Chapter VII: Front Matter (7)

Hence the theory of its causation by the presence in the system of the toxic products of bacteria rather than the bacteria themselves. (Dieckerhoff.) Cadeac supposes that any toxin which causes capillary dilatation may determine the disease, and calls attention to the fact that the injection of mallein (a vaso-dilator) aggravates the phenomena of petechial fever and determines enormous local exudations and engorgements. He notes further the potent vaso-dilator action of the products of strangles, contagious pneumonia, and influenza which are among the most frequent antecedents of petechial fever. Dieckerhoff also looks on the phenomena as the result of poisoning by the absorbed toxins of the microbes of suppuration, which modify the nutritive changes in the walls of the capillaries and determine exudations and hæmorrhages. Zschokke thinks that there is infection of the intima of the capillaries, with the formation of coagula. Clots are not found, however, apart from hæmorrhages.

The toxin theory receives indirect support from the absence of the same specific lesions in simple mechanical congestion of the capillaries and veins. Ranvier had no such results from tying the veins of a rabbit’s ear. Roger tied the auricular veins of the rabbit, and then cut the sensory nerves without effect: he then destroyed the cervical sympathetic ganglion, when there supervened marked exudation, lasting for three days. The complete blocking of veins by pressure or aseptic ligature, does not produce a spreading œdema, whereas in ordinary suppurative phlebitis, with abundance of toxins in the tissues this is a constant result.

The toxin theory does not fully account for those cases that occur suddenly, without any manifest pre-existing disease, and as the result apparently of cold and chill. On the other hand, it is only a very small proportion of horses exposed to the same degree of cold and chill that contract petechial fever, and it might well be surmised that in these few an unknown focus of suppuration or other lesion existed prior to the chill or that toxins having the requisite devitalizing and vaso-dilating properties had been absorbed from fermentations in the bowels or elsewhere. The mere exposure is harmless to the very great majority of subjects.

In any case it must be accepted that the debility and impaired local innervation, nutrition and function, that attend on the exposure to cold and toxins must be looked on as potent contributing causes. The predilection of the swellings for dependent parts (limbs, venter, face) shows the influence of gravitation and congestion. Whether there is present any special microbe which has yet eluded discovery, but which is the main pathogenic factor, must be left to the future to decide.

In cases that appear to be due to cold or chill alone, the disease is held to be _primary_; in those following on another affection, _secondary_.

Among the diseases on which petechial fever supervenes as a secondary affection contagious inflammatory affections of the lungs and air passages hold a bad preëminence. Strangles, influenza and contagious pneumonia, about in the order named, are especially causative factors or occasions of petechial fever. Among the other affections on which it supervenes may be named pharyngitis, abscess of the nasal sinuses, hepatic, renal and other internal abscesses, acute coryza, laryngitis, or bronchitis, enteritis, abortion, aggravated grease, suppurating wounds of the skin, infective abrasions by harness, suppurating sores after firing, infective arthritis with open joint, amputation of the tail, and castration.

_Lesions._ In certain cases these may be largely confined to petechiæ and slight blood extravasations, which are distributed very generally throughout the tissues, but show especially in the skin, subcutis, mucosa and submucosa of the nose, eyes, pharynx, guttural pouches, larynx, trachea, bronchia, mouth, stomach, intestine, bladder, vagina and womb; also in and on the lungs, pleura, pericardium, heart, liver, spleen, kidneys, peritoneum, pancreas, ovaries, bones, lymph glands, brain and nerves. The largest extravasations are liable to be in the softest tissues, and in the lungs they may reach the size of the closed fist, though usually they vary from a mere spot up to this. The spleen is sometimes engorged even to rupture. Beside the extravasations, and associated with them in position, and probably largely as an effect of them, there is more or less serous effusion infiltrating the tissues, congestions, suppurations, degenerations, and necrotic changes.

The _skin_, if white, and the dark skins on section, are seen to be marked by petechiæ. The cutaneous swellings may appear on any part, commencing with nodular thickenings varying in size from a pea to a walnut, and merging together into extensive elevated areas terminating abruptly at their margins in the smooth skin. The larger and more persistent engorgements settle on the lower aspect of the body and other dependent parts like the limbs and face. Cracks, oozing, deep fissure, and extensive sloughs are not uncommon. When the skin is incised it shows serous infiltration and thickening, with spots and patches of blood extravasation. The subcutaneous connective tissue is similarly infiltrated and discolored, and often in the limbs, face, and under the breast, sternum and abdomen so as to form a tremulous gelatinoid cushion of several inches in thickness. The capillaries may be distended to more than 20 times their normal calibre. The exudate may extend deeply between the muscles, and sloughs may lay these freely open and invade their substance. The muscular tissue is mottled with petechiæ, and apart from these it is pale, yellow, or grayish, having to some extent undergone granular or fatty degeneration. Detachment of the perforans and perforatus from their insertions is occasionally met with.

The _nasal mucosa_ may show only petechiæ and circumscribed blood staining, but in fatal cases it is more likely to present extensive blood extravasations involving it may be the whole mucosa, and narrowing the lumen almost to complete occlusion. Sloughing is not rare, and the resulting ulcers may extend into the subjacent tissues, so as to penetrate the septum nasi or the thin plate of the turbinated bone.

The _buccal mucosa_ and _submucosa_ are often involved in common with the skin of the lips, cheeks, and intermaxillary space, the tissues being involved in one common infiltration of blood and serum. In some cases circumscribed necrosis and ulcerations are formed.

In the _pharynx_ and _larynx_ infiltration of the mucosa and adjacent parts of a deep blood red, with or without ulceration, causes serious narrowing of the passage, that on the vocal cords threatening suffocation. Suppuration of the pharyngeal glands and guttural pouches is not uncommon. Alimentary matters are frequently found in the larynx, and bronchia.

Beside the petechiæ and hæmorrhages in the _lungs_, œdematous infiltration in dependent parts, hepatization, abscess, and limited areas of necrosis are met with. The pleural sacs often contain a sanguineous effusion.

The _stomach_ and _intestines_ are usually more or less mottled with petechiæ involving mucosa, serosa or muscular coat; they are raised in rounded or irregular elevations by œdemas; or they are the seats of more or less extensive and even perforating ulcers. The contents of the bowels may be deeply discolored by the escaping blood.

