Chapter XV: Front Matter (15)

Geographical distribution: timbered lands in the United States;
different altitudes, and geological formations; on hills and wooded
bottoms; known to Indians and pioneers; now unknown where formerly
prevailed. Contagion: through milk; no specific microbe found in every
case. Alleged causes: rhus; nickel; spirillum; bacillus. Prevails in
dry seasons; contracted under night exposure; confined to given
enclosures; to late summer and autumn. Not conveyed by contagion,
indefinitely, as are plagues. Men show very varying susceptibility;
young children may be relatively immune. Fatigue, debility, ill
health, predispose. Exertion to fatigue rouses symptoms in animal
affected. Cow in full milk eliminates toxins and does not show
symptoms; the milk infects. Steers, bulls and heifers, show marked
symptoms. Calves suffer through milk; swine through veal; dogs through
pork; buzzard through dead dog. Incubation 8 to 12 days. Symptoms:
tardy, lazy gait, drooping, anorexia, ardent thirst, inactive bowels
and kidneys, milch cows when driven or excited, tremble and may
suddenly die. Muscular debility, constant decubitus, complete apathy,
neither evades nor resents injury. Bloodshot, fixed, glazed, unwinking
eyes, pulse and breathing slow, temperature low, hebetude, torpor,
coma; death 8th to 10th day. Sheep very prostrate. Calves tremble when
sucking, vomit and perhaps die suddenly. Pigs and dogs vomit, and show
costiveness, remarkable debility and weariness. Man is weary,
languorous, weak, apathetic, loathes food, is nauseated, retches. No
fever; but ardent thirst, tremulous tongue, mawkish breath, soft
flabby belly, careless of own or family interests, forgetful of
decency. Nausea, vomiting of blueish liquid, hebetude, inactive
bowels, coma. Lesions: gastro-intestinal congestions; ingesta like
hard balls of sawdust. Treatment: charcoal, mild laxatives, elm bark,
egg nog, potassium permanganate. Prevention: clear timber land, let in
sunshine, cultivate. Insects. Sterilize the milk.

This is an infectious disease which has been found enzoötic in certain unimproved, timbered lands of North Carolina, Georgia, Tennessee, Kentucky, W. Pennsylvania, Ohio, Michigan, Indiana and Illinois. Beach says it has never been reported on any of the Western prairies, at any point west of the Mississippi River, in New England, in the Canadas, in any islands, or in any part of the Old World. Altitude appears to have no effect in its production, nor geological formation; it has been found in the wooded mountains of the Blue Ridge of N. Carolina and Georgia (Kerr, Salmon, Phillips); in the hills of Pennsylvania and Kentucky; (Beach, Phillips); on timbered uplands (Phillips); and on the wooded bottoms of the Scioto and Miami in Ohio (Phillips, Schmidt); in the timbered bottom lands of the Wabash and White Rivers in Indiana (Phillips); and in the wooded bottoms (Beardsley), and Indian Grove in McLean, Co., Ill. (Beach). The constant conditions are the heavily timbered and virgin condition of the soil.

It was much more prevalent in the time of the early settlers, than it is to-day, many infecting localities having become salubrious in connection with the clearing away of the forests and cultivation of the soil. The disease was well known to the Indians and often proved disastrous to the pioneers, whole communities being swept off as recorded of Pigeon Creek, by Nicolay and Hay in their History of Abraham Lincoln. According to these writers it was “a malignant form of fever—attributed variously to malaria, and to the eating of poisonous herbs by the cattle—attacking cattle as well as human beings, attended with violent retching and a burning sensation in the stomach, and often terminating fatally on the third day.” Even in these early days settlers were loathe to acknowledge the existence of the infection on their lands, doubtless because it depreciated them, and to-day with a better knowledge of the necessary precautionary measures, it has literally disappeared in many places, so that it is now difficult to find a case.

_Contagion._ That the disease has been transmitted through the milk from animals to man and other animals has been too painfully evident from the first, but no specific microörganism has been found to be constantly present, capable of pure culture in artificial media and of causing the disease when transferred from such media to a new victim. Naturally all sorts of theories have been advanced, no one of which has been demonstrably proved. It has been attributed to eating of poison ivy (Rhus toxicodendron) by the cattle, as this plant was usually found on the infecting lands, but rhus is also common throughout New England and the Eastern States where milk sickness is unknown. It has been claimed that it was due to mineral agents, especially nickel, in the water but the mineral salts in the water are not removed by culture of the surface soil, which puts an end to milk sickness. Phillips (1876) claimed to have found the cause in an actively motile spirillum in the blood, but he had examined the blood of but one patient, and it has not been found in other patients by subsequent observers. Bitting found a bacillus but further research has not determined its constancy.

