SEMIOLOGY OF THE ORGANS OF CIRCULATION.
The semiology of the circulatory apparatus comprises the clinical examination of the heart, arteries and veins, and the examination of the pulse and blood.
Heart. In animals of the bovine species, the heart is situated in the thoracic cavity opposite the third, fourth, fifth and sixth ribs, nearly in the median plane of the thorax, and inclined from front to back at an angle of 70 degrees.
The pericardial sac touches the extremity of the sternum where it is in immediate contact with the lower insertion of the diaphragm. This peculiar arrangement favours the development of pericarditis due to foreign bodies.
On the left side the pericardial sac may come in direct contact with the internal surface of the thoracic cavity opposite the lower extremity of the third, fourth, and sometimes fifth ribs. At all other points the pulmonary lobes, as expanded during inspiration, separate it from the thoracic wall.
Although the pericardium and heart are situated in the median plane, percussion and auscultation should be performed on the left side, since the anterior and cardiac lobes of the left lung are less developed than those of the right; but the heart can be auscultated on the right side, as is advisable at times.
In the healthy ox there exists an area of the left thoracic wall which may be called the cardiac zone, on a level with which are heard the normal heart sounds. In diseased conditions this zone or area may vary in size, and the sounds may be modified.
The heart can be examined by inspection, palpation, percussion, and auscultation.
Under ordinary conditions inspection reveals nothing in well-nourished animals; but in very thin subjects and in those suffering from recent cardiac lesions or pseudo-pericarditis, a rhythmic movement of the chest wall is sometimes detected.
Palpation is performed by placing the open hand on the cardiac zone. In this way the cardiac shock can be felt, its degree of intensity judged, and, in an imperfect manner, its rhythm.
Percussion by means of the fingers or a pleximeter discloses the extent of the physiological area of partial dulness, due to the presence of the heart, as well as its variations in pathological conditions, particularly in pericarditis with marked exudation.
Fig. 173.—Schema of a section through the chest opposite the heart. Pg, Left lung; Pd, right lung; cp, right and left pleural cavities; P, pericardium; l, l1, cardiac lobes of the lung interposed between the pericardium and thoracic wall.
In such cases there may even be complete dulness when the distended pericardium thrusts upwards the corresponding pulmonary lobe, and comes in contact with the internal surface of the thoracic wall, or, in cases of pericardial pneumatosis, exaggerated resonance, and a tympanitic sound.
Auscultation is carried out either directly or by the stethoscope or the phonendoscope. The normal or pathological sounds of the heart are thus ascertained, as well as the intensity of the cardiac beats and sounds, the frequency of the rhythm, etc.
When injuries have occurred which cause murmurs, it is best to use the stethoscope and to apply it at the points where murmurs are heard at their maximum intensity, i.e., exactly at the spot where the cardiac shock is noted, and towards the base, in the region where the great arterial trunks begin.
In the latter case it is often useful to draw the left fore leg forward.
Arteries. The arteries are rarely the seat of lesions that can be detected by examination, and therefore such examination is usually limited to noting the state of the pulse.
Arteritis and thrombosis of arteries are rare, and although lesions of atheroma have been discovered in certain chronic diseases, such as tuberculosis, chronic diarrhœa, etc., they are difficult to detect, even on examination per rectum of the bifurcation of the aorta.
Pulse. The examination of the pulse, on the contrary, is of great importance. In animals of the bovine species the pulse may be taken at a number of different points, such as the submaxillary artery, on the side of the lower jaw: in the case of very thin animals at the radial within and in front of the elbow joint; at the internal saphenous artery, at the height of the mamma or scrotum; or at the coccygeal artery, at the base of the tail.
This examination reveals the frequency (50 to 60 per minute), the quality, whether strong, feeble, imperceptible, etc., the regularity, etc., etc.
Veins. The veins are more easily examined than the arteries, on account of their superficial position in most cases.
Inspection and palpation are the only means of examination.
Inspection shows the degree of fulness or collapse, and also the existence or absence of what has been termed venous pulse.
Venous pulse occurs only at the lower extremity of the jugulars. It is very frequent in animals of the bovine species, and in thin animals is not necessarily a pathological symptom. It is due to reflux of blood in the anterior vena cava, under the influence of the expiratory effort; sometimes to emphysema, tuberculosis, etc.; in other cases to the return of blood towards the vena cava and jugulars at the moment of auricular systole, as a result of lesions of the tricuspid or auriculo-ventricular orifices.
By palpation of the veins their permeability can be estimated, also the degree of distension or obstruction, and the condition of their contents.
Capillary system. Among methods of arriving at the state of the circulatory system must be included an examination of the vascular condition of the accessible mucous membranes, such as those of the eye, mouth, nostril, vulva, etc. This examination is easy to carry out, and is of value in diagnosing congestive states, pneumonia, and local inflammation.
Blood. Examination of the blood is sometimes necessary for the exact diagnosis of certain diseases, and therefore should be carried out whenever occasion requires. The physical state, coloration, and rapidity of coagulation afford valuable data in certain diseased conditions, and indicate the approximate richness in hæmoglobin, the normal or abnormal composition of the plasma, and the richness of the blood in white corpuscles.
Microscopic examination is still more valuable, whether carried out by the moist method, in which a drop of blood is compressed under a cover glass, or the dry method with or without staining. In the latter case the specimen is fixed with a mixture of equal parts of alcohol and ether or by immersing it in a 1 per cent. solution of osmic acid.
By this means it is possible to detect the condition of the red and white blood corpuscles and hæmatoblasts; the existence or non-existence of leucocytosis and its degree, as well as the existence, for instance, of leucocythæmia.
The blood corpuscles may also be counted.
Histological examination, supplemented by suitable staining, reveals the presence of normal or abnormal blood corpuscles, parasites such as piroplasma, or microbes such as bacteria.
Such examination necessarily presupposes a knowledge of what should be looked for in the normal state.
In normal blood the red blood corpuscles predominate. They are all similar in form and, with few exceptions, of the same size. They stain strongly with acid solutions such as eosine. In pathological conditions, large or giant corpuscles may be found (macrocytes), as well as those of medium size (normal) and small size (microcytes). Some are vigorous and stain deeply; others, on the contrary, are degenerating or dead, and have no greater affinity for one constituent than for another of the double or triple stains commonly employed.
In pathological conditions the hæmatoblasts occur in very varying numbers.
The white blood corpuscles found in health may be classified as follows:—
Large and small lymphocytes, each of which has a round voluminous nucleus and a narrow border, and contains a non-granular protoplasm; their proportion varies between 22 per cent. and 25 per cent.:
Polynuclear leucocytes or polymorphous leucocytes with a single nucleus, which originate in bone marrow, stain best with neutral colours, and are present in the proportion of 70 per cent. to 72 per cent.:
Mononuclear leucocytes with an ovoid eccentric nucleus stain best with basic colours, and form about 1 per cent.:
Polynuclear leucocytes stain best with eosine or acid colours, and form about 1 per cent. to 2 per cent.
When these white blood corpuscles are in larger number the condition is known as leucocytosis, and when one or other variety is in very great excess the condition is known as leucæmia.
CHAPTER I.
CARDIAC ANOMALIES.
ECTOPIA OF THE HEART.
Ectopia of the heart, i.e., congenital malformation in which the heart is displaced from its normal position and thrust sometimes completely beyond the thoracic cavity, is not very rare. The heart may be well developed, but it is not enclosed by the thoracic walls when the thoracic cavity closes during the first stages of embryonic life. The sternum, which is cartilaginous and becomes ossified only at a later period, remains fissured along the median line, and the fissure, usually of oval form and with rounded margins, surrounds the auricles and the vessels at the base of the heart. The ventricles form a hernia projecting beyond the thorax, which then only contains the two pleural sacs and a complete mediastinal partition. The pericardium remains undeveloped.
Despite this malformation, the embryo develops. The fœtus may in due season be brought forth living, but as a rule death occurs in a few hours.
The diagnosis is easy, but this malformation cannot be treated. All that can be done is to protect the ectopiated organ against external violence in cases where the young creature is born alive.
CHAPTER II.
PERICARDITIS.
Pericarditis consists in inflammation of the pericardial sac. It is attributable to different causes, varying in importance and in causation.
Specific pericarditis may be produced by the tubercle bacillus, or it may develop during an attack of contagious peripneumonia. Tuberculous or peripneumonic forms of pericarditis as a rule form only complications of chronic pulmonary tuberculosis or peripneumonia. They are very rarely primary in character, and, like the allied forms of pleurisy, assume a vegetative and adhesive form in tuberculous cases.
Moussu has never seen the true exudative form either in acute or chronic tuberculosis, but only vegetative and caseous forms.
Simple acute pericarditis. Cases of simple acute exudative pericarditis have been described, and have been referred to chills, wounds, or injuries in the region of the heart, and in a few cases to the rheumatic diathesis.
Such forms of pericarditis may occur, but probably are very rare, for Moussu has seen but two cases. As the symptoms correspond exactly to those of exudative pericarditis produced by a foreign body, it is unnecessary to describe them specially.
The only important detail to bear in mind with this disease is the possibility of cure by suitable treatment, such as the application of stimulants or vesicants to the cardiac zone, the administration of salicylate of soda or diuretics, and complete rest.
The diagnosis, moreover, should be confirmed by making an aseptic exploratory puncture with the capillary trocar. The nature of the liquid withdrawn will indicate whether the case is one of simple acute pericarditis or pericarditis due to a foreign body.
Cancerous pericarditis is generally secondary, and is caused by development of tumours on the pericardial serous membrane, and in the myocardium. Moussu, however, has seen one case of primary cancerous pericarditis, the tumours being found only on the periphery of the myocardium. The growth assumes a vegetative form with moderate exudation. The symptoms, however, so closely approach to those of exudative pericarditis due to foreign bodies that only the latter variety, which is by far the most frequent in animals of the bovine species, need be described.
EXUDATIVE PERICARDITIS DUE TO FOREIGN BODIES.
Fig. 174.—Tumours of the surface of the heart. Primary cancerous pericarditis and myocarditis.
This condition has been erroneously described as traumatic pericarditis, but the latter term would suggest that the disease was due to an injury acting from without. It may be defined as a disease produced by the discharge into the pericardial cavity of some foreign body from the gastric compartments.
Boizy in 1858 described several cases of this kind of pericarditis. Hamon in 1866 gave an excellent table of symptoms. Roy in 1875 supplemented this with numerous observations showing clearly the possibility of recognising the disease by clinical examination. Pericarditis due to foreign bodies is to-day one of the best characterised diseases of the ox, and it is easy to diagnose.
Before approaching the etiological side of the question, it is necessary to recall in a few words the anatomical arrangement of the pericardium and its relations to neighbouring organs.
In the ox the diaphragm presents a marked concavity directed towards the abdomen. The pericardium, situated exactly in the median plane, is fixed by its point to the sternum. A fold of adipose tissue directly connects it with the anterior surface of the diaphragm. On the abdominal side the conical right compartment of the rumen is in free communication with the reticulum, which is closely applied to the posterior surface of the diaphragm on the median line opposite the spot occupied by the pericardium on the anterior surface (Fig. 176). As a result of this arrangement any object passing through the reticulum and diaphragm in the median plane would enter the pericardial cavity. These particulars indicate clearly how this form of pericarditis is produced.
Causation. One of the chief causes of pericarditis by a foreign body is connected with the way in which oxen feed. They rapidly swallow their food and any foreign bodies that may be concealed in it, submitting it later on to a second mastication in the course of rumination. This method of feeding results in bolting the food almost without mastication, hence the possibility of swallowing foreign bodies.
The proximity of the reticulum to the pericardium is also an important factor, because the foreign bodies fall into the reticulum as soon as the bolus of food begins to break up. It is important to notice, moreover, that pericarditis is commonest on farms where the oxen are attended by women, or in regions where sharp objects are to be found on roads or pastures frequented by the animals, such as the vicinity of needle, nail, and rivet factories.
The sole cause is the penetration of a foreign body into the pericardial sac.
Pathogeny. All kinds of foreign bodies are swallowed by oxen, as is abundantly shown by post-mortem examinations. These indigestible bodies pass with the food into the rumen, and accumulate in the deepest portions of that receptacle. Owing to physiological contractions the lower wall of the rumen rises to the level of the orifice of communication with the reticulum, and so passes much of the material accumulated within it into this organ.
Soft foreign bodies fall towards the lower parts of the reticulum, but sharp objects may lodge in its walls. Very often the bodies penetrate in this way without causing reticulitis or grave inflammation. The functions of the reticulum are not impeded. The commonest of such objects are needles, pins, nails, or fragments of iron wire. On account of their form, needles are the most dangerous. The sharpness of one extremity ensures its passing readily through the tissues, and as the point is the part that offers least resistance, the needle continues gradually to penetrate.
If the foreign body becomes implanted vertically in the lower wall of the rumen or reticulum it may be expelled directly through the medium of an abscess. This is a favourable termination, though it usually results in permanent gastric fistula.
More often the objects penetrate the anterior wall of the reticulum and gradually work their way towards the diaphragm, impelled by the movements of the reticulum and the other digestive compartments. They perforate the muscle and pass into the thoracic cavity, either in the direction of the pericardium or of the pleural sacs.
First as to the penetration of the pericardium. The foreign body, whatever it may be, produces by its presence alone very marked irritation, and as in addition it is always infected in consequence of its having passed through the digestive compartments, inflammation is set up to a degree proportionate to the pathogenic qualities of the infective agent.
Symptoms. The early symptoms are those of indigestion, and not of pericardial disease, a fact which is easy to understand, because at first the whole mischief is in the abdominal cavity. The patients are dull, restless, and seem to be suffering from an obscure ailment. They remain standing more than usual, show more than ordinary deliberation in lying down, lose appetite, cease to ruminate regularly, and exhibit intermittent tympanites.
The cause of these symptoms is as follows: At first the reticulum is partly immobilised by the local inflammation, and at a later stage movement of the diaphragm is checked by reflex action when the sharp body has progressed far enough to touch it. The rhythmic movements of the reticulum and the diaphragm are interfered with, rumination is disturbed, eructation ceases, and tympanites appears.
The patient often utters slight groans, particularly when forced to move; but as this is a sign common to all grave diseases it can only give rise to a suspicion as to what has occurred. In ten to fifteen days this primary phase may have terminated; but it is impossible to say how long it lasts, for it varies with each animal as with each variety of foreign body, and it may be prolonged for months.
From the moment it reaches the thoracic cavity the foreign object makes its way towards the channel formed on either side by the ribs and below by the sternum, and therefore towards the point of the heart. This is the second phase of development.
The passage of the foreign body through the diaphragm occupies a more or less considerable time, depending on its length; the beginning of this second phase is characterised by relative immobility of the circle of the hypochondrium during respiration. The abnormal sensibility and pain impede contraction of the diaphragm.
Palpation of the region of the xiphoid cartilage then reveals abnormal sensibility, and sometimes causes the animal to resent being handled.
From this time the pericardial symptoms proper commence, the foreign body having come in contact with the pericardium. This phase, unlike those which precede it, presents well-defined symptoms. The irritation of the heart and its ganglionic system by a foreign body in the pericardium is shown by considerable acceleration of the heart beats even before there is any exudation into the pericardial sac. Instead of 60 to 70 beats, the normal number, the pulse may rise to 80, 90, 100, or even 110 beats per minute. The heart sounds are tumultuous, dull and ill-defined, while the pulse appears bounding and strong.
But this period of cardiac excitement while persisting is soon complicated by other symptoms. As soon as the foreign body penetrates the pericardial sac, there is infection, which produces an active form of inflammation and abundant exudation. From this time the pulse becomes weaker and weaker, until, under the steadily increasing pressure on the heart, it is almost imperceptible.
There is only moderate fever. As soon as the exudation becomes considerable, the symptoms of pericarditis grow very marked: they may be grouped in the following order, according to their importance.
A. Cardiac symptoms. On palpation of the cardiac zone on the left the impulse of the heart is no longer felt. Percussion, which under normal circumstances reveals only partial dulness, now seems to give pain, and indicates abnormal dulness distributed in a vertical plane. The pulmonary lobes between the pericardium and thoracic walls are thrust upwards. The distended pericardial sac approaches the parietal layer of the pleura and may adhere to it, hence the dulness. This dulness extends as far back as the xiphoid appendix of the sternum, and can be detected on both sides, marginated above by a convex line.
In rare cases the dulness is absent, being partially replaced by tympanitic resonance, due to the presence of gases in the distended pericardial cavity, which gases originate in the digestive reservoirs or result from putrid fermentation of the pericardial exudate.
Simple or double pleurisy, or even pneumonia of the cardiac lobes resulting from infection by contiguity, may complicate cases of rapid pericarditis. The dulness then appears modified, as do the signs observed on auscultation.
Auscultation furnishes valuable indications. From the outset it reveals acceleration of the heart. At a later stage, but only for a short time, it permits of the detection of the pericardial rubbing sound which precedes serous exudation, and which may persist for several days when large quantities of false membrane are produced.
If exudate is present in considerable quantities a liquid sound is heard at each heart beat. The heart appears to be beating in water, but the liquid note varies considerably. It has been termed the “claclaque” sound (Lecouturier, 1846), in allusion to the sound produced by the meeting of water ripples; “clapotement” sound (Boizy, 1858), with reference to the sound produced under the influence of a light breeze on the borders of a stream; “glou-glou” sound (Roy, 1875), suggested by the noise of liquid escaping from an inverted bottle into a resonant vessel, etc. It is important, however, to remember that cases occur (principally when the pericardium is greatly distended and entirely filled with liquid) where, with the animal at rest, these sounds are difficult to detect. To render them noticeable the patient must be walked for a few yards.
Vernant, again, has described a sound as of dripping water, of quite special character; he compared it to that resulting from the fall of drops of liquid on to a marble table or into a half-filled vessel. So far as can be ascertained this sound of dripping water greatly resembles that heard in pneumo-thorax, but it is less resonant and less prolonged.
It appears to be characteristic of the presence of air in the pericardial cavity, and its special quality varies with the quantity accumulated in the pericardium. Masked by these pericardial sounds the beating of the heart seems dull, badly defined, distant and stifled.
Fig. 175.—Appearance of a patient suffering from fully-developed pericarditis.
B. Jugular symptoms. The “jugular” symptoms are secondary, and result from the accumulation of liquid in the pericardial cavity. No intra-pericardial exudate can exist without exerting pressure on the heart, and as the auricles have very thin walls and are more compressible than the ventricles, this pressure immediately causes difficulty in the return circulation, whence venous stasis, varying in intensity, but clearly visible and appreciable on account of the distension of the jugulars.
The venous stasis is general, for the pulmonary veins are as much compressed as the posterior and anterior venæ cavæ, but it is only apparent in the large superficial veins. This stasis is accompanied by venous pulse, and particularly by peripheral or internal œdema, œdema of the lung, intestine, mesentery, etc., of the submaxillary space and of the dewlap and entrance to the chest. Œdema of the submaxillary space is specially characteristic, for it appears almost first amongst external signs. That of the dewlap follows at a later stage, and extends backwards as far as the umbilicus, rising above this point as high even as the entrance to the chest and the axillary region.
C. Pulmonary symptoms. The pulmonary symptoms result from difficulty in the return circulation and from the venous stasis. They are due to passive congestion and œdema of the lung or to hydro-thorax. At rest the respiration may appear fairly regular, but at the least movement it is accelerated, and may rise to 40 or even 60 per minute.