The _kidneys_ may be pale except where blood stained and œdematous infiltration of the surrounding tissue may be marked. Serous effusion into the peritoneum is not rare.

The _eyelids_ are often implicated, infiltrated thickened, and rigid, and the conjunctiva, bulbar and palpebral, the seat of extensive petechiæ.

Barreau mentions extravasations on the divisions of the lumbosacral plexus causing sudden paraplegia.

Petechiæ and hæmorrhages mark endocardium, pericardium and cardiac muscle, otherwise the muscle is pale. The blood is sometimes in firm clot, at others diffluent or nearly incoagulable.

_Symptoms._ If hyperthermia is not already present as a feature of the pre-existing malady it usually shows itself early, at first slight, it may be (101° F.), and afterward rising in some cases to 104° to 106° F., or even higher. The general symptoms are usually those of the pre-existing disease (strangles, contagious pneumonia, influenza, nasal catarrh, pharyngitis, bronchitis, etc.), pursuing, it may be, a persistent course, or attended by special toxæmic symptoms of prostration and other signs of depression of vital functions. In some cases the hyperthermia is either absent at this stage or overlooked. On the prostration supervene the petechiæ on the visible mucosæ, and often also the swellings of the skin and subcutis. One of these may be seen before the other and it is difficult to decide whether the petechiæ always appear first as has been claimed. Cadeac claims that when œdema is first seen it has been preceded by petechiæ in that tissue (skin).

The _petechiæ_ are usually first noticed on the nasal mucosa as fine red points, pin’s heads, or up to half an inch in diameter, or a number of these have coalesced to form extensive patches, and by and by to cover the entire wall. At first the mucosa is spotted with purple, without any marked elevation of the surface, but as the lesions extend it becomes swollen and raised at the points of extravasation and immediately around them and oozes a serous, sometimes a pinkish or yellow fluid. Even in the smallest petechiæ the color is persistent and does not disappear on pressure like the blush of the adjacent mucosa.

Usually _cutaneous swellings_ coincide with the petechiæ, or appear within two days thereafter. The first manifestation is in the form of rounded abruptly elevated nodules, about 1½ inch to 3 inches in diameter, strongly resembling the eruption of urticaria. These show a certain predilection for the more dependent parts of the body,—limbs, abdomen, sheath, mammæ, sternal or pectoral region, nose, lips, face, etc.,—but they may develop on any part or on the whole surface. Neither tenderness nor heat is usually excessive. The swellings tend to run together so as to form extended elevations enveloping the entire limb up to a given point, forming a great pad under the chest and abdomen, or distending the whole face or head so that it seems more like that of a hippopotamus than of a horse. In such cases the lips and nostrils become so thick and rigid that prehension is impossible, and breathing if it can be accomplished at all is accompanied with a marked snuffling. The swollen eyelids are closed, and the general turgid surface of the face is hard and resistant and no longer pits on pressure.

Under the _chest_ and _abdomen_ the swellings show as a continuous pad or cushion, on one side mainly or extending across continuously on both sides, and from the breast to between the thighs. It usually pits on pressure, and may shed the hair and become rough and scabby or ooze a serous fluid from the surface.

On the limbs the swelling usually shows first on the fetlock or pastern and gradually extends upward until it reaches the body.

As the disease advances chaps, cracks and fissures tend to form on the swellings, showing about the head, on the lips or on the nose and maxilla where the noseband of the halter crosses; on the lower part of the body where the circingle crosses, or where the part is pressed upon in lying down, and in the limbs in the flexure of the joints—behind the pastern, or knee or in front of the hock. In many cases the skin and connective tissue sloughs, and drops off exposing the muscles, the tendons or the ligaments of the joints. In other cases the tendons are involved in the degenerative process or necrosis and become detached from their lower insertions so that the toe may be turned up or the fetlock pad may come to the ground. The matrix of the hoof wall (coronary band) may separate from the horn, leaving a gaping opening which exudes liquid freely, and if the animal survives, the entire hoof may be shed.

In other cases, and often quite early in the disease, the swellings may suddenly subside and disappear, with it may be, a recovery, or, in other cases, with an exudation into the lungs or chest, the digestive organs or abdomen. In case the lungs are attacked, there is hurried oppressed breathing merging into dyspnœa or asphyxia. In case the bowels suffer there are colicy pains more or less acute, with much constitutional disturbance, marked prostration and serous or bloody diarrhœa. These mostly prove speedily fatal. Less redoubtable are those cases in which the swellings alternately subside or moderate, and reappear or increase, without implication of the internal organs. The absence of internal lesions and the moderation and intermissions, of the external ones, give good hope of the preservation of the vitality of the tissues and of recovery.

_Course and Duration._ These vary much with the severity of the case. In subacute and tardy cases with few petechiæ and restricted swelling in the limbs, the symptoms become remittent and recovery finally takes place after one or two months. In other cases the morbid phenomena which developed rapidly may subside as quickly and recovery occurs in a few days. In the more typical case the visible lesions may encrease or remain stationary for one, two or three weeks and then terminate in death or recovery. In the most violent types death may occur within forty-eight hours. The average duration of the affection is found to be about 16 days.

_Differential Diagnosis._ In typical cases of petechial fever, diagnosis is easy. The supervention on a protracted or debilitating disease of the respiratory passages of an access of hyperthermia, and marked prostration, with the appearance on the nasal or other mucosa of petechiæ and swellings of a dark red color throughout, and of cutaneous swellings in the form of nodular elevations and more extended salient patches, having a tendency to ooze blood or serum, to crack and fissure is virtually pathognomonic.

_Acute glanders_ may resemble it but lacks the extended sloughs of petechial fever, and the nasal ulcers that form in glanders are on a yellowish base and periphery, whereas the purpura ulcer is on an uniformly dark red base, and without the elevated margin seen in glanders. In cases of doubt the mallein test is not available as the purpuric patient is already fevered, or liable to be so at any moment, and any wound in such a subject will give rise to extensive swelling.