Beach furnishes a series of observations which should be useful in seeking to estimate the value of any theory propounded. 1st. Milk sickness is a disease of dry seasons. 2. In unusually dry seasons it is dangerous to leave domestic animals out over night in the localities where the disease is prevalent. 3d. It has never been considered dangerous for animals to pasture on such lands in the day time. 4th. Cattle in one field will habitually escape, and in another with apparently exactly the same conditions and the same flora they are attacked. 5th. The disease is unknown on the open prairies of the Western States, where the domestic animals are not allowed to remain over night in the timber belts. 6th. With occasional exceptions, it is a disease of late summer and autumn. The dangerous lots can, as a rule, be safely depastured in winter and spring. 7th. The pioneers found that they could protect their stock by keeping them corralled on a “tame” piece of land from before nightfall until the fogs and dews became dissipated on the following morning.

For the land to become “tame” it was only considered necessary to cut off the timber and let the sunshine act freely on the surface. Plowing and cultivation did not seem to be requisite in all cases.

A great drawback to research is the difficulty of securing cases to study. Many lots, formerly dangerous, are no longer so, and others still infecting are kept so secluded that casual cases cannot be found, without much expense for experimental animals. Again, owners do not care to depreciate their land by acknowledging that it is infecting. The experiment stations naturally enough look askance, on the proposal to institute expensive experiments on a disease which dies out when the soil is improved. Deadly as the disease is to the individual attacked (man or beast), it is not propagated indefinitely from non-milking subjects, by simple contact or proximity after the manner of plagues. It usually comes to an end by the death or recovery of the subject that has contracted it by consuming meat, milk, butter or cheese, the product of an infected animal. The demand for sanitary police measures is, therefore, less urgent. Different observers claim that cases occur in the large cities, through the consumption of meat, butter or cheese, sent from infected localities, but that the city physician fails to make a correct diagnosis. These must, however, be comparatively rare.

In addition to ingestion as a cause, certain accessory causes ought to be noted. Some men eat the infecting material with impunity, while others succumb to the deadly disease. As the observations have all been made in or near the infecting localities, individuals may be immune through a previous attack and recovery, or there may be a native immunity through unknown conditions. Young children often suffer less than adults, possibly because of the greater activity of their emunctories and consequent elimination of the toxic products and the comparative absence of exhausting or depressing conditions. Their purely animal food (milk) may exercise an influence, and this may assist in explaining the fact that certain adults appear to be refractory.

Fatigue, debility and ill health are said to predispose the system. Milk sickness attacks most violently those that have been subjected to overwork or severe exertion of any kind, especially in hot weather, those suffering from want of sleep (sitting up with the sick), those having a special cause of mental depression, those suffering from some illness—constipation, indigestion, malaria, etc.

Milch cows are probably more open to the attacks of the germ because their systems are reduced by simultaneous milking and breeding through a number of years. Exertion or fatigue has a potent influence in developing the symptoms, so that it is a common practice in the vicinity of infected localities to subject animals to a good run before purchasing. Paradoxically enough the infected milch cow which is distributing the infecting element freely in her dairy products usually shows, in herself, no distinct symptoms of the disease. If she is dry or farrow she suffers like any other animal, but if in full milk, the toxins, and even the hypothetical microbe, seem to escape in that secretion, which proves highly poisonous to other animals, while the cow retains her spirits, vigor and outward appearance of health. Steers, bulls and heifers, on the other hand, show violent symptoms.

Calves suffer so long as they suck the milk. The dead calf is eaten by swine, which suffer in their turn, and the dog contracts the disease by eating one of these animals, or by taking infected milk or cheese. The buzzard eats the dead dog and dies as the result.

_Incubation_ is from 8 to 12 days, though it may be reduced to two. (Beach.)

_Symptoms._ In the domestic animals the first indication of illness is a lazy, tardy disposition, The subject stands apart from the herd, with drooping head and ears, listless, indifferent to all around him, and often without appetite; or, in cattle or sheep, rumination. There is usually extreme thirst, but without correspondingly free urination or defecation. Peristalsis is virtually abolished and nothing whatever passes from the bowels. The patient is likely to be found lying down and it is difficult to get him up, and when raised he moves stiffly and with reluctance.

In milking cows there may be no symptoms until the animal is excited or fatigued by violent or continued exercise, as a hard run, or a drive of four or five miles. This developes the tremors alike in milch cows and in the mild cases in dry cattle or sheep. The subject stands still and trembles in a striking way, the action resembling the muscular contractions seen after the removal of the hide in an animal newly killed. The head and ears are drooped, movements are uncertain and stiff, and the animal may even drop dead on the spot.

As the disease advances the muscular debility becomes so great that the animal lies down if possible, and if once down he seldom rises again. The decubitus is extended, the head being stretched on the ground. There is a most complete apathy, the subject showing no fear, no apprehension, no disposition to escape or resent injury. The wildest or most timid steer can be freely handled, and there is no disposition to flight or retaliation. The eyes are bloodshot and become fixed and glazed, winking ceases, the breathing is slow, pulse infrequent, and temperature often subnormal. The extremities and surface of the body are cool, the muzzle dry, the coat usually stares, the apathy merges into a complete hebetude, torpor and coma, in which condition the animal often dies on the eighth or tenth day. Violent exercise precipitates the death at once. Recoveries are infrequent and attended by no critical discharge from bowels or kidneys, only by a slow, at first almost imperceptible, resumption of natural action.