Percussion reveals lessened resonance of the parts, and in the case of hydro-thorax dulness marginated by a horizontal line, as in pleurisy.
On auscultation the vesicular murmur may sometimes have diminished or even disappeared, while the respiration may be blowing, as in active congestion, and in exceptional cases a tubal souffle may be observed. In most cases the animal has a paroxysmal, somewhat frequent cough, due to reflex irritability of the pneumo-gastric.
Cruzel in addition mentions a double respiratory movement like that produced in the horse by broken wind. This is really the result of hydro-thorax, and is not a constant symptom.
D. General symptoms. When the disease has lasted a certain time the patients show certain well-marked general symptoms: they remain standing in one position for long periods, with the head and neck extended, the front legs thrust outwards from the trunk and the body rigid, as though the least movement caused them pain. The general attitude expresses anxiety, the animals lie down with great care and seldom remain long in this position, which interferes with the functions of the heart and lung. In the last stages the animals remain constantly standing, appetite is almost entirely lost, and they waste rapidly.
The course of pericarditis due to foreign bodies is very variable. Sometimes death occurs in eight or ten days. In other cases the animal may survive for weeks, provided it is well tended. Everything depends on the rapidity with which the foreign body moves and on the character of the infectious organisms which it introduces into the pericardium. Death is the inevitable termination, and occurs as a consequence of cardiac and respiratory syncope. It may follow suddenly as the result of a simple forced movement, even when the animal still seems to retain some amount of strength. When the organisms introduced into the pericardium are of marked virulence, complications such as septic pleurisy and pneumonia may be observed, and death soon takes place.
It has been suggested that recovery might follow a return of the foreign body towards the reticulum. This view can only have been advanced as a consequence of errors in diagnosis, either as to the existence of pericarditis or as to its nature. Pericarditis due to cold or rheumatism sometimes becomes cured spontaneously.
Death, again, may suddenly occur by syncope when the foreign body penetrates the myocardium, passes through it, and enters the ventricular cavities.
The return of the foreign body is not conceivable, at all events after it arrives in the pericardial cavity. Up to that time the only disturbance is of a digestive character; no pericarditis exists. But when for example the disturbance is due to long fragments of iron wire which may extend from the reticulum as far as the pericardium, it is clear that the pericarditis is of a kind which cannot be cured without leaving traces. In our opinion, natural recovery is impossible.
Diagnosis. The diagnosis of pericarditis cannot be made until such pericarditis actually exists, i.e., until the disease has arrived at the third stage of development mentioned above.
As long as the symptoms point only to the first or second stage, the logical diagnosis is reticulitis produced by a foreign body. At this time the development of pericarditis, although possible, is not inevitable.
When, on the other hand, one knows how the digestive disturbance has originated and developed and thereafter notes signs of cardiac irritation, disappearance of the cardiac impulse, dulness of the heart sounds, venous stasis, etc., the diagnosis is easy even thus early.
Mistakes are not very likely. Only in some cases are they liable to occur, as in acute peripneumonia of the anterior pulmonary lobes, causing compression of the pericardium of the anterior vena cava and producing secondarily venous stasis and œdema of the dewlap. Cases of specific pericarditis due to peripneumonia also occur, and under such circumstances a mistake would be even more excusable. Nevertheless, the temperature curve in itself is a sure indication, for whilst in peripneumonia the fever is always very marked, it is scarcely noticeable in pericarditis due to a foreign body.
When the diagnosis of pericarditis has been arrived at it is desirable to determine the exact nature of the disease, for whilst cases of pericarditis due to foreign bodies are incurable and in the interest of the owner the animals should be slaughtered, pericarditis due to cold or rheumatism may be successfully treated. Rheumatism generally affects the synovial membranes even before it produces pericarditis, and this indication, supplemented by the history of the case usually ensures one against mistakes regarding the initial cause.
It is much more difficult to distinguish pericarditis due to a foreign body from pericarditis due to carcinoma and from the forms of pseudo-pericarditis produced by lesions in the neighbourhood of the heart. When considering the latter we shall deal with this particular point.
Prognosis. The prognosis is always fatal.
Lesions. When the foreign body is very thin and sharp, the reticulum may not become attached to the diaphragm. In such cases its passage has been rapid and the tissues have healed.
Usually the reticulum, diaphragm and pericardium are united by a mass of fibrous tissue as thick as a man’s arm. It resembles a fibrous sleeve surrounded by an œdematous zone, usually of slight extent. This mass of new fibrous tissue is traversed by a sinuous tract resulting from the irritant action of the foreign body on the surrounding tissues. All writers describe this fibrous sleeve, which, however, only occurs in cases where a very long foreign body has occupied a considerable time in passing from the reticulum to the cavity of the chest.
In very exceptional cases the sinuous tract is ramified, possibly as a result of displacements of the foreign body.
The orifices of the tract are to be found, one in the reticulum, the other in the pericardium. On the side of the reticulum there is never more than one opening, and in many instances the tract is already closed on that side, either by exuberant granulations or by a cicatrix.
On the contrary, the fistula is more frequently open in the pericardial cavity. Its walls are of very varying appearance, depending on their age: they may be red, greyish, soft or hard, and when the lesion is of old standing they may have been converted into a sclerotic tissue.
Fig. 176.—Appearance of the lesions in a case of fatal pericarditis. P, inflamed pericardium, distended with exudate and adherent to the neighbouring pulmonary lobes; 1, posterior lobe; 2, cardiac lobe; 3, anterior lobe; Fp, pleural false membranes.
The pericardium appears distended with a considerable quantity of liquid of a special character—sometimes sero-sanguinolent, sometimes almost or entirely purulent; sometimes yellowish, or greenish-grey; sometimes frothy, inodorous, or very fœtid.
These characters depend on the nature and number of the germs which have invaded the pericardial cavity. They also vary with the gravity and number of the hæmorrhages produced by the action of the foreign body on the myocardium.
The quantity of liquid also varies within very wide limits. There may be scarcely any exudation. In that case the pericarditis is of a partially adhesive character, with abundant false membranes. As a rule the quantity of fluid exudation varies between seven and eight quarts, but sometimes the quantity is much greater. Trasbot described an instance in which the united weights of the heart and pericardium exceeded 36 lbs. Hamon mentioned a case of pericarditis in which the liquid exudate exceeded twenty quarts.
“When inflammation is first set up the liquid is serous, yellowish, or reddish yellow. It contains fibrinous flocculi in suspension. Little by little this exudate becomes purulent, whilst the internal layers of the pericardial serous membrane undergo desquamation. These are next covered with false membranes of varying appearance; the fibro-albuminous exudation is wrinkled, villous and tufted. The two layers of serous membrane are connected at certain points by this exudation, the adhesions being sometimes very extensive. The pericardial sac properly so called becomes the seat of marked lardaceous thickening, due to inflammation. The heart appears entirely covered with a layer of greyish or earthy-coloured granulation tissue, which appears as though baked, and was compared by Hamon to the back of a toad. It is atrophied as a consequence of prolonged compression.
Under the influence of the eccentric pressure of the liquid the pericardial sac is distended and comes in contact with the walls of the chest, to which it may adhere. The foreign body, especially if small, is not always easy to find.
The myocardium often displays interesting lesions. At first there is thickening, or more commonly sclerous degeneration, of the superficial layers covering the ventricles, and then appears a crop of little miliary abscesses. Abscesses of considerable size have several times been detected in the walls of the ventricles and in the interventricular septum.
The foreign body, moreover, may not only injure the myocardium, but may even perforate it completely and produce ulcerative endocarditis (Cadéac). In this case infectious germs very rapidly invade the circulation and all the tissues, and the animal dies of pyæmia.
These essential lesions are accompanied by others of varying importance. Thus the lung is congested throughout, and by contiguity of tissue inflammation may extend from the pericardium to the lower part of the pulmonary lobes and to the pleura.
Interference with the return circulation induces lesions due to venous stasis: dropsy of the chief serous membranes, œdema of the connective tissue, pleural and peritoneal exudations, etc. If the hind limbs never become swollen it is because the skin covering them is very resistant and does not readily yield. The liver becomes hypertrophied, congested and engorged with blood, and when the animals live for some weeks, shows the appearances known as cardiac or nutmeg liver.
Treatment. The treatment of pericarditis due to the presence of foreign bodies is at present merely palliative. Often the only thing to be done is to slaughter the animal.
We need not go back to the methods formerly recommended. All are illusory or mischievous, such as the use of purgatives to arrest or reverse the progress of the foreign body, removal of the foreign body after opening the rumen, puncture of the pericardium, etc.
In 1878 Bastin successfully opened the pericardium and extracted the foreign body through a window produced in the thoracic wall.
This operator recommends that after drawing the left limb forward and incising the skin and muscles, the operator, with his hand bound round with a cloth, should perforate the pleura, and then having found the foreign body, proceed to extract it. By this method it seems difficult to cause perforation of the pericardium, which would certainly lead to the production of pneumo-thorax complicated with fatal septic pleurisy.
It must be borne in mind that the two pleural sacs, right and left, descend as far as the sternum (Fig. 173), and that it is not possible to touch the pericardium directly without perforating the pleura.
Moussu has drained the pericardium through the pleura in the hope of relieving the pressure on the heart and facilitating the reabsorption of the œdema, in order to permit of the subsequent slaughter of the animal, but has had unsatisfactory results. Lastly, he has practised median trepanation of the sternum in the infra-pericardiac region. Here again the operation is difficult, because of the œdematous infiltration of all the substernal region, while it is so dangerous to the patient, which must be cast and may suddenly succumb, that it is of no use in ordinary practice.
There is probably only one condition in which it would be possible to attempt intervention with a fair chance of success, that is, when there exists a fibrous connection between the pericardium, lung, and wall of the chest on the right or left side.
In such cases aspiratory puncture or incision of the pericardium in an intercostal space might prove of service, because it would not expose the animal to the danger of pneumo-thorax.
The only difficulty lies in ascertaining beyond all question the existence of such an adhesion before attempting operation, and this is really very great, even having regard to the form of the dulness and the absence of all respiratory sound in the lower third of the thoracic cavity and cardiac zone. The pulmonary lobe between the heart and chest wall may be thrust upwards and be partially adherent to the pericardium and to the parietal pleura, and at the same time it may be impossible to avoid producing operative pneumo-thorax when the cartilages are resected to admit of incising the pericardium.
The only logical method seems to be puncture of the pericardium through the xiphoid cartilage, as described below.
The topographical anatomy of the thoracic viscera shows that the point of the pericardium extends along the sternum to a point close to the lower insertion of the diaphragm, and that the pericardial sac is only separated from the xiphoid region, or rather from the region of the neck of the xiphoid appendix of the sternum, by the fatty cushion at the point of the heart.
Fig. 177.—Lesions of exudative pericarditis produced by a foreign body. Relation of the pericardium to the sternum and ensiform cartilage. Pericardium opened. D, diaphragm; Œ, œdema of the dewlap, Ax, ensiform cartilage; F, liver; Vb, gall bladder; 1, posterior lobe of the lung, drawn backwards; 2, cardiac lobe; 3, anterior lobe; E, spot where the foreign body penetrated, towards the point of the pericardium, between the neck of the ensiform cartilage and the circle of the hypochondrium.
A glance at the annexed diagram (Fig. 177) will show this.
The diagram, carefully reproduced from an anatomical preparation of an animal which succumbed to pericarditis, shows that the distended pericardium extends close to the neck of the xiphoid cartilage.
First stage. Identify the three following anatomical guiding points:—
(1.) Xiphoid appendix and white line. (2.) Point at which the circle of the hypochondrium becomes attached to the sternum. (3.) Point at which the external mammary vein penetrates the abdominal wall (Fig. 178).
Lines uniting these three points enclose a right-angled triangle, which the operator must imagine to be bisected by a third line.
The incision, which should be about 8 inches in length, follows this bisecting line at an equal distance between the white line and the circle of the hypochondrium, to a point within about 8 inches of the anterior margin of the mamma. All these points are readily observable before the animal is cast.
Fig. 178.—Seat of operation for puncturing the pericardium by way of the ensiform cartilage. L B, White line; H, line of the hypochondrium; V. M.a., anterior mammary vein; P, point where the pericardium is punctured through the incision.
The cutaneous incision affords exit to large quantities of fluid, and the pectoral muscles attached to the neck of the ensiform cartilage can then be divided with the bistoury. The area of operation is thus uncovered.
Second stage. The second phase comprises incision of the tissues opposite the neck of the ensiform cartilage, about 8 inches in front of the base of the triangle and at equal distances from the points Nos. 1 and 2; incision through the skin for a distance of 8 inches, and dissection of the muscles of the ensiform region exposed at the neck of the cartilage.
By means of the index finger or the index and middle fingers of the right hand the mediastinal space is explored, and the fatty masses round the base of the heart broken through. If the pericardium is greatly distended, the point of the sac can be felt with the tip of the finger, or its position can be recognised, even from a little distance, on account of the fluid contents transmitting the impulse of the heart. The sensation conveyed to the finger is very clear.
The right index finger is then replaced by the left, and, a trocar about 10 inches long and ¼ inch in diameter being introduced along the index finger used as a director, the pericardial sac is reached. The exudative fluid transmits the impulse due to the beating of the heart, and the pulsations can be clearly distinguished when grasping the handle of the trocar.
Third stage. Digital exploration of the course of the puncture and fatty cushion at the base of the heart, with the object of discovering the position of the pericardium.
Fourth stage. Puncture with a trocar about 10 to 12 inches in length, puncture of the pericardium, irrigation and dressing.
Fig. 179.—Photograph of a patient immediately after operation. Extensive œdema of the dewlap and neck.
The trocar is inclined in a slightly oblique direction from without inwards and forwards towards the median plane, in order that the point may not deviate towards the left pleural sac; the left index finger is then withdrawn, and by a sharp thrust of the right hand the trocar is pushed forward about 1 to 1½ inches and the pericardial sac is entered.
The position of the canula should not be altered whilst liquid is escaping, for if it is thrust in too far a considerable quantity of fluid may remain in the deepest portion of the sac.
The cavity having been drained, a long strip of iodoform gauze is introduced into the track and a protective surgical dressing applied over the incision in order to prevent infection by the litter.
In consequence of the introduction of the fingers into the track caused by puncture and the escape of pericardial liquid along the canula or after removal of the canula, the operative wound is necessarily infected; but this is of little importance, because the opening is inclined downwards, and also because it is impossible to hope for aseptic healing.
The dressing is renewed after forty-eight hours, and every three or four days afterwards.
The œdematous infiltration about the front portion of the body disappears rapidly in two to three days, and should the animal be slaughtered the meat is quite sound in appearance.
This operation does not aim at effecting a cure, but is simply for the purpose of allowing animals which would otherwise be valueless to be slaughtered and sold.
Fig. 180.—Photograph of the same subject as Fig. 179, taken six days later.
CHRONIC PERICARDITIS.
Pericarditis when due to tuberculosis may assume the chronic form. Tuberculous pericarditis, at least in a large number of cases, is only accompanied by slight exudation, which might remain unnoticed unless the animals were carefully examined; but it causes the internal surface of the pericardial sac and the surface of the myocardium to become covered with exuberant vascular growths, which by setting up adhesions lead to partial or generalised union of the heart and pericardial sac. Between these adhesions, which form partitions, are found little cavities filled with sero-sanguinolent, grumous, or caseous liquid. In time the adhesions increase in number, pericarditis obliterates the free space, and the heart becomes wholly adherent to the pericardium.
As in acute pericarditis, the fibrous layer undergoes thickening and hardening processes. The superficial layers of the myocardium undergo sclerous transformation, and the tissues forming the adhesions themselves may assume the characters of fibrous tissue.
In one solitary case Moussu saw another form of chronic pericarditis with complete adhesion of the heart and pericardial sac, without any exudation and almost without any false membranes. He was unable to determine the exact cause, but was strongly inclined to regard the disease as having followed pericarditis à frigore or pericarditis of a rheumatic character.
Fig. 181.—Schema of a subpleural abscess on the right side which produced symptoms of pericarditis (pseudo-pericarditis). Po, Right lung, partly splenised and thrust upwards; Pl, parietal pleura separated from the wall of the lower half of the chest; A, cavity of the subpleural abscess.
Adhesions between the heart and pericardial sac are also said to be the inevitable though delayed result of all punctures of the pericardium through the ensiform cartilage in cases of pericarditis due to a foreign body.
Symptoms. If the chronic pericarditis is limited to a few partial adhesions, it remains unnoticed; but when it is more marked it offers certain signs of acute pericarditis, such as partial dulness of the cardiac area, which is more extensive than usual, disappearance of the cardiac shock, weakening of the sounds, feebleness of the pulse, very marked venous pulse, moderate stasis, extremely rapid and aggravated dyspnœa when the animal is forced to walk, threatened asphyxia if exercise is prolonged, and complete asystole.
All these symptoms are due to the existence of adhesions between the heart and pericardium, which, by destroying the interpericardial space, interfere with diastole while preventing regular systole.
Sudden death is a frequent consequence.
The diagnosis of chronic pericarditis is very difficult. The prognosis is extremely grave, and we do not possess any means of dealing with the condition.
PSEUDO-PERICARDITIS.
Under this title we purpose grouping a certain number of pathological accidents due to different causes, but manifesting themselves by identical symptoms, which symptoms offer so marked a resemblance to those of pericarditis produced by foreign bodies as to suggest the presence of that disease. This refers to accidents by which the foreign body closely approaches, without actually touching, the pericardium, the lung or the pleural sacs, but in which it causes purulent collections which displace the pericardium, indirectly compress the heart, and finally cause symptoms of an apparently pericardial character.
Causation. During the development of pericarditis the foreign body perforates the reticulum and diaphragm, passing along the middle line of the body, without which it would not come in contact with the pericardium. If the perforation, however, occurs to the right or left of the median plane, the foreign body moves forward just as easily, but it misses the pericardium and passes either into the lung, where it causes fatal pneumonia; or the pleura, where either it sets up septic pleurisy in the subpleural connective tissue or produces an abscess.
The abscess is generally lateral, situated in the right subpleural region, or it may develop below the pericardium. These are the two varieties of pseudo-pericarditis seen by Moussu.
There is, however, a third variety, which might be called “parasitic pseudo-pericarditis.” It is extremely rare, and Moussu has only seen one case. It was due to the presence of an enormous hydatid cyst of the right lung as large as a man’s head, which was situated towards the mediastinal plane of the lung and pressed on the supero-posterior surface of the heart and pericardium. In consequence of the permanent downward pressure which it exercised it interfered seriously with the heart’s action and caused symptoms of pseudo-pericarditis.
Symptoms. The general and external symptoms are those of pericarditis—viz., dulness, diminution in appetite, irregular rumination, wasting, œdema of the dewlap, distension of the jugulars, marked venous pulse, great anxiety and dyspnœa when the patients are forced to move, etc.
But the cardiac symptoms differ notably, and moreover vary, according to the nature of the lesions. Speaking generally percussion reveals complete dulness on one or both sides, and auscultation always indicates the absence of sounds due to extravasated fluid in the pericardial sac.
When the abscess is situated below the pericardium, a condition difficult to diagnose, the dulness seldom extends very high on either side of the chest, and the sounds heard over the cardiac area, while much weaker than usual, are audible above the normal points.