In glanders the nodular submaxillary enlargement is almost pathognomonic and still more so if the facial lymphatic vessels are thickened (corded) and both symptoms fail in purpura. In cutaneous glanders with swollen joints or limbs the attendant pain is much more severe, and the farcy buds, forming on the thickened and indurated lymph vessels, bursting and discharging an albuminoid fluid like oil have no counterpart in petechial fever. In cases of doubt the search for the glander bacillus, and above all the inoculation of a male Guinea pig in the flank and the discovery of the bacillus mallei in the resulting exudate and diseased testicle will decide.

From _anthrax_ and _emphysematous anthrax_ petechial fever is distinguished by the absence of the large bacilli of these respective diseases from the exudate. It is not communicable, like anthrax, to the sheep, Guinea pig and rabbit, and does not crackle on manipulation, like emphysematous anthrax. The swellings are much more generally diffused than in anthrax and the hyperthermia much less.

_Urticaria_ furnishes a skin eruption which may be indistinguishable from the earlier skin lesions of petechial fever, but these lesions are not associated with the petechiæ in the nasal and other mucosæ, and the swellings do not advance to great sanguineous engorgements, cracks, fissures, necrosis, and deep and extensive sores as in purpura. Urticaria is, moreover, usually traceable to some digestive disturbance and fault in feeding.

_Malignant œdema_ is usually confined to the seat of the inoculation wound and an extension around that, the exudate is very watery and may be mixed with fetid gas bubbles, so as to crepitate slightly, and it contains an abundance of its specific, round ended bacillus, often in chain form. The carcass putrefies with great rapidity.

_Horse pox_ affecting the pastern and limb with attendant swelling is distinguished by the absence of petechiæ on the mucosæ, and by the formation on the affected part of little pea-like papules, which early exude an abundant liquid, the concretion of which on the hairs forms a remarkable yellowish encrustation, embedded in the angry red sores beneath.

_Mortality._ _Prognosis._ The mortality has generally averaged about 50 per cent. Much, however, depends on the violence of the attack, and the reduced and worn out condition of the patient. The most hopeful cases are those in which the temperature remains near the normal, the strength and appetite are well sustained, the swellings are comparatively slight, and there is no indication of any internal complication. The unpromising symptoms are: persistent high temperature; complete anorexia; great dulness and prostration; excessive swellings not only cutaneous but in the nose and throat as well; a marked oozing from the swellings with a tendency to form cracks, fissures and sloughs; the serious obstruction of breathing and prevention of hæmatosis by blocking of the nose, pharynx or larynx by sanguineous and serous exudate; the appearance of oppressed breathing and other indications of exudate with the lungs and chest, or of colics, diarrhœa, and other suggestions of effusion on the bowels or in the abdomen. Extreme fetor of the expired air and of the fæces is a bad symptom, though not always a fatal one. Sudden retrocession of the cutaneous swellings, may be the precursor of internal exudations and death, yet in the absence of marked acceleration of the pulse, and of the objective symptoms of disease of the chest or abdomen, it is rather to be taken as a herald of recovery.

_Treatment._ Whatever may be the precise cause of petechial fever it is largely connected with and maintained by an unhealthy condition of the blood, and especially with the presence of toxins and waste products in that liquid. The first consideration is to secure for the patient the best possible sanitary conditions. A roomy loose box, dry, clean, well lighted and well aired, nourishing, easily digested food—green food, carrots, turnips, or mashes—and pure water are desiderata. A sunny exposure is desirable especially in winter, and everything like chill should be guarded against. Blanketing may be called for in cold weather, but the circingle like the halter should be avoided as being calculated to cause indentation, cracking or sloughing of the swellings.

A moderate action of the bowels should be secured by the nature of the food (linseed meal or tea), or by small doses of saline laxatives (sodium sulphate) or calomel. Suppression of the urine too, must be counteracted by diuretics (saltpeter, oil of turpentine) when necessary.

Further internal medication has been aimed to correct the dilatation of the capillaries, and to prove antidotal to or to eliminate the poisons present in the blood.

As _vaso-motor_ stimulants have been employed ergot, belladonna, tannic, sulphuric and hydrochloric acids, oil of turpentine, iron sulphate, potassium bichromate and chlorate, quinia sulphate, and strychnia sulphate and arsenate. The value of any one of these is dependent on its early employment, the slight character of the lesions and the remissions that so often occur even in severe attacks. None are of much account in a violent attack at its worst.

In the slighter cases _ergotin_, 5 grains daily in two doses, has been apparently useful. An objection is that its continued action on the nerve centres and digestive organs is liable to prove depressing and injurious. Of the acids, _tannic_ is liable to engender constipation, locking up the injurious products to which, however, it acts to some extent as an antiseptic. _Sulphuric_ and _hydrochloric_ acids have a tonic effect, and the latter is a stomachic under ordinary conditions. The same may be said of the _iron salts_ and to some extent of _oil of turpentine_, which have both proved useful in favorable cases. Cadeac condemns ol. terebinth as calculated to abolish kidney secretions. The _potash salts_, _bichromate_ and _chlorate_, and _quinia sulphate_ are decided antiseptics and though the admissible dose would not ensure the destruction of bacteria, yet, acting in the system, with leucocytes and leucomaines, they may serve by keeping them in check. The _chlorate of potash_ is given to the extent of an ounce the first day, and of half an ounce on succeeding days. The _quinine_ salt is given in half ounce doses once or twice daily. In combination with bitters they seem to be of material value. _Nux vomica_ (1 dram) or _strychnia sulphate_ or _arsenate_ (2 grains) given twice daily has seemed to be among the most promising agents of this class. As a potent vaso-motor stimulant, a bitter tonic and stomachic, strychnia has seemed at times to rouse the vitality and enable the system to throw off the load of poison that depresses it. The wonderful power of _adrenalin chloride_ as a vaso-motor stimulant more than warrants its use both locally and generally. In using any one of these agents, we should not neglect concurrent attention to the bowels and kidneys, to antisepsis internally and externally, to hygienic and tonic measures generally.

_Antiseptic agents_ have been given by the alimentary canal, the skin, the subcutis, and the air passages.

By the _stomach_ the following have proved more or less useful in checking gastro-intestinal fermentations, and perhaps in hindering absorption of toxins from the specific lesions on this track: _phenic acid_, _creolin_, _lysol_, _ichthyol_, _boric acid_, _salicylic acid_, _sodium salicylate_ and _hyposulphite_, and _calomel_.