The milder cases, those that show no appreciable symptom when at rest, are seized with trembling or rigor when made to undergo the slightest exertion; they appear haggard, stupid and spiritless, drag their limbs slowly and stiffly and quickly stop from pure weariness and debility.

The prostration is even more marked in _sheep_, which often seem unable to rise, or lack the nervous energy to do so.

_Calves_ tremble while sucking, and will sometimes leave the teat, vomit the contents of the stomach, fall down and perish.

In _Vomiting Animals_ (_pig_, _dog_,) emesis usually occurs, and torpor of the bowels or obstinate constipation is present. _Pigs_ burrow under the litter and are driven out with difficulty, and _dogs_ when called on to follow, do so reluctantly, slowly and stiffly and fail to keep pace with their master (“the Slows”).

In all animals alike active or continued exertion rouses or intensifies the symptoms.

In _man_ there is at first extreme langour, weariness and weakness, the patient cannot be troubled to move, he loses appetite, loathes food, and soon has nausea and retching—often from the first. There is no chill, rigor nor violent headache as in other fevers; but insatiable thirst; large, flabby, tremulous, moist tongue, coated a dirty white; cold nose, ears and general surface; dry skin; sweet, mawkish or offensive breath; flat, flabby empty belly; without peristalsis or defecation. Respiration becomes very slow, pulse weak and compressible, heart action tumultuous and labored, temperature often below normal, and though sometimes 99° or 100° F., never higher. The patient takes to bed in four or five days, or, after exertion or fatigue, in a few hours becomes profoundly apathetic, expresses no concern for his business, his own future or that of his family, is intolerant of bed clothes or other covering and utterly oblivious of the demands of decency. Nausea continues, but retching becomes weaker, and comparatively ineffective, or brings up a little liquid which has been compared to blueing water of the laundry. The apathy merges into a state of hebetude and this into coma, with fixed, glazed eyes, absence of all winking, and insensibility to irritants and death takes place quietly without a moan or struggle.

Recovery is slow, and improvement for a time is almost imperceptible. In some cases there remains a nervous atony, and in man, a lack of mental and bodily vigor, and a disposition to relapse under exposure to intense heat or fatigue has been noted, but in many cases recovery is complete and permanent without lasting weakness.

_Lesions._ Both in man and animals, congestions of the gastric and intestinal mucosæ have been noted, usually with a dark firm condition of the membrane, but in some cases with capillary stasis, and sloughing. Beach never saw indication of tenderness in the abdomen or elsewhere, nor did he ever find blood nor stercoraceous matter in the vomited material. The contents of stomach (paunch in cattle) and bowels formed hard balls like cemented sawdust, firmly adherent to the dry mucosa.

_Treatment and Prevention._ Treatment by the Indians consisted in giving large doses of powdered charcoal suspended in milk. The early physicians attempted to open the bowels by calomel and jalap, olive oil, magnesia citrate, and even croton oil, but the last generally with fatal results. Milder and hardly less effective treatment consisted in large doses of elm bark. Beach believed he got better results with quinine and egg nog. It might be suggested to try such antiseptics as potassium permanganate, peristaltic stimulants like eserine or pilocarpin, as an eliminating agent pure water or weak diuretics, and nerve stimulants nitroglycerine or ammoniacal preparations.

_Prophylaxis._ The time-honored resort of clearing the timber and brush land so as to let the sun act freely on the soil, and the putting in of cultivated crops, is proved reliable and permanent. The other precautions in use are valuable in protecting the herd, but lack the merit of thoroughness and permanence and thus fail to strike at the root of the trouble. They are: 1st. the exclusion of domestic animals from the infected woods in late summer and autumn and in very dry seasons; and 2d. the exclusion of stock from such pastures from before nightfall until after the dews have evaporated on the following morning.

The danger which attends on passing the night in the forest, strongly suggests the intervention for the transfer of the poison of some nocturnal animal, perhaps a night-flying insect, like the anopheles, which transmits the plasmodium of malaria. If the germ and its intermediate bearer (if any) were demonstrated, probably other and simpler means of prevention could be adopted.

The fact that the propagation of the disease is not constant and wide spreading, like a genuine plague, lessens the urgency for a rigid sanitary police, yet animals kept on such infected farms, should be tested by long or vigorous driving before they are killed for food, and all milk devoted to the production of butter and cheese should be Pasteurized or sterilized before use. It might well be questioned whether the clearing and exposure of infecting places should not be undertaken by the state as a sanitary measure.

In view of the fact that a milch cow may not show symptoms of the disease, and yet yield deadly milk, and considering that the owner cannot always tell whether she has been in the infecting woods, or having been in, whether she is infected, it becomes an important public health question whether such a source of deadly disease should be perpetuated, where human food is open to contamination.

VARIOLA: POX.

