retracts, until, in horseman’s parlance, “the belly is up to the back,” even in cows of four, seven, and eight years’ bearing.
The diarrhœa is serous, always fœtid, and without tenesmus.
The fæces may either be very soft or be passed in veritable jets. They are always a little discoloured, and frequently contain grain or undigested forage. They always contain numerous bubbles of gas.
The wasting during later periods of the disease is absolutely characteristic, and different from that of other wasting diseases, such as chronic broncho-pneumonia, tuberculosis, etc. The patients finally become walking skeletons. The red corpuscles of the blood progressively decrease, until the number may fall as low as 800,000 or even 500,000 red corpuscles instead of six millions, the normal figure. The œdema common to wasting conditions appears, and the animals die without suffering, in a condition of absolute exhaustion.
Fig. 72.—Appearance of a portion of the small intestine in chronic diarrhœa.
Complications are rare, though occasionally intestinal hæmorrhage or broncho-pneumonia occurs. The temperature, which remains normal or shows very slight changes throughout the course of the disease, may then oscillate between 101° and 103° Fahr. (38° and 39·5° C.).
Fig. 73.—Atheromatous lesions of the aorta in chronic diarrhœa.
Lesions. At the first glance no lesions can be detected on post-mortem examination except those of generalised wasting, but when the autopsy is carried out immediately after death all the interior of the intestine appears affected. The mucous membrane of the abomasum and the mucous folds appear infiltrated, thickened, and with moderate sub-epithelial congestion. The intestine seems friable, and tears with the slightest traction. The sub-epithelial portions of the mucous folds are infiltrated and congested, while the more prominent parts of the folds, which are exposed to the friction of semi-digested food, become eroded.
Throughout the length of the jejeunum and ileum the mucous membrane exhibits multitudes of small ulcerations.
Histologically, the epithelium and the glands seem atrophied, without any inflammatory change having occurred in the mucous or submucous coats.
The colon and the cæcum show similar lesions, and in addition brown deposits of pigment under the mucous membrane and along the course of the small blood-vessels. This lesion resembles that found in chronic dysentery in man, and suggested to Moussu a possible connection between the two diseases.
The liver is less than the normal size. In the heart Moussu has seen one case of sclerosis of the auricles and calcareous infiltration of the sub-endothelial lining of the aorta.
In several instances he has noted calcareous infiltration of the mesenteric lymphatic gland.
Diagnosis. It is easy to diagnose this condition, and quite possible to distinguish it from the diarrhœa of tuberculous enteritis, infectious hepatitis, and other conditions.
Prognosis. The prognosis is very grave, and the disease almost always proves fatal.
Treatment. At the present moment no curative treatment is known. Lignières’ treatment—viz., the injection of physiological salt solution and serum from healthy oxen, and saline solution or defibrinated blood—has never given permanently successful results.
All the drugs usually employed against diarrhœa, the antiseptics, astringents, etc., fail, or confer merely momentary benefit. Economically, nothing is to be gained by keeping the patients alive. With great care existence may be prolonged for months, or even for several years, but the animals never regain condition, and are never of any use.
The most rapid and lasting good effects follow the administration of 2½ to 8 fluid drachms of hydrochloric acid per day, given in two portions and very freely diluted.
DYSENTERY IN CALVES.
This disease sometimes appears on the first day after birth, frequently on the second or third. It may be mistaken for septicæmia of umbilical origin.
Symptoms. The young animal may be born vigorous and in good condition, though this is exceptional. More frequently it is puny and below normal weight. The first evacuation (of meconium) may exhibit the diarrhœic character; in other cases this peculiarity only appears on the second or third day, when half-digested milk is passed. The fluid is greyish, extremely fœtid, and rapidly becomes brownish and blood-stained. Evacuation is frequent and accompanied by tenesmus.
The patients at once become very dull, refuse to suck, and resist efforts to feed them by hand. The temperature rises, and the diarrhœa, which at first was of an alimentary character, becomes mucous, serous and blood-stained. The little patients appear “tucked up,” the flanks sink in, the strength diminishes, and in twenty-four hours, or two or three days at most, they die of exhaustion.
Recovery is exceptional, and when the disease assumes this character it usually attacks a considerable proportion of the other animals in the byre.
Causation. The exact cause of this form of dysentery in new-born calves has not yet been identified, but the disease is undoubtedly a microbic enteritis, and may even be a primary septicæmia of puerperal origin.
For a very long time this dysentery was mistaken for simple diarrhœa, though it exhibits neither the characteristics, course, nor termination of the latter disease.
The co-existence of epizootic abortion and dysentery in certain byres has led some authors to believe that a connection exists between the two diseases, and that the young are infected with dysentery at birth. Evidently, intra-uterine infection is not exceptional, and it seems quite natural that the new-born calf may equally suffer when the fœtal envelopes and fluids are infected before parturition. Epizootic abortion is probably not the only disease which may produce this condition.
The diagnosis is very simple. The course of the disease and its rapid development prevent it from being mistaken for ordinary diarrhœa. It is more difficult to distinguish from septicæmia of umbilical origin, although this disease also has well-marked characteristics.
The prognosis is not hopeful. Statistics show that almost all the affected animals die, and that those exceptional cases which survive remain puny and sickly. There is no economic advantage in attempting to save them.
The mothers of affected calves seldom show any sign of illness, though the after-birth is often retained.
Lesions. The macroscopic lesions are of very trifling importance compared with the gravity of the disease. The digestive tract appears congested throughout. The intestinal mucous membrane is moderately swollen, but without gross lesions. The intestinal contents exhale a sickly, fœtid odour. The smaller vessels and capillaries forming the peripheral vascular network appear distended, as in septicæmia. The carcases putrefy with extreme rapidity.
Curative treatment is very uncertain. Varying results have been obtained with doses of 4 to 5 drams of slight purgatives like borotartrate of potassium, sodium sulphate, and magnesium sulphate; small doses of intestinal antiseptics like salicylic acid, 15–grain doses of salicylate of soda, 45 to 75 grains of carbolic acid, 2 per cent. carbolic solution in doses of 7 to 12 drams; 1 per cent. Lysol solution in doses of 2 to 4 ounces; benzo-naphthol, lactic acid 45 to 75 grains, tar water, lime water, etc. Although all these preparations, when carefully used, generally give good results in the early stages of simple diarrhœa, they appear to fail in dysentery of new-born calves.
Prophylactic measures are more reliable. They consist:
(1.) In scrupulous disinfection of the byres when the first case of abortion occurs;
(2.) In successively isolating cows which are about to calve in a small specially detached stable;
(3.) In carefully disinfecting the genital organs of cows which have aborted, firstly with boiled water at a temperature of 100° Fahr., and then with 1 per cent. iodine solution.
Calves which are infected when born cannot be saved, but abortion can be prevented and dysentery so stamped out.
DIARRHŒIC ENTERITIS IN CALVES.
This disease is usually called “simple sporadic diarrhœa.” It may appear at any time before weaning, and can usually be cured if treated early before the patients show bodily wasting.
Causation. Indigestion from failure of the abomasum to deal with the milk usually precedes diarrhœic enteritis; it may terminate without complications, but very often is followed by diarrhœa. Anything which produces milk indigestion, therefore, favours the occurrence of enteritis. Such predisposing influences include over-distension of the abomasum, milk of bad chemical composition, milk tainted by keeping or by storage in dirty and infected pails, etc. The addition to the milk of nutritive substances which the abomasum and intestine are not yet capable of digesting, such as wheat, rye, barley, or maize meals, very often produces diarrhœa even when the meal is well cooked.