To the _superficial swellings_, _fissures_ and _sores_ the same agents may be freely applied, alone, or combined with astringents, such as _alum_, _lead acetate_, _aluminum acetate_. In the hot season they may be applied cold, whereas in the cold weather hot applications are often preferable. Aruch claims excellent results from covering the engorged head with a woolen cloth and irrigating it with cold water.

The question of drainage of the worst cutaneous swellings by _scarification_, has been variously dealt with, Dieckerhoff advocating deep incisions, while Friedberger and others forbid them as encreasing the tendency to necrotic infection and sloughing. In the slighter cases it can well be omitted, but in extensive swellings the disintegrating and debilitating action on the tissues is so great as to well warrant its prevention by incisions and drainage. It is well to first give the surface a soapy wash, then apply a mercuric chloride or carbolic acid lotion and lance it in the prominent and tense portions. As a further precaution against septic infection it may then be covered by cotton soaked in one of the above lotions and covered with a bandage. For swellings beneath the abdomen or chest this may be held in place by loose circingles. Scarifying becomes imperative in case of paraphymosis arresting the flow of urine. Deep fissures and sores following sloughing may be treated with mercuric chloride solution, (1:1000), creolin or phenic acid (2:100), iodoform, dermatin, naphthalin or salol.

Disinfection of the _nasal passages_ has been attempted by pervading the air with carbolic acid, creolin, cresyl, lysol, or naphthalin, by hanging saturated cloths in the stall, or spreading them on the floor. Perhaps a better method is to flush out the nose, by injecting each chamber in turn with a piece of rubber tubing, one end of which is introduced into the nose, and the other raised four feet and furnished with a funnel. The injection may be 1 dram creolin to 2 quarts water, or carbolic acid or alum may be substituted or alternated.

The swelling of the nostrils may be so great that it becomes requisite to hold them open mechanically. The suture of the two altogether, across above the nose has been practiced, or a tube of light wood or aluminum can be inserted in each nostril.

_Injection of the trachea and bronchia_ with a solution of iodine 1 part, potassium iodide 5 parts, and water 100 or 200 parts, was advocated by Dieckerhoff and met with a fair measure of success in mild cases. In some cases, however, granular tracheitis and bronchitis followed, and in others necrotic tracheitis and pulmonary gangrene, so that the method has not been widely accepted. If resorted to, the weaker solution is to be preferred, and may be injected through a tracheal ring, or the membrane between two rings twice a day in doses of 3 to 5 centigrammes (45 to 75 drops).

_Injection into the veins of Argentum Colloidale_, 1 per cent solution in doses of 1⅔ oz. (50 grammes) at intervals of 2 hours has been very strongly advocated by Dieckerhoff who in four successive cases had complete recoveries in from three to six days. After disinfection of the skin a small trochar and cannula, or a hypodermic needle is introduced into the jugular and the injection made. Local treatment for the swellings was also applied.

Injection subcutem of the _antistreptococcic serum_ of Marmorec, has been lauded as promptly overcoming the capillary dilatation, and enabling the leucocytes to neutralize the toxins.

Finally Menveux recommends an artificial compound as possessing all the good qualities of the antistreptococcic serum. This is composed of sodium chloride 5 grammes, sodium phosphate 1 gramme, sodium sulphate 20 centigrammes, sodium carbonate 1 gramme, caffein chlorhydrate 10 grammes, boiled filtered water 100 grammes. Inject daily in three doses 135 grammes.

PETECHIAL FEVER IN CATTLE.

Synonyms. Causes: microbes, maturity, hard work, chill, poor hygiene,
drying of damp lands in summer and autumn, impermeable soils, corrupt
water, bacillus, diplococcus; resemblance to hæmorrhagic septicæmia.
Lesions: petechiæ and hæmorrhages on mucosæ, serosæ and skin;
gelatinoid exudates gravitating to the lowest parts of face, chest,
belly and legs; chaps, oozing, sloughs, depilation, exudate in tongue,
bloody diarrhœa, duration 14 to 40 days, mortality light; indurations.
Diagnosis: from anthrax, black quarter, malignant œdema and acute
hæmorrhagic septicæmia. Prevention: avoid infecting soils in summer
and autumn; drainage, cultivation; chills. Treatment: venesection:
laxatives, diuretics: intratracheal injections of iodine: colloidal
silver. Locally: antiseptic astringents: remove eschars: facilitate
breathing by surgical or mechanical means: good hygiene.

_Synonyms._ Purpura Hæmorrhagica. Anasarca. Inflammatory Œdema. Yellow Water. Morbus Maculosus.

This malady presents phenomena very similar to those found in the horse, and shows itself in mild and severe types. It has been noted by writers on diseases of cattle from Vegetius down, though under quite a variety of names.

_Causes._ These are uncertain, though much seems to point to microbian invasion or intoxication by microbian poisons. In France, it has been seen mainly in mature and robust working oxen after a hard day’s work, when the animal has had time to cool off. Also in cows used in the yoke and milked at the same time. Poor food, starvation and low condition have also been cited as causes. In other cases, high feeding and plethora have been incriminated. It shows itself most commonly in summer and autumn, so that cold or chill must be looked on as a cause secondary to another—probably microbian or toxic. Again, it is by far the most common in the adult animal. What is more suggestive is its relative frequency in localities characterized by swamps, springy fields, hollow basins, damp hill-foots, bottom lands, and damp, impermeable or undrained soils. Again, on heavy clays where the water is preserved through summer in open ponds and often in a very corrupt condition. This at once accounts for its common appearance in summer and autumn when the offensive products of fermentation are most abundant, and corroborates the doctrine of a toxic ferment. But its origin has not been definitely traced to such products as yet. This, notwithstanding that Kolb attributes it to _bacillus hæmorrhagicus_, and Robert, Fabert, and Dinter found the exudates swarming with _diplococci_. This may assimilate it to _septicæmia_ hæmorrhagica.