An abscess developing beneath the pleura on one side displaces the heart in the opposite direction. The cardiac beat is weakened by the compression, but, nevertheless, transmits an impulse to the purulent fluid, which in its turn conveys it outwards through the intercostal spaces in the form of movements corresponding in rhythm with the beating of the heart, so that at first glance one might imagine an aneurism existed at the base of the large arterial trunks. The lower pulmonary lobe is thrust upwards, and over the area of dulness pulmonary sounds completely disappear.
When the heart is compressed by a large hydatid cyst or other lesion, the general and external symptoms are similar to those above described.
Finally, one last symptom, which appears of some importance, may be mentioned. When animals suffering from pericarditis due to a foreign body are forced to move, the heating of the heart becomes so tumultuous that it can no longer be counted, and even in a state of rest it may rise to 140 or 150 beats per minute. In cases of pseudo-pericarditis it rarely rises above 90 or 110.
Fig. 182.—Appearance of an animal suffering from pseudo-pericarditis (infra-pericardial abscess). The dotted outline indicates the space occupied by the heart, which is thrust upwards.
Diagnosis. The attempt to diagnose this condition accurately must not be regarded merely as a result of scientific curiosity. Under certain circumstances the diagnosis may be of very great importance. While the patient affected with pericarditis due to a foreign body is beyond all hope of recovery, certain cases of pseudo-pericarditis appear amenable to treatment.
The diagnosis, therefore, is of great importance, and the practitioner should spare no effort to confirm it, bearing in mind the symptoms enumerated, and remembering that the normal sounds of the heart never completely disappear.
An aseptic exploratory puncture with a long, fine needle will sometimes prove of great assistance.
Prognosis. Although grave, the prognosis is less so than in true pericarditis.
Treatment. If clearly recognised, both subpleural and subpericardial abscesses seem curable. By freely puncturing the pus-filled cavity through an intercostal space, the liquid may be evacuated and recovery may occur. Healing is favoured by carefully washing out the cavity with a non-irritant disinfectant.
The only precaution required in making such punctures is to avoid the internal thoracic artery and vein, the intercostal artery, and the lower cul-de-sac of the pleura.
CHAPTER III.
ENDOCARDITIS.
If the symptoms of pericardial diseases are well defined, we cannot say the same of diseases of the heart, properly so-called. Such affections often pass unnoticed, being detected only on post-mortem examination. Moreover, cardiac diseases are rare. Very frequently they are only of a secondary nature, accompanying or following better recognised conditions, such as infectious diseases, post-partum infections, etc.
Causation. Endocarditis, i.e., inflammation of the endocardium and valves, is rarely primary, simple and benign. It was formerly thought to be the result of chills or of the rheumatic diathesis. These simple forms of endocarditis usually escape observation, though careful examination in the first instance reveals them.
Much more frequently, however, endocarditis is secondary, malignant, infectious and infecting. This variety occurs as a complication of post-partum infection or of very serious general conditions, such as peripneumonia, gangrenous coryza, aphthous fever, tuberculosis, etc. To detect it, not only must the original disease be accurately diagnosed, but all the changes the disease is producing in important organs must be followed.
While it is generally admitted that all forms of endocarditis, even of the most benign character, are originally due to infection, it is certain that in those of the second group the organisms which have entered the bloodstream through a lesion of the uterus, lung or other tissue, are endowed with very great virulence. They attack some point on the endocardium, and produce either ulcerations which become covered with fibrous clots, or exuberant new growths of a pathological nature, which generally are papilliform, fragile, and prone to become detached by rupture of their pedicle and thus to be launched into the general circulation and to form emboli. The surface of these infected vegetations, like that of the ulcerations, becomes covered with fibrinous clots, which are readily loosened, form emboli in their turn, and infect distant organs.
Symptoms. The general symptoms of infectious endocarditis are by far the most important. They consist of prostration, loss of appetite, severe thirst, and high temperature. The local symptoms consist principally of murmurs: soft murmurs due to insufficiency of the auriculo-ventricular valves, heard during systole, particularly opposite the point of the heart where the cardiac shock is most clearly felt. This fact differentiates them from the murmurs of chronic endocarditis, which are usually due to aortic contraction, and are accompanied by a systolic sound heard at the base of the heart, more in advance and at a higher point than those now under consideration.
These murmurs or souffles furthermore vary in intensity and in character, according to whether the endocarditis results from post-partum infection, pyæmic disease, or some other cause.
Diagnosis. The diagnosis of endocarditis has not yet been the object of really careful study in bovine pathology, but there is no doubt that it can often be detected by patient examination.
Prognosis. The prognosis is very grave, and patients may die in a few days.
Treatment comprises vigorous local stimulation over the cardiac area, the administration of antithermic and antiseptic drugs, such as salicylate of soda, or of digitalis, sparteine or other cardiac tonics.
Pathologists have also described, chiefly as post-mortem curiosities of interest to pathological anatomists, various diseases and lesions due to insufficiency or contraction of the auriculo-ventricular, aortic, and pulmonary openings, lesions due to infectious myocarditis, to the presence of parasites and to other causes.
The symptoms of these various diseases or lesions in bovine animals are still too imperfectly understood to permit of more than a very limited description.
In the present state of our knowledge, diagnosis would always be of an uncertain character, and for this reason we do not propose to deal with them at present.
CHAPTER IV.
DISEASES OF BLOOD-VESSELS.
Diseases of vessels, arteries or veins, in animals of the bovine and ovine species are frequently nothing more than localisations of grave general disorders, and rarely admit of treatment. This is specially the case in regard to arteries, but a study of the diseases of veins has some practical importance.
PHLEBITIS.
Phlebitis, i.e., inflammation of a vein, is of interest only in the case of bovine animals. In them certain conditions may occur which the practitioner should understand, with a view either to prevention or treatment. Inflammation of the veins may be due to external causes, such as surgical or accidental wounds (phlebotomy wounds, accidental wounds, local inflammations, etc.), or to internal causes of infectious origin (general infection, puerperal infection, etc.).
ACCIDENTAL PHLEBITIS.
The jugular vein may become inflamed as a result of accidental wounds or of phlebotomy, but the mammary vein in cows is much more frequently affected. In both cases the disease is due to infection of the clot which seals the vessel; it may assume the form of either adhesive phlebitis or suppurative phlebitis. Whether produced directly by the use of infected instruments or whether it is of a secondary character, traceable to the clot being infected by germs entering from without being conveyed to the wounds by the head-stall chains, by litter, manure, etc., the result is the same. The inflammation, at first confined to the endothelium, extends to the wall of the vein and causes fibrin to be precipitated over the inner wall of the inflamed vein for a distance varying with each case.
If the microorganisms do not produce suppuration, the vein appears simply thrombosed and inflamed, the phlebitis remains of an adhesive character, and may disappear spontaneously, provided the animal be kept quiet. If, on the other hand, suppuration is set up, the clot gradually breaks down, the internal surface of the vein develops granulations and undergoes suppuration, and the phlebitis is then said to become suppurative. The clot may even become entirely detached, transforming the suppurative phlebitis into a very grave form of hæmorrhagic phlebitis.
The jugular is the commonest seat of adhesive phlebitis, the mammary vein of suppurative phlebitis.
Symptoms. The symptoms are easy to recognise. The accidental or instrumental wound is the seat of a painful œdematous swelling. It discharges a reddish offensive serosity, or exhibits blackish-violet bleeding granulations surrounding a little central sinus.
The affected vein, whether the jugular or mammary, soon becomes swollen, is sensitive to the touch and very rapidly becomes indurated in the direction of its origin for a greater or less distance.
Phlebitis has then set in, and according as one or other complication predominates, it is described as suppurative or hæmorrhagic.
Diagnosis and prognosis. The diagnosis presents no difficulty. In phlebitis of the jugular the neck is held stiffly, and the jugular furrow is partly obliterated.
The prognosis is somewhat serious, particularly in phlebitis of the mammary vein, for obliteration of the vein interferes with the function of the venous plexus from which it springs, and, although there may be a limited vicarious circulation, the secretion of milk is indirectly and secondarily checked owing to difficulty of irrigation.
The extension of phlebitis of the jugular towards the head and the venous sinuses of the cranial cavity, is quite exceptional.
When the mammary vein is inflamed it appears collapsed in the direction of the heart and swollen, indurated, and painful in that of its origin in the mammary gland.
Treatment. The first point requiring attention is so to fix the animal as to prevent the clot from being pressed upon or crushed, though, unfortunately, this cannot always be properly done. The difficulty is obviated by applying vesicants, which cause swelling and pain, and so reduce natural movement of the parts to a minimum.
At first, when the parts surrounding the operative wound are simply swollen and phlebitis is threatened, repeated application of tincture of iodine or a liquid vesicant is useful, and may prevent the disease developing.
In existing cases a blister applied over and around the whole of the hardened tract may prevent the mischief from proceeding beyond the adhesive stage. In such case the clot becomes organised, the vein remains obliterated, and recovery follows.
Similar treatment may also be employed in suppurative phlebitis, but as the clot gradually breaks down in consequence of the action of bacteria it is useful and almost indispensable to disinfect the vessel. For this purpose the opening of the sinus must be enlarged, and, by means of a sterilised or very clean syringe with a curved nozzle, the parts washed out daily with warm boiled water, followed by an antiseptic injection containing 2 per thousand of iodine, 3 per cent. of carbolic acid, or, better still, glycerine containing 1 per thousand of sublimate.
If in spite of this treatment the phlebitis extends towards the origin of the jugular or mammary vein, a counter-opening may be made at the point where the clot still remains adherent, and a strip of iodoform gauze saturated with tincture of iodine or with blistering ointment diluted to one-eighth with oil may be passed. Needle firing is also of value. Finally, as a last resource, a ligature may be applied to the vein above or beyond the clot.
This operation, which in the horse is confined to hæmorrhagic phlebitis, is especially applicable to phlebitis of the mammary vein in the cow. As the vein is subcutaneous, the operation may easily be performed in the standing position; the successive stages are as follows:—
The patient is firmly secured and its hind limbs hobbled by passing a rope around the hocks in a figure of eight. It is steadied on one side by an assistant who presses on the quarter.
One cubic centimètre of a 10 per cent. solution of cocaine is subcutaneously injected on each side of the vein at the point chosen. Ten minutes later a button-hole incision is made through the skin and a loop of thick catgut passed around the vein by means of a curved needle. The ligature is tied firmly with a surgical knot and the little wound afterwards covered with a mass of cotton wool secured by collodion.
INTERNAL INFECTIOUS PHLEBITIS (UTERO-OVARIAN PHLEBITIS).
The internal forms of phlebitis of parasitic or infectious origin are as yet little understood, but mention may be made of phlebitis of the utero-ovarian veins which frequently follows parturition and post-partum infection. This is probably in many instances the real cause of the post-partum paraplegia without gross or apparent material lesions.
This form of infectious phlebitis may extend to the large internal and external iliac veins and produce embolism and septicæmia, as is shown by recorded cases.
The mechanism of the disease is easily understood. The infective agents penetrate the veins of the uterine mucous membrane and pass from the lumen into the wall of the vein. Here they cause inflammation of the vascular endothelium, followed by the deposit of a fibrous clot of cylindrical form, which sets up partial thrombosis of the vein. This thrombosis becomes complete by the formation of a central clot due to venous stasis.
It is not necessary for the germs to penetrate at a number of points. The thrombosis progresses until it gains a large trunk beyond the original point of infection.
Symptoms. Phlebitis of the veins of the pelvis is frequently misunderstood or overlooked, because the practitioner is apt to confine his attention to external signs, the paresis and paraplegia of the hind quarters.
The symptoms usually appear from five to eight days after normal parturition or parturition in which there is retention of the after-birth followed by metritis. The animals show fever and lose appetite, signs which may be due to metritis, but soon after they experience difficulty in rising, and some days later remain permanently recumbent.
The circulation is weak, and the entire intra-pelvic region painful; the large nervous trunks are affected, exertion becomes difficult, and the animals refuse to rise. At this stage they should not be forced to do so.
In two to three weeks improvement may occur and lead to recovery but in many instances various complications in the nature of purulent infection or septicæmia set in, or the animals are previously slaughtered.
Diagnosis. The diagnosis can only be determined after the symptoms develop. Confirmation might in some cases be obtained by rectal exploration made methodically and gently.
Prognosis. The prognosis is grave.
Treatment. Treatment should be based on disinfection of the uterus by injections of boiled water or warm iodised solutions and drainage by means of strips of iodoform gauze. The animals should be placed on a thick and scrupulously clean bed, and as far as possible be spared any considerable exertion for a fortnight. By changing their position once or twice a day complications may be avoided.
UMBILICAL PHLEBITIS OF NEW-BORN ANIMALS.
One of the most serious conditions met with in practice is that known as umbilical phlebitis of new-born animals. Whilst in fact it is easy to deal with phlebitis of the jugular or mammary vein, surgical or medical assistance becomes extremely difficult in this case, because the inflamed vein is deeply situated in the abdomen and passes through one of the most important internal organs, viz., the liver. When it is added that umbilical phlebitis is in 95 per cent. of cases of a suppurative character, the reader may form some idea of its gravity.
Unless the condition is early diagnosed and measures are at once taken, such complications as infectious hepatitis, purulent infection, and septicæmia cannot be avoided. Death is then inevitable.
In order clearly to understand this phlebitis, however, it is necessary to recall the anatomical formation of the umbilical region in the new-born animal.
At birth the umbilical cord is represented by a cylindrical mass, surrounded by the terminal portion of the amnion. It enters the abdomen through a circular perforation in the abdominal wall known as the umbilical ring. This ring may be divided into two parts, one deeply seated, the fibro-aponeurotic ring, consisting of an aperture in the white line; the other the superficial or cutaneous ring, formed by the skin, which is wrinkled all round it, and constitutes a kind of sleeve about an inch in length. This cutaneous sleeve is continuous with the amniotic tissues. The entire umbilical cord is therefore enveloped in an amniotic-cutaneous sheath.
Fig. 183.—Position of the abdominal viscera in a new-born animal: Ru, rumen; E, epiploon; Rg, left kidney; Ig, small intestine; C, abomasum; U, ureter; O, urachus; R, rectum. Umbilical cord: Vo, Umbilical vein; Aa, allantoid arteries; Va, allantoid veins; O, the urachus.
It is composed of four principal structures—the umbilical arteries, the umbilical vein, the urachus, and the interstitial mucous tissue.
The umbilical arteries and vein consist of two parts—the extra-fœtal part, which co-operates in forming the cord, and the intra-fœtal part.
The first is formed of two arteries and two veins, in contra-distinction to the condition in solipeds, where the cord only contains one vein. In the second, the arrangement is as follows: The two umbilical allantoid arteries on entering the abdomen curve backwards towards the entry of the pelvis, passing over the sides of the bladder enveloped in the lateral ligaments, and extend upwards towards the bifurcation of the aorta, finally pouring their contents into the internal iliac arteries. In the adult they may still be traced as annexes of these latter vessels. The two umbilical veins on passing through the ring unite to form one within the abdomen. This vessel passes forwards, rising along the lower abdominal wall, then becomes lodged in the thickness of the inferior middle ligament of the liver, and finally penetrates that organ where it unites with the portal vein. It is also connected with a vessel known as “the vein of Arantius,” which places it in communication with the posterior vena cava, a vein not found in solipeds.
The fœtal blood is purified by exchanges between it and that circulating in the maternal placenta, and when re-arterialised it returns by the umbilical vein.
The urachus, found in the embryo and fœtus, eventually gives rise to the bladder. In new-born animals this viscus is therefore open at its base, and communicates with the allantoid cavity through the urachus. The urachus starts from the base of the bladder, and, extending along the median plane of the lower abdominal wall between the two umbilical arteries as far as the umbilical opening, takes its place in the cord alongside the vessels. Through it the secretions of the fœtal kidneys drain into the allantoid cavity. The interstitial mucous tissue, also called “Wharton’s jelly,” is a gelatinous material which unites these different vessels and helps to support and protect them in the umbilical cord. It is particularly abundant opposite the umbilicus.
Immediately after birth the umbilical cord ruptures of itself as a result of the fall which the young animal experiences or of movements made by the mother, as for instance when she attempts to rise. In certain other cases it is divided by the mother biting it, or it may be ligatured by some person present. However the rupture may be brought about, it always occurs at a distance of 2 to 4 inches from the umbilicus. The immediate result is to produce thrombosis of the umbilical vessels and obstruction of the urachus. The two umbilical arteries rarely bleed, for hæmostasis is brought about by stretching, and these arteries, being very elastic, almost immediately retract and close. The umbilical veins simultaneously become blocked, and the single intra-abdominal vein having no further raison d’être, gradually becomes obliterated. The urachus should normally be obliterated at the moment of delivery (Colin and Saint-Cyr), or at any rate soon afterwards, as a consequence of rupture of the cord (Chauveau and Zundel).
Immediately after delivery another change sets in. The extra-fœtal portion of the cord, which remains attached to the umbilicus, dries on contact with the air, the Wharton’s jelly retracts, the whole undergoes a kind of necrosis, assumes the appearance of a dry scab, and in eight or ten days falls away, leaving in its place the umbilicus, which should be half cicatrised on the fall of the cord. Thus the umbilical cord presents an extra-fœtal degenerated portion and a persistent portion about ½ to 1 inch only in length, buried in the cutaneous ring of the umbilical region.
If all the changes indicated occur normally and physiologically, the little wound in the region of the umbilicus cicatrises in a perfectly regular way. But unfortunately this is not always the case. At times the cicatrix becomes contaminated by manure, urine or dust, suppurates, and may then become the seat of various complications, such as umbilical phlebitis, omphalitis or persistence of the canal of the urachus.
UMBILICAL PHLEBITIS OR OMPHALO-PHLEBITIS.
History. Umbilical phlebitis, and in a more general sense all pathological conditions of the umbilicus, in new-born animals have been the object of numerous investigations by Lecoq, Bénard, Loiset (1843), Bollinger (1874); and more recently by Morot (1884), Uffredizzi (1884), Chassaing (1886), etc.
Omphalo-phlebitis may occur as a primary condition or may appear as a complication of omphalitis and of persistence of the urachus. It consists essentially in suppurating inflammation of the umbilical vein, but is not infrequently accompanied by omphalitis, arteritis, peritonitis, and cystitis.
Causation. The disease results from infection of the (normal) clot and of the wound resulting from severance of the cord. The infection may only cause simple phlebitis of the umbilical vein, but if the organisms are virulent the phlebitis almost inevitably degenerates into suppurative phlebitis.
Formerly omphalo-phlebitis was thought to be caused by the mother licking the foal, by irregular tearing of the cord, by crushing and separation of the obliterating clot, etc. The truth is that all these causes favour infection of the umbilical wound, which is the primary cause, suppurative phlebitis being secondary only.
When the cord is ruptured both the veins and arteries become plugged, and bleeding ceases. This plugging should end in organisation of the clot and obliteration of the vessels. If, however, the wound is infected, microorganisms make their way between the clot and walls, and extend along the inner surface of the vein, infecting first the clot and then the vein, and thus setting up suppurative phlebitis.
If suppuration does not continue, recovery may occur spontaneously. Infection may be confined to the clot, producing simple phlebitis, but it often extends along the umbilical vein to the liver, causes infectious hepatitis and purulent infection or septicæmia. Similar results may be produced by infection of the arteries, the organisms making their way as far as the bifurcation of the aorta, and thus gaining the general circulation. Moussu believes that this is the commonest method by which septicæmia is produced in calves.
Symptoms. In these cases it is usually the general symptoms which first attract attention, the local lesion passing unnoticed for a greater or less time.