Chills, privations, irregular feeding, and badly-managed weaning may facilitate its development, but none of these causes, however important they may be, seem to play any other part than that of favouring the multiplication of the numerous varieties of microbes to be found in the intestinal tract. Vascular disturbance occurs, either as a result of direct irritation of the intestinal mucous membrane or of the action of toxic products contained in milk which has served as a culture medium for these microbes; this is followed by secretory disturbance, and the intestinal contents being modified in character, the microbes normally present undergo changes in number and quality. Inoffensive organisms assume pathogenic qualities and secrete toxic principles, normal digestion is disturbed, the intestinal defence becomes less perfect, toxic principles which the liver is incapable of destroying are absorbed, and diarrhœic enteritis is set up.
Symptoms. Diarrhœic enteritis appears during the second week of life, towards the end of the first month, or even later. It is characterised by the passage of fæces consisting of mucus and containing little clots of milk.
This is the first stage of alimentary diarrhœa, also termed “white diarrhœa” or “white scour.” It may prove unimportant; it may last a day or two and then cease. Most commonly diarrhœa increases and assumes a mucous and then a serous character, whilst the dejecta exhale a very characteristic repulsive smell. The excrement becomes greenish brown, and after several days or a week or more may appear blood-stained. The number of evacuations varies enormously, depending on the gravity of the condition. The ejected material is irritant, and the parts soiled by it, like the perineum, hocks, and back of the cannon bones, become slightly inflamed as though blistered; later, the hair falls away.
The general health then begins to suffer. Fever remains moderate, but the mouth is pasty, the tongue coated, and the breath fœtid.
The patients become thin, and lose their appetite and spirits. Palpation of the abdomen, especially of the right flank, is slightly painful, and the pulse is accelerated.
The diarrhœa may spontaneously diminish if the animal’s constitution prove sufficiently strong; but if it follows its course, the little patient becomes weaker, eats less, the evacuations increase and are accompanied by tenesmus. In seven to eight days, in rare cases in four to five, the animal dies from toxi-intoxication of intestinal origin, or from infection resulting from intestinal germs, particularly the bacterium Coli communis, obtaining entrance into the circulation. On the other hand, the diarrhœa may continue for weeks.
The diagnosis is easy, and there should be no difficulty in distinguishing this disease from dysentery and from umbilical phlebitis, which are also accompanied by diarrhœa.
The prognosis is grave, unless treatment is early undertaken. In the latter case there is a good chance of recovery.
Lesions. The macroscopic lesions are not of much interest, being confined to congestion of the intestinal mucous membrane, superficial desquamation of the epithelium, small vascular erosions, and general wasting.
The mesenteric lymphatic glands are swollen and œdematous.
After death from general infection, it is not uncommon to find pleural, peritoneal, and pericardial exudation or even endocarditis.
Even in cases where no post-mortem change has had time to occur cultures from the blood yield varieties of the bacterium Coli communis.
Treatment. The meals should be given at fixed hours, and regulated both as regards quantity and quality. These precautions alone suffice to prevent the appearance of diarrhœic enteritis.
Curative treatment has every chance of succeeding when undertaken at the outset. Delafond and Trasbot recommend mild purgatives, which act more rapidly than intestinal antiseptics. These comprise borotartrate of potash in doses of 4 to 5 drachms, sodium sulphate in doses of 2½ to 4 drachms, sulphate of magnesia, etc. By evacuating the bowel and removing a large number of the germs which have multiplied there, they arrest intoxication and prevent infection. Nevertheless, they should not be administered for long, and after one or two doses should be followed by antiseptics like benzo-naphthol, in doses of 15 to 30 grains, salicylic acid in doses of 5 to 10 grains, or salicylate of soda 45 to 60 grains. Mucilaginous and sweetened drinks containing lactic acid in doses of 45 to 75 grains per day may be given between the meals, or at intervals if the calf is sucking.
Laudanum in doses of 6 to 10 drops per day administered in rice water, extract of opium, weak solutions of tannin, etc., are also of value. Filliàtre has successfully used tar water in the first stages. The solution consists of vegetable tar 6 drachms, boiling water 1 quart. This solution is used tepid in the proportion of 1 part to 3 parts of warm milk.
Decoctions of spiked purple loosestrife, willow bark, etc., are also of great value in certain districts.
The drug which appears least dangerous, however, is that so often successfully used in young children—viz., subnitrate of bismuth. It can be given in doses of 30 to 45 grains per day, with lactic acid in doses of 75 to 150 grains, according to the size of the patients. If the animals are greatly exhausted and have been ill for some time there is less chance of recovery, and under these circumstances Dr. Lesage’s anti-colic serum might be used.
It gives excellent results in infants, and it has proved successful in simple diarrhœa of calves.
CHAPTER VII.
POISONING.
Accidental poisoning is frequent in domesticated animals. It may present no visible lesions, and it is therefore very important to recognise the symptoms which indicate the secret lesion.
POISONING DUE TO FOOD.
Under this title are included all forms of poisoning resulting from the ingestion of bad fodder. Such expressions as “intestinal typhus” and “typhic gastro-enteritis” only indicate a special stage in the condition, which is never twice the same.
Causation. The most important changes in the food ingested do not consist in a mere modification in its chemical composition, but in the presence of various parasites which develop in grain and forage, after moistening, or after abnormal fermentation in the interior of the grains. These parasites are chiefly represented by fungi belonging to the genus Mucor: Aspergillus or Penicillium; blight—Puccinia graminis, Uredo linearis; smut—Tilletia caries, Ustilago segetum, Ustilago maydis; yeasts of different kinds resulting from the fermentation of brewers’ grains; and, finally, unrecognised microbes which act by means of the poisons they secrete.
The symptoms are always very vague. At first the only marked symptom is loss of appetite, accompanied by dryness of the mouth and muzzle, depression and constipation. The animals never clearly show signs of gastro-enteritis; nevertheless, the changes in general health point very clearly to a digestive origin.
In cases of acute poisoning the symptoms develop rapidly. Torpor becomes more marked, the movements of the heart tumultuous, and the temperature rises to 105° Fahr. (40·5° C.), diminishing later until death occurs.
In chronic forms of poisoning constipation is present at first, but is soon followed by profuse, fœtid, blackish diarrhœa, sometimes containing streaks of blood and accompanied by abdominal pain.
In exceptional cases these digestive symptoms are amplified by the presence of broncho-pneumonia, pleuro-pneumonia, nephritis, and cystitis, as in poisoning by tannin and essential oils. These complications are of infectious origin.
In young animals, like lambs and young pigs, still with their mothers alimentary intoxication may also occur though the mothers show no signs of illness. The passage of poisonous principles into the milk cannot be disputed. Moussu has seen numerous cases of alimentary intoxication in lambs whose dams were fed with decomposed beet pulp, and in sucking pigs whose mothers had received bad maize, turnips, etc.
Diagnosis. Careful examination of the substances with which the animals are fed, and consideration of the history, prevent confusion with ordinary poisoning. Anthrax as a cause can easily be eliminated.
The prognosis is grave, unless the practitioner is summoned early.
The lesions are those of acute gastro-enteritis—congestion of the mucous membrane, abomasum, and intestine, submucous infiltration, shedding of the epithelium, which sometimes attains the stage of ulceration, suffusion and intestinal or superficial hæmorrhage, dilatation of the capillaries, etc.
The symptoms of poisoning are produced by the absorption of toxic products, which pass from the intestine into the blood current.