_Lesions._ In cattle killed during the early stages, circumscribed hæmorrhages and petechiæ are found in the nose, trachea, bronchia, gastric and intestinal mucosæ, cerebral membranes, pleuræ, peritoneum, bladder, and skin. In many cases these are accompanied by congestion and thickening of the walls of the lymphatics, and effusion in and under the skin in different parts of the body, but especially along its lower aspect—(belly, sternum, dewlap, limbs, lower jaw, tongue)—of a gelatinoid exudate, which raises the skin abruptly in the form of a thick cushion. At first this is soft and tremulous, but later it may have coagulated giving a great degree of resistance to the structure. Extensive cracks, fissures, and sloughs, and unhealthy sores form on these swellings. Franck especially notes the enlarged tongue gorged with blood and yellowish exudate as in gloss-anthrax. The blood extravasation may be further evidenced in the black or blood-streaked fæces, the reddish urine, and a rosy tint of the milk.

_Symptoms._ The animal is dull, sluggish, moves stiffly and with difficulty, and shows hyperthermia, (102° to 106° F.), inappetence, impaired or suspended rumination, heat of the roots of the ears and horns, and of the dry muzzle; the spine, and usually certain points beneath the sternum or abdomen at which swellings are about to appear, are tender to the touch. On the affected parts of the skin the temperature is raised, and there may be detected pea-like elevations which become surrounded and enveloped in extensive swellings that pit on pressure. The swellings show a preference for the thinner and looser parts of the skin, and gravitate rapidly toward dependent parts. Thus, the eyelids, roots of the ears, intermaxillary space, throat, muzzle, dewlap, ventral aspect of the body, axilla, mammæ, scrotum, groin, thigh, knee and hock are favorite spots, the liquid rapidly gravitating downward through the loose connective tissue to the lowest points. The face becomes infiltrated to unsightly dimensions, interrupting prehension and threatening suffocation, the dewlap swells up to a great size, the forearms or thighs become rounded and tense, and a thick pad forms along the ventral aspect of the body. The white skin on such swellings becomes red, they may ooze a yellowish liquid or blood, the surface becomes depilated, scaly and rough, chaps and cracks appear, going on, it may be, to deep fissures, more particularly at the flexures of the joints, on the throat or muzzle, or on other points that are subjected to pressure. Necrosis of great patches of skin is not uncommon, and these sloughing off leave large wounds with unhealthy, indolent surface and little disposed to rapid healing.

The petechiæ show early on the muzzle, the nasal and buccal mucosæ, and on other mucous membranes. Exudations also appear and a serous, often bloody, discharge escapes from the nose and concretes in colored encrustations around the nostrils. The nose may be obstructed causing the animal to breathe through the open mouth, protruding the tongue which is often also the seat of extensive swelling, discoloration and induration.

As the disease advances there is encreased dullness and prostration, marked emaciation, and anæmia, sunken eyes, encrusted eyelids, extensive areas of depilation including even the long hairs of the tail, and quite often an abundant bloody diarrhœa.

The affection may last for 24 to 40 days and under rational treatment the majority survive. There remains, however, in a certain number of cases, a permanent enlargement and fibrous induration from the organization of the exudate.

_Diagnosis._ A fully developed case is easily recognized. The fever and constitutional disorder, complicated by petechiæ on the mucosæ and skin; the extensive swellings suddenly formed, oozing serum or blood, and tending to fissures and necrosis; and the discharge of blood from the nose, bowels, kidneys and udder, in the absence of the bacilli of anthrax, emphysematous anthrax, malignant œdema, and wildeseuche; the slower progress; the low mortality; the occurrence on a damp, springy, or impermeable soil, or one known to produce this disease; and especially if in late summer or autumn, become virtually pathognomonic.

_Prevention._ Seclude cattle in late summer and autumn especially, from soils known to be productive of this affection and above all from damp wet clays, underlaid by hardpan, from swamps, from drying up ponds and basins, from wet river bottoms and deltas and from springy fields generally. Fields of this kind may be reserved for cultivated crops or for raising hay. The fundamental remedy is thorough drainage, and a subsequent abandonment of the land for a year or two to other crops to allow of a dissipation of the poison. Sudden chills after being heated or fatigued, and exposure in the pasture in cold nights are to be avoided.

_Treatment._ The French writers up to the present extol bleeding for the early stages. Its benefit must apparently depend on the diminution of the blood tension allowing the distended capillaries to resume their normal contractility, and in the lessening of the tendency to exosmosis, and the encrease of endosmosis so that much of the poison in the blood is removed and what remains is largely diluted and rendered comparatively harmless. However well this may operate in the strong and plethoric, it cannot be considered as applicable to the weak or anæmic, nor to advanced cases in which the vital powers are already seriously reduced by the abundant exudations and extravasations, and by the narcotic and devitalizing action of the circulating toxins.

With us the demand is usually met by laxatives and diuretics, under the idea that these are less debilitating and that if the morbid process can be arrested recovery is more prompt and perfect. A purge of sulphate of soda is followed by full doses of nitrate or acetate of potash, in combination with iodide of potassium, or chlorate of potash; or bicarbonate of soda associated with hyposulphite of soda. These or other diuretics should be pushed so as to produce free diuresis. Stimulating antiseptic diuretics like ol. terebinth, may be added. Iodine solutions injected into the trachea have been recommended as for the horse (Huber, Heuberger, Rohr,) and the serum or silver preparations or adrenalin may be tried.

_Locally_ astringents and antiseptics have given good results. Solutions of alum or lead acetate with carbolic acid and iodine; frictions with soap liniment, with a mixture of aqua ammonia, oil of turpentine and oil, or with mixtures of oils of origanum, cajeput and peppermint, and iodine, or simple painting with tinct. of iodine may be cited. Fissures and open sores may be dressed with mercuric chloride solutions (1:1000), Lugol’s solution, phenic acid lotion, solution of creolin, lysol, or chloronaphtholeum, camphorated spirit, or other antiseptic agent. The nose should be injected, cleared of eschars, and if necessary propped open.

An abundant, wholesome, easily digested diet, pure air, a dry stall and protection against cold are essential.

CHICKEN CHOLERA. FOWL CHOLERA. CHICKEN TYPHOID. CHICKEN PASTEURELLOSIS.

