10. In the cases of some species of fluke there is reason to believe that before the Cercariæ gain access to their final or definitive host they re-enter the bodies of the mollusks. This they accomplish by means of a boring apparatus, and having previously cast off their tails they encyst themselves beneath the surface of the skin. In this new situation they develop into the so-called pupa, which is at length passively transferred with the fodder, or drink, to the digestive organs of the host. In the case of Fasc. hepatica, as probably obtains also with many other flukes, I think there can be no doubt that the Cercariæ pass directly into the bodies of ruminating animals. The circumstance that flukes of this species have been found beneath the human skin shows how considerable are the boring powers of the armed Cercariæ.
In regard to the possibilities of fluke development, that will be best understood by glancing at the constitution of the zoological individual. The sum total of the products of a single germ may be tabulated as follows:—
| Zoological individual (Fasciola hepatica). | |||
| a. | Ovum in all stages, |
| First “biotome.” |
| b. | Ciliated free-swimming embryo, | ||
| c. | Nurse, germ-sac, sporocyst (redia), |
| Second “biotome.” |
| d. | Active, migrating, tailed larva (cercaria), |
| Third “biotome.” |
| e. | Encysted, resting larva (pupa), | ||
| f. | Sexually-mature fluke (fasciola). | ||
This is a fair representation of the life-phases of the fluke. The life-phases are rarely less numerous or complicated than here indicated, but Pagenstecher’s researches tend to prove that under certain climatal conditions the number of larval forms may vary considerably. In other words, the fluke individual does not comprise any definite number of “zoöids,” although the kinds of zoöids are limited. I recognise three “biotomes.” The first includes only one temporary, independent life-phase, this is the ciliated animalcule, which I call a “protozoöid.” The second “biotome” may comprise only a solitary simple sporocyst or germ-sac (deuterozoöid), but an almost indefinite multiplication of new and independent germ-sacs, as well as other more highly organised “nurse formations,” may also be developed from the primary sporocyst (secondary and tertiary “deuterozoöid”). The third “biotome” embraces a large but variable number of “tritozoöids” (cercariæ), an equal number, whatever that may be, of “tetartozoöids” (pupæ), and, therefore, also, a similar number of “pemptozoöids” (flukes).
Practically, other curious results arise out of the foregoing considerations. For example, a single sheep may harbor 1000 flukes. Each fluke will develop 10,000 to 40,000 eggs. Each egg may give rise to 370 zoöids. It thus appears that, if all the conditions were favorable, a single fluke might originate between three and four millions of individualised life-forms, whilst the solitary sheep itself would, under the same circumstances, be the means of causing the production of at least 3,000,000,000 fluke zoöids! Happily, no such results as this can possibly occur in nature, since interfering agencies reduce the favorable conditions. However, the balance of parasitic forms from all sources is usually sufficient to destroy thousands of sheep annually. The virulence of rot-epizoöty is entirely due to the presence of conditions favoring the development of fluke larvæ.
As regards the injurious action of this parasite on animals, it is well known that in particular years, in England alone, hundreds, and even thousands, of sheep have been destroyed in a single season. A writer in the ‘Edinburgh Veterinary Review’ for 1861 states that in the season of 1830–31 the estimated deaths of sheep from rot was between one and two millions. This would, of course, represent a money loss of something like four million pounds sterling. As affording additional striking instances of the disastrous effects of rot, I may cite the statements of Davaine. Thus:—“In the neighbourhood of Arles alone, during the year 1812, no less than 300,000 sheep perished, and at Nimes and Montpellier 90,000. In the inner departments, during the epidemic of the years 1853–54, many cattle-breeders lost a fourth, a third, and even three fourths of their flocks.” In like manner our English authority, Prof. Simonds, furnished a variety of painful cases. Thus, on the estate of Mr Cramp, of the Isle of Thanet, the rot epidemic of 1824 “swept away £3000 worth of his sheep in less than three months, compelling him to give up his farm.” Scores of cases are on record where our English farmers have individually lost three, four, five, six, seven, and even eight hundred sheep in a single season; and many agriculturists have thus become completely ruined.
Remarkable periodic outbreaks of this disease are recorded by Simonds as occurring in England in the successive years of 1809, ’16, ’24, ’30, ’53, and ’60; whilst, for France, Davaine mentions 1809, ’12, ’16, ’17, ’20, ’29, ’30, ’53, and ’54, as the most remarkable years. It would be interesting to know how far these outbreaks tally with the similar outbreaks which have occurred in Holland, Germany, and other European districts. The disease was prevalent during four separate years in France and England at one and the same time. This, indeed, is no more than we would naturally expect, considering that the extent of the development of the larval forms must, in a great measure, be dependent upon atmospheric conditions. A warm and moist season would alike prove beneficial to the development of the larvæ and their intermediate molluscan hosts. Their numbers would also multiply enormously; for, as already remarked, the degree of non-sexual production of trematode larvæ within their sporocysts is materially affected by climatic changes. On the other hand, a fine, dry, open season will tend to check the growth and wanderings of the larvæ, and thus render the flocks comparatively secure.