Poisoning is frequently complicated by infection produced in a similar manner.
Treatment. The first point is to change the food. This alone is often sufficient to dispose of the digestive disturbance in a week or two. In addition, mustard plasters may be applied, and purgatives, stimulants and mucilaginous drinks may be given. Finally, diuretics are useful in eliminating the toxic products accumulated in the blood. They comprise general stimulants like wine, alcohol, tea, coffee, etc. Subcutaneous or intravenous injection of physiological salt solution is indicated.
POISONING BY CAUSTIC ALKALIES.
The cause consists in the administration of insufficiently diluted solutions of ammonia in cases of tympanites, or the ingestion of quick-lime, used for disinfecting stables, by animals suffering from depraved appetite.
The symptoms indicate injury to the anterior part of the digestive tract. They consist in salivation, loss of appetite, colic, indigestion, diarrhœa, and progressive loss of strength.
Diagnosis is only possible when the history is clear.
The prognosis is grave if the doses swallowed have been so large as to cause severe burning of the mouth, œsophagus, rumen, etc. The local lesions are grey and soft.
Treatment consists in immediately giving acidulated draughts containing vinegar or 1, 2 or 3 per cent. of hydrochloric acid, and emollient, mucilaginous drinks containing opium for the purpose of calming the irritation.
POISONING BY CAUSTIC ACIDS.
Cases of this kind are rare. Gerlach described a case of poisoning by straw which had been removed from sulphuric acid carboys. Abadie saw a number of cases which were traced to the unskilful treatment of two empirics.
The symptoms point to the existence of stomatitis, œsophagitis, and gastro-enteritis. Death occurs rapidly, with a running-down pulse. On post-mortem examination one discovers more or less deep burning of the mucous membrane of the digestive tract.
The diagnosis is difficult in the absence of information.
The prognosis is grave.
Treatment comprises administration of alkaline draughts, solutions of bicarbonate of soda, calcined magnesia, etc., and of mucilaginous drinks containing opium, chalk, etc. This may produce temporary relief.
Water mixed with whipped whites of eggs is also extremely valuable, but it is often better to slaughter the animal as soon as the condition is diagnosed.
POISONING BY COMMON SALT.
This form of poisoning is rare in oxen on account of the large quantity of salt which can be ingested without producing bad effects. It is commonest in animals to which old brine has been given or which have received rough salt containing toxic substances (sheep and pigs). Beef, pork, or fish brine, four or five months old, is especially dangerous because of the toxins it contains. Half a pint is a fatal dose for a pig (Reynal). The symptoms include marked thirst, vomiting and diarrhœa; at a later stage motor and nervous disturbance appears, resulting from poisoning of the cerebro-spinal system. Paralysis, epileptiform convulsions, trismus, coma and death characterise extremely acute cases.
To the naked eye, the lesions are those of acute gastro-enteritis; and, in many cases, of marked congestion of the brain and medulla and of the mucous membrane of the bladder.
The treatment is prophylactic and hygienic. Old brine and salt of doubtful purity should be avoided. The symptoms should be treated by administering diuretics, preferably soda bicarbonate, which does not irritate the kidney, and by giving mucilaginous drinks with anodynes.
POISONING BY THE NITRATES OF POTASH AND SODA.
This form of poisoning has frequently been described as following the ingestion of water used for washing sacks which have contained chemical manures. Occasionally it results from the administration of medicines containing excessive doses of nitrate of potash. The symptoms vary in severity with the purity of the salt, with its nature, and with the degree of concentration of the solution: nitrate of potash is more dangerous than nitrate of soda.
The chief symptoms may be grouped as follows:—
Salivation, indigestion and tympanites, nausea, vomiting, diarrhœa, and (especially) intense polyuria: the kidney may be irritated to such a degree as to produce albuminuria and hæmaturia. Intense dulness and general weakness precede death, which sometimes occurs in four to twelve hours after the poison has been taken.
The lesions are to be found in the digestive and urinary apparatus. The kidneys are congested and hypertrophied, or present changes indicating epithelial nephritis. The ureters and the bladder may show similar lesions.
Treatment comprises removal of the cause, and the administration of emollients, narcotics, and diffusible stimulants.
POISONING BY TARTAR EMETIC.
Tartar emetic is sometimes given for the purpose of favouring secretion and restoring rumination; occasionally the proper dose is exceeded and poisoning occurs. Given repeatedly, tartar emetic is apt to accumulate in the deeper portions of the gastric compartments and to produce general symptoms of super-purgation, and such local symptoms as ulceration and even perforation of the walls of the stomach, which in turn is followed by abscess formation in the abdominal wall.
Diagnosis is easy. The prognosis is grave.
Treatment is confined to the administration of mucilaginous and diuretic fluids. Tannin has been recommended.
POISONING BY ARSENIC.
Overdoses of Fowler’s solution produce rapidly fatal results, in twenty-four to forty-eight hours. Lesions are little marked.
Arsenious acid acts like tartar emetic by accumulating and producing local gastritis; it may also cause acute poisoning, being in that case characterised by severe colic with tympanites, salivation, and fœtid, sometimes blood-stained, diarrhœa. The urine becomes albuminous, and remains scanty. Incomplete paralysis is sometimes produced, and various forms of hæmorrhage result from changes in the constituents of the blood.
If the gastric compartments are perforated, an abscess may develop in the abdominal wall. The lesions are those of acute gastro-enteritis. The contents of the stomach exhales an odour resembling garlic. The parenchymatous organs—the liver, kidney, and heart—show fatty degeneration in chronic cases.
In prescribing arsenic, one should begin with small doses, which can gradually be increased as the animal becomes accustomed to the drug. Curative treatment consists in administering antidotes, such as hydrated oxide of iron, sulphate of iron, and calcined magnesia.
Haubner described a form of chronic arsenical poisoning produced in the neighbourhood of blast furnaces near Freiberg. Similar forms of poisoning may perhaps occur in the neighbourhood of chemical and smelting works in England.
PHOSPHORUS POISONING.
Though the chronic form is common in men, phosphorus poisoning only occurs accidentally in animals through eating phosphorus paste, used as a poison for rats, or as a consequence of excessive doses given medicinally. Some cases have been described by Maury.
The symptoms comprise salivation, loss of appetite, alliaceous odour of the buccal cavity, arrest of intestinal peristalsis, indigestion, colic, diarrhœa, exhaustion and death in a state of coma. Albuminuria and icterus also occur.
The lesions are the same as those of arsenical poisoning—viz., stomatitis, pharyngitis, and gastro-enteritis. The specific changes consist in fatty degeneration of the liver and kidneys, and the peculiar odour resembling garlic exhaled by the flesh.
Death is a consequence of deoxygenation of the blood, which appears black, and when spectroscopically examined reveals only the lines of reduced hæmoglobin.
Treatment. Oil and milk dissolve phosphorus and render it more easily assimilable; they should never be administered. Large doses (up to six fluid ounces) of essence of turpentine have been recommended. This prevents the phosphorus absorbing oxygen at the expense of the blood. Saline purgatives assist in eliminating the poison.
MERCURIAL POISONING.
Mercurial poisoning may result either from the administration of medicines or from accident. Cases of the former kind follow the internal use of sublimate or calomel. Doses of 2 to 2½ drams of calomel, if repeated for a certain time, may prove toxic in the ox. Accidental poisoning results from the use of mercurial ointment as a parasiticide over large surfaces. Poisoning, however, rarely occurs unless the animal is able to lick the parts. Some authors have tested this point by freely applying mercurial ointment over parts likely to absorb it readily, without having seen any bad effect.