Definition. Historic notes. Bacteriology: Bacterium choleræ
gallinaceæ, nonmotile, with polar stain, bleached by iodine,
non-liquefying, causes septicæmic lesions. Lignieres’ bacillus,
culture features non-gasogenic, acidifies dextrose; vitality in
disinfectants; survives drying. Accessory causes: new birds in flock,
or eggs for hatching, mingling of flocks, manure, watershed, streams,
ponds, dust, wild birds, buzzards, rabbits, insects, infected soil.
Susceptible animals: hens, doves, peafowl, pheasants, parrots, ducks,
small birds, guinea pigs, rabbits, white and gray mice. Effect on
sheep, horse, man, cow, frog. Incubation 18 to 48 hours. Symptoms: in
fulminant cases rarely seen, in acute, anorexia, depression, debility,
apathy, ruffled feathers, sunken head, neck, wings, tail, tremors,
nasal and buccal discharge, hyperthermia, sighing, violet comb and
wattles, thirst, pultaceous fæces, later glairy, green and fetid.
Temperature becomes subnormal, inability to rise, stupor, convulsions,
death in 1 to 3 days. Mild cases last 7 days. Cases caused by one
microbe have slough only. Lesions: congested, petechiated, hæmorrhagic
intestinal mucosa; contents of bowels watery, frothy, bloody;
epithelial degeneration and desquamation; abrasions, croupous
exudates, enlarged congested lymph glands, fermenting contents of
crop. Petechiæ general, spleen and liver swollen, congested, friable;
kidneys congested; lungs hyperæmic or blood gorged. Blood diffluent
with microbe. Anæmia. Emaciation. Arthritis. Diagnosis: by rapid
spread, infection origin, early excessive mortality, hæmorrhagic
lesions, microbe in blood and liquid ingesta. Prognosis: Mortality 90
to 95 per cent. at outset. Prevention: Quarantine new birds, inside
screens in summer; burn or acidify manure; exclude buzzards, vermin,
wild birds, and visitors; separate sick, kill, burn, disinfect; divide
infected flock in small lots; prevent wandering in fowls, destroy
insects. Phenic acid subcutem. Immunization: inoculate in breast with
one microbe (Salmon): or with weakened virus (Pasteur). Limitations.
Treatment: gastric and intestinal disinfection—copperas, mineral
acids, carbolic or salicylic acids, aromatics, quinine, naphthol, tar,
phenic acid subcutem.

_Definition._ A febrile hemorrhagic septicæmia of chickens and other fowls (pigeons, ducks, geese, parrots, etc.) communicable to certain rodents and other animals, and characterized by a short incubation, rapid progress, great prostration, violent diarrhœa usually greenish, and a high mortality (90 to 95 per cent.).

_History, Geographical distribution._ It is quoted as prevalent in Lombardy in 1789, in East India in 1817, in France in 1825, and generally in Europe and America in the last half century.

The _losses_ from the ravages of this disease are far greater than the average value of the individual animal would lead one to suppose, but with domestic fowls numbering 300,000,000 and a yearly egg crop bordering on a billion dozens it may well be called enormous.

_Bacteriology._ Chicken cholera is caused by a very small ovoid bacterium (B. Choleræ gallinaceæ) about 0.3 to 1.8μ long, as found in the blood and tissues of the fowl. It has the general characters of the groups which cause hemorrhagic septicæmia, thus: 1. It fixes, above all at the poles, the ordinary anilin colors; 2. It is decolorized by the methods of Gram and Wiegert (iodine solutions); 3. It grows on gelatine without liquefying it; 4. It produces acute septicemic lesions; 5. It tends to polymorphism when grown under different conditions. In the peritoneum of the guinea pig it forms cocco-bacilli tending in acute and violent cases to diplococci. Fed to rabbits it appears in the fæces as a minute bacillus. Even the mode of staining causes a difference in appearance. Fixed in alcohol-ether, and then stained in Ziehl’s phenated preparation, coloring is polar, and the central area clear. If in place of Ziehl’s fluid, hot fuchsin solution is used warm for ½ a minute, bacillus or cocco-bacillus is shown (Lignieres). It is nonmotile, though some observers have been misled by Brownian movements. There are no flagella. In old bouillon cultures short chain forms are met with. No spores are formed.

From fresh cultures, in flask or in animals, the bacterium grows readily in alkaline culture media. In _bouillon_ a turbidity ensues, and after some days pellicles form on the surface and walls, and the liquid slowly clears. The addition of a little blood serum, sugar or glycerine encreases and hastens the growth, while acid retards or prevents. This is common also to other septicemic germs. In _gelatine_ growth is tardy, but in two or three days there are whitish glistening colonies, becoming opaque later, and appearing granular if slightly magnified. In punctures minute colonies form along the line of culture and one at the surface, at first translucent; later opaque. On _agar_ the colonies grow faster with similar appearance. On _gelose_ at 37° C. the colonies are blueish and iridescent, at first, and later opaque. If the germ has been repeatedly passed through the Guinea pig, they are more translucent. On _potato_ with alkaline surface, there is a delicate grayish yellow growth after 48 hours; if acid, growth ceases. In _milk_ there is no coagulation nor acidification for four weeks; then it becomes slowly clear and opalescent. With _sugars_ it is not gas producing. With dextrose it forms an acid solution; with saccharose or lactose an alkaline one. Cultures in peptone gave a strong _indol_ reaction (V. A. Moore). Lignieres found no indol in cultures in pancreatic bouillon.

The bacterium perishes when heated to 58° C. for fifteen minutes. It dies in carbolic acid solution (1:100) in five minutes; in sulphuric acid solution (0.25:100) in ten minutes; in lime water in ten minutes; and in sulphur fumes in three hours. Easily destroyed by disinfectants, it remains potent for months in flasks or buildings that are not subjected to disinfection. It is not killed by drying (T. Smith and V. A. Moore) nor by zero temperature maintained for seventeen hours.

The cultures, especially those made in agar have a very characteristic odor.

