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Text Book of Veterinary Medicine, Volume 3 (of 5) · James Law — chapter 56 of 126 · ~2,452 words · public domain

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We are not however limited to the womb as the only possible field of a pathogenic microbian growth. The frequent presence of microbes in the sphincter of the teat, in the galactophorous sinus, and in the milk ducts inside the mammæ is absolutely proved. Guillebeau found on the mucosa in cases of mammitis three forms of bacillus, to which he attributed the disease. In the New York State Veterinary College we have found mammitis usually associated with a streptococcus in the milk. In one cow in the University herd which gave abundance of good milk, and rarely showed any sign of congestion, streptococcus was constantly present. In cows producing “gassy” curd, V. A. Moore and A. R. Ward found in the milk a bacillus which morphologically and in cultures resembled the colon bacillus (evidently one of the colon group). In the milk and mammary gland tissue got from other (slaughtered) cows, a micrococcus growing in yellow or buff-colored colonies predominated. (Moore and Ward). That the colon bacillus, so constant in the intestines and manure, is not always found in the milk ducts, would show that in its normal condition it is not adapted to this habitat, but when a variety appears that is so fitted, it appears to be able to maintain its place indefinitely.

With such facts before us, we must allow the possibility of poisoning by toxins of bacteria in the udder, or by compounds formed by the synthesis of such toxins and the leucomaines of the expanding udder, or by the union of the udder toxins with those from the womb. The whole subject of microbian and leucocytic causation of parturient fever is still hypothetical, yet enough is known to show the high probability of such source, and to demand a thorough investigation which will place the subject on a substantial and assured basis.

Nature. Theories of the nature of this disease are numerous and varied, and are largely based upon some restricted or one-sided view of phenomena and lesions. Coutamine considers it as the reaction of the surplus of nerve force, which was not used up in the easy parturition. The theory is somewhat fantastic as an explanation of the rapidly developing asthenia and paralysis. Billings explains the cerebral anæmia as due to vaso-constriction of the nervous capillaries produced by the exaggerated excitability of the uterine nerves. But with the easy parturition, and delivery, and the moderate contraction of the womb, without violence or spasm, the theory seems rather insubstantial. Trasbot looks on the affection as a congestion of the myelon, apparently shutting his eyes to the far more prominent encephalic symptoms. Haubner considers it as a cerebral anæmia induced by the vaso-dilatation in the portal system and abdominal viscera generally, the result in its turn of the vacuity of the abdomen, from the expulsion of the fœtus and its connections. But the womb is often found contracted and comparatively exsanguine, the plethoric condition of the cow, suddenly increased by the great mass of blood from the uterine vessels, maintains a marked general blood tension, and finally, the closed box of the cranium cannot have its blood so completely drained from it as can a part outside such a cavity. Stockfleth attributed the malady to a metro-peritonitis, and the absorption of the morbid products and poisoning, but neither a metritis nor peritonitis is a common accompaniment of the affection.

Franck who accounts for the asthenia by an anæmic condition of the brain, explains the anæmia by a pre-existing congestion and œdema of the rete mirabile at the base of the brain. He claims that sows which have also a rete mirabile in this situation sometimes suffer from parturient fever. He fails to adduce cases in the sheep and goat which also have retia mirabilia. The pregnant sheep may die of an asthenic affection, but usually before parturition. Franck’s theory is plausibly based on the anatomical and physiological conditions, for the elaborate network of vessels at the base of the brain, undergoes great distention under increased arterial tension, and with the serous effusion, compresses the brain and drives out its blood.

Palsy of the ganglionic system has been invoked, with succeeding congestion of the myelon and encephalon (Barlow, Kohne, Carsten Harms, etc.). Explanation is made that the supposed excess of nervous force fails of distribution through a lack of conductility of the nerves, and the nerve centres suffer. Binz has even found the spinal roots of the sympathetic surrounded by a thick gelatinoid exudate. The theory is, however, essentially speculative and fails to explain the origin of the disease or its connection with the recognized conditions of its occurrence.