_Definition_: Structure of lesion. Nomenclature. History, smallpox,
sheeppox, cowpox, horsepox. Animals susceptible: Man, sheep, cow,
goat, horse, pig, dog, buffalo, camel, monkey. Microbiology: A pure
contagium, particulate contagium, cocci, sporidium vaccinale.
_Horsepox_: Early history, means of infection. Symptoms: Vesicles on
lips, on heels, concretions, treatment. _Cowpox_: Relation to
horsepox. Causes. Relation to smallpox. Observations of Ceely,
Fletcher, Thiele, Klein, Martin, Reiter, Chauveau, influence of
vaccination, of spring parturitions, of infected stables. Symptoms:
Incubation, seat and nature of vesicle, inoculations for vaccine.
Diagnosis from aphthous fever, rinderpest, eruption of mastfeeding,
false cowpox, streptococcus eruption. Duration. Course. Prognosis.
Treatment. _Sheeppox_: Synonyms. Definition. Pathogenesis: Sheep,
goat, ox, dog, pig, horse. Forms: Discrete, confluent, hæmorrhagic.
Distribution. Causes. Contagion; extends on air; experiments on blood;
wool, hides, litter, buildings, yard, parks, railway cars, boats,
clothes, manure, wine, milk, men, dogs, cats, birds, vermin, flies.
Receptivity. Overcrowding, filth, starvation, neglect, wars, commerce.
Recovered sheep. Disinfectants. Incubation 4 to 7 days; conditions
affecting. Symptoms: Hyperthermia, general disorders, rigors,
anorexia, skin blush on parts devoid of wool, red points, papules,
vesicles, pustules, desiccation. Successive crops. On eye, nasal
mucosa, mouth, pharynx, intestines, lungs. Confluent cases. Lesions.
Prognosis. Mortality. Depreciation. Treatment. Prevention: By
segregation, slaughter and disinfection; by ovination. Technique of
ovination. Resulting immunity. _Sheeppox in Goat_: Danger of infection
to sheep. _Goatpox._ _Swinepox_: From man, sheep, goat. Symptoms.
Forms: Discrete, confluent. Susceptibility of young. Treatment.
Prevention. _Dogpox_: From man; from sheep. Other eruptions in dog.
Symptoms: Fever, flushed skin, red points, papules, vesicles,
pustules. Discrete. Confluent. Treatment. Prevention of infection of
man and sheep.

By the generic name _Variola_ is understood a febrile malady attended by a characteristic eruption on the skin, at first papular, then becoming vesicular and finally pustular. The structure of the vesicle is so characteristic that it may be taken to indicate the variolous eruption as found in man and a variety of the domestic animals. The first indication of the lesion is the appearance on the skin of fine points of congestion like fleabites. This is followed by active diapedesis and proliferation of cells in the papillary layer and rete mucosum, constituting the nodule or pimple stage. In smallpox this is so firm and definitely outlined that it has been compared to the presence of a shot in the skin. As the proliferation of cells increases these form in separate clusters or groups, isolated from each other by septa or walls largely made up of the epidermic cells. In the next stage, therefore, when exudation takes place the lymph accumulates in the spaces occupied by the clusters of growing cells, and is found in a series of chambers more or less perfectly separated from each other, so that to evacuate the whole vesicle, each minute sac must be punctured independently. The vesicles thus differ from others caused by ordinary irritants in that each is chambered, instead of forming one common undivided sac, which may be emptied by a single puncture. In the next stage, when suppuration ensues, the septa usually undergo liquefaction, so that the liquid occupies one individed cavity in each pustule. For this reason the central depression seen in the larger vesicles (cowpox) in their early stage tends to disappear in the pustule. It may reappear later in the resulting scab. Desiccation, scabbing and desquamation complete the course of the affection, a distinct _pit_ being left as a result of the destruction of the superficial layer of the dermis.

_Nomenclature._ The term _variola_ is believed to come from the Latin varius (variegated, spotted) and _pox_ from the Saxon pock (pouch). The specific names, drawn from these tongues sustain this view: As, _variolæ vaccinæ_, _cowpox_, _kine-pox_; _variolæ equinæ_, _horsepox_; _variolæ ovinæ_, _sheeppox_; _variolæ caprinæ_, _goatpox_; _variolæ suillæ_, _swine pox_; _variolæ caninæ_, _dog pox_. The term _smallpox_, (_petite verole_) is deduced from the small size of the vesicle as compared with that of cowpox, just as the same has originated the term _smallpox_ in sheep.

_History._ Variola has undoubtedly existed from very ancient times. Moore found it referred to in Chinese records of 1122 years before Christ, but it was only clearly described early in the tenth century by Rhazes an Arabian physician. Gregory, however, found the name _variola_ in Latin manuscripts in the British Museum of a much earlier date. The early epidemics of small pox have usually extended from the east, and the disposition has been to refer its origin to the crowded communities of central Asia, but nothing is certainly known as to such origin and the lack of definite recognition and description cannot be taken as implying that the disease did not exist. The extension of small pox to America in 1520 was distinctly traced to a sick negro slave landed in Mexico, and the way in which it swept the continent killing the Indians by tens of thousands, speaks strongly for its prior absence and the extraordinary susceptibility of the hitherto unaffected Indian races.