The animal shows intense fever, due to either suppurative phlebitis, infectious hepatitis, or, as often happens, to generalised infection. Appetite is lost, diarrhœa is abundant, the respiration and circulation are accelerated, and the temperature rises to 104° Fahr., or even 105° Fahr.
The local symptoms are those usually associated with omphalitis or phlebitis. An examination of the umbilical ring reveals an œdematous, hot, sensitive swelling, the lower part of which exhibits a chronic, suppurating, fungoid, blackish wound of unhealthy appearance.
This wound is the seat of one or more sinuses which penetrate the vein, arteries, or urachus. If only one sinus exists, it always passes upward and forward into the umbilical vein. The utmost precaution should be employed in examining the parts. Should it be thought desirable to probe the sinus in order to discover its direction, the probe must be very cautiously introduced, and only for a short distance, because rough handling would tear the tissues and carry infective material to deeper seated points.
Complications. These are numerous and very grave. Long ago Lecoq described a disease suggestive of laminitis, which beyond doubt was only a form of purulent infection. At a later date Loiset studied a disease following omphalitis, in which interstitial abscesses developed in the cord. This also was simply purulent infection.
More recently complications such as pleurisy, pneumonia, infectious endocarditis, diarrhœic enteritis, and especially suppurative polyarthritis of young animals have been referred to omphalo-phlebitis. All these complications result from infection. The microorganisms themselves or the toxins they secrete appear to have a particularly injurious action on the serous membranes, a fact which throws light on the frequency of such complications as pleurisy, peritonitis, endocarditis and arthritis.
Intoxication also plays a certain part, and microbic toxins are responsible, at least at first, for the uncontrollable diarrhœa, arthritis with sterile exudations, etc.
Diagnosis. This presents no difficulty. The alarming general symptoms seen at the outset immediately suggest in the case of young animals the possibility of disease in the umbilical region.
Prognosis. The prognosis is grave, it may be said very grave, because treatment is difficult to apply, and dangerous complications, which almost always prove fatal, may already have been set up.
One must always distinguish, however, and take into account in forming the prognosis, the special characteristics of the phlebitis, and weigh carefully the signs of complication. The fistula should be cautiously explored, and its depth, etc., noted, while the temperature, circulation, respiration, etc., should be carefully studied.
Treatment. A very important item of treatment consists in regularly and scrupulously cleansing the region of the umbilicus after the cord has separated and until the wound has completely cicatrised. The parts are washed with boiled water and dusted with boric acid, iodoform, etc.
A still better plan, and one that almost certainly guards against this disease, is to apply an antiseptic dry dressing as soon as the new-born animal has become dry. This need only consist of a small sheet of antiseptic cotton wool fixed to the umbilicus by four pitch bandages or by two pieces of webbing passed over the back. In this way contamination of the cord and the risk of infection are avoided.
In cases of fully-developed phlebitis the old generation of practitioners used to recommend local dressings with adhesive plasters, astringent and vesicant applications, etc. All such methods are useless, because they only act on a part of the diseased structures and cannot reach the blind ends of the sinuses. The classic treatment of suppurative phlebitis also is out of the question.
All that can be done, therefore, is slightly to open up the sinuses and wash them out frequently with antiseptic solutions, such as boiled water, sublimate glycerine, carbolic glycerine, etc., afterwards applying antiseptic dressings. These methods, however, are scarcely likely to put an end to infectious complications such as suppurative polyarthritis.
There is no danger in using strong carbolic solution, 3 per cent. creolin, 4 per cent. chloride of zinc, sulphate of copper, etc. Should there be several sinuses and should one of them extend in a backward direction, it is necessary to make certain that no communication exists between the urachus and the bladder. For this purpose some boiled water may be injected into the sinus. If a communication exist, this water will fill the bladder and distend the urachus. The treatment necessary in this case is similar to that of persistence of the urachus.
It is well in all cases to be guided by the following principle: never to resort to treatment unless suppuration has occurred and the sinus is blind. To check suppuration a blister may be applied around the umbilical region while means are taken to prevent the animal licking the parts.
Chassaing in 1886 suggested a rather original method of operation which deserves description. It is founded on the permanent treatment of sinuses, and consists in introducing a flexible osier stick, a kind of bougie, enveloped in tow and moistened with the following mixture:
| Collodion | 3 parts. |
| Sublimate | 1 part. |
This is introduced for a distance of 3 to 4 inches into the fistula, and is fixed to the skin with gutta-percha or pitch. The dressing is renewed every five or six days, and healing takes place, it is said, in one, two, or at most three weeks.
It is very likely that if the sinuses were previously cleared and simply plugged with antiseptics or treated by introducing pencils of salol, nitrate of silver, sulphate of copper, iodoform, etc., at least as good results might be obtained.
CHAPTER V.
DISEASES OF THE BLOOD.
SEPTICÆMIA OF NEW-BORN ANIMALS.
The above title is given to that exceedingly fatal disease commonly known as “white scour,” etc., the mortality in which often rises to 95 per cent.
The disease was studied by Poels in Holland in 1889, Dèle in Belgium in 1891, Perroncito in Italy, Galtier in the centre of France in 1891–92, and quite recently by Nocard in Ireland in 1901.
It occurs throughout all the breeding districts of France, and in some parts causes enormous losses, the mortality comprising two-thirds or even three-fourths of all new-born calves. In certain breeding establishments in Normandy all the new-born animals without exception die unless special precautions are adopted.
In foals, septicæmia of the new-born is very rare, because horse-breeding establishments are much better cared for, and breeding mares are segregated. In byres, on the other hand, the greatest promiscuity exists. The disease is equally uncommon in lambs, although it makes numerous victims in folds which have once been attacked. It is, however, quite common in young pigs.
Symptoms. The development and course of the disease are in certain respects characteristic.
The disease usually appears within two or three days after birth, and only in rare cases after the second week. Calves which at birth appeared vigorous and in good health are found dull on the second day; after the second or third meal they suffer from diarrhœa, and from that time refuse all nourishment, lie down as though exhausted, and sometimes die very rapidly.
Some even perish in ten to twelve hours without showing diarrhœa; although apparently well at night, they are found dead or dying the next morning. This is the peracute form.
Most frequently the young creatures suffer for two or three days, sometimes a week. Appetite is partly preserved; at first the diarrhœa resembles that due to inability to digest milk, but the fæces soon become greyish or blackish and very fœtid. The hair of the tail, quarters and hocks is soiled and matted, the skin irritable and reddish; the patients lose strength, appear unsteady on their limbs, and develop rapid respiration and tumultuous action of the heart.
They take little food, become weaker by degrees, and die in a condition of exhaustion.
Fever, well marked at first, frequently diminishes, and the temperature may remain normal for several days, falling to 97° Fahr., or even 95° Fahr., twenty-four hours before death.
This is the commonest form of the disease. It lasts three to five days, and is always grave.
Cattle-men recognise the disease chiefly by the diarrhœa and loss of appetite.
Lastly, a third and rarer form occurs during which appetite is maintained in spite of the diarrhœa. The animals remain thin, develop poorly, but survive for a month, six weeks or two months. The diarrhœa diminishes or disappears, but its disappearance is followed by complications such as broncho-pneumonia, pleuro-pneumonia, endocarditis, acute arthritis, etc., a fact which led Prof. Galtier to give the disease the name of “septic pleuro-pneumonia in calves.” These complications, again, are extremely grave, and generally prove fatal after a period of varying length. They are due to local development of microorganisms of the kind which produce septicæmia, and similar to those described under the name of broncho-pneumonia of intestinal origin in sucking calves.
They differ, however, as regards their cause, from the primary affection, and may be due to very varied organisms, the commonest being those of suppuration. These organisms, in fact, are alien to the primary disease, and obtain entrance from without, very probably by the tracheobronchial tract.
In young pigs septicæmia assumes the same forms as in the calf. In lambs the chronic form seems more frequent than the peracute and the ordinary forms.
Causation. The septicæmia of calves, and possibly of all new-born animals, of whatever species, is produced by a microbe which flourishes in the manure and litter of stables, and which Nocard included in the group of Pasteurella. It can be found in the blood from the moment the first external symptoms appear until the time of death. During the last hours, however, the bacterium Coli communis also invades the circulation in many instances, and if cultures are not made until some hours after death, the colon bacillus and bacteria of putrefaction are more particularly discovered.
The microbe of calf septicæmia can be readily cultivated in jelly or in ordinary liquid media. Injected into the veins of experimental animals, it reproduces the clinical symptoms, and causes death more or less rapidly, according to the dose injected.
The virulence of cultures grown in defibrinated calf’s blood seems more intense, and Moussu has been able to reproduce the clinical form of the disease by applying to the umbilical cord of a new-born animal a pledget of cotton wool saturated with such a culture, and covering it with a dressing. The germs of the disease are spread throughout the byres through the medium of fæces. When the umbilical cord has become dry, that is, after the third day, the application of virulent cultures to the stump no longer causes infection.
Pathogeny. The pathogeny of this septicæmia of calves and of new-born animals is easy to explain.
At birth the young animals fall on the litter, and the umbilical cord becomes contaminated. The infective agent, finding an excellent culture medium in the tissues of the cord, at once begins to develop, increases in enormous numbers, steadily ascends along the cord, and sets up septicæmia. It grows in the gelatinous Wharton’s jelly and in the fibrinous plug closing the arteries and umbilical vein, and soon enters the true circulation. Septicæmia is then fully established, general disturbance sets in, and with it the diarrhœa by which it is externally indicated.
It is important to remember, however, that infection occurs most readily through the medium of the cord, and during the first few days after birth: it may occasionally be brought about towards the eighth or tenth day, when the shrivelled portion of the cord falls; in this case its entrance is effected through the little umbilical wound.
Lesions. The lesions are sometimes so obscure that the practitioner may hesitate to deliver an opinion.
In acute cases, where death occurs in two or three days, or even in ten to twelve hours, post-mortem examination reveals only increased vascularity of the serous membranes—the peritoneum, pleura, pericardium, etc.; and it may be almost impossible to discover anything abnormal in the cord, for although the clots closing the arteries and veins are infected, they are neither separated from the walls of the vessels nor broken up.
On the surface of the urachus, at the base of the bladder, and in the depths of the peritoneal folds supporting the allantoid arteries (sometimes also the hepatic vein), unequivocal signs of local ascending infection may, however, almost always be found, together with intense injection of the capillaries, little hæmorrhagic spots, and commencing formation of false membranes, etc.
The infection extends also by the lymphatic vessels contained in these peritoneal folds, and finally attains the sublumbar region.
When the disease develops less rapidly the peritoneal cavity contains a certain quantity of blood-stained serosity, as do the pleuræ and pericardium, whilst vascular engorgement of the serous membranes is extremely marked. The intestine shows traces of congestion and inflammation throughout its length, and its contents contain the specific organism in very large numbers.
Finally, in the chronic forms, the serous membranes and the intestine seem only slightly attacked, possibly because the lesions have undergone retrogressive changes. The striking features are the secondary lesions, such as those of pneumonia, broncho-pneumonia, pericarditis, and abscess formation in the lung.
Nocard gives the following description of the lesions found during his investigation of “white scour” of calves in Ireland (Veterinarian, April, 1902, p. 171; see also Prof. Mettam’s paper, Veterinarian, June, 1902, p. 307):—“The lesions found on autopsy vary according to whether the evolution of the disease has been rapid or slow. One lesion, however, is never absent—that of the navel and the navel vessels. In all the calves attacked we found a large umbilicus with hardened coats enclosing a clot easily broken down, sometimes soft and purulent. In every case, also, we observed blood suffusions, often very extensive, along the course of the umbilical vessels and of the urachus, invading often the posterior third of the bladder. In cases where the evolution had been rapid we found the lesions of true hæmorrhagic septicæmia. All the viscera were congested to excess; their surface was studded with petechiæ, ecchymoses, or subserous blood suffusions. The capillary network of the peritoneum, pleura, and pericardium appeared strongly injected. This lesion was especially marked on the epiploon. The intestine was the seat of intense congestion, especially at the level of the ‘floating colon.’
“The mucous membrane was thickened, gorged with blood, and friable; the solitary glands, thick and protruding, were sometimes transformed into a kind of bloody magma, or they were ulcerated, as in anthrax; the contents of the bowel were mixed with a large quantity of blood. The mucous membrane of the fourth stomach was altered nearly to the same degree; it was studded with interstitial hæmorrhages, especially above the level of the open edge of its folds. The mesenteric glands—especially those of the colon—were enormous, gorged with blood, reddish, and often hæmorrhagic. The mucous membrane of the bladder was often covered with petechiæ, the urine which it contained was clear and limpid, but always rich in albumen. [In one sample which was analysed, the urine contained more than 4 grammes of albumen to the litre.] The lungs were gorged with blood, like the intestines; sometimes they were manifestly œdematous, but generally their tissue was still supple, elastic, permeable, and without apparent lesion.
“In the subacute forms the lesions are much less marked. The mucous membrane of the intestine is less congested; sometimes œdema of the submucous tissue exists. The mucous membrane of the fourth stomach is often punctuated with brownish-red patches, traces of the capillary hæmorrhages which were produced at the onset of the disease. The mesenteric glands are swollen, gorged with serum, but not hæmorrhagic; the liver is large and of a yellowish tint; the spleen is little altered; the urine always contains albumen; the lungs are seldom quite sound; they usually contain here and there small diffuse centres of catarrhal pneumonia, of nodular bronchial pneumonia, or simply of atelectasis.
“These lesions are more constant and more dense if the animals have resisted the disease for some time; they then constitute the transition stage between the simple collapse at the beginning of the disease and the suppurating lesion of lung disease. The joint lesions when they exist are very interesting. At the beginning all the periarticular tissues are infiltrated with a yellowish gelatinous serosity. The synovial membrane is covered with vascular aborisations of an extreme richness, which extend on to the articular cartilages. The synovial capsules are distended by a considerable quantity of thick synovia of a deep yellow or brownish tint, holding in suspension flakes of fibrous exudate more or less dense and abundant. When the lesion is older the synovia is replaced by a thick fibrous exudate, which fills sacculations, and extends between the articular surfaces. In this case the lesion appears identical with that of the arthritis seen in pleuro-pneumonia of sucking calves.”
Diagnosis. The diagnosis presents no difficulty, for the development and acute course of the disease (the majority of patients die within a week of birth) leave little room for doubt.
This disease is easily distinguished from dysentery in new-born animals, which appears at birth, as also from simple diarrhœic enteritis; in the latter disease the symptoms are delayed, sometimes occurring only when the animals are weaned; moreover, the disease is never so grave as that now under consideration.
Should, however, the post-mortem appearances seem indecisive, the diagnosis can be based simply on the high mortality.
Prognosis. The prognosis is extremely grave. About 95 per cent. of the animals attacked die, and among those which survive many show thoracic complications, that render them useless.
Treatment. Treatment of animals already affected is useless, and, moreover, too costly. Drugs administered through the digestive apparatus to a large extent miss their mark, because the digestive symptoms are secondary, primary infection having occurred through the circulation. The administration of purgatives and internal antiseptics can, therefore, only prove illusory.
On the other hand, prophylactic treatment is of the greatest value; all that is necessary is to prevent the umbilical cord from becoming infected.
The great mortality, which causes such severe loss to breeders, is simply due to want of proper care of new-born animals. Even in carefully kept byres the mortality may be high, for the specific agent develops in litter contaminated with fæcal matter, by lying on which young animals become fatally infected.
Fig. 184.—Dressing for umbilicus of new-born calf.
To check or prevent this septicæmia in breeding establishments, it is merely necessary to take the same precaution as is taken in dealing with young children, i.e., to apply an aseptic or antiseptic dressing to the stump of the cord after ligation. As soon as the young animal has been dried by the mother or by artificial means, a carefully boiled ligature is applied to the cord at a distance of about 1 inch from the umbilical ring. The portion of the cord below the ligature is snipped off, the remaining part is carefully washed with boiled water or boric solution, and is surrounded with a mass of iodoform wool, kept in place by a bandage passed over the back.
The cord will shrivel a little less rapidly than it would if exposed to the air, but will be protected from all infection. The young animal should be separated from the mother to prevent her from displacing the dressing by licking the parts.
In a few days all danger is at an end. This method is very simple, and can be carried out even by the breeder and in an infected byre. Nocard recommends the use of umbilical dressings containing collodion, and the practitioner can choose whichever method he pleases.
In grave outbreaks involving large establishments, the byres should be rigorously disinfected, and it is sometimes well to segregate cows about to calve in a special byre, from which the calves are not allowed to pass until the umbilicus is cicatrised.
TAKOSIS: A CONTAGIOUS DISEASE OF GOATS.[[4]]
[4]. Annual Report, U.S.A. Bureau of Animal Industry, 1902, p. 354 (Mohler and Washburn).
This disease has been seen in Angora goats brought from Texas into Pennsylvania, U.S.A.
Symptoms. The disease presents many of the symptoms usually accompanying a parasitic invasion, and is characterised by great emaciation and weakness, with symptoms of diarrhœa and pneumonia. In the early stages of the affection there is usually little to indicate that anything is seriously amiss with the animal. The first observable symptom manifested is the listless and languid appearance of the animal, evidenced by its lagging behind the flock, and is usually accompanied by a drooping of the ears and a drowsy appearance of the eyes. The pulse is slow and feeble, and the temperature is elevated slightly at first, but becomes subnormal a few days before death. The highest temperature observed in the natural disease was 104·1°, and the lowest, in a prostrated animal a few hours before death, registered 99·7° Fahr. Snuffling of the nose, as in a case of coryza, with occasional coughing is sometimes in evidence.
As the disease advances the animal moves about in a desultory manner, with back arched, neck drawn down toward the sternum, and with a staggering gait. Rumination is seldom impaired. The appetite, while not so vigorous, is still present, though capricious, and the affected animal shows plainly that the ravages of the disease are rapidly overcoming the restorative elements derived from the food. The fleece is usually of good growth, and presents a surprisingly thrifty appearance when the condition of the animal is taken into consideration. All the exposed mucous membranes appear pale, and the respirations are accelerated and laboured. The goats finally become so weak that they are readily knocked down and trampled upon by their fellows. If picked up they may move off slowly and eat a little, but within a few hours are down again, and in this way linger for several days, shrinking to about half their natural weight, and occasionally bleating or groaning, with head bent around on the side or drawn down to the sternum. A fluid discharge from the bowels of a very offensive odour is usually observed in the last few days of life, but this symptom is not constant.
Course and Susceptibility. This disease may assume a subacute or chronic type, usually the latter. The animal dies of inanition in from eight days to six or eight weeks. Several owners have reported deaths after only two or three days of illness, but the goats doubtless had been affected for a longer period, although not noticed on account of their mingling in the flock. Many of the animals live for weeks, but gradually become weaker and more debilitated, finally dying in a comatose condition. In no instance has the natural recovery of an animal after once the symptoms of takosis were noticed been observed or heard of.
The younger goats seem to be the most susceptible to the disease, although the old animals are by no means immune.
Pathological Anatomy. As already indicated, the general appearance of the carcase simulates that produced by a wasting disease. The visible mucous membranes are pale and anæmic, while the fleece, which appears somewhat dry and lustreless, furnishes a shroud for the extremely emaciated condition, that becomes plainly perceptible on skinning. The same anæmic condition of the subcutaneous and muscular tissues is observed on eviscerating the carcases. The lungs in most cases are the seat of a peculiar diversified inflammation, never of a remarkable extent. The external appearance of these organs is at times mottled, caused by a few congested areas, several patches of an iron-grey colour similar to areas of pneumonia during the process of absorption, and normal tissue. On section through the reddened patches, a frothy mucus may exude from the bronchioles, and in one case numerous punctiform hæmorrhages were observed on the sides of the incision. This tissue, while not so buoyant as a normal portion would be, nevertheless floats when placed in water.
