Part 55

The rapid growth of multiple =tumors= as of melanosis in gray horses has been noticed to cause profound anæmia (Bouley).

Perhaps no cause is more potent than the attacks of =parasites= and especially such as live by sucking the blood. The numerous strongyli of the lungs, stomach, and intestine, the tricocephalus, and allied round worms, the trematodes of the liver, and the cytodites of birds furnish striking examples of the bloodless and debilitated condition which they may produce. In man ankylostomata causes anæmia in Egypt, Italy (St. Gothard) and elsewhere, and bothriocephala in different countries.

=Chronic exhausting diseases= especially those which affect the digestive organs and mesenteric glands are prolific causes. So with Bright’s disease.

Connected with these are =defects in diet or hygiene=. Starvation, unsuitable, innutritions, or indigestible food, too laxative food, damp, dark, draughty or unventilated stables, and irregularity in feeding, watering and work are all potent factors in inducing anæmia.

=Diseases of the masticatory apparatus= (broken jaw, diseased teeth,) preventing the preparation of food, and pharyngeal troubles interfering with deglutition are other causes. Finally overwork is not to be forgotten.

=Toxic anæmia= may occur from the ingestion of lead, mercury, or arsenic.

Symptoms. These may be little marked at the outset in slowly developing cases. Extra pallor of the mucous membranes, fatigue and even breathlessness on slight exertion, a small, weak, pulse, with a tendency to become rapid, with violent heart beats, when excited.

At a more advanced stage the mucosæ, especially the buccal, are pale and thin, the muscles are soft, flabby and weak, fatigue and perspiration are easily induced, the feet are advanced more nearly in the median line of the body, and the toes strike on any obstacles, the pulse is weak, small and quick, and the heart easily excited even to palpitation, and with an occasional anæmic murmur with the first heart sound. Arterial and venous murmurs may be present. The hairs are easily detached. Appetite and digestion fail, there is costiveness, a full secretion of urine of a clear aspect, the subcutaneous fat disappears and the skin feels thin and limp (paper skin in sheep), the hair dry and lusterless, the wool flattened (clapped). The weakness and emaciation go on increasing and dropsies appear in the limbs, under the trunk and jaw and in the internal cavities.

Pathology. Lesions. Apart from the causes, the morbid conditions are mainly found in the blood. The watery state of the blood, the lack of red globules (even to but 2,000,000 per cubic millimeter), the absence of albumen (76 per 1000 in place of 83), the loose coagulum with excess of buffy coat, and the excess of serum are characteristic. The presence of large, nucleated (myelogenous) red cells, of spherical bodies smaller than the normal red cells (microcytes), and of irregularly shaped red cells (poikilocytes) is characteristic, the latter especially of pernicious anæmia. As the disease advances fatty degeneration of heart, liver, kidneys, and other organs are complications and tend to aggravate the disease, by counteracting repair of the globules—thus establishing a vicious circle. All the organs are pale and flaccid, the arteries empty, the veins contain a little blood, forming pale clots. In the cases considered, all the result of another disease, the lack of blood and of the solid and vital elements in that which remains, entails imperfect function in all the vital processes, including sanguification itself, and in this way an anæmia once established tends to perpetuate and aggravate itself.

Treatment. The anæmia above considered being largely symptomatic, or resultant from other diseases, the first consideration as regards both prevention and treatment is to prevent or cure such diseases. Where dietetic or hygienic, a liberal diet, and good hygiene will meet every demand in the early stages. In the warm season an open air life is most important. In case of a drain by over-secretion (milk) this must be judiciously checked. In bitches it will often be needful to wean several of the puppies. A rich and very digestible diet (oats, beans, linseed, oil meal, milk, gruel), in small compass, and suited to the genus and individual, with iron and bitters, and in the herbivora carminatives, will suit many cases. Muriate of iron, with strychnine or nux vomica; iron sulphate, sodium chloride and nux; or dialysed iron, or some other soluble ferruginous salt, with quinia, gentian, or some other bitter will serve a good purpose. For the dog saccharated carbonate of iron or citrate of iron and ammonia with quinia or strychnine, in pill form, is convenient. With poor digestion muriatic acid and pepsin may replace the iron at first. Beef teas may often be given with advantage, even to the herbivora, and injections of defibrinated ox blood night and morning have proved of service. In extreme anæmia, as from hæmorrhage, transfusion, or its equivalent, must be resorted to. A normal saline solution (0.6 per cent. NaCl), boiled, may be thrown into the peritoneum or subcutaneous connective tissue, or defibrinated blood, may be injected into the peritoneum. Transfusion is the dernier resort.

PROGRESSIVE PERNICIOUS ANÆMIA. IDIOPATHIC ANÆMIA.

Definition. Causes, obscure, faulty diet, hygiene, microbes, glycerine, pyrogallic acid, hæmoglobin, deranged sanguification, parasitisms. Symptoms, of anæmia of obscure origin. Treatment as for anæmia, special measures, for intestinal fermentations, dietetic.

Definition. Anæmia which is without any pre-existing appreciable cause.

Causes. As in the corresponding disease in man the real starting point of pernicious anæmia is unknown. Faults in diet and in general hygiene have been adduced, and while in Berne this appears to be sustained, in Ireland, in the poorest classes, the disease is little known, and in Montreal, it find its victims largely in a class of well to do artisans (Osler.) In the domestic animal it is described on all soils, and on the most varied dietary (Bouley and Reynal). Zschokke and Friedberger and Fröhner in cases occurring enzootically in stables, found a minute bacillus in the patients, which would remove these cases into the list of symptomatic anæmia. The same is true of the anæmia (Surra) of horses and mules in India and Siberia, in which Evans, Burke, Steele and Ignatovsky, found a motile spirilloid organism which destroys the red globules. Other forms that are apparently purely idiopathic have been attributed to a failure in the cytogenic processes in the bone marrow especially. Back of this we know only of the various debilitating causes in food, hygiene, building, location, work, etc., operating on a specially susceptible system, in which, once started, the morbid process tends to perpetuate itself and increase.