The variolæ of animals are not recorded until later, the mildness of the forms attacking cattle and horses, and the lack of close observation of the diseases of sheep furnishing a reasonable explanation. We must pass over as uncertain the _lues ovium_ of Thomas Wallsingham, (Historia Anglicana), imported in a _rotten_ Spanish ewe in 1274, and which prevailed for 25 years destroying nearly all the sheep of the kingdom, also the reference to the “pockes” of sheep in Chaucer’s “Pardoners’ tale” as highly uncertain. Laurent Joubert in his work on the “_peste_” mentions _sheep pox_ as prevailing in 1567, and Rabelais speaks of it as prevailing in France in 1578. It prevailed in Padua in 1649, in Venice in 1664, 1672, and 1674 (Bottani), in Italy in 1690 (Ramazini), in Germany in 1687–8 (Stegman), in England in 1711, in Hungary in 1712, in France, Italy, etc., in 1714 (Kanold), in Venice and Bohemia in 1719 (Bottani), in Saxony in 1720, in Venice and France in 1723–24 (Bottani, Astruc), in Thuringia in 1725, in Siberia in 1771 (Pallas), and in Persia generally at the beginning of the 19th century (Bruce). Great Britian, long protected by her insular position, was infected by sheep from Germany in 1847 and again in 1862. Under ovination the first invasion prevailed for four years causing wide spread destruction; under strict separation based on thermometry, the second lasted but four months.

_Cowpox_ has existed in England for centuries, but it has only attracted general attention since the introduction of vaccination by Jenner in 1796. _Horsepox_ has existed concurrently with cowpox, the infection being habitually transferred by the hands of the milkers from horse to cow and vice versa. Jenner found it so common in the Valley of Gloucester, that he considered it as the habitual source of cowpox. Sacco recognized it at the beginning of the 19th century, Hertwig in Berlin in 1830, Röll in Vienna in 1855, and Bouley and others later in different parts of Europe.

_Animals Susceptible._ Variola in some form affects man, sheep, cattle, horses, goats, pigs, dogs, buffaloes, camels and monkeys.

_Microbiology and Infection._ It has long been well established that variola is due to contagion alone. The habitual dread of contact with a smallpox patient, shows the general appreciation of the danger of contagion, and the many epidemics, started by the introduction of a smallpox patient and thereafter spreading from that as a centre, together with the long continued immunity of certain insular or trans-oceanic countries illustrate this. One of the most striking examples is the immemorial immunity of the New World until the landing of the variolous slave in Mexico in 1520, and the immediate, rapid and destructive spread of the disease among the native tribes. Sheeppox offers a no less striking example. Prevailing for centuries in Asia and Europe, its extension to a new district was always the manifest result of the movement of infected sheep; England remained immune until her first invasion in 1847, and the second in 1862, in both cases the source was easily traced, and the disease completely extinguished by the destruction of the infection in its circumscribed area; the more distant sheep raising countries, America, North and South, Australia, Tasmania, New Zealand, South Africa, in the absence of importation of infected sheep remain free to the present time. For horsepox and cowpox the demonstration is more difficult as limited outbreaks, have occurred at intervals in different localities, traceable more or less clearly to infection from vaccinated persons, yet often mistakenly attributed to spontaneous developments of the disease. Before the days of Jenner however it prevailed habitually in certain dairying districts (Gloucestershire), and I can point to localities in New York, in which the infection is manifestly laid up in the stables, and the disease develops yearly in the heifers coming into milk for the first time and in newly purchased cows, that have not been previously exposed.

The contagion varies greatly in force in the different forms of variola, the milder horsepox or cowpox, requiring actual contact (inoculation) while in smallpox and sheeppox, infection may take place at some distance from the patient (in sheep over 200 yards).

A particulate infecting material was demonstrated by Chauveau, who filtered the virus and inoculated the filtered liquid without effect, while the solids retained on the filter invariably produced the disease.

The identity of the microbe of variola has been much discussed. Guttmann and Grigorjew found in the lymph a coccus (Staphylococcus albus variolæ), Ruete a very motile diplococcus, and others streptococcus, but in cutaneous lesions it is very difficult to exclude such elements. Pfeiffer, Guarnieri, Van der Loeff, Wasielewski and others have drawn attention to small protoplasmic bodies (manifestly protozoa) found in the vaccine lymph, and which appear to be the infecting agents. Wasielewski cultivated these on a rabbit’s cornea to the 48th generation, and from the last successfully inoculated a calf and several children.

Funck finds this _sporidium vaccinale_ constantly in the vaccine lymph and surrounding tissue, as a refractile, amœboid, spherical organism (spore) 1 to 3μ in diameter, and, less abundantly, a round or ovoid spore cyst 25μ. These cysts are either smooth or uneven like a raspberry, and have a single or double contoured membrane. They are easily stained with Sudan III. Examined in hanging drops they are seen just under the cover glass, not on the surface of the drops. Larger flattened bodies found in the lymph, with many included spores are manifestly epithelial cells. Copiman cultivated the organism in glycerinated collodion capsules in the peritoneal cavity of rabbits and dogs, producing zoöglœea masses staining peripherically with methylene blue, and which caused typical vaccinia in calves. He found the same elements in variola of man.