The heart in all cases is pale and dull, its tissue soft and flabby, while inflamed areas, more or less penetrating, are present at times on the epicardium about the auricular appendages, and at other times on the endocardium, especially that lining the ventricles. These hæmorrhagic patches consist of either pure extravasated blood or blood mixed with serum, which gives them a more diffuse appearance and a gelatinous consistence. The pericardium is slightly thickened, and usually contains a small increase of fluid tinged with blood. The liver usually appears normal, although the gall bladder is frequently distended with pale-yellow watery bile. The kidneys are anæmic and softened. The cortex appears slightly thicker and paler than normal, and contrasts strongly with the darker pyramids. The capsule strips off easily from the parenchyma of the organ. In one instance several pale areas simulating anæmic infarcts were observed under the capsule extending into the cortex, which probably resulted from the compression of the capillaries by the swollen parenchymatous cells. The presence of albumin in the urine was detected by the nitric-acid test. The spleen appears atrophied and indurated, and on section the fibrous tissue far exceeds the splenic pulp. Attachments by fibrous adhesions may fix the spleen to the diaphragm or the neighbouring organs. The intestines may contain normal fæcal matter or semi-fluid fæces of a disagreeable odour. The surface of the mucous membrane is at times covered with a slimy mucus or plastic exudate, and the appearance is that of a chronic catarrh associated with necrosis of the mucosa.
Bacteriology. Examination of cultures and slides showed the presence of a micrococcus, usually arranged in the form of a diplococcus, which was found in pure cultures from the heart’s blood, spleen, kidneys, and pericardial fluid, and essentially so in the tubes inoculated from the other organs.
The specific organism of takosis appears in fresh bouillon cultures as a spherical or oval micrococcus with a diameter of 0·8 to 1 µ. In these cultures it is single or in chains of two, three, or four elements, but most frequently in pairs, as diplococci, with a diameter transverse to the axis of the chain greater than the longitudinal diameter.
Treatment: Prophylaxis. Sudden climatic changes should be avoided as far as possible, and when shipments of goats for breeding purposes are to be made which necessitate their transportation over considerable distances the changes should be made during the months of summer or late spring, and not in the fall or winter, when the contrast of temperature will be so much greater.
Angora goats should be provided with stables that are thoroughly dry, erected upon ground that has perfect natural drainage.
As a third measure of prevention may be mentioned careful feeding.
The segregation or isolation of all affected animals as soon as they evince any symptoms of the disease will be found a most valuable means of protection for those that remain unaffected, and a strict quarantine over all of the diseased members of the flock should be maintained so long as the disease remains upon the premises.
Medicinal treatment has proved unsatisfactory in many of the cases of takosis to which it has been applied. The best results have been derived from the administration of calomel in 0.1 gram doses twice daily for two days, followed by arsenic, iron, and quinine, as follows:
| Arsenious acid | 1·40 | grams. |
| Iron, reduced | 12·00 | „ |
| Quinine sulphate | 6·00 | „ |
Mix and make into twenty powders, giving one to each adult goat morning and evening at the conclusion of the administration of calomel. After an interval of two days this treatment is repeated. In case the diarrhœa persists, the sulphate of iron has been substituted for the reduced iron, with beneficial effects.
Conclusions. After preliminary investigation, the following conclusions have been reached:—
(1.) The disease described as takosis has appeared in many parts of America, but particularly in the Northern States, where it has caused great loss to many breeders of Angora goats.
(2.) It is a progressive, debilitative, contagious disease, characterised by great emaciation and weakness, with symptoms of diarrhœa and pneumonia, and causes a mortality of 100 per cent. of those affected and from 30 to 85 per cent. of the whole flock.
(3.) From the carcases of numerous animals that have succumbed a new organism, Micrococcus caprinus, has been recovered in purity, and is presumably the etiological factor.
(4.) This micrococcus possesses pathogenic properties for goats, chickens, rabbits, guinea-pigs, and white mice, but not for sheep, dogs, or rats.
(5.) Medicinal treatment was attempted with varying success, while the immunising experiments thus far conducted (although too few to permit of any conclusive statement or accurate estimate as to their protective value) have shown highly encouraging results. When accompanied with measures of isolation and disinfection, the treatment may prove of great assistance in the suppression and eradication of the disease in an infected flock.
BLOOD POISONING (MALIGNANT ŒDEMA) IN SHEEP AND LAMBS IN NEW ZEALAND.
This disease, which occurs during the operations of shearing sheep and of castrating and docking lambs, is the cause of considerable loss annually to sheep breeders in several districts of New Zealand. In 1893 J. A. Gilruth, Chief Veterinarian for New Zealand, issued a leaflet dealing with the disease and the preventive measures to be adopted. Generally the first thing that draws the owner’s attention seriously to the condition of his flock is the discovery, in from thirty-six to forty-eight hours after docking or shearing, of a few dead sheep lying in various parts of the paddocks. Next morning he finds a few more dead, and so on for three or four days, when, as a rule, the mortality ceases.
Symptoms. In the early stages of this disease the animal seems listless, disinclined to move about, and, if the sun is shining strongly, prefers to lie in the shade. If forced to move, the hind legs are drawn forward with a peculiar stiff, dragging motion, as if there were no joints. There are slight muscular tremors all over the body, which become spasmodic as the disease progresses. If the flock be driven about much, the diseased animal soon shows signs of great fatigue, ultimately dropping to the ground thoroughly exhausted. The breathing is fast and painful, being maintained more by a series of spasmodic jerks than by any regular act. The pulse is quick and weak; the temperature is very high, registering 106° to 108° Fahr., showing acute fever; the eyes close, and the whole face is expressive of pain. Gradually the spasms cease and coma sets in, resulting in death. The scrotum and surrounding skin right along the floor of the abdomen and between the hind legs become swollen and black. This gangrenous tissue, when present before death, can be peeled off without pain to the animal. On post-mortem examination various conditions are met with. The animals are generally found to be among the best of the flock and in fairly good condition. The scrotal and perineal regions in lambs (between hind legs and below tail) are always, or almost always, gangrenous, this condition extending along to the floor of the chest, and sometimes implicating the tail. Many of the muscles, generally those of the shoulders, haunches, and loins, are dark in colour and infiltrated with a black, watery fluid. The intestines are generally healthy, though sometimes the peritoneum is inflamed. The spleen and liver are in the usual condition after death, due to febrile disturbance. In the chest, either the pleuræ (coverings of the lungs) or pericardium (covering of the heart) are often inflamed, with occasionally a fibrinous exudation, causing surfaces to adhere.
Cause. In Gilruth’s report for 1900 he demonstrated the cause of blood poisoning to be a microbe known as the malignant œdema bacillus (Vibrion septique of Pasteur). This organism, which is found in many dirty yards, swampy soils, etc., on gaining entrance to the system of almost any animal by means of a wound, rapidly increases in numbers, producing gangrene, or death, of the part affected first, and ultimately the death of the animal.
Curative treatment is practically useless.
Preventive measures. Destruction of the carcases of animals which have succumbed to this disease by efficient burial or by fire. Disinfection of surface soil of yards, etc., by quick-lime. Cleansing of floors and walls of sheds with strong hot lime wash containing crude carbolic acid in the proportion of 1 to 50. Disinfection of flesh cuts made by the shears or the docking or castrating knife. Boiling of docking and tailing knives before use. Observance of antiseptic applications even when temporary yards are employed. Sheep and lambs after operation to be kept in a paddock free from swampy patches.
PIROPLASMOSIS.
Under the title piroplasmosis is included a group of diseases caused by hæmosporidia, and found in animals of the bovine and ovine species. These affections are far from having the same importance in temperate as they have in tropical countries; nevertheless, it is very important to be able to recognise them.
BOVINE PIROPLASMOSIS.
Bovine piroplasmosis has been described under different names, such as hæmoglobinæmia, hæmoglobinuria, Texas fever (U.S.A.), tick fever (Australia), tristeza (Argentine Republic), African coast fever, East Coast fever, redwater, Rhodesian fever (Cape), and bovine malaria.
Fig. 185.—Angora goats affected with takosis (photographed twenty-four hours before death).
(Ann. Rep. U.S.A. Bur. An. Ind. 1902.)
Fig. 186.—Angora goat six days before death from takosis.
(Ann. Rep. U.S.A. Bur. An. Ind. 1902.)
Fig. 187.—Angora goat (photographed three days before death).
(Ann. Rep. U.S.A. Bur. An. Ind. 1902.)
Fig. 188.—The same goat as shown in Fig. 187. Position assumed after exhaustive efforts to regain its feet. (Ann. Rep. U.S.A. Bur. An. Ind. 1902).
Fig. 189.—Portion of a steer’s hide, showing the Texas fever tick (Boophilus annulatus) of the United States. Natural size. (Styles. Ann. Rep. Bur. An. Ind. 1900.)
Fig. 190.—Two female ticks (Hyalomma ægyptium) ovipositing. Natural size. (Photograph by J. E. Emery. Annual Report, U.S.A. Bureau of Animal Industry, 1900.)
It was first described by Babès in 1888, in animals inhabiting the Danube Valley, and was termed by him bacterial hæmoglobinuria of the ox. Afterwards it was well described by Smith and Kilborne (in 1889) under the title of Texas fever. It was rediscovered in Finland by Krogius and Van Hellens in 1894; in Sardinia by San Felice and Loi; in Australia in 1895 by Pound; and it has been the object of remarkable investigations by Koch in South Africa (1898–1904).
Fig. 191.—Dorsal view of larva of Boophilus annulatus of North America. Greatly enlarged. (Stiles, Ann. Rep., U.S.A. Bur. An. Ind., 1900, p. 388.)
Nicolle and Adil-Bey (1899) state that it exists in a latent form in European Turkey and Asiatic Turkey; and Lignières (1900), after a series of researches in Argentina, suggests the final solution of the questions which it raises.
Symptoms. Babès describes it as an acute febrile disease, clinically distinguished by the passage of blood-stained urine. The urine is coloured by dissolved hæmoglobin; red blood corpuscles are not found. Smith and Kilborne, and afterwards Stiles, described two forms: an acute, rapidly fatal form, in which the Piroplasma bigeminum is found in the blood of the general circulation, in the spleen and kidneys; and a chronic form, in which, notwithstanding the absence of clinical signs, the parasites may be discovered in the blood under the form of diplococci.
Lignières describes a grave and a benignant form. The grave form is indicated by dulness, loss of appetite, and considerable fever. In twenty-four hours the temperature rises to 104° or 105° Fahr., and the pulse to 100 or 120 per minute, while the respiration is greatly accelerated.
The urine is of a light-red or brownish-red colour, resembling coffee-grounds, but it contains no blood corpuscles. The animals die in from three to eight days with symptoms of asphyxia; but this termination is not inevitable, and recovery may occur spontaneously. Improvement is indicated by a fall in temperature, disappearance of the blood-stained urine, and a return of appetite, together with marked thirst.
Fig. 192.—Ventral view of larva of Boophilus annulatus of North America. Greatly enlarged. (Stiles, Ann. Rep., U.S.A. Bur. An. Ind., 1900, p. 388.)
Drs. Smith and Kilborne describe the symptoms as follows:—“The beast when first observed to be amiss appears to be dull and sluggish, with a disinclination to move, and hence it is generally found apart from the rest of the herd. The hair stands erect like that of an animal on a cold day (a staring coat), the ears hang, and the eyes have a dull and lustreless appearance. In some cases the animals cease to feed, or ruminate, in others they continue to nibble at the herbage until nearly the last, but in a languid, indifferent manner, indicating that they have little relish for their food, and they fall off very rapidly in condition. There is generally a dribbling of saliva from the mouth, the muzzle may appear quite moist during the early stages of the disease, but it invariably becomes dry and crusty as the disease advances. Later on the animal manifests a strong reluctance to move, and when compelled to do so, it walks with a dragging, straddling gait, as if weak across the loins. In severe cases, when the sick beast is left undisturbed, it will remain almost constantly in one place, standing with its head depressed and ears hanging in a drowsy semi-comatose condition, looking the very picture of complete nervous prostration. Other animals will lie down the greater part of the time and scarcely move, and when dead the limbs will be found in their natural position, and the head doubled round on the shoulder as if asleep. On making a post-mortem examination of some of these cases the carcase was found to be pale and bloodless, as if the animal had been bled to death.
Fig. 193.—Scutum and scutellum of female Boophilus annulatus, showing mouth parts, porose areas (p. a.), and eyes (e). Greatly magnified. (Stiles, Ann. Rep., U.S.A. Bur. An. Ind., 1900, p. 392.)
“In other acute cases a twitching and quivering of the muscles will be observed, especially of those situated in the flank and behind the shoulder. The pulse and breathing are much quickened, and the animal will stand and grind its teeth and curl up its upper lip, indicating great uneasiness and pain. The fæces during the early stages of the disease are very often soft, with a tendency to diarrhœa, more especially in transport oxen on the road, but they invariably become hard as the disease advances; but whether hard or soft, they have generally a brownish tinge, and often mixed more or less with blood and mucus. In some severe cases which recover, the favourable crisis is often ushered in by a salutary diarrhœa.”
In the benign form the animal for the space of about a week shows indifference to its surroundings, loses its appetite, wastes, and, less frequently, has slight feverish symptoms, without discoloration of the urine. The only reason for the belief that this trifling disturbance is due to piroplasmosis is furnished by examination of the blood, in which the parasites may be found in very small numbers in certain blood corpuscles.
Calves seldom take the disease except in the benign form.
Fig. 194.—A, red blood corpuscles containing pear-shaped Piroplasma bigeminum (the typical form); B, red blood corpuscles containing round Piroplasma bigeminum. (After Lignières.)
Lesions. At first glance the lesions appear to resemble those of anthrax, but may be differentiated from them in many details.
The skin is covered with ticks or shows traces of their punctures.
Fig. 195.
The myocardium appears as if boiled, the spleen is invariably hypertrophied and two or three times as large as in the normal state.
The kidneys are violet in colour and congested, and the adipose layer surrounding the kidney is infiltrated with a yellowish serosity. The urine may present a variety of tints, derived from hæmoglobin. The liver is often engorged with blood and the gall bladder always distended.
When convalescence sets in, icterus appears; but it is a special kind of icterus, depending on changes in the hæmoglobin—in fact, a hæmaphæic icterus. Histological examination of the blood furnishes the explanation of the disease by revealing the presence of the parasite.
Fig. 196.—Slow formation of free germs. 1, Pear-shaped organisms with large chromatic element and a flagellum; 2, newly-developed round cell without chromatic element; 3, 4 and 5, formation of the chromatic elements; 6, the germs about to escape; 7, the germs freed. (After Lignières.)
Pathogeny. The parasite is the Piroplasma bigeminum, which is easily demonstrated by drying the blood, fixing it and staining with very weak methylene blue. The blood is light in colour and pale, and the serum is tinted by the dissolved hæmoglobin. The blood corpuscles diminish in number with extreme rapidity while the parasites are developing, and in twenty-four or forty-eight hours may fall from some six millions and a half, the normal number, to one million or even to two or three hundred thousand red blood corpuscles per cubic millimètre.
Fig. 197.—Rapid formation of free germs. 1, Newly-developed round parasite without distinct germs; 2, round parasite with two germs; 3, the germs approaching the surface and undergoing development; 4, the germs beginning to grow outwards preparatory to forming new round parasites; 5, the process previously noted is becoming more marked; the protoplasm of the cell is undergoing degeneration, and scarcely stains at all; 6, round parasites. This completes the cycle. These parasites (6) are similar to (1). (After Lignières.)
This destruction is due to the action of the piroplasmata, as may be shown by staining with a ·5 per cent. methylene blue or carbolised thionine. These parasites usually assume a simple pyriform shape, and two or three may be found in one blood corpuscle. The number of parasites and infected blood corpuscles is generally in direct ratio to the intensity of the infection. These parasites are found throughout the blood, but principally in that of the spleen, kidneys, and mesenteric veins. They are only abundant whilst the temperature is rising or at the moment when it reaches its highest point, and they often disappear before death or convalescence.
The pyriform shape is only temporary, and corresponds to the acute phase of the disease, but the parasite assumes the round form as soon as convalescence sets in. This round form gives birth to one, two or three spherical spores, which are set free in the plasma after the destruction of the maternal protoplasm, and are able after transference to a fresh red blood corpuscle to again assume the pyriform shape peculiar to the grave forms of disease.
The parasite can only be cultivated in defibrinated blood from a hæmoglobinuric subject, and the cultures do not always yield more than reproductions of the round form, the pear-shaped form only being produced with red blood corpuscles in the living animal body.
Regarding the method of growth of the piroplasma in the body and in cultures, Lignières believes that the parasite may produce two forms of spores differing in their nature. One, the active spore, has little resisting power. It soon degenerates outside the animal body, forms rapidly at the expense of one of the pear-shaped parasites, and may immediately reinfect another red blood corpuscle. The other, called the passive spore, is very resistant, and retains its vitality for a long time outside the body, being produced at the expense of spherical parasites already withdrawn and incapable of producing the disease.
The form of piroplasmosis at present under consideration is peculiar to the ox, and none of the other domestic animals or experimental subjects can be inoculated with it.
Subcutaneous or intravenous inoculation of the ox with 5 to 10 cubic centimètres always gives positive results when made with blood or active products, such as the pear-shaped parasites or active spores, but is ineffectual when the parasites have already begun to retract in order to form passive spores.
Calves seldom contract more than the benign form of the disease, and do not die.
In the grave form following experimental infection the temperature begins to rise between the third and sixth day, and corresponds with a marked increase in the number of parasites to be found within the red blood corpuscles. The urine at first becomes albuminous, then hæmoglobinuric, whilst the red blood corpuscles diminish in number to a very marked extent, falling from about six or seven millions to one million, or even a few hundred thousands, in the course of a few days. The temperature, which may previously have risen to above 105° Fahr., suddenly falls, indicating the approach of death.
If an immediate autopsy is made, the spleen is always found to be enlarged, the intestinal mucous membrane reddish in tint or blood-stained, and the serous membranes, particularly the endocardium, covered with petechiæ.
Few or no parasites can be discovered except in the blood from the cardiac muscle and the kidneys.
The grave form may end in recovery. This end is indicated by the temperature remaining normal after defervescence, the appearance of hæmaphæic icterus of an obstinate character, and the progressive return of appetite.
The disease is usually transmitted by adult and larval ticks carrying the parasite from infected animals. Lignières has proved that this transmission occurs through the medium of passive spores, which, though themselves incapable of producing the disease, become active and infective in consequence of the local irritation produced by the poisonous saliva of the ticks.
The pathogeny of Texas fever may be shortly summed up as follows:—Animals suffering from the disease carry in their blood a protozoan organism called the Piroplasma bigeminum, analogous to the parasite of human malaria; once introduced into the blood, this organism remains there in an active condition throughout the animal’s life; it is transferred to susceptible cattle either within or without the infected district by the Southern (U.S.) cattle tick Boophilus annulatus; Southern cattle, although carrying the protozoa, are harmless unless infested by this particular tick: the mature ticks and their eggs contain the protozoa, and the mystery of certain grounds over which infected animals have passed being first dangerous, then harmless, and again dangerous depends on—(a) the infestation of the ground with mature infected ticks; (b) the destruction or death of the mature ticks; and (c) the hatching out of new (infected) ticks from the eggs laid on the ground by the mature female ticks.
