Part 14

Causes. In Oneida, the subjects were dairy cows, which in the early spring, when the frost went out of the ground, had to wade through chilly soft mud reaching to the knees or above, and mixed with small stones with sharp edges, and with semiliquid manurial products. The abrasions made by these stones furnished convenient infection atria for septic microbes in the manure. In the pus obtained from the ulcers were found in abundance the bacillus coli commune, and a long streptococcus representing on an average from 20 to 40 cocci in a chain. Dr. Moore made pure cultures of these and produced the same symptoms in a cow by injecting the streptococcus subcutaneously in the back of the pastern, and in another animal by simply abrading the surface and rubbing on the streptococcus culture. As the inflammation, suppuration, and resulting ulcers implicated not only the skin but also the subcutaneous connective tissue, the affection had many of the characters of erysipelas.

Symptoms. The affection commenced by swelling in the region of the fetlock, pastern, metacarpus or metatarsus, and exceptionally, the forearm or tibial region, and advanced to a tense swelling, which pitted on pressure, and the formation of centres of suppuration, which burst and discharged. If the exposure to the septic mud were continued the sores ulcerated and extended both in the skin and subcutaneous connective tissue, but when the dry weather came and the mud disappeared, the tendency was to spontaneous recovery. In some instances ulceration extended beneath the hoof threatening its evulsion, and in other cases it extended deeply to the tendons and ligaments.

Treatment. The main object should be prevention, to be secured by protecting the stock against contact with septic mud, and especially such as is near the freezing point and intermixed with such sharp stones and pebbles as would wound the surface and open channels for infection. When infection has taken place we should seek to limit it by lotions of an antiseptic character. Bandages soaked in a solution of hyposulphite of sodium, 1 dr. to the ounce will often succeed. A more potent application is iodized phenol, prepared as follows: tincture of iodine 2 drs., carbolic acid crystals 4 drs., glycerine 1 oz., alcohol 1 oz., water 8 ozs. When applied on a bandage this may be diluted with water to make 1 pint. For circumscribed application to forming sores the undiluted iodized phenol, made of one part each of iodine and carbolic acid crystals, may be applied twice a day with a glass rod. Other favorite applications are a lotion of lead and laudanum; a saturated solution of boric acid; ninety-five per cent. alcohol; a mixture of creolin 1 part, iodoform 4 parts, and lanolin 10 parts; ichthyol and collodion; ichthyol and vaseline; or iodol, iodoform, salicylic acid or resorcin as dusting powders.

Internally, tincture of muriate of iron 3 drms. every three hours helps to keep the affection in check.

GANGRENOUS INFECTION OF THE CORONET. HORSE. POTCHETCHOUI.

Seen on rich, damp lands. Symptoms: lameness, small areas of congestion, erection of hairs, vesiculation, pustulation, gangrene as deep as tendons, depilation, desquamation, fistulæ, slough of hoof, early fever, impaired appetite, recovery in 14 to 21 days in most cases. Staphylococcus and streptococcus. Prevention: segregation, different attendants, avoidance of infecting land while damp, smear limbs with antiseptics. Treatment: antiseptic bandages.

Under this name Sotsevich describes an infectious disease of the horse, which prevails in the Don province, and especially on rich, low, damp lands. Before the appearance of any local lesion, the horse goes very lame on one limb. Afterward there appears, usually on the coronet or pastern, an area on which the hairs stand erect, with elevation of the epidermis and the formation of vesicles as large as barley corns, filled with a yellowish white liquid and later with pus. Gangrene follows, extending from the skin to the subcutaneous connective tissue, aponeurosis and tendons, and forming large sores, one to two inches in diameter and discharging an abundant yellow, fœtid pus. The adjacent skin takes on a yellow tint and sheds its hair and epidermis. The disease may extend into the interphalangean joints or under the hoof, leading to offensive fistulæ or evulsion of the hoof. If it extends to the higher parts of the limb it becomes less destructive.

At the onset there is some fever (101° F.), dulness and inappetence, but these gradually subside, and in favorable cases complete recovery has taken place in two or three weeks.

Bacteriological investigation has detected in the contents of the vesicles, staphylococcus pyogenes aureus, and streptococcus pyogenes.