HORSE POX. VARIOLA EQUINÆ.

This was recognized toward the end of the 18th century, in the valley of the Severn, England, by Jenner, who believed it to be the origin of cowpox, but failed apparently to distinguish it from ordinary “_grease_”. To-day, when we must trace each case to a preëxistent one in some animal, and ignore the question of primary origin, we must still recognize that it passes readily from horse to cow, and from cow to horse, through the hands of milkers and stable-men, but that it also has the source of vaccinated persons in the families of those handling the horses. Whether it was also often derived from the very prevalent small pox in past times is doubtful, yet it appears to have been much more common about the year 1800 than it is to-day. When once started in a stable it passes readily from horse to horse, through the hands of shoeing-smiths and grooms, including of course their aprons, brushes, sponges and rubbers, and also through blankets, bandages, litter and other things on which the virus has been received. The susceptibility of the skin in the hollow of the pastern depends mainly on the frequency of chaps and abrasions, and to a certain extent on contact with the road-mud infected by other passing animals. At times the suffering animal licks the affected part, and determines the eruption on the mouth, lips and nose (see contagious pustular stomatitis). Megnin saw cases affecting the external generative organs and transmitted between the sexes by coition. (See vesicular eruption on the genitals). All such cases should be identified by inoculation.

Hertwig, as early as 1830 recorded the existence of horsepox in Berlin, where it has been seen frequently since, and noted its transmission to man. Bouley gave evidence of its special prevalence at Paris, and of the production of typical vaccine vesicles in man by its inoculation. More recently it has been frequently observed and studied by inoculation and otherwise.

_Symptoms._ These, whether seen in horse, cow or man, do not differ from those of cow pox, with which it may be held to be identical. The observations of Chauveau, Warlomont, and Pfeiffer that experimental infection, intravenous, subcutaneous, intratracheal (inhalation), or by feeding almost always failed to give the general eruption which characterizes small pox and sheep pox. It remains strictly local except when inoculated on other parts of the skin or mucosa. It must be added, however, that small pox or sheep pox, when inoculated successfully on the horse, as a rule remains confined to the seat of inoculation. The constitution of the horse, like that of the cow, tends to resist its virulence.

The affected horse may show preliminary febrile symptoms, but these are usually too slight to be noticed. They are followed by heat, tenderness and swelling of some part of the skin, usually in the hollow of the pastern and perhaps the back part of the metatarsal region, with more or less (sometimes extreme) lameness. On the swollen skin may be detected nodules, which may pass early into vesicles and pustules. The eruption varies, however, as developed on the comparatively hairless lips or nose, or on the densely pilous pastern.

On the lips, or other part lightly covered with hair, one can easily follow the successive formation of the round nodule, the distinct (sometimes umbilicated) vesicle, with its clear translucent straw-colored contents, and the pustule, which bursts, forming a sore, or dries up forming a dense scab, like that of cowpox.

On the heels, or on any part thickly covered with hair, the vesicle or pustule is rarely recognized, the exudate on the contrary takes place mainly on the surface, which becomes encrusted with an abundant yellowish concretion, matting the hairs together, and sometimes literally covering them. This may be very misleading to the practitioner who expects to see the succession of fully developed vesicle and pustule, and overlooking the true nature of the malady he may allow it to spread widely in a stable.

Describing his inoculation cases, Chauveau gives the following successive phenomena:—

“From the fifth to the eighth day the points of inoculation become distinctly papular. As far as about the tenth day, the papules encrease, and become more prominent, taking the form of an extremely wide cone, with a base of ⅓ to ½ inch. During this period these large conical papules are resistant and painful on pressure, but show no elevation nor change in the epidermis, save a slightly reddish reflection in animals with white skins. Afterward supervenes a new stage which may be called the _period of secretion_. This commences from the ninth to the twelfth day. The epidermis, slightly raised upon all the papule, sweats out numerous drops of a limpid, very slightly yellow serosity. These drops soon concrete into yellowish, transparent crusts covering the whole surface of the pustule:—a species of characteristic crystallization, very different from the crusts that succeed the vaccine pustules in mare and cow. The secretion, which continues several days, is terminated from the thirteenth to the seventeenth day after inoculation. If then the crust is raised there is exposed a humid, pink, granular surface not projecting beyond the surrounding skin. This surface is hollowed out by a very deep central cavity, a sort of umbilicus, in which is inserted, like a nail, a projection from the deep surface of the crust.”

I would add that after recovery the hair in the seats of the nodules has a lighter color and, on the shanks and higher, remains dappled for the season.

No _treatment_ is demanded. The application of a solution of sodium bisulphite once or twice a day, or continuously on a bandage, will greatly modify the intensity of the inflammation, and ward off complex infections. If the skin is left tender or with a disposition to crack, treat it as advised under chapped heels.

COWPOX. VARIOLA VACCINÆ.

This is manifestly the same disease, and due to the same microbe as horse pox. The disease of the one genus is easily transmitted to the other and the lesions and symptoms are the same, as if the virus were derived from an animal of the same species. Differences in the local manifestations appear to be due rather to the varying conditions of the skin and hair follicles, than to any material distinction in the virus.