Dr. Salmon states that in Texas a successful method of protection is in practice based on the observations that young cattle do not suffer so severely as adults, and that the disease always assumes a milder form in winter. Young animals introduced during the winter are inoculated with virulent blood. They contract a mild form of disease, and afterwards resist. In this way the losses, which previously amounted to 90 per cent. of all freshly introduced stock, have been reduced to about 10 per cent.
A remarkable and very interesting observation (if absolutely reliable) deserves to be mentioned, viz., that the ticks develop regularly in the natural prairie, but do not develop in parts artificially sown with grass such as lucern, and that when contaminated or diseased animals are transferred to artificial meadows they do not convey the disease to other animals already there; the latter are proof against it.
Diagnosis. The disease is so typical that it cannot be mistaken for anthrax. In anthrax the urine is never hæmoglobinuric and very rarely hæmaturic, and the fæces are sometimes blood-stained, a symptom never present in piroplasmosis. Anthrax can be transmitted to experimental animals, but piroplasmosis cannot.
Prognosis. The prognosis is generally grave.
Treatment. Van Hellens recommends the use of quinine in large doses. He give 5 drachms in one dose, and repeats it for the next two, three, or four days.
Lignières says that he has never obtained the slightest success with quinine, though it is true he has never given higher doses than 2½ drachms.
Attempts have been made to confer immunity by injecting animals with serum from others which have recovered. Vaccination with the blood of patients arrived at the period of convalescence has also been tried. The results, however, have not been very satisfactory.
Lignières has formulated an efficient method of vaccination, of which he has not yet published the full details, but which appeared by reason of its simplicity likely to render great service. Nevertheless, his most recent reports seem to show that vaccination is not always efficacious, and that in the Argentine Republic alone several varieties of the disease exist, two being caused by allied but different parasites. The vaccine used against one variety is powerless against the other. The problem of vaccination would therefore appear to be much more complex than in the case where one form only occurs in any particular country.
The immunity arising from attacks of piroplasmosis is in direct ratio to the gravity of the disease, and according to Lignières’ views this acquired immunity is due to the secretion by the piroplasma of a substance which is toxic for the red blood corpuscles. This toxic substance provokes, as in other diseases, an organic antitoxic reaction.
BOVINE PIROPLASMOSIS IN FRANCE.
Until recent years it did not seem that piroplasmosis occurred in France. It had been detected in Algeria, although its existence had not been conclusively proved. Mathis claims to have met with it in the department of the Loire in 1896 and in the Ain in consequence of the importation of Algerian cattle, but its ravages were comparatively trifling.
Having good reason to suspect that certain morbid conditions, known as mal de Brou, might be due to piroplasmosis, Lignières endeavoured to verify his theory, and discovered that sometimes, but not often, this disease was mistaken in France for anthrax and mal de Brou. Piroplasmosis in France appears less grave than in America, and is rarely fatal.
As regards its symptoms, it usually develops suddenly with fever, loss of appetite, acceleration of the pulse and respiratory movements, suppression of the milk secretion, and the passage of red hæmoglobinuric urine. In exceptional cases death may occur in from three to five days.
On post-mortem examination a varying number of ticks (Ixodes hexagonus) are found on the skin, the spleen is always increased in size, and the kidneys are black and hæmorrhagic.
The disease transmitted by ticks, as in Texas fever, seems due to the presence of a round parasite, different from the well-known Piroplasma bigeminum.
The elucidation of this disease, which occurs towards the northern frontier of France in the neighbourhood of Maubeuge, calls for further investigation. It never appears to be very fatal, and it attacks more especially animals imported into the infected region. A method of vaccination identical with that used by Lignières against one of the forms of the American disease may perhaps in the future prove available against the disease in France. Until then the best treatment would appear to consist in free subcutaneous injection of saline solution and the administration of evacuants, sulphate of quinine, and laxatives.
OVINE PIROPLASMOSIS.
Causation. The existence in France of this disease has not yet been clearly established, for in the only communication on the subject (by Leblanc in 1899) the writer seems to have confused the toxic hæmoglobinuria produced by feeding on decomposed beet pulp with the parasitic hæmoglobinuria due to piroplasmosis.
In Italy ovine piroplasmosis was described by Bonomo in 1896 under the title of parasitic icteric hæmaturia of sheep. It is said to be due to a parasite of the red blood corpuscles (Amœba sporidium polyphagum), the said parasite being of oval form, very refractile, always occupying an outer position near the free margin of the corpuscle, and sometimes floating freely in the plasma.
According to Babès, who described it under the name of gurceac du mouton, the same disease appears to occur in the islands and low parts of the Danube valley.
Symptoms. The development of this parasite produces in the patient loss of appetite and high fever, accompanied by the passage of dark coloured hæmoglobinuric urine. Icterus is frequently present. The animals rapidly become exhausted, collapse and die.
On post-mortem examination carried out immediately after death the spleen is found to be large, the pulp being like wine lees. The liver is soft and yellowish; the kidneys are soft and black.
The disease is said not to be transmissible by direct transfusion (?).
It would appear that this disease has also been seen in Turkey by Nicolle and Laveran, near Constantinople, in 1899. The parasites (Piroplasma oris) are round or slightly elongated and occur near the periphery of the red blood corpuscles. It is to be hoped in the interest of breeders in localities where this disease rages that Lignières’ method of vaccination against bovine piroplasmosis may prove reliable and equally applicable in the case of sheep.
DISEASES PRODUCED BY TRYPANOSOMATA.[[5]]
[5]. An interesting article and a series of figures on the “Evolution of the Trypanosoma Evansi” were published in the Jour. of Comp. Path. and Therap. for September, 1904, p. 210. The same number also contained articles on several piroplasmic diseases.
In 1904 Professor Koch delivered an address, from which the following is a summary, to the Berlin Medical Society regarding his experiences and observations on diseases produced by trypanosomata in Africa:—
A wide field of study has recently been opened by the discovery of various pathological protozoa. Three discoveries especially have directed attention to these special disease organisms—
(1.) Laveran’s discoveries regarding malaria. Ross has shown that the malaria parasites are carried by mosquitoes (Anopheles claviger).
(2.) The discovery of the protozoa of Texas fever by Smith. In this case ticks (Rhipicephalus (boophilus) annulatus) convey the disease.
(3.) The discovery of the trypanosoma of the tsetse disease, which is conveyed by a stinging fly (Glossina morsitans).
These discoveries were followed by numerous others indicating protozoa as causes of disease.
The trypanosomata are morphologically distinguished by the existence of a flagellum. When fresh blood is examined it is scarcely possible to overlook the protozoa in the preparation, for attention is at once attracted by the energetic way in which the red blood corpuscles are continually being displaced. The peculiar form of the protozoa, however, can only be detected in stained preparations. Romanowsky’s staining method is probably the best. Trypanosomata stained by this method show a fish-shaped body, the front end of which carries a flagellum. The body of the trypanosoma is coloured blue. At the anterior end may be seen a red-stained nucleus; at the opposite end a much smaller red spot, which has been termed the nucleolus, but is more properly described as the centrosome. From the centrosome a red thread extends along the outer margin of the body as far as the front extremity, where it becomes continuous with the flagellum.
The trypanosomata increase by longitudinal fission. The centrosome and then the nucleus divide, and finally a second flagellum is formed. Sometimes the young trypanosomata remain connected, producing the so-called “rosettes.”
The disturbance produced by trypanosomata seldom becomes acute, but often continues for years. The only sign of disease consists in ill-defined fever with long intermissions. The destruction of the red blood corpuscles causes anæmia, the animals or men become weak and waste away, œdema and sometimes erythema occur at varying points in the body, and occasionally the lymphatic glands become swollen.
The classical land of the tsetse disease is in the neighbourhood of the Zambesi. There it was seen and very well described by Livingstone; but, unfortunately, further investigations have shown that tsetse disease extends over the whole of Africa.
Whilst the trypanosomata of rats can only be conveyed to the one species, those of tsetse disease thrive in all mammals, particularly in the horse, mule, ox, dog, rat, and mouse.
The tsetse organism has been shown to kill both horses and mules, but to be less dangerous for oxen. A certain relative immunity exists in some races. As regards the ass, observers are not agreed; Koch failed to infect it. Sheep and goats are also but slightly susceptible. The conveyance of trypanosomata from the blood to uninfected animals occurs through the medium of a stinging fly (the Glossina morsitans).
Surra is endemic in the Philippines, Java, and the island of Mauritius. Koch regards the trypanosomata of surra as strictly analogous with the parasites of tsetse disease. Horses (and, in India, elephants) especially suffer from surra. Although the Glossina morsitans does not occur in India, other stinging flies replace it and convey the disease.
Another variety of trypanosomiasis is mal de caderas, seen in South America, particularly in Argentina and Brazil. It affects horses. According to Koch, the parasites of mal de caderas exactly resemble the tsetse and surra parasites. Other observers, however, declare that the mal de caderas parasites are distinguished from those before mentioned by their particularly small centrosome. Mal de caderas affects not only horses, but all the other animals which suffer from tsetse.
Another variety of trypanosoma, the trypanosoma Theileri, is especially striking on account of its size. It is only found in oxen, and exhibits a very slight degree of virulence.
Koch divides trypanosomata into two great groups.
The grouping is based on three important peculiarities: firstly, the morphology of the parasite; secondly, its virulence; and, thirdly, its relation to the host.
The first group only exists in one species of animal. They have become so completely accustomed to this method of life that they cannot exist under other circumstances. Their virulence is slight but constant. This group comprises the trypanosoma of rats and the trypanosoma Theileri.
The second group (to which all other trypanosomata belong) shows great variation in virulence and in form. These trypanosomata are not peculiar to any one species, but may affect dogs, rats, horses, etc. Their morphological peculiarities also vary according to the animals in which they are found. Thus, the tsetse parasites when cultivated in the bodies of dogs and rats become much smaller than usual, and the centrosome appears near the end; when cultivated in horses the end appears pointed, and the centrosome lies near the centre; in the pig the parasites lose their peculiar short flagellum. Their virulence also varies within wide limits.
It has been found possible, as in the case of bacteria, to modify the virulence of trypanosomata by successive passages through different animals. By inoculating dogs with comparatively innocuous trypanosomata and conveying the disease from dog to dog the virulence is markedly increased. On the other hand, parasites which prove very virulent for oxen become much less active for these animals after passages through rats and dogs. This apparently trifling discovery laid the foundation for protective inoculation experiments. Parasites of the second group can also exist in the bodies of almost all mammals.
Koch is of opinion that the parasites of surra in India and of tsetse disease in Africa are absolutely identical. Laveran, on the other hand, states that he has protected animals against tsetse, and that they have nevertheless suffered from surra.
That this in no way disproves the identity of the two parasites is shown by other experiments.
Koch, whilst in Dar-es-Salaam, made some interesting experiments for the purpose of discovering a method of protective inoculation. He had found that the virulence of the ox parasites could be modified. He therefore inoculated oxen first with these weakened parasites and afterwards with others of high virulence. All the control animals died while those treated as above remained alive.
Veterinary Surgeon Schmidt kept these animals under observation, and reinoculated them from time to time with highly virulent material, notwithstanding which they were still perfectly well six years after the first inoculation.
In practising this method, however, the trypanosomata used for the first inoculation must not be unduly weakened. The method would have appeared fully successful were it not for the fact that the protected and apparently quite vigorous animals still suffered from the presence of parasites in the blood. To extend its use, therefore, meant that one would not suppress, but would spread the disease. The effect would be to produce herds harbouring the parasite, which herds, though exhibiting no signs of illness, would nevertheless in a sense be propagating the active cause. Further observation has also shown that the protection so conferred is only relative. Dogs can always be infected with the blood of such animals. It has long been known in Africa that antelopes and buffaloes harbour trypanosomata in their blood without showing external signs of disease.
Another method of protection must therefore be sought, such as destroying the various stinging flies; but this offers little hope of success. Koch admits that he sees no method of dealing with them. The other method is directed against the parasite, and here he seems more hopeful. The disease can be rooted out by killing all diseased animals suspected of disease. The line of procedure is indicated by the experience gained in Mauritius and Java. When surra broke out in Mauritius almost all the oxen died in two years. In Java the nature of the disease was early recognised, and all suspected animals were at once slaughtered or isolated until slaughtered; in this way the disease was soon stamped out.
LOUPING-ILL.
The close analogy between the convulsive form of the disease described as “trembling” (which disease is well known in France) and the condition known in Britain as louping-ill lead us to give here a short account of the latter condition. For a great part of what follows we are indebted to articles by Meek and Greig Smith, published in the Veterinarian, Vol. LXIX, Nos. 820 and 840.
Nature and Symptoms of the disease. The disease known usually as louping-ill or trembling has long been of annual and sometimes of biennial recurrence in certain parts of Great Britain. In these places sheep farmers look for the appearance about the middle of April, to its continuation during May, and to its gradual disappearance early in June. Lambs are most liable, but sheep are also quite susceptible to the disease, and in both the symptoms are the same. The disease under consideration is rendered quite distinct by certain well-known symptoms. Though these have been described in various ways, the disease can be recognised by the more or less complete paralysis of the body and limbs. Symptoms may succeed one another very rapidly, or may be spread over some length of time. The animal at first loses control over the muscles, which are seen to twitch convulsively. It may fall down and struggle on the ground, sometimes jumping up again, often to some height. Between the fits it is often seen to stand trembling. These symptoms are frequently accompanied by frothing at the mouth. Some such appearances are the usual onset to the disease, and are followed by a paralysis which usually affects the hind limbs, but may also include more or less of the body and the head and neck. The fore limbs are often similarly paralysed. The affected limb or limbs become cold to the touch. The paralysis necessarily brings the animal to the ground, though it may be able to crawl about by the aid of the unaffected legs. When the head and neck are affected the former is usually drawn to one side, and the eyes often become oblique. Excitement is greatly increased when the animal is disturbed. The symptoms, then, in a few words are more or less complete paralysis, preceded as a rule by fits and trembling.
The small number which recover present “a wry neck, stiff joint, high back, or other deformity.” During recovery swellings occur at the joints; these may be pierced with good results, giving a large discharge of pus. According to Fair, in the Veterinarian, Vol. VIII., “these abscesses usually appear in the neighbourhood of the joints, but sometimes above the arms, the brisket, or any neighbouring part of the body.”
While the disease is characteristically a sheep ailment, other animals are also liable. Swine fed with the carcases or blood of sheep which have succumbed to louping-ill die with every characteristic of the disease in a short time. If the carcase has been boiled this does not occur. Swine will also frequently take the malady if allowed access to the grass of affected fields. Cattle are said to take the disease, and in the North Tyne district it is said that if a cow takes louping-ill, the milk will give the illness to a calf or lamb. One or two cases of horses being attacked are also reported.
Regarding the infectious character of louping-ill, the following is very well known. Sheep bred on diseased places are not nearly so liable to the disease as sheep which have been introduced from unaffected places. Louping-ill may be introduced into a new place, but in such cases, unless the importation from affected farms be continued, the malady may disappear.
Distribution of the disease. In Great Britain it is confined to the North Tyne district of Northumberland and to the contiguous border counties of Scotland, extending into Kirkcudbrightshire and certain valleys of Dumfriesshire. It is rare in Berwickshire, common in the north and west of Roxburghshire and the similar hilly districts of Selkirkshire and Peeblesshire. It occurs in Ayrshire, to a slight extent in Lanarkshire, and is found in the western parts and islands of Argyleshire and Inverness-shire.
Not only is the disease very circumscribed in its distribution as a whole, but locally in the places mentioned infected and non-infected spots are pointed out. These may be quite contiguous. The flocks in the North Tyne district feed up and down the hills in limited “cuts,” and it is one of the features of the illness that certain “cuts” are very liable to it, while others, even on the same farm, are just as free. In many cases the nature of the pasture is such as to suggest to an experienced man the probability of its being subject to the disease. A dry and foggy pasture seems best suited for harbouring the cause of the malady. These infected places have remained wonderfully constant, but a peculiar feature about them is that some may be very bad for louping-ill one year, and others bad another year. Of two adjoining farms, one may be badly attacked and the other mildly, while in the following year the conditions may be reversed. Districts may present the same peculiarities. Thus, though the disease is essentially endemic, it is not absolutely constant in its recurrence. There seem to be certain circumstances capable of favouring or retarding it.
Fig. 198.—Larva of the grass tick.
Length, ¹⁄₄₀th of 1 inch.
Fig. 199.—Pupa of the grass tick.
Length, ¹⁄₁₈th of 1 inch.
Lesions. The chief lesions are localised in the membranes of the brain and spinal cord, which are congested or inflamed, and contain an increased amount of cerebro-spinal fluid or a jelly-like, sometimes blood-stained exudation. Softening and hardening of the spinal cord have both been observed. Inflammation of the pleura and pericardium, with fluid or jelly-like exudation, are common; lobar congestion of the lungs, endocarditis, gastritis, and enteritis have all been described; some observers have mentioned congestion of the kidneys and liver and swelling of the spleen. Lesions of the nerve-centres are the most constant and reliable.
Etiology. Depressing and weakening influences of all kinds have been blamed for producing the disease, but the general consensus of opinion points in the direction of infection with microorganisms carried and introduced into the sheep’s system by the common sheep tick or “grass tick” (Ixodes redurius). The following remarks on, and illustrations of, this parasite are from an article by Mr. Wheeler, of Alnwick (Veterinarian, Vol. LXXIII., No. 867, p. 141).
Life History of the Grass Tick. Sheep ticks (which must not be confused with the sheep-ked, or keb, a wingless six-legged fly, universal on sheep everywhere) are allied to the spiders. They pass through four stages of existence: the egg—the six-legged larva—the eight-legged pupa—and, finally, the eight-legged adult male or female.
Fig. 200.—Adult male of the grass tick. Length, ⅑th of 1 inch.
Fig. 201.—Adult female. Length, ⅐th of 1 inch.
In each of the three stages of larva, pupa, and adult female, all species of ticks attack some “host” or animal, either beast, bird, or reptile, to which they attach themselves by the “rostrum” or beak, and become greatly distended by suction of the host’s blood. When replete they fall to the ground—if a larva or pupa, in order to undergo its metamorphosis to the next stage of its existence, and afterwards seek a fresh host; if an adult female, to lay its eggs amongst herbage. The adult male is not capable of distension by suction, though it equally attaches itself to a host.
After undergoing metamorphoses, grass ticks, with the exception of males, are light in colour, soft and lethargic, and remain concealed for some time while recovering strength before seeking a fresh host.
Professor Neumann alludes to the fact that a fresh host is sought by ticks three several times during their existence.
The Larva. When first hatched out from the eggs, which are supposed to be laid at the roots of coarse herbage, the young ticks are white and soft, but soon gain strength. Provided the weather is favourable, they climb up the stems, and, holding by their two posterior pairs of legs, await the passing of a host, employing their two front legs as insects use their antennæ.
In this, as in other “free living” stages of their existence, the young larvæ show great activity, attaching themselves and clinging tenaciously to any moving object. They appear to be more numerous on the rank rushes growing in damp, undrained places.
Fig. 202.—Partially distended female. The dotted white line represents the size of the tick before distension.
On finding a host, larvæ attach themselves by the rostrum, and remain there for about two days, by which time they are distended, black and globular. At this time they are easily detached from the host, and have lost their activity and clinging habits.