Symptoms. Free salivation, the saliva gradually becoming fœtid and blood-stained. The slight irritation of the buccal membrane first seen is soon replaced by congestion of the gums, then by gingivitis and periostitis, with local ulceration and hæmorrhage. The portion of the gums surrounding the teeth becomes violet, and suppurative alveolitis may follow.
As a consequence of disturbance in the digestive secretions digestion ceases, defæcation becomes irregular, the fæces are often hard and coated, and can only be passed with difficulty, though sometimes there is profuse fœtid diarrhœa.
Respiration is difficult, jerky, or even dyspnœic, and is accompanied by discharge from the nose and by expectoration. The gait is irregular, and paralysis may follow. Finally the skin shows an eruption resembling that of impetiginous eczema; vesico-pustules, covered with yellowish crusts, appear over the entire surface of the body.
Lesions. The lesions of hæmorrhagic gastro-enteritis are sometimes accompanied by catarrhal tracheo-bronchitis, and even intra-pulmonary hæmorrhage. The muscles are discoloured, appear as though boiled, and are covered with ecchymoses. Blood effusions occur beneath the eczematous crusts, but the rest of the skin is anæmic.
Treatment includes administration of raw eggs, or, better still, of white of egg beaten up in water; the albumen in coagulating imprisons the mercury. Failing these, other bodies, like flowers of sulphur and iodide of potassium, which with mercurial salts form soluble and harmless compounds, may be given. Chlorate of potash has also been recommended.
Complications like stomatitis and gastro-enteritis are treated by the usual methods.
LEAD POISONING: SATURNISM.
Lead poisoning is very rare, and seldom occurs except near camps or factories. It then results from swallowing lead “spray” mixed with the grass or from inhalation of lead vapour.
The symptoms comprise salivation, nausea, colic, obstinate constipation, tympanites, and arrest of milk secretion. A peculiar form of trembling affects the head; epileptiform convulsions, amaurosis, and paralysis may also occur. General sensibility diminishes, and death follows.
The disease may assume a chronic form, characterised by a blue line around the gums, changes in the joints, albuminuria, and bodily wasting.
The lesions are those of ulcerative stomatitis, anæmia of the mucous membranes, and fatty degeneration of the epithelium. In the chronic form the kidneys are atrophied.
Treatment consists in giving substances which form insoluble compounds with lead. It comprises the administration of dilute sulphuric acid, solutions of sodium sulphate or magnesia, milk, eggs, and iodide of potassium.
COPPER POISONING.
This is a rare form of poisoning. It may follow ingestion of food stored in copper vessels, licking of ointments containing copper salts, or ingestion of vine leaves, or leaves of other plants which have been sprayed with sulphate or acetate of copper to prevent “mildew.”
The symptoms comprise vomiting of green-coloured material, colic, diarrhœa, muscular weakness, and convulsions. The urine contains dissolved albumen and hæmoglobin.
The lesions are those of acute enteritis and dilatation of the stomach. The essential lesion consists in decomposition of the blood with the formation of methæmoglobin. Nephritis and granular degeneration of the muscles form secondary symptoms.
Treatment consists in administering raw eggs, albumen, milk, mucilage, flowers of sulphur, or calcined magnesia.
CARBOLIC ACID POISONING.
Carbolic acid poisoning sometimes follows the use of carbolic acid solutions in the form of injections, enemas, or baths.
Symptoms. Administered in over-doses or for too long a time, carbolic acid produces stomatitis, œsophagitis and vomiting.
True poisoning is characterised by changes in the kidneys and bladder; the urine becomes brown and turbid, and possesses a well-marked carbolic odour, the animals suffer from severe trembling and appear stupid, and coma and paralysis precede death.
The specific lesions consist in parenchymatous nephritis, sometimes accompanied by renal hæmorrhage, cystitis and hyperæmia of the lung and brain. The flesh has an odour of carbolic acid, which renders it unfit for human consumption.
Treatment consists in giving stimulants and slight diuretics, such as ether, alcohol, wine, coffee, saline sulphates, or Glauber’s salt. The last named forms phenyl-sulphuric acid, which is not toxic. Olive, rape, or linseed oil has been recommended. All these drugs are useless if the kidney lesions have become too pronounced.
POISONING BY ALOES.
This form of poisoning is caused by administering over-doses of aloes.
Apart from the accidents possible in pregnant female animals, large doses of aloes produce symptoms of super-purgation—profuse diarrhœa, running down pulse, and nervous prostration.
The lesions are those of gastro-enteritis, the intestine being empty, and its mucous membrane of red colour.
Treatment is confined to administering drugs like camphor, rice, bismuth, opium, chloral, and emollients, which diminish peristalsis and lessen secretion.
IODOFORM POISONING.
The causes are limited to the licking of wounds which have been dressed with iodoform.
The symptoms include gastric disturbance, somnolence, coma, and the signs of iodism.
The only lesions are those of fatty degeneration of the kidneys and liver.
Treatment comprises the exhibition of vomitants, stimulants, and diuretics.
IODINE POISONING: IODISM.
Death by iodine poisoning is absolutely exceptional: the complications described under the name of iodism are rather to be referred to saturation of the organism than to true poisoning.
The cause of iodism is unduly prolonged administration of iodide of potassium, or of iodine in solution.
The symptoms include discharge from the eyes, coryza, hypersecretion from all the mucous membranes, and gastric disturbance. The cutaneous eruption exhibits special peculiarities, including desquamation of the epidermis in the form of branlike scales, and pruritus.
The first indications in treatment are to discontinue the drug and to administer stimulants and nutrients like milk, cod liver oil, etc.
STRYCHNINE POISONING.
Strychnine poisoning is most commonly due to over-doses of the drug accidentally given during treatment.
The symptoms comprise tetanic convulsions, hyperæsthesia and dyspnœa. As a result of muscular rigidity, the ribs cannot be moved, and death by asphyxia follows.
Treatment comprises the use of anæsthetics, and the administration of chloral hydrate, as long as the contractions continue. Bromide of potassium, tobacco, tannin, etc., are also useful.
The chief part of the botanical descriptions in the following list have been extracted, by permission, from the Annual Report for 1898 of the United States Bureau of Animal Industry, p. 392. To Dr. D. E. Salmon, who gave this permission, and who also kindly supplied the blocks, the writer (Mr. Dollar) desires to express his very sincere thanks. Considerable modifications have been made, and in the case of the more important poisonous plants, details of symptoms and treatment have been added.
LIST OF PLANTS POISONOUS TO STOCK.[[2]]
[2]. The names of plants proved beyond doubt to be poisonous to stock are marked with an asterisk. The evidence in regard to the toxic properties of others is not in every case entirely convincing, though there is good ground for strong suspicion.
PERISPORACEÆ (ROT-MOULD FAMILY).
Aspergillus glaucus.—This is the common flocculent woolly mould which sometimes develops to a dangerous extent on corn, oats, and other food grains which have either been harvested before full maturity or been stored in a damp place. The mouldy growth is pure white at first, but changes with the ripening of the spores to gray and then green. The spores are apparently the cause of the so-called enzootic cerebritis, or “staggers,” of horses, which, during the winter of 1898–99, was reported as having caused very heavy losses in the southern portion of the United States. European investigators have shown that the spores of this mould will grow within the living body if they are introduced into the blood. Death is probably caused by some poison which is simultaneously produced with the mould in the body of the animal.
HYPOCREACEÆ (ERGOT FAMILY).