_Accessory Causes._ Birds sent to poultry shows will often contract the disease and introduce it into the home flock on their return. It may also be imported in newly purchased birds, or on eggs obtained for hatching. It is even alleged that it has been propagated by feeding healthy hens on the eggs of diseased ones. When chickens run at large it passes easily from flock to flock in the immediate vicinity. The infected manure is, however, the most common channel of infection. Carried on the feet or bill this contaminates the food and drinking water, and washed into streams and ponds, it finally in any case reaches the alimentary canal of the susceptible bird. Or drying up and raised as dust it is inhaled into the lungs. Or finally from any such source it infects any open sore. As granivorous birds, wild and tame, suffer from fowl cholera, it is often introduced by the wild, especially coming from infected poultry yards. Predatory birds, like hawks and buzzards, but the latter especially, are common bearers of infection. Rabbits, which contract the affection so readily, transmit it equally with birds, but man or beast, soiled by the manure will convey it. Insects are among the most prolific bearers, hence, as noted by Salmon, the infection may fail to overstep a close fence in winter, but is subject to no such limitation during the fly season. In this respect chicken cholera agrees with Asiatic cholera, typhoid fever and other affections in which the virus abounds in the alvine discharges. The sale and transportation of the guano from the infected poultry yard is a direct cause of new outbreaks. Feeding on the carcasses or offal of the infected birds is a further cause. It must not be forgotten that the microbe is largely saprophytic, living indefinitely in the organic matter in soils, and determining new outbreaks when brought in contact with susceptible animals. Thus a period of immunity may be followed by infection when new birds are brought in or when young and susceptible ones grow up.

_Susceptible Animals._ Fowl cholera is preëminently a disease of chickens, but the microbe is successfully transferred to pigeons, peafowl, pheasants, parrots, ducks, canaries, sparrows and other small birds, also to Guinea pigs, rabbits, white and gray mice. Guinea pigs have abscesses in the seats of inoculation (Pasteur); the same is alleged of sheep and horses (Kitt), and man (Marchiafava, Celli). Injection into a cow’s teat caused chronic catarrhal mammitis in which the microbe persisted for a long while (Kitt). Like other members of the group of microbes causing septicæmia hæmorrhagica, the pathogeny and even the morphology are liable to material modification as grown in different environment (genera). Some of the forms of cholera occurring among domesticated birds and held to be distinct diseases may find in this an explanation. Rabieaux claims that under favorable conditions it has been transmitted to the frog.

_Incubation._ This varies from 18 to 48 hours, the usual being 24 hours.

_Symptoms._ In some _fulminant cases_ the animal is found dead a few hours after apparently blooming health; it may even have died on the nest or fallen dead from the roost. Cadeac speaks of transient symptoms even in such cases—extreme dulness, prostration, somnolence, seclusion in a cool, dark place, ruffling of feathers, sinking of the head between the wings, drooping, trailing wings and tail, violet comb, gaping, discharge of glairy mucus from the bill, convulsions and death. These symptoms last from two to five hours.

In _acute_ but less fulminant forms there is loss of appetite, depression, debility, apathy, erection of the feathers, sinking of the head, swaying when made to walk, drooping wings and tail, sitting on the breast, convulsive tremblings, discharge of filmy or frothy mucus by the nose or mouth, vomiting, hyperthermia (108° to 111° F. ), sighing, breathing, inflation of the crop, violet colored comb, wattles and mucosæ, great thirst and diarrhœa, at first pultaceous and light yellow, later glairy, green and fetid. The feathers round the anus become soaked and matted with the discharge. Temperature becomes subnormal, the patient falls and is unable to rise, and finally dies in a stupor or convulsions, the illness having lasted 1 to 3 days.

_Milder cases_ occurring chiefly towards the end of an outbreak when the less susceptible animals only are left, or when the microbe has become less virulent, show a larger ratio of recoveries. These show a lack of spirit and vigor, impaired appetite, diarrhœa, emaciation, dulness, prostration, moping, ruffling of the plumes, dark discoloration of the comb, and often swelling of one or more important joints (femoro-tibial, etc.). These may burst and discharge a reddish pus, or simply form dark or grayish swellings. These cases may drag along for a week or more and finally die in marasmus. The minute bacillus is not obtainable from these (Lignieres).

Cases inoculated in the pectoral muscles with only one or two microbes usually have only a circumscribed slough, with loss of condition, and after the elimination of the slough and the healing of the sore the bird proves immune.

_Lesions._ The alimentary canal is the main seat of morbid changes. The intestinal walls, and especially the mucosa, have points and patches of blood extravasation, extensive areas of congestion with ramified redness, exudation and thickening. The intestinal contents are watery, frothy, browned or blackened by effused blood, and swarming with ferments including the specific bacterium. The mucous surface is brownish or blackish, and epithelial degeneration and desquamation with abrasions are not uncommon especially on the summits of the duodenal folds and villi. Croupous exudates and swelling or ulceration of the follicles are met with. The lymph glands at the base of the cæcum are often enlarged and congested. The crop is full of watery, pulpy, frothy or slimy contents, and its mucosa and that of the pharynx may be deeply congested.

Elsewhere the lesions suggest rather the action of destructive toxins and the profound changes in the blood. Pericardium and endocardium are usually studded with dark petechiæ, and congestion and even slight exudation may be present. The spleen is enlarged, soft, and gorged with blood. The liver is swollen, congested, extremely friable, and mottled, grayish white from degenerations. The kidneys are dark red, and friable. The lungs may show slight hyperæmia only, or a blood engorgement and consolidation, and are then easily reduced to a dark red pulp. Friedberger and Fröhner say that respiratory changes are most frequent in land birds; and intestinal and cardiac in water fowl.

The blood is diffluent coagulating loosely if at all, of a brownish red color, reddening slowly and imperfectly in contact with air, and like the tissues contains an abundance of the characteristic bacterium staining deeply at the poles and clear in the center.

In birds that survive a few days there are marked anæmia and emaciation, and the muscular system is of a grayish red color, with fatty degeneration. In acute and fulminant cases on the other hand the muscles may be full and of the normal red color.

In arthritic cases the congestion and thickening of the soft tissues, and the excess of synovia, are supplemented by destruction of the articular cartilage and by areas of bone abrasion. In the more tardy cases collections of caseous matter are found.

_Diagnosis._ This is based on the demonstrably highly contagious character of the disease, its rapid spread in a flock, and from the first to nearby adjoining flocks in summer, the short period of incubation, the constancy and nature of the diarrhœa, the speedy and great mortality, and the hemorrhagic lesions of comb, bowels, heart, lungs, liver, kidneys, spleen, and serous membranes. The demonstration of the bacterium in the blood and affected tissues is conclusive. Kitt points out that inoculation of a pigeon kills the bird in 12 to 48 hours, with dry yellow exudate in patches of from ½ to ¾ inch in diameter on the surface of the muscles, and yellow discoloration and nodular induration beneath.