_Causes._ Aside from the germ (Sporidium vaccinale) the conditions which favor infection are: the milking of susceptible cows with imperfectly washed hands, after dressing legs, the seat of horse pox eruption; the milking of healthy cows after those affected with cowpox; and the milking with hands contaminated with the exudate in cases of vaccination of man. That susceptible cows may also be inoculated successfully from smallpox patients, under given conditions appears to be true, but in Western Europe and America this is very uncommon, and would be much more so if vaccination were universally carried out. Among those who claim the identity of small pox and cow pox may be named Ceely, Reiter, Babcock, Thiele, Voigt and Klein.

Ceely alleges the infection of five cows and one heifer, in 1839, in England, from chewing the flock of a bed on which a small pox patient had died. In 12 or 14 days they had tender congested udders, with hard pimples imbedded in the skin, followed by blisters, and brownish scabs. The milk diminished, saliva drivelled from the mouth, the cheeks were inflated and retracted, the coat stared, their feet were drawn together, and the back was arched. The disease was communicated to the owner. This was clearly an outbreak of aphthous fever, which invaded England in that year, and was still an unknown disease to medical men. The implication of the heifer which would not have been inoculated with variola through the hands of the milker, and the salivation which is unknown in cow pox, but points directly to the buccal vesicles of foot and mouth disease, are conclusive on this point.

Ceely later, after many fruitless attempts to convey smallpox to the cow, at last met with results which indicated cowpox, and which he thereafter passed from cow to cow with the characteristic cowpox eruption.

Fletcher further reports the transmission of smallpox through the horse to the cow, and thence to the child in the form of cowpox.

In 1836, Thiele, Kasan, S. Russia inoculated some cows on the udder with smallpox lymph, and conveyed the lymph of the resulting vesicles back to man, and from man to man for seventy-five generations of the virus without finding any variation from the type of the true vaccine disease. He repeated the experiment with equal success in 1838.

Such experiments, made before the days of careful antiseptic, or aseptic, laboratory methods, by men who were daily engaged in making vaccinations, cannot be very implicitly relied on, yet the success of Thiele in Central Asia, the early home of variola, may indicate the possibility of a transition, under given eastern conditions, which, to say the least, is exceedingly rare in Western Europe or America.

The experiments of Klein, conducted under modern methods, are more conclusive, and seem to imply the possibility of smallpox passing into cowpox, in the bovine system, under some not yet clearly defined conditions. Until such conditions are sufficiently well known, so that they can be controlled at will, no one can be justified in attempting to produce lymph for vaccination by simply passing smallpox virus through the system of the cow.

It seems important to note one or two instances of the evident transmission of smallpox from man to man through the bovine system.

In 1860, Martin inoculated variolous matter, from a man who had just died of smallpox, on a cow’s udder, and subsequently inoculated about fifty persons from the eruption caused in the cow. Most of those so inoculated had unmistakable smallpox and three died.

Reiter had a very similar experience.

Chauveau (French Commission) inoculated twelve susceptible cattle with smallpox virus and produced, in all but one, small conical (smallpox) papules and vesicles, and in ten of these, on subsequent inoculation with cowpox, six proved immune, three had rudimentary pustules, and one had a distinct cowpox eruption.

A milch cow and two heifers were inoculated with smallpox and cowpox on two sides of the vulva, with the result that each disease appeared in the seat of its inoculation, with its characteristic vesicles, and the two developed side by side. The smallpox vesicles were by inoculation conveyed from ox to ox with steadily decreasing activity. Inoculated from the cow on a child, it caused great hyperthermia, vomiting, one large vesicle like vaccinia and a general eruption like varioloid. Inoculation from this child upon another produced a mixed eruption of cowpox and varioloid. Inoculation from the second child on a bull and heifer produced papular eruption only.

Smallpox virus, inoculated on a horse produced a papular eruption, but failed to affect another horse that had been previously vaccinated. Cowpox virus inoculated on the first horse which had had the papular eruption, caused a second papular eruption (not cowpox). The virus from a vesicle in the first horse caused a similar eruption in another horse, on which it was inoculated. The lymph from the papular eruption led to a similar eruption in cattle, on which it was inoculated, but did not protect against cowpox, subsequently inoculated.

The lymph from the papular eruption in the horse, inoculated on two children, produced fever, vomiting, a general papular (smallpox) eruption, in which a few of the pustules only showed a tendency to umbilication. A child and its mother in the same ward contracted varioloid. A child inoculated from one of the first named children, had six large umbilicated vesicles like cowpox and a general papular (smallpox) eruption. Another child inoculated from the last had six large umbilicated vesicles, and a general papular (smallpox) eruption. From the papular eruption of one of these children a horse and seven cattle were inoculated and in all a varioloid eruption resulted.

The rational conclusion is, that while there is every indication of a primal identity of the two diseases, and indeed of all forms of variola, as shown by a disposition of the virus from one genus, when inoculated upon a totally different genus, to show some indication of the characteristic eruption of the latter, yet the generic type, which comes from the long continued growth in the one class of animal, becomes so fixed, that it cannot be overcome at once, and sometimes apparently not at all, by transferring it to an animal of another class.