The Pupa. The possession of eight legs distinguishes the pupa easily from the larva. The extra pair are placed behind the others. After the metamorphosis, the pupa takes up its position on the stalks of herbage, just as the larva had done, for another chance of attachment to a host. But whereas adult grass ticks seem to confine themselves mostly to sheep, cattle, and deer, the larvæ and pupæ attach themselves very readily to various hosts, such as horses, dogs, and even human beings. After about four days the pupa is again replete with blood, black and opaque, and again drops to the ground to undergo its second and final change.
Adults. On reaching the adult age, both males and females again wait on herbage for a passing host. At this time, as well as after distension of the female on the host, an action which appears to be sexual intercourse freely takes place, even in confinement. On the host the females gradually distend (Fig. 202), and in the course of so doing vary much in colour and appearance. When fully replete, the female Ixodes reduvius becomes globular and black. One taken in this condition on April 15th commenced to lay on May 12th, and a few others taken at the same time commenced shortly afterwards.
Grass ticks never remain on the host to undergo metamorphosis or to lay eggs. They must therefore during their cycle of existence contrive to find a fresh host no fewer than three times.
In an article published in the Transactions of the Highland and Ag. Soc. for 1902 Mr. Wheeler draws attention to the close points of resemblance between louping-ill, Texas fever, tsetse fly disease, surra, heart-water, yellow fever, and malaria.
In the article previously referred to he summarises his conclusions as follows:—
One species only of tick, Ixodes reduvius, commonly known as the grass tick, has been found to carry the louping-ill bacillus to the sheep. It is easily recognised by the red body of the young females, the legs, shield, etc., being dark brown.
It lays its eggs, and undergoes its metamorphoses, in coarse herbage, and after each change seeks a fresh “host” on which to distend itself to a large size by suction of blood.
Fig. 203.—Female, under size.
Fig. 204.—Headless female.
In all stages grass ticks abstain from all food except when on a host, and they are endowed with extraordinary powers of fasting until a host is found.
Ticks soon die of drought where there is no good harbourage among rank vegetation.
Judging from analogy, it is probable—
That the bacillus can only be obtained from a diseased sheep, and inserted by the tick into another sheep.
That ticks convey the bacillus through their eggs to their offspring, as well as retain it through their metamorphoses.
That there is no danger in removing sheep from foul ground to cultivated lowlands, but that the disease is easily imported from one hill farm to another.
Strong and fat animals are nearly as susceptible to attack as weakly ones.
If the land is once free of disease, it can only be re-imported by diseased sheep, or ticks taken from them.
SUGGESTED MEASURES FOR PREVENTION.
Burning and cutting of long grasses, bracken, rushes, etc.
Salt and sulphur given to the sheep.
Inoculation.
Removal of all diseased sheep to a separate inclosure, where hand-picking and dipping are carefully attended to, the pasture is kept short, and damp places are drained. The sheep to be confined to this inclosure so long as the tick season lasts.
Immediate slaughter and burial of all affected sheep.
BRAXY.
[The following is a very condensed account of a paper published by C. O. Jensen on the above disease. It first appeared in English in the Veterinarian, Vol. LXIX., No. 825, p. 621, along with the original illustrations.]
The name Braxy is applied to a disease in some respects resembling anthrax, which appears as an epizootic, and is best known in Iceland, the Faroe Islands, and parts of Norway, though it also occurs in Scotland and Cornwall. Krabbe describes the disease as infectious, very acute in its course, and as proving fatal within a few hours of the appearance of certain characteristic swellings about the posterior parts of the body. Post-mortem reveals extensive dark purplish staining of the abomasum and distension of the digestive canal with gas, while decomposition of the cadaver occurs with excessive rapidity, the liver and kidneys undergoing softening, the skin assuming a bluish tint, the wool becoming loose, and the entire carcase giving off a most offensive stench. Krabbe states that the disease was regarded as a form of anthrax—a view, however, in which he does not coincide. Somewhat later Messrs. J. Sigurosson, S. Jönsson, and Einarsson, all natives of Iceland, and the Norwegian State Veterinary Surgeon, Ivar Nielsen, carefully described the disease, throwing considerable light both on the conditions in which it appears and on its etiology.
According to them, braxy is an acute, or even exceedingly acute, infectious disorder, which begins as a hæmorrhagic inflammation of the mucous membrane of the abomasum, is accompanied by excessive development of gas in the digestive canal, especially in the stomachs, and proves fatal in some cases by a kind of general infection, in others by a specific intoxication, or by dyspnœa due to tympanites.
Braxy commits its chief ravages during the winter months: appearing first in autumn, the cases increase as winter approaches, to diminish again in spring; in summer they are exceedingly rare. This fact explains why the disease was so long regarded as due to climatic influences. Even at the present day, when it is known to be due to a specific organism, the action of temperature, etc., must still be regarded as probably playing an important part in infection. The disease is said not to occur in mild weather; but whether or not this be true, every one is agreed that it is principally seen during frost, especially when frost is unaccompanied by snow.
From experience gained both in Iceland and Norway, the disease appears to be often localised in certain districts and fields—a fact largely accounted for when we learn that up to the present little or no attempt has been made to prevent the spread of infection from the dead bodies.
Braxy chiefly attacks young animals, and is rare in those over three years of age. Hjaltelin estimates the number of deaths in a single district during the years 1849–1854 at approximately 6,000, made up as follows:—
| Yearling lambs | 2,440 |
| Two-year sheep | 2,460 |
| Three-year sheep | 1,020 |
| Animals older than three years | 80 |
The younger animals suffer most, and in Norway Nielsen directs attention to the heavy fatalities amongst lambs.
Symptoms. The sheep suddenly appears ill, is dull, lies about, and cannot be induced to rise; all movement seems to give pain, and from time to time the animal groans; the posterior parts of the body become swollen, and a little froth often escapes from the mouth. The pulse varies between thirty and thirty-five per minute, and is often imperceptible in the extremities; the temperature may rise to 105° or even 108° Fahr. This condition may last some hours, and always ends with the animal’s death; sheep, which overnight had shown no signs of illness, are often found dead in the morning. The incubation period is from forty-eight to sixty hours, but ordinary cases seldom live longer than from five to eight hours after the symptoms declare themselves.
The striking post-mortem appearances, especially the hæmorrhagic inflammation of the abomasum, were early the subject of remark. This appearance is very characteristic.
If the animals are slaughtered, the most important change is found to be a purplish, dark, somewhat swollen patch in the abomasum; during the course of the disease this increases in size, and if the animal should be allowed to die of braxy the entire abomasum shows hæmorrhagic or sero-hæmorrhagic infiltration; the abomasum and the first part of the small intestine usually contain no food, but may often show a certain amount of bloody fluid. This hæmorrhagic inflammation may extend in a forward direction, implicating the other stomachs, or backward, invading the small or both small and large intestines. The other parts of the intestinal canal are congested. The pleural and peritoneal cavities contain a little serous fluid. The blood is dark in colour, but may be clotted; the spleen is at times somewhat swollen, at others normal. The liver is usually light-coloured, soft, and degenerated; occasionally this degenerative process is extremely marked, but due allowance should always be made for post-mortem change. The kidneys may appear degenerated; in many cases they are enlarged and soft, or almost fluid in consistence. The carcase decomposes very rapidly; within a short time of death the belly is distended with gas, the rectum protrudes at the anus; the skin assumes a bluish colour in places, and the wool falls out; sometimes the skin bursts, revealing the presence in the subcutaneous tissue of a sero-hæmorrhagic fluid.
Fig. 205.—The shaded areas of the above map indicate the distribution of braxy.
Braxy is, then, a primary violent hæmorrhagic inflammation of the abomasum, with or without secondary general infection.
From careful study it seems quite certain that the Scottish “braxy” is identical with the Norwegian and Icelandic “bradsot”; it appears at the same season, and is intimately connected with climatic influences; it runs its course so rapidly that animals left healthy at night are found dead in the morning; and the pathological anatomy of braxy is the same as that of “bradsot.”
To Ivar Nielsen, of Bergen, must be ascribed the honour of elucidating the etiology of braxy. During the course of investigations, published in 1888, he found, partly in the local lesions of the intestinal track, partly in the capillaries of the internal organs, a special bacillus, easy to distinguish from that of anthrax, of which he gives the following description:
“The bacilli (B. gastromycocis-ovis) are oval, of a length varying from 2 to 6 micromillimètres, and a thickness of one micromillimètre. They are often in pairs, arranged in a straight line or meeting at an angle; in the former case, and especially if deeply stained, the pair may present the appearance of a single bacillus. Occasionally they form long chains. Near the centre of the bacillus, but not always centrally placed, may often be found a zone measuring more than half the total length of the bacillus, and exhibiting little or no colouration. It appears as though the stained portions gradually contracted, finally forming two deeply coloured masses at the poles of the lemon-shaped bacillus, which then somewhat resembles the bacillus of rabbit septicæmia, except that the unstained part of the braxy bacillus is larger and more rounded, appearing to be bulged out laterally. In dry preparations the bacillus is easily recognised on account of the highly refractile character of the colourless portion; but in sections careful search is often required, especially if the section be somewhat thick. Whether the colourless portion represents a spore cannot at present be said, though such appears probable. The bacillus is always found in the mucous membrane of the abomasum, and especially in the submucous and subserous connective tissue. In the other organs the bacillus may be present in considerable numbers, or, on the other hand, may be impossible to detect.”
The same bacillus has been found in the tissues of affected sheep both in Norway and in Iceland; the bacillus, when subcutaneously injected, produces a violent hæmorrhagic inflammation of the same character as one finds in the abomasum in cases of spontaneous braxy, and the local changes at the point of inoculation may, just as in spontaneous braxy, be accompanied by a general infection with degeneration of different organs, and with softening of the kidney substance.
The bacillus of braxy is anaërobic. In cultures it develops considerable quantities of gas, just as it does when inoculated into the tissues. It is closely related to the bacillus of symptomatic anthrax, which it somewhat resembles in general appearance, and of which it reminds one by its ability to produce hæmorrhagic inflammation in the muscular tissues. It is distinguished from the last named, however, by being pathogenic to swine, mice, pigeons, and poultry, which are not killed by the bacillus of symptomatic anthrax.
The bacilli of braxy, malignant œdema, symptomatic anthrax, together with Ivar Nielsen’s shortly described bacillus of whale’s septicæmia, and Thoma’s bacillus of malignant emphysema (found in extensive subcutaneous inflammation and emphysema in man), and certain others less well known, form a group of closely allied bacilli resembling one another in form, in being anaërobic, and in producing a sero-hæmorrhagic inflammation and emphysema, but differing in the manner of producing their effects.
Experience and analogy both seem to indicate that young animals occasionally suffer from mild attacks of braxy from which they recover. Such animals afterwards exhibit a well-marked immunity against the disease.
Ivar Nielsen attempted to vaccinate against braxy by a method resembling that used in black-quarter. He dried the diseased kidney tissue, and injected subcutaneously small quantities of the material thus obtained suspended in water. A slight local inflammation followed, which appeared to protect against later “spontaneous” infection. He has used this method in his own district, and states that it is also practised to some extent in Iceland. As far as one can judge—and of course a just opinion is very difficult to form—these inoculations appear of value.
The result of experiment, considered in conjunction with the good results of inoculation for black-quarter, would seem to indicate that Nielsen’s method of vaccination against braxy may yet prove of the greatest possible value, although the method will doubtless require modification in its details.
These modifications Jensen enumerates at some length.
(Mr. Dollar has been informed that Professor Hamilton and Dr. McCall have been engaged in an investigation regarding the possibility of conferring immunity against braxy, and that a Government report will be issued on the subject. Up to the present time however—April, 1905—he has not been able to obtain this report or any advance proof sheets of it.)
BILHARZIOSIS IN CATTLE AND SHEEP.
This disease is caused by the bovine blood fluke (Schistosoma bovis) of cattle and sheep. Synonyms: Bilharzia bovis; Bilharzia crassa; Gynæcophorus crassus; Gynæcophorus bovis; Bilharzia hæmatobia crassa; Schistosomum bovis.
Geographical Distribution. Egypt, Italy, Sicily, India (?).
This parasite was discovered by Sonsino (1876) in Egypt in the portal veins of the ox, and later he found it in sheep, while Grassi and Rovelli afterwards found it in about 75 per cent. of the sheep slaughtered at Catania, Sicily.
Source of Infection. Clinical observation and analogy point to unfiltered drinking water as the source of infection.
Position of the Parasite. The worms are found in the veins of the abdomen, the vena porta, vena linealis, vena renalis, and the venous plexus of the bladder and of the rectum.
Symptoms. The young parasites appear to do no injury; in fact, even the adult worms seem to be inoffensive in themselves. The eggs, on the other hand, armed with a sharp point, are the exciting cause of the disease. The position of the parasite in the venous system, and the consequent location of the agglomeration of eggs, determine the particular symptoms. Either the genito-urinary system is attacked, in which case hæmaturia is one of the first symptoms, or the large intestine is attacked and blood is noticed in the fæces.
Fig. 206.—The bovine blood fluke (Schistosoma bovis), male and female. × 9. (After Leuckart, 1894, p. 467, Fig. 204 A.)
Fig. 207.—Cross-section of bovine blood fluke (Schistosoma bovis), showing the position of the female in the gynæcophoric canal. × 200. (After Leuckart, 1894, p. 472, Fig. 209.)
If the parasites are lodged in the venous plexus of the genito-urinary system, the chief symptoms are: hæmaturia, pains in the lumbar region, the left iliac fossa, the thigh, or in the vulva, which may be spontaneous or may accompany micturition; cystitis, vesical calculus, urinary fistulæ, vaginal verminous tumours, nephritis.
The eggs accumulate in the capillaries, which they rupture; they traverse the mucosa and fall into the bladder, thus causing more or less hæmorrhage; in this way the hæmaturia is established, which is often the initial symptom. At first the urine is quite bloody, but it gradually becomes clearer, and it is only at the end of micturition that muco-purulent flakes are expelled, in which numerous eggs and even embryos are found; the urine contains also epithelial cells, more or less pus, eggs, and occasionally embryos. On micturition sharp pains are felt at the base of the penis or at the gland, possibly due to the passage of eggs. The passage of eggs through the walls of the bladder gives rise to cystitis; blood becomes more abundant in the urine after fatigue or coitus; clots may form and cause retention of urine; chronic urethritis may develop, evidently due to the presence of the eggs. In Egypt 80 per cent. of the cases of vesical calculus in man coincide with bilharziosis; the formation of the calculi evidently results from the presence of the eggs, for the central nodule always contains one or more of these structures. Urinary fistulæ, opening on the perineum, more rarely into the rectum, occasionally form. The mucosa of the vagina, also of the uterus and bladder, becomes impregnated with calcareous salts. Nephritis develops in grave cases.
Fig. 208.—Eggs of bovine blood fluke (Schistosoma bovis), showing the peculiar process on the end. a, b, Layers of the oviduct; c, eggs in the oviduct × 180; x, eggs deformed by pressure; y, spinous process on end of egg × 700. (After Sonsino.)
If the parasites lodge in the veins of the rectum the lesions caused are analogous to those described for the genito-urinary tract.
The heart, lungs, and liver generally remain normal.
Pathology. The bladder is reduced in size, while its wall is greatly thickened, due chiefly to hypertrophy of the muscularis; the mucosa is also thickened, and at certain points it is indurated by uric or calcareous deposits, but the principal lesion consists in ulcerations covered with sanious pus. Lesions analogous to those of the bladder are also observed in the lower third of the ureters, and may extend as high as the kidney; the ureter is enlarged and tortuous; the mucosa irregular; its lumen may remain nearly normal in size, but its wall becomes very thick: the flow of urine may be obstructed; in short, a veritable hydro-nephrosis obtains, which results in atrophic lesions of the kidney, and may finally end fatally.
The mesenteric lymphatic glands may hypertrophy, their substance becoming tumefied, presenting small hæmorrhagic centres, and containing eggs. The liver may contain eggs and become somewhat cirrhotic; the eggs accumulate in the branches of the portal veins, or after piercing the walls they lie in the hepatic parenchyma. The lungs may also contain eggs.
Diagnosis. The diagnosis may easily be made by a microscopic examination of the urine to determine the presence of the egg.
Prognosis, etc. The severity of the disease varies directly with the number of parasites (and hence the number of eggs) in the body. Fortunately, in the majority of cases, the number of parasites is small, though it may increase from repeated infections to 500 or more. In cases of comparatively light infection the disease is reduced to a slight chronic cystitis, with now and then exacerbations, in course of which a slight amount of blood and pus is passed in the urine. The disease may last for years without apparent increase. In the most severe cases death may occur from various causes, rupture of the bladder, ascending pyelo-nephritis, uræmia, albuminuria; the patient may die in marasmus, being exhausted by the dysentery or the anæmia.
Bilharziosis is accordingly not such a fatal disease as has sometimes been supposed.
HEAT STROKE—OVER-EXERTION.
In oxen and sheep heat stroke is rare as a primary accident, but it is frequently produced by over-exertion resulting from the combined action of the sun’s rays, heat, and fatigue due to work or travelling.
It is commonest during the hottest months of the year in oxen doing hard work or in flocks which have been travelled considerable distances. It may also be seen during cooler seasons as the result of exceptional fatigue.
The disease results from a general intoxication which reacts most markedly on the cerebro-spinal centres. It is in fact a complex intoxication resulting from failure of the natural excretory organs to perform their function completely, and from excessive central heat acting on the nervous centres.
Fat animals out of condition are more readily attacked than working animals or sheep reared in the open air.
The symptoms are very characteristic. Oxen when attacked first of all show extremely rapid respiration and dyspnœa, announcing progressive asphyxia. They move with the nostrils dilated, the eyes prominent and injected, the mouth open and the tongue lolling out. Then all of a sudden they come to a stop beside a wall, or, if at liberty, in a ditch, and refuse to move. They may die rapidly with symptoms of asphyxia if they are forced to move until completely exhausted. In others, after a rest of several hours, the breathing becomes slower, the anxiety less and normal conditions return.
In sheep the same general signs may be seen: panting respiration, cyanosed mucous membranes and extreme anxiety, while death follows rapidly in the same way, with symptoms of asphyxia.
The diagnosis is extremely easy. The prognosis is grave.
Treatment consists in prompt and free bleeding to prevent pulmonary congestion. The animals should be rested in a shady, sheltered spot. They should have cool drinks and be sprinkled over the head, neck, or entire surface of the body with cold water.
To prevent such attacks, fat animals should not be moved for long distances, or during the hottest hours of the day, while difficult and prolonged exertion should be avoided.
CHAPTER VI.
DISEASES OF THE LYMPHATIC SYSTEM.
Diseases of the lymphatics are numerous, highly important, and still imperfectly understood. They follow various accidents, local inflammations, certain specific diseases, such as tuberculosis, and may occur in an isolated form without involving any other part of the body.
Fig. 209.—Superficial lymphatic glands of the head and neck. P, parotid gland; Gl.SM, submaxillary gland; GaSG, subglossal gland; GaPPA, preparotid gland; GaSA, subatloid gland; GaPS, prescapular gland; GaPPE, prepectoral gland; J, jugular; 1re C, first rib.
Inflammation, usually of infectious origin, may attack lymphatic vessels (lymphangitis) or lymphatic glands (adenitis), giving rise either to simple lymphangitis, suppurative lymphangitis, or again to simple or suppurative adenitis.