Plethora with Arterial tension and all conditions contributing to this, as already set forth under causes must be allowed a prominent place in considering the nature of the disease. The blood globules in my experience are somewhat smaller than normal, implying the density of the plasma, and implying a direct influence on trophic and metabolic processes. Under these influences the congestion of the encephalic circulation, and notably of the rete mirabile, and a serous effusion, tend first to prostrate the nerve force, and second to render the other intracranial structures anæmic.

The direct action of a narcotic poison, leucocytic or microbian, though as yet a hypothesis merely, has much in its favor, on considerations drawn from the observed immunity in particular buildings, the sudden prostration, the promptitude of certain recoveries and the favorable results of the iodine mammary injections. The presence of sugar in the urine, most abundantly in the worst cases, implies a profound disorder in glycogenic centres (medulla, liver), and primarily no doubt in the bulb.

Lesions. These are exceedingly variable in successive cases. Congestion and effusion in the meninges, cerebral or spinal, in the rete mirabile and choroid plexus have been often noticed, and exceptionally clots of extravasated blood. In certain cases congestion and pink discoloration of portions of the brain substance (cerebral convolutions, bulb, ganglia) with marked puncta vasculosa, are found, while in others the greater part or the whole of the encephalon is anæmic. The puncta in such cases, large and dark, on the surface of the section, promptly enlarge until they may form distinct drops.

In the lungs areas of collapse, and of dark red congestion and infiltration are common, mostly as the result of the entrance of alimentary or medicinal matters into the bronchia owing to palsy of the pharynx. Such materials can be found in the bronchial tubes.

The third stomach and the large intestine may be impacted, the contents more or less baked and glossy on the surface, and coincident congestions of the mucosa are not uncommon. In some instances, however, the contents are soft and pultaceous and the absence of mucous congestions is remarkable.

The womb rarely shows characters differing from the condition which is normal to the first few days after parturition.

The blackness and thickness of the blood has been noted by practically all observers. This is partly the result of its density, but doubtless also of the undetermined toxins which are operative in the disease.

Yellowish gelatinoid exudates have been found in the subdorsal and sublumbar regions, as well as the cranium and spinal canal.

Glucose appears to be constantly present in the urine, and in excess in the more violent and fatal cases: from 1.19 grm. per litre in slight cases to 41.8 grms. in a fatal one (Nocard). Albumen may be present, though probably only when local inflammation has supervened.

Symptoms. The conditions of the attack should be noted. This is a disease of the first six days after parturition, rarely seen in the second week, and never after the fourteenth day. It is very exceptional before parturition, yet Müller quotes 47 cases in 1107 births. The breed, condition, milking qualities, plethora, feeding, etc., of the patient are, as already noted important data in diagnosis. The onset is sudden without premonitory symptoms.

Two very distinct types are met with, the comatose and violent or spasmodic, which, however, merge into each other by insensible gradations, and may follow each other.

From twelve to seventy hours after an easy parturition there suddenly appear signs of discomfort. Feeding and rumination cease, the calf is neglected, there may be plaintive moaning, the eyes seem dull and clouded, the eyelids drooped, the conjunctiva red, the pulse normal for parturition, sometimes extra strong, the breathing excited often with moans or grunts. The senses are dulled, the walk is unsteady, the feet being abducted and planted like clumps, or the legs sway, perhaps cross each other, remain semi-bent, and soon give way leaving the animal prostrate, resting on the sternum and abdomen, or later on the ribs, with head extended. Attempts may still be made to rise, but this is rarely accomplished unless when improvement sets in. This is the condition in which the patient is usually found, being the first to be noticed by the owner. The bowels are torpid, the urine retained in the bladder, and the animal may remain thus in a drowsy condition, without changing from the sterno-ventral decubitus, or dropping the head on the ground until improvement sets in. The head rests on the shoulder or upper flank. If held outward or forward the upper border of the neck has an S shaped outline.