Ponfick induced anæmia experimentally by the intravenous injection of glycerine, pyrogallic acid, solutions of hæmoglobin, etc., which dissolve the blood globules. This suggests the probable pathogenesis by the production of unidentified blood solvents in cases of deranged sanguification, but it still leaves us in the dark as to the exact seat of such derangements (liver, blood glands, bone marrow, etc.) and as to the cause, parasitic or otherwise, which determines such disorder. Pathological investigation has enabled us to differentiate, according to their respective causes, a number of diseases (distomatosis, lung worms, ankylostomiasis, internal acariasis, chronic trichinosis, strongyliasis, etc.,) which were formerly classed as anæmias, and it seems altogether probable that the onward progress of medicine will enable us to go farther in the same direction and to allot the remaining unclassed anæmias to their proper etiological places. Some may be unrecognized helminthiasis, others microbian disorders, and still others, disorders in nutrition and sanguification from different causes.

The Symptoms are those of other forms of anæmia, but being more obscure in origin and therefore less open to corrective treatment, it is more likely to grow to an extreme development and fatal issue. The weak pulse, irritable heart, debility, unsteady walk with the hind limbs, hurried breathing and sweating under exercise, watery, puffy eyes, dropsies in limbs and dependent parts of the body, progressive emaciation, and weakness are even more marked than in symptomatic anæmia.

The treatment is in the main as for the other form alike in its hygienic and medicinal bearing. In man recoveries have taken place under arsenic combined with the iron. Arseniate of potash and ferrum redactum in pill form, or tincture of chloride of iron, and Fowler’s solution in food or water, continued for a length of time. Phosphated pepsin, and peroxide of hydrogen have seemed to do well in some instances, and phosphorated oil is another resort. W. Hunter attributes idiopathic anæmia to toxins derived from microbes in the alimentary canal, as Sir Andrew Clark ascribes chlorosis to a similar cause. He prescribes beta-naphthol as the least soluble and best antiseptic, in a dose of 5 grains daily in mucilage for man (1 drachm for horse or ox). Hunter further found that a farinaceous diet protected the globules against destruction while a nitrogenous diet favored this. It may be noted that long ago Delafond attributed anæmia in animals to the extension of the use of artificial fodders of the natural order leguminosæ which are rich in nitrogen.

CHRONIC ANÆMIA. DROPSY IN CATTLE AND SHEEP.

Definition. Causes, parasitic and microbian. Symptoms. Treatment.

Definition. A progressive anæmia in ruminants and other animals, resulting in general anasarca, and dropsies of the internal cavities.

In veterinary works published on the European Continent this affection is given a special place apart from the same train of symptoms which mark distomatosis, taeniasis, and strongyliasis. The disease is described as prevailing in wet years, after inundations, when the vegetation is rank and aqueous, and of course largely aquatic, in animals that are turned out in early morning before the dew has evaporated, in the conditions, in other words, that favor the ingestion of parasites. It prevails also in work oxen fed on the refuse of sugar factories (beets, turnips) in which the nitrogenous materials are held to be deficient, but in Great Britain where cattle are often fattened on an exclusive diet of turnips, containing even a larger proportion of water, this non-parasitic disease is unknown. It is also ascribed to close, ill-ventilated, unwholesome buildings, and to over-kept and tainted fodder, and so far as a separate disease exists, it seems more reasonable to charge it to the toxins produced by bacterial ferments or cryptogams than to causes which elsewhere appear to be inoperative.

The symptoms are essentially those of distomatosis, and the treatment, apart from the parasiticides, is the same. When helminthiasis can be certainly excluded prevention would include the avoidance of the factory refuse, especially when in a state of decay.

MELANÆMIA. BLACK PIGMENT IN BLOOD.

Definition. Melanin, in normal tissues, abnormal. Melanosis. Bisulphide of carbon subcutem. Decomposition of hæmoglobin in leucocytes. Coloration of tissue.

Definition. Accumulation of granules and scales of blood pigment (melanin) in the circulating fluid, and in various organs (spleen, liver, bone marrow, brain, etc).

=Melanin=—C{44.2}, H{3}, N{9.9}, O{42.6}—or black pigment (a close relative of hæmatin) occurs physiologically in epithelium (choroid, retina, iris, in the deeper layers of epidermis, and on the surface of the dog’s lung and of the sheep’s brain) and in connective tissue corpuscles (lamina fusca of the choroid).

Pathologically it is found in the blood of the victims of malarious fever, often in great abundance, and in the spleen, liver, bone marrow, brain, lymph glands and some other organs. It is formed abundantly in the black pigment tumors (melanosis) of man and animals, and in extensive melanosis is present in the blood of both man and horse (Schimmeln). So far it has not been found in connection with the extensive destruction of red globules which takes place in anæmia. Schwalbe has developed malanæmia experimentally by the hypodermic injection of bisulphide of carbon in rabbits.

According to one view the melanin is produced in connection with the destruction of red globules in the liver, spleen, etc., and is thence carried into the blood. This is in keeping with the local formation of the pigment in melanosis. Arnstein however urges that in malarious cases the destruction of the red cells takes place in the blood, and that the hæmoglobin, absorbed into the leucocytes, is transformed into melanin, and finally deposited in the tissues by the migrating white corpuscle. Why the hæmoglobin set free in anæmia is not similarly transformed, does not appear. The pigmented organ may be quite black in the immediate vicinity of the blood vessels, and in its general aspect in chronic cases reddish brown, dark gray, or dark olive.