Prevention is largely secured by a rigid separation of the diseased from the healthy. Other obvious precautions would be to exclude those dressing the sores from handling other horses until after thorough disinfection of the hands, and to keep the sound animals, during wet seasons, from the damp infecting soils, or when they must work on these, to smear the lower parts of the limbs with antiseptic ointments (tar, carbolic, iodine, mercuric, etc., etc.)

Treatment with sublimate bandages proves very satisfactory, yet any comparatively non-irritating antiseptic lotion may be used.

STRANGLES, INFECTIOUS RHINO-ADENITIS.

Synonyms. Definition. Historic notes. Bacteriology: streptococcus coryzæ contagiosæ equi in pus, chains of 3 and upward, free cocci, arthrospores, clumps, ærobic, growing freely in serum, or glycerined bouillon; pathogenic to horse and white mouse; relation to other streptococci; clinical evidence; accessory causes, youth, primary susceptibility, dentition, training, impure stable air, grain ration, excitement, sudation, fatigue, chill, change of climate, trading, crowding, sea voyage, catarrh of air passages. Infecting products, pus, ingesta, blood, manure, fodder, litter, water, secretion of mucosa of healthy. Wounds, castration, mangers, racks, troughs, buckets, poles, shafts, harness, halters, twitches, blankets, rubbers, combs, brushes, men, etc. Pathology: infection of lymphatics, through inhalation, sore, ingestion, congenital, milk; congestion of nasal mucosa, epithelial degeneration and desquamation, discharge little viscid, corded lymphatics rare, submaxillary swelling rarely small or nodular, pus creamy, indolent cases, pharyngeal, thoracic, buccal, gastro-intestinal, hepatic, pancreatic, splenic, muscular, arthritic, cutaneous, nervous. Forms: mild, malignant, regular, irregular. Incubation 3 to 5 days. General symptoms: hyperthermia, dulness, apathy, costiveness. Specific symptoms: nasal, congestion, sneezing, purulent discharge; epiphora, submaxillary phlegmon; pharyngeal and laryngeal; parotidean; pulmonary; abdominal, hepatic, pancreatic, splenic, perirenal, cutaneous, genital, nervous, septicæmic. Diagnosis, from catarrh, glanders. Prognosis, favorable, apart from malignancy. Prevention: exclude strange equine animals; avoid public stables, yards, drinking troughs and buckets; also manure, stable utensils, hay, fodder, litter, or watershed from infected places; disinfect cars, wagons, etc. Seclude inmates of infected stable, yard, park, etc., temporarily close public drinking and feeding places, make sale or exposure of infected animal penal; temporarily close dealers’ stables; sale with general guarantee only. Disinfection. Immunization; inoculation from mild case. Treatment: hygienic, antipyretic, eliminating, antiseptic, surgical, tonic, antisuppurant.

Synonyms. Distemper; Coryza Contagiosa Equorum; Gourme (Fr.); Druse (Ger.); Cimurro (Ital.).

Definition. An infective, streptococcic, febrile disease of solipeds, usually manifested by a catarrhal inflammation of the upper air passages, and phlegmon of the adjacent lymph glands, or less frequently by phlegmonous inflammation of lymph glands elsewhere or of the skin.

Historic Notes. Strangles was fairly indicated in the writings of the ancient Greek veterinarians, and was clearly described and attributed to contagion by Solleysel in 1664. It was so evidently infectious that it was experimentally inoculated by Lafosse in 1790, by Viborg, in 1802, and later, by Erdelyi (1813) and Toggia (1823) and others. Rivolta, in 1873, found a streptococcus in the pus of its abscesses, and to this the contagion was definitely assigned by Baruchello (1887), Schütz, Sand and Jensen (1888). Priority in this demonstration is accorded to Schütz.

Bacteriology. The streptococcus coryzæ contagiosæ Equi (Streptococcus rhino-adenitis or S. equi) is easily found in the pus of gland abscesses sometimes in pure cultures (impure in the nasal discharge), stains readily in aniline colors and in Gram’s solution so that it stands out clearly among the pus cells. The decolorizing agent must be weak (not muriatic acid) and applied only for a very short time. Beside the chain forms, there are isolated, oval cocci, some of which, larger than others and more elongated, have been held to be arthrospores or mother cells. The number of elements articulated in a chain varies from two to four and upward. The chains are straight or sinuous, and may be grouped in bundles, radiating masses, or clumps like staphylococci.