* Claviceps purpurea.—This, the most common species of ergot, infests various species of native and cultivated grasses. It sometimes causes great losses of stock.
POISONING BY ERGOT OF RYE: ERGOTISM.
Causation. This form of poisoning is due to the presence of ergot in grain or forage.
Symptoms. The symptoms are seldom very marked. In mild cases pregnant females may abort; grave cases are indicated by local gangrene of the mucous membrane and gangrene of the extremities, particularly in poultry, in consequence of the constrictive action of the drug on the peripheral blood-vessels, on the vaso-motor centres, and on unstriated muscular fibres.
Treatment. The use of chloral and morphine has been suggested in this condition; but as the lesions when discovered are established and permanent, this treatment seems illusory. More is to be expected from preventive measures and the avoidance of ergotised food.
USTILAGINACEÆ (SMUT FAMILY).
Ustilago maydis.—The black powdery fungus known as corn smut is common throughout the corn-producing districts of the central United States, and is occasionally reported as being fatal to stock. Experiments made in Wisconsin and elsewhere show that it is not a very active poison when eaten in moderate quantity. When given in gradually increasing amounts up to 2 lbs., no effect was noted, but 4 lbs. on each of two successive days caused the sudden death of one cow. Since corn smut has been shown to be less fatal when wet, it seems probable that its physical and not its chemical character may be responsible for the death of cattle which have eaten it in considerable quantity.
Fig. 74.—Fly amanita (Amanita muscaria). a, Mature plant; b, top view of cap showing corky, patches—both one-half natural size.
POISONING BY SMUT OF BARLEY.
Causes. The presence of smut in straw, in millers’ grains, or in damaged kiln-dried grains which have fraudulently been added to grain sold for feeding, represents the principal source of this form of poisoning.
The symptoms are very vague. There is indigestion, with a tendency to nausea, and vomiting. Diarrhœa may be present: At a later stage the heart and nervous system are affected. The gait becomes hesitating, the animals show general dulness and spasm of the pharynx; death, when occurring, is by cardiac or respiratory syncope.
Treatment consists in giving an entire change of food, and administering stimulants and purgatives.
AGARICACEÆ (MUSHROOM FAMILY).
Amanita muscaria.—The well-known fly amanita (fly fungus; deadly amanita) may be found from spring to early winter in pine forests throughout the United States. Cows are supposed to be killed by eating it, and almost every year the daily papers chronicle the death of several human beings who were led to eat the fungus through mistake for some edible species. The fresh cap is frequently rubbed up with milk and used to poison flies.
PHALLACEÆ (STINK-HORN FAMILY).
* Clathrus columnatus.—In an article published in the Botanical Gazette (Vol. XV. p. 45), Dr. Farlow, of Harvard University, gives an account of an investigation of a case of poisoning in hogs which was caused by eating this peculiar fungus. It grows in patches in oak woods and openings, and is quite common throughout the Southern States.
POLYPODIACEÆ (FERN FAMILY).
Pteris aquilina.—In July, 1895, nineteen cattle died in Maryland, which were supposed to have been poisoned by eating the common bracken fern. Very few similar cases are on record, but one European authority cites one in which five horses were killed by eating hay contaminated with this fern, and another states that cases are quite frequent among cattle in England.
EQUISETACEÆ (HORSETAIL FAMILY).
Equisetum arvense.—The field horsetail was reported from Connecticut in 1871 as being poisonous to horses. Cases are very rare, and it is probable that this plant is deleterious only when eaten in considerable quantity, and then perhaps only on account of its physical character. Experiments made in Europe show that a similar species (E. palustre) is fatal to horses when fed in considerable quantity with hay.
TAXACEÆ (YEW FAMILY).
Taxus minor.—The common yew, or ground hemlock, is called poison hemlock in some places. The leaves of this shrub are probably poisonous to stock, as are those of the European yew. This species is more accessible to stock than the western yew (Taxus brevifolia), which grows only in deep cañons.
YEW POISONING (TAXUS BACCATA).
The leaves of yew, when eaten in any considerable quantity, are very poisonous. Two ounces to eight ounces, according to the size of the animal, slow the heart’s action, produce weakness, staggering, and apoplectic congestion, which may have a fatal result in less than an hour. The bark is less injurious, and the fruit is scarcely poisonous at all.
The early symptoms, which are only seen in chronic cases, consist in excitement, followed by somnolence and muscular weakness, with slowing of the respiration and circulation.
POACEÆ (GRASS FAMILY).
Lolium temulentum.—The seed of the darnel, or poison rye grass, an introduced annual especially abundant on the Pacific Slope, is considered poisonous to both man and animals.
Stipa robusta.—This is a perennial plant which is known in Arizona and New Mexico as sleepy grass. It produces a narcotic effect on horses and cattle that feed upon it, but stock bred in that region rarely touch it.
Zea mays.—The numerous deaths that are frequently attributed to Indian corn are mostly due, not to any poison inherent in the plant, but rather to parasitic or saprophytic fungus growths, as noted under Aspergillus and Ustilago. The green fodder is very apt to cause severe and even fatal tympanites if the animal’s diet is not properly regulated. Death has also been attributed to the presence of nitre (potassium nitrate) in the growing stalks. It is supposed that in very rich soil this substance will sometimes accumulate in the stalks in considerable quantity during prolonged drought.
POISONING BY THE MALE TUFTS OF MAIZE.
The green tufts alone are toxic; the toxicity disappears after drying. Prolonged administration produces nephritic colic and renal lithiasis.
POISONING BY SWEET SORGHUM GRASS.
This form of poisoning is characterised by attacks of trembling, tympanites, and frequent attempts to urinate. The heart beats feebly, and the pulse grows progressively weaker, until at last it becomes imperceptible.
MELANTHACEÆ (BUNCH-FLOWER FAMILY).
* Chrosperma muscætoxicum.—The bulbous portion of the fly poison, or crow poison, an eastern plant, is sometimes eaten by cattle with fatal results. The bulbs, when crushed with molasses, are used to stupefy flies.
Fig. 75.—False hellebore (Veratrum viride), one-third natural size.
Fig. 76.—Lily of the valley (Convallaria majalis), one-third natural size.
* Veratrum viride.—The leaves of the common swamp hellebore (American white hellebore; false hellebore; Indian poke) of the eastern and northern portions of the United States have proved fatal to man and to horses. Sheep eat the young leaves and shoots with apparent relish. The seed is poisonous to chickens.
Zygadenus venenosus.—The name death camas has been applied to this plant in the North-West of America to distinguish it from the true camas (Quamasia quamash), which is highly esteemed for food by the Indians. In Oregon it is erroneously called “lobelia” by most stockmen and farmers. Horses, cattle, and sheep, as well as man, are poisoned by eating the bulb.
Zygadenus elegans.—The bulbs, and perhaps the leaves, of the Glaucous zygadenus, or alkali grass, are poisonous to cattle.
CONVALLARIACEÆ (LILY OF THE VALLEY FAMILY).
Convallaria majalis.—All parts of the lily of the valley are powerfully poisonous, and are liable to injure cattle and horses.
HÆMODORACEÆ (BLOODWORT FAMILY).
Gyrotheca capitata.—This is the red root, or paint root, of the Atlantic coast and Cuba, so called on account of the red colour of its sap. White hogs are supposed, throughout the Southern United States, to be particularly subject to the poison contained in the plant.
FAGACEÆ (BEECH FAMILY).