More commonly the somnolence increases, passing into a complete torpor and insensibility, the eye may be touched without causing winking, pricking or other injury causes no further response, the patient turns upon its side, with its head extended on the ground. She may lie in this condition with no sign of vital activity save pulsation and breathing, and the latter is liable to be slow and stertorous by reason of the paralysis of soft palate and larynx. The jugulars usually show a venous pulse. Fermentations in the inactive paunch cause the evolution of gas with tympany, which still further obstructs the breathing, and reacts injuriously on the nerve centres. The normal eructations from the rumen may continue, with liquids and floating solids, and in the paralytic state of the throat these too often pass in part into the bronchia, causing septic bronchitis and pneumonia. The same is liable to follow the administration of liquids, the irritant drugs passing into the larynx, trachea and lungs. The pulse becomes soft, small and finally almost imperceptible. It may be 50, 60 and upward.

In favorable cases, defecation may still occur, or the rectum once emptied may fill again through the continuance of peristalsis, the milk continues to be secreted, and in one to four days, spontaneous defecation and micturition may be resumed, and the patient may get on its limbs and commence feeding. There is usually at first a little weakness of the limbs, but this is transient and health is restored in a very short time. The suddenness of the improvement is often as marked as of the attack. The patient is left prostrate and insensible, without giving any response when the eyeball is touched and in two or three hours it is found on its feet, eating, with eyes bright and clear.

Some patients, however, are restored to ordinary sensation, intelligence and appetite, while the hind limbs remain paralytic, or paretic, and the station and gait both weak and uncertain for days or even weeks. In such cases there have been presumably structural changes in the nerve centres, which require time for repair.

In fatal cases, death may occur quietly from apoplexy, cerebral compression, or narcotism, or it may be preceded by a period of marked excitement or disorderly muscular movements. Lifting of the head, throwing it alternately on the shoulder and on the ground, trembling of head, members and body, cramps or jerking of the limbs or of other parts, drawing the hind limbs up against the abdomen, and again extending them, rolling of the eyes, loud, noisy, irregular, embarrassed breathing and a running down pulse are often marked features.

The temperature range is peculiar. At the start there may be some hyperthermia 103° or 104°; with the advance of the disease it tends to become lower, 98°, 96°, or 94°. When improvement sets in, it rises again promptly to the normal.

Cadeac describes a special form which is ushered in by great restlessness, bellowing, throwing the head to right and left, grinding the teeth, sucking the tongue, salivation, licking of certain parts of the body, spasms in the neck, back or limbs, and prompt recovery, or lapse into the comatose condition as above described. It proved less fatal than the ordinary comatose type, but seems to depend on similar conditions.

Prognosis. Mortality. The disease is very deadly, the mortality in time past having reached 40, 50 or even 60 per cent., the gravity increasing as the disease set in nearer to parturition. Cases occurring on the first or second day were mostly fatal, those at the end of the first week were hopeful, and those occurring during the second week were very hopeful. With the Schmidt (iodine) treatment the mortality is claimed to be reduced to 16 or 17 per cent.

Prevention. Measures directed toward the lessening of plethora tend to remove one of the most fruitful causes of the disease and though not invariably successful, are yet of great value. The most direct is the abstraction of blood in the last fortnight of pregnancy, to the extent of 6 or 8 quarts. This tends to secure a lessening of the blood tension, and blood density, but there is the drawback of a created tendency to a subsequent increase in blood formation to make up the loss. This measure should be reserved for cows that are very plethoric, extra heavy milkers and such as have already suffered from the disease.

Purgatives will measurably secure the same end without the same degree of danger. One to two pounds of Epsom or Glauber salts in the last week of gestation, or at latest when labor pains set in, tend not only to remove solid or impacted masses from the first and third stomachs, and inspissated contents from the large intestines, but to secure a free depletion from the portal system. If not before, this should always be given immediately after parturition to cows in extra high condition, heavy milkers, and that have had a short and easy delivery.

Restriction of food for a week before and as long after parturition is of equal importance. A very limited supply of aqueous, easily digested, and laxative food (roots, sloppy bran mashes, fresh grass, ensilage) will meet the demand.

Exercise in the open air is of great value in giving tone to the muscles, and especially the nervous system, and in stimulating the emunctories and other functions.

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