They are ærobic (facultative anærobic), grow freely as transparent droplets on blood serum at 99° F., and in glycerine bouillon, and less vigorously on agar and gelatine. On agar the colonies reach the size of a pin head in two days with projecting alæ, and on gelatine in three to five days, and then dry and shrink. Multiplication takes place by transverse division, and at such a time the organism may seem to be a chain of diplococci.

Pathogenesis. Inoculation of cultures on a susceptible horse produces the unquestionable phenomena of strangles, and solipeds alone take the disease casually. In white mice it produces abscess in the seat of puncture and in the adjacent lymph glands. If the action is delayed the abscess may be in lung, spleen, kidneys, liver, or other distant organ. Rabbits, Guinea pigs, pigeons, pigs and cattle are immune unless large doses are employed. Intravenously large doses kill the lamb.

The identity of the microbe with other streptococci of animals and man has been claimed. Arloing alleges that, by culture of the microbe in the blood or peritoneum of the live rabbit, he exalted the virulence, and obtained in succession a streptococcus capable of producing erysipelas; gangrenous erysipelas; suppurating, sloughing erysipelas; pseudo-membranous peritonitis; metastatic abscesses; and fulminant septic peritonitis. Hill, Jensen and Sand, and Lignieres, as the result of cultures and inoculations claim that strangles streptococcus is identical with that of contagious pneumonia. Courmont, on the other hand, as the result of his cultures and inoculations, concludes that the microbe of strangles and that of erysipelas are independent organisms.

The clinical evidence is decidedly against the theory of identity. In epizoötics of strangles we meet with a constant succession of cases of strangles and in districts into which contagious pneumonia has never been introduced, no single case of that disease ever comes in to break the monotony of the sequence and to start a series of cases of the latter affection. Conversely, in an outbreak of contagious pneumonia in a locality heretofore free from strangles, strangles do not develop. Again, no matter how prevalent nor how constant strangles may be in a locality, and how habitually men have their wounded hands covered with the pus of the abscesses, no epidemic of erysipelas is entailed in man. Strangles spreads with remarkable rapidity through a stable, but not to the often more than equally exposed human attendants, nor to any animal apart from the genus equus. The absence of strangles from Iceland (Jonsson) endorses that view.

As a practical question of sanitary science, we occupy a sound position in differentiating the germs of strangles and contagious pneumonia, and further that of erysipelas of man, as a wise health officer would differentiate the microbes of cowpox and smallpox. Whatever may be true or false as to their primary identity, or as to the transition of one to the other in successive inoculations on animals of other genera, they are essentially diverse pathogenically as we meet with them in practice, and our measures may be safely based on this practical diversity.

Accessory Causes. Youth strongly predisposes, most cases occurring between two and five years, and seventy per cent. before five years. It may, however, appear at any age, being congenital in some cases (Nocard, etc.), in others appearing a few weeks after birth, and in still others at over twenty years, if the subjects have not contracted it earlier.

Dentition which is active in these early years, induces congestion about the head and general constitutional disturbance, which make the system more receptive.

Training or breaking is another reason for the predisposition in the young. The first experience of the hot, impure, infected air of the stable, the unwonted grain feeding, the excitements and perspirations attendant on the first handling all contribute to temporary loss of resistance.

Fatigue like other weakening conditions lays the system open to attack.

Chill is a most efficient cause, hence the disease often prevails most extensively in spring and autumn, at the time of changing the coat, and of passing from stable to field and the converse. Joly relates that in Russia where large numbers die of strangles through imperfect stabling in winter, immunity is sought through a milder first attack, brought on in the milder autumn weather by turning the young animals into a deep pool for half an hour and then exposing them freely to cold winds and giving cold water to drink. The omnipresent germ takes occasion to attack the cold debilitated system.

Any change of latitude or of locality acts in the same way. Riquet even alleges that this will bring about a second and even a third attack. It is common, he says, for newly bought young horses to have the disease at Hamburg, and after recovery to have a second attack at Hanover and finally a third one after they join the regiments in France. A similar exhaustion of immunity has been repeatedly noticed in the case of canine distemper.