Quercus sp.—In Europe the acorns of various species of oak cause sickness and death in hogs and cattle. This effect may possibly be due to tympanites, but may also be due in some way to the tannin or the bitter principle which they contain.
POISONING BY ACORNS.
The acorn, or fruit of the oak (Quercus robur and Quercus sessiliflora), is much valued as a food for swine. “A peck of acorns a day with a little bran will make a hog, ’tis said, increase a pound weight per diem for two months together.” Though largely consumed by swine with no apparent ill effects, acorns constitute a dangerous food for young cattle, especially when eaten before they are ripe and when herbage or other feeding is scanty or restricted.
The symptoms comprise dulness, loss of appetite, constipation, followed by diarrhœa, with straining and colicky pains, head carried low, eyes retracted, with mucus about the eyelids and blood-stained discharge from the nose. Frequently the abdomen is distended. Temperature normal.
The lesions are, abrasions of the buccal membrane on the palate, cheeks, etc.; impaction and intense congestion of the omasum.
Treatment. Change of pasture. Alkalies—potash or soda bicarbonate, magnesia; tonics and stimulants.
URTICACEÆ (NETTLE FAMILY).
* Urtica gracilis.—The slender nettle covers thousands of acres of reclaimed swamp land in Michigan and Wisconsin, which is made nearly worthless by its dense growth, horses refusing to pass through it to cultivate the soil.
CHENOPODIACEÆ (GOOSEFOOT FAMILY).
Fig. 77.—Slender nettle (Urtica gracilis).
Sarcobatus vermiculatus.—Black greasewood, or chico, is a scraggy shrub which grows in strongly alkaline soil in the south-western and western portions of the United States. A correspondent in New Mexico states that on one occasion he counted as many as 1,000 sheep that had been killed by eating the leaves of this plant. It is claimed that cows are not affected by eating it at any time, and that sheep can eat it quite freely in winter. Death is perhaps due more to tympanites rather than to any poisonous substance which the plant contains.
PHYTOLACCACEÆ (POKEWEED FAMILY).
* Phytolacca decandra.—The leaves of the common pokeweed (poke; garget; American nightshade) of the eastern half of the United States is occasionally eaten by cattle with fatal results.
ALSINACEÆ (PINK FAMILY).
* Agrostemma githago.—The common corn cockle (cockle; mullein pink) is a weed common to both the United States and Europe. Poultry and household animals are occasionally poisoned by eating the seeds or the bread made from wheat contaminated with the seeds.
MAGNOLIACEÆ (MAGNOLIA FAMILY).
Illicium floridanum.—The leaves of this species of anisetree are supposed to be poisonous to stock.
RANUNCULACEÆ (CROWFOOT FAMILY).
* Aconitum napellus.—Aconite (monkshood; wolfsbane) is very commonly cultivated in gardens, and is therefore capable of doing great damage to stock. Horses and cattle have frequently been poisoned by eating the leaves and flowering tops.
* Aconitum columbianum.—The Western aconite, or monkshood, is native in the north-western portion of America, where it sometimes poisons sheep.
Anemone quinquefolia.—The common wind flower, which grows throughout most of the United States, is extremely acrid and poisonous. Cattle seldom touch it. The plant loses most of its poison in drying.
Fig. 78.—Pokeweed (Phytolacca decandra), one-half natural size.
* Delphinium tricorne.—The dwarf larkspur, or stagger weed, of the north-eastern quarter of the United States has been especially reported from Ohio as fatal to cattle in April, when the fresh leaves appear.
* Delphinium consolida.—The seeds of the commonly introduced field larkspur are well known to be poisonous; the leaves are known in Europe to be fatal to cattle.
* Delphinium menziesii.—The purple larkspur of the north-western quarter of the United States is very common throughout Montana. In one case of poisoning reported by Dr. E. V. Wilcox, of the Montana Experiment Station, over 600 sheep were affected, 250 of which were claimed to have been killed by the weed. An experiment made by Dr. S. B. Nelson, Professor of Veterinary Sciences in the Washington State Agricultural College, shows that it is possible to feed as much as 24¾ lbs. of the fresh leaves to a sheep within a period of five days without any apparent ill effect taking place. An experiment made by Dr. Wilcox shows that the extract from less than an ounce of the dried leaves killed a yearling lamb in two hours, the dose having been given by way of the mouth.
Fig. 79.—Corn cockle (Agrostemma githago). a, Sprays showing flowers and seed capsule, one-third natural size; b, seed, natural size; b′, seed, four times natural size.
Fig. 80.—Aconite (Aconitum columbianum). a, Flowering plant; b, seed capsule—both one-third natural size.
LARKSPUR POISONING IN SHEEP.[[3]]
[3]. The following account is summarised from a bulletin of the Montana Experiment Station by Dr. Wilcox.
Severe losses have from time to time been recorded, especially in America, from larkspur poisoning, the number of animals lost amounting to thousands. The first signs of poisoning are slight general stiffness and straddling gait, especially of the hind legs. The stiffness becomes more and more pronounced, until walking is difficult and evidently painful. Soon there are manifested various involuntary twitchings of the muscles of the legs and sides of the body, and loss of control or co-ordination of the muscles. Ordinarily there is no increase in the quantity of the saliva, no dribbling of saliva from the mouth, no champing of the jaws or attempts at swallowing. The sheep manifest none of the mental disturbances frequently seen in cases of poisoning from other sources, as for example loco weed and lupine. There is no impairment of the special senses. The sheep seem to hear and see as well and as correctly as under normal conditions of health.
No indications of any disturbances of the digestive functions are to be seen. The appetite remains good, and the sheep eat up to the very last. They were observed eating industriously during the intervals between the attacks of spasms which they have during the last stages.
At first the frequency of the pulse and of the respiratory movements is lessened and the temperature is lowered. The pulse remains very weak, but in the later stages becomes very rapid, in some cases 130 per minute. Toward the last also the respiration is very shallow and rapid. During the final convulsions the respiration is sometimes 120 per minute, but so shallow that the air is simply pumped up and down the windpipe. The air in the lungs is therefore not renewed, and the animal dies by asphyxia or suffocation.
So long as the sheep can stand on its feet, or walk, it keeps up with the flock as nearly as possible. The exercise, however, excites it, makes its respiration more rapid, and it has frequently to lie down for a moment and then get up and hobble along after the flock. The worst cases can thus easily be detected, since they straggle behind the rest of the flock.
The later stages follow rather rapidly. The involuntary movements become more frequent and more severe. All four legs tremble and shake violently. In fact, all the muscles of the body contract spasmodically until the animal totters over on its side and dies in the most violent spasms.
Larkspur has the effect of arresting the heart’s action and respiration and of paralysing the spinal cord.
Treatment. Place the animal by itself in a cool, quiet, shaded place and avoid all excitement. Of the drugs tested, atropine sulphate dissolved in camphor water has given the best results. Wilcox (Bull. 15, Montana Ex. Station) recommends for sheep from ¹⁄₂₀ to ¹⁄₁₅ grain in the earlier, and ⅙ to ¼ grain in the later convulsive stages. Cattle require from four to five times these doses. Inhalations of ammonia vapour, and small doses of alcohol and ether, are also useful.
Fig. 81.—Delphinium menziesii.
(To illustrate “Larkspur Poisoning.” From the Annual Report, U.S.A.
Department of Agriculture, 1898.)
Fig. 82.—Delphinium menziesii.
(To illustrate “Larkspur Poisoning.” From the Annual Report, U.S.A.
Department of Agriculture, 1898.)
Fig. 83.—Delphinium scopulorum.