It is unnecessary to emphasise this point in general surgical pathology, for it is identical with that which is observed in other domestic animals, but in order properly to detect the glandular symptoms in certain diseases peculiar to the lymphatic apparatus, and in certain specific diseases, such as tuberculosis, farcy of the ox, etc., it is necessary to understand thoroughly the topography of the lymphatic system.
Topography of the lymphatic glandular apparatus: Examination. The lymphatic glands are in some cases superficial, in others deep seated, and are arranged symmetrically on either side of the body.
Fig. 210.—Deep-seated lymphatic glands of the head and neck. The posterior portion of the lower jaw removed. P, pharynx; GRp, retro-pharyngeal gland; GC, deep cervical glands (cervical chain); NS, spinal nerve; NP, pneumo-gastric nerve; GCs, superior cervical nerve ganglion; NMi, inferior maxillary nerve.
Beginning with the head and fore quarters, the lymphatic apparatus comprises a subglossal, a preparotid, a subatloid, a prescapular and several prepectoral glands (Fig. 209).
None of these glands are very deeply placed, and all are easily accessible to palpation, provided their exact position is known and the animals are not too fat.
The subatloid is a little more difficult to detect, but in thin animals the tips of the fingers can easily be passed under the wing of the atlas so that the condition of the gland can be examined.
In a normal condition, any gland on being examined conveys a sensation of softness and elasticity of a special character which never varies. Palpation is painless.
When, however, the gland is diseased, palpation causes pain in the case of all acute affections. It may, indeed, be impossible to reach the glands, as they are buried sometimes in œdematous swellings of varying size. On the other hand, they may be painless on being touched, but swollen, hypertrophied, indurated, hardened or caseous.
The deep-seated glands of the fore portion of the body comprise the retro-pharyngeal and the cervical chain running along the posterior border of the trachea. Normally these glands cannot be examined (Fig. 210); but when the seat of certain morbid processes, they may be so enlarged as even to be readily visible. The larynx and pharynx are then displaced downwards, the depression between the head and upper extremity of the neck disappears, together with the depression known as the jugular furrow. Such deformities may be either perfectly symmetrical, as in lymphadenia, or (as is more commonly the case) asymmetrical, as in tuberculosis; and if inspection leaves any doubt, the glands may be further examined by palpation.
Fig. 211.—Lymphatic glands of the hind quarter. GG, Precrural lymphatic gland; GF, lumbar lymphatic; GP, popliteal lymphatic (deep-seated); GI, ischiatic lymphatic (deep-seated); GA, anal lymphatic (deep-seated).
To obtain the fullest information both hands should be used, one arm being passed over the neck and the fingers engaged behind the trachea. The operator may also stand in front of the animal, whose head should be lifted so that the points of the fingers can be thrust deeply inwards on either side of the trachea in the direction of the vertebral column.
In the posterior portion of the body the number of glands that can be examined is much smaller. The gland of the stifle, also called “gland of the flank,” is, so to speak, the only one which can readily be detected by examination or palpation. Nevertheless, in cases of lymphadenitis, tuberculosis of the glands, etc., it becomes easy to detect lymphatic glands in the loose fold of skin known as the flank. These glands are very small, and three in number. They are arranged in a triangle, one being much more prominent than the two others. In exceptional cases, little nodular glands, indistinguishable at ordinary times, may become hypertrophied. This is particularly true of the small glands in the neighbourhood of the last rib.
Fig. 212.—Lymphatic glands of the thoracic and abdominal cavities. T, Trachea; C, heart and pericardium; Bd, right bronchi; O, œsophagus; A, posterior aorta; VCp, posterior vena cava; R, rectum; VIe, external iliac vein; AIe, external iliac artery; GA, aortic lymphatic gland (anterior mediastinum); GM, mediastinal lymphatic glands (posterior mediastinum); GSL, sublumbar lymphatic glands (part of lumbar chain); GSS, subsacral lymphatic glands; GI, iliac lymphatic glands.
The retro-mammary glands need only be mentioned, but it is important to know that a deep-seated popliteal gland also exists above the semi-tendinosus and semi-membranosus muscle in the thickness of the muscles of the thigh; as also an ischiatic gland opposite the ischiatic notch, which can only be examined by internal palpation from the pelvis, and an anal gland situated deeply on the sides and in front of the sphincter ani.
With the exception of those of the pelvis and of the sublumbar region, the glands of the thoracic and abdominal cavity cannot be examined, but change in them is indicated under certain circumstances by clearly defined clinical symptoms, and moreover it is necessary to be able to detect changes in these glands on post-mortem examination.
In the thoracic cavity the lymphatic apparatus comprises the mass of the prepectoral glands, which extends into the anterior mediastinum between the first ribs (glands of the entry to the chest), the aortic lymphatic gland situated beneath the dorsal portion of the spine opposite the bifurcation of the aorta, and the lymphatic glands of the posterior mediastinum, one of which is relatively small and is lodged in the concavity of the posterior aorta, the other large, elongated and situated immediately above the œsophagus in front of its passage through the diaphragm.
In the abdominal cavity a sublumbar chain is found situated on the sides of the lumbo-sacral portion of the vertebral column, the mass of the subsacral lymphatic glands, and, at the entrance to the pelvis, extending on either side along the course of the external iliac arteries and veins and resting on the shafts of the iliac bones, the iliac glands.
All these glands are partly accessible to examination by the rectum.
Last of all, we may mention the gland situated on the hilum of the liver, the mesenteric glands, and the little lymphatic glands above the sternum.
In the front limb the only glands of importance from a clinical standpoint are those of the internal surface of the shoulder, close to the divisions of the brachial plexus.
When enlarged or invaded by any specific organism, they may, by compressing the nerve trunks, cause lameness.
THE LYMPHOGENIC DIATHESIS.
(LYMPHADENITIS, LYMPHO-CYTHÆMIA, MYELO-CYTHÆMIA.)
It has been questioned whether the term “lymphogenic diathesis,” which was employed in human medicine by Jaccoud to describe certain morbid conditions also found in animals of the bovine species, should continue in use. At the present moment it is difficult to determine the question. Under any circumstances it has the advantage of including diseases of the lymphatic system, indicated by hypertrophy of the lymphatic glands (adenitis) or by an exaggerated production of white blood corpuscles (leucæmia), and the passage into the general circulation of products derived from the lymphatic apparatus. For these reasons it may be employed here.
Clinical investigation long ago demonstrated that in man certain pathological conditions were characterised by a peculiar colour of the blood, due to the presence of white blood corpuscles in excessive quantities, whence the names “leucæmia” (Virchow) and “leucocythæmia” (Bennett). In the same way it has been shown that the change in the blood characterised by a superabundance of white blood corpuscles generally coincides with engorgement or more or less marked hypertrophy of the lymphatic system and of the adenoid tissue of the body (lymphatic glands, spleen, bone marrow, and, in exceptional cases, liver, kidneys, etc.)—leuco-cythæmic lymphadenitis; but that many cases also occur in which this hypertrophy of the adenoid tissue or of the lymphatic gland tissue may exist, without any excessive number of white blood corpuscles in the blood, whence the name “aleucæmic lymphadenitis or pseudo-leucæmia.” Cases of true leucæmia without adenitis are much rarer, the lesions therein being confined to the adenoid tissue of the bone marrow.
These three morbid conditions—leucæmic lymphadenitis, or leucocythæmia; aleucæmic or pseudo-leucæmic lymphadenitis, or more simply adenitis; and true or simple leucæmia—are frequently found in the bovine species. Whilst stating that these diseases are frequent, we must, however, be understood to except the numerous cases of tuberculous lesions formerly included under the same head.
Jaccoud has shown that in reality the causes of these three morbid conditions are very similar, and that a case which at first appears to be of the nature of aleucæmic lymphadenitis may later become transformed into leucæmic lymphadenitis; or, inversely, that a case which at first appeared to be a simple leucæmia might often become complicated with lymphadenitis: hence the grouping of these different morbid conditions under the heading of lymphogenic diathesis.
Investigations have now thrown more light on the subject because of the more perfect recognition of the varieties of white blood corpuscles, and the above-mentioned morbid conditions may be defined as follows:—
(1.) The first variety consists of a more or less marked adenitis or lymphadenitis without leucæmia (aleucæmic lymphadenitis).
(2.) The second variety, consisting of leucæmic lymphadenitis, or leucocythæmia, is a lymphatic lucæmia or lympho-cythæmia, the anatomical characteristic of which is enlargement of lymphatic glands, and the histological characteristic increase in number of the large and small lymphocytes.
(3.) A third variety, formerly regarded as simple leucæmia without lymphadenitis, is myelogenic leucæmia or myelo-cythæmia, the anatomico-pathological characteristic of which is to be found in myeloid hypertrophy of the bone marrow, giving to the bone marrow on post-mortem examination a puriform appearance, and in the myeloid condition of the spleen.
Histologically this variety is characterised by an absolute increase in numbers of the large mono- and poly-nuclear eosinophile leucocytes.
Symptoms. Simple lymphadenitis begins in an insidious manner, and is characterised by weakness, anæmia, paleness of the mucous membranes, and wasting without apparent reason, although the appetite is preserved. It is only at a later stage that the glandular enlargements are discovered (adenitis), and often this discovery is not made until the veterinary surgeon is called in.
The existence of the disease is indicated by enlargement of the superficial glands, and this enlargement, which may commence at any point, extends along the course of the lymphatic vessels to the neighbouring glands, until in a shorter or longer time it involves all the lymphatic glands in the body.
The enlargement of the glands is usually symmetrical, and on clinical examination it is sometimes easy to detect at the outset an increase in size of the retro-pharyngeal glands, the glands of the neck, the prescapular glands, the glands of the flank, etc.
Rectal exploration reveals hypertrophy of the glands of the pelvis and of the sublumbar region, etc. The animals waste very rapidly, and sometimes in a few months become incapable of standing. They develop cachexia, and die in a state of exhaustion, with no other lesions than those of lymphatic hypertrophy. Neither do they exhibit any marked increase in the number of white corpuscles in the blood.
In lympho-cythæmia the beginning of the disease is often identical with that of simple lymphadenitis, the increase in the number of white blood corpuscles not occurring until later. In other cases, on the contrary, leucæmia appears first, and the enlargement of the lymphatic gland follows; but what characterises this form and allows of it being distinguished from myelo-cythæmia is the great increase in the number of large or small lymphocytes. The development is identical with, and sometimes much more rapid than, that of the preceding form. The animals waste away and become anæmic and cachectic, dying at last in a state of absolute exhaustion.
Post-mortem examination reveals, as in the previous condition, symmetrical hypertrophy of all the lymphatic glands; the spleen is very often enormous, and the liver is sometimes affected, as are also, in exceptional cases, the kidneys.
It may happen that the spleen alone appears affected, or at least that it has been first attacked, a fact which explains the existence of leucæmia before any enlargement of the lymphatic glands.
Causation. The causes of lymphadenitis and of lympho-cythæmia are unknown in veterinary as in human medicine. Apparently these diseases are more common in adults than in young animals. Some regard them as infectious in character, but this can hardly be the case, as all experimental attempts to transmit the diseases have failed. It is more plausible to compare the development of these morbid conditions with that of malignant tumours, and although some doubt still exists, simple lymphadenitis may be described as an aleucæmic lymphoma or lympho-cytoma, which has gradually become generalised, spreading by way of the lymphatic channels from the gland first affected through the surrounding glandular system. Lympho-cythæmia, on the other hand, may be said to be a leucæmic lympho-cytoma, which spreads both by the blood circulation and by the lymphatic paths (spleen, hæmatopoietic glands and organs).
This view of the development of the lesions enables us to class lympho-sarcomata with lymphomata and lympho-cytomata. The malignant character and extremely rapid development of lympho-sarcomata appear due to its extending by contiguity of tissue, and simultaneously by the lymphatic paths.
This new grouping would consequently place on one side myelogenic leucæmia, also called myelo-cythæmia, which is perhaps a different morbid species. This would destroy the unity implied in Jaccoud’s theory of the lymphogenic diathesis; but for all that this method of grouping might be justified by reference to specific cellular characteristics. In myelo-cythæmia the disease appears to commence as a lympho-cythæmia, i.e., it is unaccompanied by enlargement of lymphatic glands or hypertrophy of the spleen or liver, though the blood appears leucæmic. The condition is not a leucæmia due to lymphocytes, but rather a leucæmia produced by mono- and poly-nuclear eosinophile leucocytes, i.e., leucocytes derived from the bone marrow.
The patients are carried off rapidly after persistent wasting, decline and cachexia, whilst on post-mortem examination the puriform aspect of the bone marrow is an extremely striking characteristic.
Diagnosis. There is rarely much difficulty as regards the diagnosis. The enlargement of the lymphatic glands, for instance, can readily be detected, and the only disease with which this can possibly be confounded is tubercular enlargement.
With the means at present available for diagnosing tuberculosis, such as microscopic examination of the discharge, inoculation with discharge, examination of material from the glands, injection of tuberculin, etc., the nature of the disease can always be placed beyond doubt.
In lympho-cythæmia and in myelo-cythæmia, the whitish-violet lactescent appearance of the blood is of unmistakable significance, particularly when the manifest progressive wasting of the whole system is taken into account.
Histological examination of the blood after fixation and staining will in the former cases reveal the presence of very large numbers of lymphocytes, and in the latter an absolute increase in the number of the mono- and poly-nuclear lymphocytes. It should be easy, therefore, to distinguish the two diseases, especially as other symptoms vary.
In the early stages leucæmia may be mistaken for the leucocytosis seen in infectious diseases. These forms of leucocytosis are very common in animals of the bovine species. They occur in certain forms of tuberculosis, in uterine infections, in cases of internal suppuration, in tumour of the heart, the rumen, etc., and vary in so far as one style or another of white blood corpuscle predominates. The diagnosis, therefore, necessitates that the white blood corpuscles should be counted, and whenever it is found that their variations in number are no more than between 5,000 and 15,000 per cubic millimètre, the case may be regarded as one of temporary leucocytosis.
If, on the other hand, those corpuscles number more than from 15,000 to 20,000, or, as may sometimes happen, they attain to from 200,000 to 300,000 per cubic millimètre (one white to two or three red blood corpuscles), the case is one of leucæmia, and, according to the predominance of the particular type of cell, it is a lympho-cythæmia or a myelo-cythæmia.
In leucæmic conditions the red blood corpuscles are also present in fewer than the normal numbers. They are more irregular, assume giant and dwarf forms (macrocytes and microcytes), sometimes exhibit lacunæ, and are always polychromatophile, i.e., without special affinity for any particular constituent of double or triple stains.
Prognosis. The prognosis of diseases included in the lymphogenic diathesis is extremely grave, and in the present state of our knowledge it may be assumed that sooner or later death is inevitable.
Treatment. Treatment can scarcely be considered to exist, for at the best it can only delay the development of the disease. Nevertheless, and with this reservation, it is certain that preparations of iron, iodine and arsenic have a certain effect, probably by acting on the hæmatopoiesis.
CASEOUS LYMPHADENITIS OF THE SHEEP.
In the sheep the lymphatic glands are sometimes the seat of peculiar changes, which do not appear to have any marked effect on the general condition. Thus a post-mortem examination or an examination of animals in the slaughter-house sometimes shows a certain number of isolated or symmetrical glands, such as the mediastinal, tracheal, inguinal, pelvic or sublumbar glands, to be greatly enlarged and completely degenerated. The precrural, prescapular, and popliteal glands are said to be most frequently affected. Their contents are caseous and yellowish, enveloped in a fibrous sheath, and show no signs of peripheral inflammation. The other organs and viscera may either be healthy or exhibit caseous lesions identical with those found in caseous broncho-pneumonia.
The causes of this disease are imperfectly understood, although Cherry and Bull (1899, the Veterinarian, Vol. LXXII., No. 860, p. 523) have isolated from the lesions an organism identical with Preisz’s bacillus and with the microbe of ulcerative lymphangitis in the horse.
Norgaard and Mohler (Annual Report, United States Bureau of Agriculture, 1899, p. 638) have studied the disease. In June, 1897, Turski, at Danzig, found about 150 breeding ewes, from eight to twelve years old, suffering from nodules or abscesses the size of a child’s fist in the inguinal and prescapular regions. They had been sold for slaughter, and many were in very poor condition. The disease occurs in Europe, Western America, South America, and Australia. Several thousand cases are annually seen in the slaughter-houses of the United States.
The symptoms generally escape notice, and it is only by accident that one sometimes detects marked enlargement of the lymphatic glands of the neck or of the superficial inguinal glands. The patients, moreover, may remain in very good bodily condition, so that the lesions are only discovered on the meat being inspected.
Having regard to our imperfect knowledge of this disease, it is impossible to express an opinion as to its importance or treatment.
GOITRE IN CALVES AND LAMBS.
Although not strictly relevant to the foregoing matter, a few remarks may here be made on the subject of goitre.
True goitre consists in hyperplasia of the follicles of the thyroid gland, with colloid change of their contents, which are chiefly albuminous. The swelling is mainly due to enlargement of the follicles, and is termed struma follicularis. It may attack the entire organ or only one-half; less frequently it is confined to certain sections. Other varieties of goitre are recognised, such as fibrous, varicose and cystic goitre. (For fuller details see Möller and Dollar’s “Regional Surgery,” p. 149.)
Fig. 213.—Calf showing swelling due to goitre.
Treatment by injection of thyroid juice or by feeding on thyroid extract has given better results than drugs.
The following account of an outbreak in New Zealand is summarised from the Annual Report of the Chief Veterinarian of New Zealand, 1901:—
The calves affected were born with enlarged thyroids. The farm is of rich alluvial deposit, and rather below the level of the river, which it borders. The land has been in occupation, however, for many years, and no similar condition had been previously noted. At first, as calves only were affected, it was thought possibly to be due to the bull, a two-year-old animal, but when a foal was born suffering from a similar malformation this theory naturally fell to the ground.
The land had been ploughed with a special plough 20 inches deep, but this is no uncommon practice in the island.
About the same time, a similar disease was discovered affecting lambs at a farm near Outram. From 450 ewes, 150 lambs had been lost, the glands being enlarged to the size of a cricket ball. A few had been born dead, many only lived a few hours, others lived several days, and a considerable number recovered. There was no connection, directly or indirectly, between the two farms, they being at least fifty miles apart. A few of the calves died or were killed, the remainder recovered, and the foal grew rapidly better. The land on both farms is very similar in composition.
Mr. Wilkie states, from observation of previous cases in lambs, that “it appears to be always associated with malnutrition and a condition of anæmia in the parent, induced in most cases by feeding with watery, innutritious foods.”
Specimens were forwarded, from a calf and from a lamb, of enlarged glands. The gland of the calf was enormously enlarged, being at least twice the size of an orange, dark in colour, flabby in consistency, and on section a mucous material exuded copiously from the cut surface. Micro-examination showed the acini to be larger than normal, filled with the usual mucous material, and lined with cubical epithelium. The connective tissue surrounding the alveoli was, however, crowded with round-cells, so much so that the whole parenchyma seemed to be practically composed of these cells.
A specimen of an enlarged thyroid from the lamb was about the size of a sheep’s kidney, and very much the same shape and colour. Sections microscopically examined showed a different condition to that of the calf’s thyroid. Here the acini were filled with epithelial cells loosely arranged as if the lining epithelium had been proliferating rapidly, while the connective tissue surrounding the acini was fairly normal. The section had a somewhat adenomatous appearance.