_Prognosis._ The mortality reaches 90 to 95 per cent. The negative chemiotaxis exerted on the leucocytes by the microbe, precludes defensive phagocytosis, and the progress of the deadly microbe is comparatively unhindered. Toward the end of a severe outbreak, and in certain mild epizoötics the recoveries are much greater.

_Prevention._ All birds bought or otherwise acquired and all birds returning from shows should be quarantined for one week before being allowed to mingle with the flock. In summer this should be conducted inside fly screens. The manure should be burned, carefully secluded, or treated with dilute sulphuric acid. Buzzards and vermin as possible bearers of the infection should be excluded from poultry yards. So with human beings, dogs, etc., coming from infected places. In an infected flock the sick should be at once separated, killed and burned or treated with sulphuric acid. All manure should be treated in the same way. Buildings, yards and runs should be thoroughly cleaned and liberally sprinkled with a dilute sulphuric acid (2:100). If the birds can be divided up in small groups (say of 5) the appearance of the disease will only endanger that group. In small flocks or with very valuable birds it may even be well to take the body temperature morning and night and separate at once any bird showing a rise. Any diseased or suspected flock should be kept where its manure will not be washed into wells, running streams or ponds to which other birds have access. In a locality where the disease exists fowls should not be allowed to run at large. In winter this is very effective; in summer owing to the danger from insect bearers, it must be supplemented by the most scrupulous cleanliness of poultry houses and yards, and by a liberal sprinkling with dilute sulphuric acid, or other disinfectant, to be made especially abundant and frequent on the manure. Nocard cuts short the disease by injections, subcutem of a 5 per cent. solution of carbolic acid.

_Immunization._ With valuable birds it may be desirable to secure immunization by non-fatal inoculations. Salmon secured this by first estimating the number of microbes in an mm. of the blood, then diluting until five drops would contain but one, or at most two of these organisms, and injecting this amount into the pectoral muscles. A sequestrum forms in the muscle and is gradually sloughed out, and the cavity heals, with resulting immunity.

Pasteur produced a weakened virus by exposing the artificial bouillon cultures to air for from three to ten months, the strength decreasing with the length of exposure. The weaker form produces slight illness only, from which recovery is prompt. A second and stronger virus is used ten or twelve days later and produces a real immunity.

The drawbacks to these methods are: 1st; that fowls are of too little value, to warrant inoculation in healthy flocks; 2d; that in infected flocks, where it is employed, the more susceptible birds are usually already contaminated, and a large proportion die in spite of it; and 3d; that it becomes a means of planting the infection in new localities (Kitt).

_Treatment._ The disease is so deadly that little can be hoped from medicinal treatment. It has been directed mainly to gastric and intestinal disinfection. Copperas and sulphuric or hydrochloric acid in the drinking water ½ to 1 per cent. of each is at once prophylactic and curative. Friedberger and Fröhner add fennel or peppermint, and give a tablespoonful every hour to an affected chicken. Other agents recommended are: carbolic acid (5:100) by the mouth or subcutem (Nocard), salicylate of soda, quinia (Cadeac), tannic acid (2:100), salol, naphthol, tar water, etc.

DISTEMPER IN DOGS AND CATS.

Definition. Synonyms. Animals susceptible: dog, fox, jackal, hyena,
wolf. Historic notes. Causes: contagion, inoculation, immunity,
contact with sick, clothing, bedding, kennel: infection fixed—little
diffusible, dogs at large, chill, domestication, high breeding,
special breeds, shows, public conveyances, vegetable diet,
debilitating conditions, catarrhs, change of climate, recurrent
attacks, youth, native susceptibility, teething. Microbiology:
micrococci, bacilli, mixed cultures, Shantyr’s observations,
Lignieres’. Virulent products—all secretions and exudates. Vitality:
virus survives drying, freezing, dilution in water. Destroyed by
disinfectants. Forms of distemper: catarrhal, ophthalmic, cutaneous,
gastro-hepatic, bronchitic, pulmonary, nervous. Duration 20 to 30
days. Mortality 20 to 70 per cent. Prognosis: unpromising conditions.
Incubation 4 to 7 days. Symptoms: hyperthermia (103° to 104°),
dulness, debility, anorexia, staring coat, tremors, seeking warmth,
early fatigue, dry burning nose and footpads, irregular temperature,
simultaneous congestion of all visible mucosæ; Respiratory phenomena;
sneezing, congestion of nose, discharge, blocking, snuffling, rubbing,
cough, retching, vomiting; percussion flatness in lungs, in islets or
along the lower part; auscultation râles, wheezing, crepitus,
creaking, etc.; epiphora, swollen eyelids, weeping, photophobia,
muco-purulent discharge, sticking of lids together, opacities,
vesicles, ulcers; red, hot, buccal mucosa, costiveness, fetid
diarrhœa, tenesmus, weakness, emaciation; skin eruption, on delicate
areas, papules, vesicles with colored contents, pustules, sticky,
greasy exudate; irritability, restlessness, taciturnity, depraved
appetite, spasms, delirium, paresis, epilepsy, chorea. Lesions:
inflammation, degeneration, ulceration on air-passages, alimentary
tract, lymph glands, kidneys, liver, cerebral and spinal meninges,
leucocytic infiltration: offensive odor. Lignieres’ views of microbes.
Prevention: quarantine new dogs for 14 days, wash, disinfect all
collars, etc., avoid shows and meetings, exclude street dogs, protect
against mice, rats, birds, shut up all dogs during an epizoötic;
separate a pack into small lots; seclude the sick and all belonging to
them. Immunization: by lung exudate, by weakened cultures. Treatment:
hygienic, dietetic, warm baths, antipyretics, antiferments, calomel,
phenic acid, eliminants, expectorants, collyria, emetic, demulcents,
bismuth, etc., pepsin, quinine, nerve sedatives, tonics.

_Definition._ A contagious, febrile affection attacking dogs (and by inoculation cats), and tending to local inflammatory and degenerative lesions in the mucosæ, lungs, bowels, liver, skin, kidneys, and nervous system,—a first attack usually immunizing against a second.