(To illustrate “Larkspur Poisoning.” From the Annual Report, U.S.A.
Department of Agriculture, 1898.)
In other cases very good results have been obtained from giving permanganate of potash in the form of a drench: 5 to 10 grains for an adult sheep or pig, 15 to 20 grains for a horse, and 30 to 50 grains for an ox, dissolved in a pint or two pints of water.
Fig. 84.—Dwarf larkspur (Delphinium tricorne), one-third natural size.
Fig. 85.—Cursed crowfoot (Ranunculus sceleratus.)
* Delphinium geyeri.—The Wyoming larkspur is well known throughout Wyoming, Colorado, and Nebraska under the name of poison weed. It is reported to be the most troublesome plant to stock in Wyoming, the dark-green tufts of foliage being especially tempting in spring when the prairies are otherwise dry and barren.
Delphinium recurvatum.—This species of larkspur grows in wet subsaline soil in the southern half of California. It has been reported from San Luis Obispo county as fatal to animals.
Delphinium scopulorum.—The tall mountain larkspur of the Rocky Mountains has been reported to the Canadian Department of Agriculture as poisonous to cattle in the high western prairies of Canada.
Delphinium trolliifolium.—This plant is common throughout the coast region of northern California, Oregon, and Washington. In Humboldt County, Cal., it is known as cow poison, on account of its fatal effect on cattle. Its toxic character has been questioned. Perhaps it is not equally poisonous throughout all stages of its growth.
* Helleborus viridis.—The green hellebore is a European plant, sometimes self-sown from gardens. All parts of the plant are poisonous. Cattle have been killed by eating the leaves.
POISONING BY HELLEBORE.
Fig. 86.—Mandrake (Podophyllum peltatum).
This form of poisoning is of slow progress, the plant producing irritation of the digestive mucous membrane. The symptoms consist in loss of appetite, blackish, glairy diarrhœa, and intermittence of the pulse.
* Ranunculus sceleratus.—The cursed crowfoot, or celery-leafed crowfoot, is found throughout the eastern half of the United States and also in Europe. Cattle generally avoid all of the buttercups, but fatal cases of poisoning from this plant are recorded in European literature. When dried in hay, the plant appears to be non-poisonous. The bulbous crowfoot (R. bulbosus) and the tall crowfoot (R. acris) are well-known to be very acrid in taste, and it is probable that all of the species which grow in water or in very marshy land are poisonous.
POISONING BY RANUNCULACEÆ.
Poisoning only occurs when the green plants are eaten. Drying causes certain essences contained in them to disappear, and thus destroys their toxicity.
This form of poisoning is indicated by yawning, colic, blackish, fœtid diarrhœa, and rapid loss of strength.
The animals suffer from stertorous breathing, weakness of the pulse, and aberration of vision. They die in convulsions.
BERBERIDACEÆ (BARBERRY FAMILY).
Podophyllum peltatum.—The leaves of the common mandrake, or May apple, of the eastern half of the United States, are sparingly eaten by some cattle. Cases of poisoning are very rare, but the experience of one correspondent shows that the milk from a cow that had been feeding on the plant off and on for about three weeks was so extremely laxative as to be positively poisonous. The accident occurred to a baby, fed exclusively on cow’s milk. The physiological effect of the milk was precisely like that of mandrake. It was shown that the cow ate the plant, which was abundant in one pasture, and when the animal was removed to a pasture free from the plant the child’s illness stopped at once.
BUTNERIACEÆ (STRAWBERRY-SHRUB FAMILY).
Butneria fertilis.—The large oily seeds of the calycanthus, or sweet-scented shrub, contain a poisonous alkaloid, and are strongly reputed to be poisonous to cattle in Tennessee.
PAPAVERACEÆ (poppy family).
Argemone mexicana.—The Mexican poppy is reputed to be poisonous to stock both in the United States and in New South Wales. The seeds are narcotic, like opium.
* Chelidonium majus.—The yellow milky sap of the celandine, an introduced weed common in the eastern United States, contains both an acrid and a narcotic poison. Both are powerfully active, but cases of poisoning are rare, as stock refuse to touch the plant. Reeks, of Spalding, however, describes (J. Comp. Path. and Therap., Dec. 1903, p. 367) an outbreak of poisoning by common celandine in which twenty-one valuable cows were affected and three died. The symptoms comprised excessive salivation and thirst, convulsions, unconsciousness and epileptiform movements.
* Papaver somniferum, opium poppy, or garden poppy: P. rhœas, field poppy, red poppy, or corn poppy.—These plants are sometimes self-sown from gardens. Both contain acrid and narcotic poisons, and European literature records the death of various animals from eating their leaves and seed pods.
POISONING BY POPPIES.
The consumption of poppies causes arrest of peristalsis, secretion of foamy saliva, colic, depression, coma, and in severe cases death by stoppage of respiration.
PRUNACEÆ (PLUM FAMILY).
* Prunus caroliniana.—The laurel cherry, or mock orange, is native in the south-eastern quarter of the United States, and is there often cultivated for hedges. The half-withered leaves and the seeds yield prussic acid, and are poisonous when eaten by animals.
Fig. 87.—Black cherry (Prunus serotina), one-third natural size.
* Prunus serotina.—The wild black cherry is a valuable forest tree which ranges throughout the eastern half of the United States. Cattle are killed by eating the partially withered leaves from branches thrown carelessly within their reach or ignorantly offered as food. The leaves of various other wild and cultivated cherries are probably poisonous to cattle in the same way.
VICIACEÆ (PEA FAMILY).
Aragallus lambertii.—The Lambert, or stemless loco weed, is, next to the following species, the best known representative of a large group of closely related plants which are native to the western half of the United States, and are known as loco weeds on account of the peculiar excited condition which they induce in animals that eat of their leaves. Horses and cattle are both affected, but the chief damage is done to horses. After being permitted to graze on any of these plants the animal acquires an unnatural appetite for them, and soon refuses all other kinds of food. It rapidly becomes unmanageable, shows brain symptoms, and finally dies from lack of proper nourishment.
Astragalus mollissimus.—This, the woolly loco weed, is perhaps the best known of all the loco weeds. It is the species most abundant in Colorado, where from 1881 to 1885 nearly $200,000 was paid out in bounties in an attempt to exterminate it. The plant is still abundant in that State, and reports of the damage done by it continue frequent. Specimens of the three following species of Astragalus have been forwarded to the Division of Botany with the information that they were causing great financial loss in the districts noted. It is quite probable that other species are dangerous also.
Fig. 88.—White loco weed (Aragallus spicatus) in flower.
(From the Annual Report, U.S.A. Department of Agriculture, 1900.)
Fig. 89.—White loco weed (Aragallus spicatus), showing seed pods.
(From the Annual Report, U.S.A. Department of Agriculture, 1900.)
Fig. 90.—Loco weed (Astragalus splendens).
(From the Annual Report, U.S.A. Department of Agriculture, 1900.)
POISONING BY WHITE LOCO WEED (ARAGALLUS SPICATUS).
Fig. 91.—Stemless loco weed (Aragallus lambertii). a, Flowering plant; b, seed pods; c, cross-section of seed pod—all one-third natural size.
Fig. 92.—Woolly loco weed (Astragalus mollissimus). a, Whole plant; b, section of pod—both one-third natural size.