Considerations like these sufficiently explain many of the crude theories which were early propagated concerning the causes of this disease, and in particular, the very generally prevalent notion that water, and water alone, was the true source of the disease. Intelligent cattle-breeders and agriculturists have all along observed that the rot was particularly virulent after long-continued wet weather, and more especially so when there had been a succession of wet seasons. They have likewise noticed that flocks grazing in low pastures and marshy districts were much more liable to invasion than sheep which pastured on higher and drier grounds, but noteworthy exceptions occurred in the case of flocks feeding in the salt-water marshes of our eastern shores. The latter circumstance appears to have suggested the common practice of mixing salt with the food of sheep and cattle, both as a preventive and curative agent; and there can be little doubt that this remedy has always been attended with more or less satisfactory results. The intelligible explanation of the good effected by this mode of treatment we shall find to be intimately associated with a correct understanding of the genetic relations of the entozoon, for it is certain that the larvæ of Fasciola hepatica exist in the bodies of fresh-water snails. As already hinted from Willemoes-Suhm’s observations, it is not improbable that the larvæ are confined to gasteropod mollusks belonging to the genus Planorbis.
The symptoms produced by rot are very striking. When the disease has far advanced it is easy to know a rotten sheep, not only by its very look, but still more convincingly, as I have myself tested, by slightly pressing the hand over the region of the loins. In this region the diseased animal is particularly weak, and the pressure thus applied instantly causes it to wince. At the same time the hand feels a peculiar sensation very unlike that communicated by the spine of a sound animal. In bad cases the back becomes hollow, and there is a corresponding pendulous condition of the abdomen. The spinal columns ultimately stick out prominently, forming the so-called “razor-back.” As Professor Simonds has well observed, in an earlier stage of the disease, “an examination of the eye will readily assist in determining the nature of the malady. If the lids are everted it will be found that the vessels of the conjunctiva are turgid with pale or yellowish colored blood, the whole part presenting a peculiar moist or watery appearance. Later on, the same vessels become blanched and scarcely recognisable.” The skin also becomes harsh and dry, losing its natural tint, and the wool is at length rendered brittle, either becoming very easily detached or falling off spontaneously.
The first thing noticeable in dissecting a rotten sheep is the wasted and watery condition of all the tissues. There is a total absence of that firm, fresh, carneous look which so distinctively characterises the flesh in a state of health. Not only is the rigidity and firm consistency of the muscles altogether wanting, but these structures have lost that deep reddish color which normally exists. When the abdominal cavity is opened a more or less abundant, clear, limpid, or yellowish fluid will make its escape, and the entire visceral contents will, at the same time, display a remarkably blanched aspect. These pathological changes are also shared by the important organ especially affected, namely, the liver. This gland has lost its general plumpness, smoothness, and rich, reddish-brown color, and has become irregularly knotted and uneven both at the surface and the margins, its coloring being either a dirty chocolate brown, more or less strongly pronounced at different parts, or it has a peculiar yellowish tint, which in places is very pale and conspicuous. To the feel it is hard and brawny, and when incised by the scalpel, yields a tough and, in places, a very gritty sensation. On opening the gall-ducts a dark, thick, grumous, biliary secretion oozes slowly out, together with several distomes, which, if not dead, slowly curve upon themselves, and roll up like a slip of heated parchment. On further slitting open the biliary passages, they are found distended irregularly at various points, and in certain situations many flukes are massed together, having caused the ducts to form large sacs, in which the parasites are snugly ensconced. The walls of the ducts are also much thickened in places, and hardened by a deposit of coarse calcareous grains on their inner surface. Mr Simonds says, that the “coats of the ductus hepaticus, as also of the ductus communis choledicus, are not unfrequently so thick as to be upwards of ten times their normal substance, and, likewise, so hard as to approach the nature of cartilage.” Respecting their numbers, the greatest variation exists. The presence of a few flukes in the liver is totally insufficient to cause death; consequently, when a sheep dies from rot, or is killed at a time when the disease has seriously impoverished the animal, then we are sure to find the organ occupied by many dozen, many score, or even several hundred flukes. Thus from a single liver Bidloo obtained 800, Leuwenhoeck about 900, and Dupuy upwards of 1000 specimens. Even the occurrence of large numbers only destroys the animal by slow degrees, and, possibly, without producing much physical suffering, excepting, perhaps, in the later stages. Associated with the above-described appearances, one also not unfrequently finds a few flukes in the intestinal canal, whilst a still more interesting pathological feature is seen in the fact that the bile contained in the liver ducts is loaded with flukes’ eggs. In some cases there cannot be less than tens or even hundreds of thousands. Not a few may also be found in the intestinal canal and in the excrement about to be voided. Occasionally dead specimens become surrounded by inspissated bile, and gritty particles deposited in the liver ducts, thus forming the nuclei of gall-stones. Mr Simonds mentions a remarkable instance, “where the concretion was as large as an ordinary hen’s egg, and when broken up was found to contain about a dozen dead flukes. It was lying in a pouch-like cavity of one of the biliary ducts.”