This is an erect tufted perennial, 4 to 18 inches high, with pinnately divided leaves and spikes of white or cream-coloured flowers, shaped like those of the pea. The pod is one-celled, and when shaken produces a rattling sound, which gives the plant the name of “rattle weed” in some localities. The white loco weed is exceedingly common throughout Montana. It occurs most abundantly on the northern slopes of foothills up to an altitude of about 8,000 feet. Its preferred habitat is for the most part in rather dry situations. The habit of the plant varies in different parts of Montana. In some localities the flowers are pure white, while in others they are decidedly yellow.
In Colorado the plant which is most ordinarily known as loco weed is Astragalus mollissimus, while in Montana the species already named is perhaps most important; but there are others which have a rather wide distribution and are known to produce the same effects. Among these may be mentioned A. splendens, A. lagopus, and A. besseyi.
The losses caused from the loco disease are very heavy in nearly all the Rocky Mountain States. The locoed condition is so commonly observed among sheep and horses that cases are not reported, and it is practically impossible to learn the exact extent of the disease. In the Judith Basin one prominent stockman was nearly ruined financially by the prevalence for a number of years of the loco habit among his sheep. In another instance the raising of horses was abandoned over a large tract of country on account of the loco weeds.
The loco disease occurs under two forms—an acute and a chronic. An acute case of loco disease was observed by Dr. Wilcox in a two-year-old ewe with a lamb at its side. The ewe was observed eating large quantities of white loco weed on May 22nd, 1900. During the afternoon of the same day it became unmanageable, and the lamb was badly affected. An examination of the ewe at this time showed that it was completely blind and was affected with dizziness. It walked around in long circles to the right, and after a short period remained standing for a few moments in a sort of stupor. At the beginning of each attack the head was elevated and drawn to the right; eyelids, lips, and jaws were moved rapidly. Each attack lasted from one to two minutes and the intervals between the attacks lasted about five minutes. The second day the attacks became more severe and of longer duration, the head being turned more decidedly to the right and the animal sometimes falling upon the ground. Similar symptoms, accompanied by digestive disturbances, were manifested by the lamb during the second day, and it died during the afternoon. On the morning of the third day it was found that the ewe was pushing against the fold, and had apparently been in that position during the greater portion of the night. The animal then began to whirl round to the right. Later it became unable to stand, and the spasmodic movements were largely confined to the legs. On the morning of the fourth day it died. The pupil of the eye was at no time dilated, and the expression was nearly normal. The pulse was at first very irregular, but on the second day became again regular and of normal frequency. The only remedy which was tried was frequent injections of one-quarter grain doses of morphine, but this was without effect. Two other ewes ate smaller quantities of loco weed at the same time and were similarly affected, but less severely. In these cases morphine was tried with better success. The lambs, however, died from the poisonous properties contained in the milk of the mother.
The general symptoms of loco disease are quite familiar to all stock raisers. Perhaps the most characteristic are those of cerebral origin, and are shown in peculiarities of gait and action, which may be compared to a drunken condition. The brain disturbances may consist in impairment of the special senses or in irregular motor impulses, which produce incoherent muscular action. In some cases the animal becomes blind. More frequently the animal makes errors in judgment of the size and distance of objects. These visual disturbances are often quite ludicrous. The animal often takes fright, apparently at imaginary objects, or at objects which under ordinary circumstances would cause no alarm. Locoed horses are somewhat dangerous for driving purposes on account of their tendency to run away. Such horses are frequently attacked with kicking fits without any apparent cause. The sense of hearing is often affected, and the response to sounds is irregular and out of proportion to the volume and character of the sound. Irregularities in muscular movements of sheep may assume a variety of forms. The animal may simply carry its head in an extended or otherwise unnatural condition. In some cases the back is arched. Trembling is a characteristic symptom. In locoed horses a great difficulty is sometimes experienced in persuading them to go backward. Locoed sheep are exceedingly difficult to manage. The different members of the flock may suddenly take a notion to run away in different directions, with the result that it is almost impossible for the shepherd to prevent their becoming separated. In cattle the disease appears to be rare, although symptoms, so far as observed, are essentially the same as those in sheep and horses. Occasionally locoed cattle manifest dangerous symptoms, and attack men and other animals.
In chronic cases of loco the animal gradually becomes more emaciated and crazy. In sheep the fleece may be shed in patches or as a whole. The animal becomes unable to care for itself, and is apt to fall into the water while attempting to drink. Fits of trembling are of frequent occurrence, and the animal finally dies of inadequate nutrition and total exhaustion. In chronic cases of loco disease in horses the animal is usually left to its own resources on the range. During the later stages it may remain for weeks at a time upon a small area of ground without taking water. Dr. Wilcox saw a number of such cases in horses that were almost unable to walk. Under such circumstances the animals seldom or never lie down. One horse which was seen remained for a period of two weeks, in 1897, upon a piece of ground about 150 feet square. During this time the horse had no water.
Numerous autopsies on locoed sheep and horses revealed slight congestion of the brain membranes in all cases. The lungs and heart were in normal condition. Fatty tissue was considerably reduced in quantity, and the muscles were paler in colour than under normal conditions.
The most serious mistake in connection with loco disease is made in allowing locoed sheep to remain with the rest of the flock. The loco habit is apparently learned by imitation of locoed animals, and so long as locoed sheep are allowed to remain with other sheep the loco habit rapidly spreads. An experienced sheep raiser, after being nearly ruined financially through the loco disease, adopted the method of immediate isolation and the feeding of locoed sheep for mutton. His stock was replaced with sheep that were free from the loco habit, and the trouble has been entirely eradicated from his range.
No specific remedy for the loco disease has been discovered, and in the nature of the case no such remedy is likely to be found. In the present state of knowledge concerning the subject the only rational treatment to be recommended is that of confinement and feeding with a nutritious diet. By separating the locoed sheep at once from other sheep the spreading of the habit will be prevented, and the locoed animals may be fattened and thus prevented from becoming a total loss. Although locoed animals may readily be fattened and sold for mutton, their recovery from the loco habit is apparent only, and is due to their inability to obtain the loco weed. Such animals when allowed to run upon the range again almost invariably return to their old habit of eating loco weed. Animals which have once been locoed are, therefore, unsuitable for stocking the range.
In combatting the loco disease the most rational methods include providing salt for the sheep, the immediate removal of locoed sheep from the band, confining them in a fold, and feeding them upon a nutritious diet. They may thus be fed for market, and their pernicious habit will not spread to other sheep. In the case of locoed horses, an apparent recovery takes place if they are confined in a stable and fed on ordinary cultivated forage or allowed to run in pastures where no loco weeds are found. Such horses are always somewhat dangerous, and more apt to run away or become unmanageable than horses which have not become affected with this disease.
* Crotalaria sagittalis.—The rattlebox (rattle weed; wild pea) is an annual weed which grows on sandy soil throughout most of the eastern half of the United States. In some years it is especially abundant in the bottom lands of the Missouri Valley. Horses and sometimes cattle are killed in this region by eating grass or meadow hay which is contaminated with the plant.
Fig. 93.—Rattle box (Crotalaria sagittalis). a, Whole plant; b, cross-section of seed pod—both one-third natural size.
Lupinus leucophyllus.—This herbaceous shrub is a representative of a very large genus of plants, many of which are widely and abundantly distributed throughout the western United States, and are generally known as lupines. The above species is very abundant in Montana, where it is said to have caused the death of a very large number of sheep. There is some question whether the animals are killed by a poisonous constituent of the plant or merely by tympanites. The seeds of all the lupines are probably deleterious in the raw state. In Europe, however, the seeds of Lupinus albus, after the bitter taste has been removed by steeping and boiling, are eaten by human beings as well as by cattle.