If the unfortunate results obtained by Martin, Reiter, and Chauveau, are insufficient to deter from the use of smallpox lymph which has been passed through the cow, the long experience with humanized vaccine, which in its inoculation from man to man for a century has shown no tendency to revert to smallpox virus should be a sufficient warning against such dangerous optimism.

No deduction can be safely drawn from the comparative mildness of most of the cases caused by reinoculation from cow or horse to man, inasmuch as that all forms of variola can be rendered less severe by resorting to inoculation, which was extensively practised to limit the ravages of smallpox before the days of vaccination, and is still largely resorted to in the case of sheeppox in Europe. In each of these diseases the mortality can easily be reduced to 2 per cent. instead of the 20 to 50 per cent. which are lost when the disease is contracted casually.

As occurring casually, cowpox like horsepox is rare. Yet in Denmark, a dairying country, 1,037 cases were reported in 1877–8, and 878 cases in 1888–9. I have found some outbreaks explainable, through the existence of vaccinations in the families of the milkers, and Bollinger says that in Germany, most outbreaks take place in spring, the time when children are vaccinated. He should have added that this is the usual time of parturition in the cow, the time when primipara are first subjected to the danger from the hands of the milker, and when the cow from the noninfected district is brought into an infected stable for the season’s milking. In a dairying district in Tompkins Co., N.Y., the affection appeared every spring, in the same barns, in heifers with their first calf and in newly bought cows. All older cows, bulls, steers and unimpregnated heifers escaped.

_Symptoms._ The period of incubation is two days, after inoculation, and though it may appear to extend to a week when the disease is contracted accidently, it is impossible in such cases to state the exact date of infection. The preliminary fever is not always present, or recognized, yet there may be slight encrease of temperature, partial impairment of appetite and rumination, extra firmness of the fæces, a higher color of the urine, and above all a slight diminution of milk, which is a little more watery and coagulates more readily, than the normal.

This is followed by heat and tenderness of the udder and the appearance on the teats of small, pale red nodules the size of a pea or larger. In one or two days more the nodule, largely encreased in size, presents in the centre a depressed or _umbilicated_ bluish white portion, with a firm yellowish, reddish or reddish blue margin, and outside this a soft pink areola, shading off into the white skin. The epidermis is raised at points by a viscid, yellowish lymph, enclosed in a series of saccules (multilocular vesicle). The vesicle encreases to 8 or 10 lines in diameter by the eighth or tenth day, and exceptionally, the umbilication is effaced by the excessive production of lymph. If left unbroken a brownish shade appears in the centre and gradually extends toward the periphery, the contents becoming purulent, and the pustule gradually drying up to form a crust. The drying and thickening of the crust goes on until the fourteenth day and the crust is usually detached by the twentieth, leaving a pale rose colored, smooth, shallow depression, which forms the permanent pit left after the skin has healed. The primary scabs usually show the central umbilication, and always the conical projection in the center of the deep aspect, and corresponding to the pit.

Vesicles on the mammæ may pass through the above stages, but those on the teats are usually ruptured by the hands of the milker as soon as the liquid is thrown out, and this gives rise to troublesome sores, with complex infections, at times implicating the gland tissue so as to cause destructive mammitis with loss of one or more quarters, and in any case abraded and irritated at each milking, so that the animal resists handling, the milk is drawn off imperfectly, and dries up or the cow becomes an inveterate kicker. If the milker has not been vaccinated he is liable to contract the disease.

A succession of vesicles often appear on the same animal, so that they may be found in all different stages of vesicle, pustule and crust on the same bag at one time. The later eruptions may be the result of inoculation from the earlier ones, and tend to prolong the attack materially.

In inoculation of the bovine animal for the production of lymph for vaccination, the skin of the abdomen from the symphysis pubis to the umbilicus is shaved, or in other cases the skin between the thighs, or in still others the skin on each side over the loins, and the virus applied in 50 to 200 points, by preference scraped until liquid oozes, but without any escape of blood. In a warm room the eruption matures in four or five days, its form taking on an appearance approximating that seen on the hairy skin of the horse. The individual lesions are somewhat extended corresponding in form and size to the abrasion on which the lymph was applied, and usually present the appearance of a raised patch, covered by a grayish film of epidermis, on the removal of which there is seen a raw alveolated surface filled with the amber-colored lymph.

_Differential Diagnosis._ From _aphthous fever_, cowpox is clearly distinguished by (a) the multilocular structure of the vesicle, while that of aphthous fever is a single undivided cavity which can be drained completely by a single needle prick; (b) by the pitting or umbilication, the aphthous vesicle being uniformly rounded and convex; (c) by the absence of vesicles or sores on the mouth and feet, which are rarely wanting in the aphthous eruption; (d) by the comparative absence of hyperthermia and constitutional disturbance, which is better marked though still slight in aphthous fever, and (e) by the absence of the intense and subtle infection of aphthous fever, which quickly attacks a whole herd and extends with equal rapidity over sheep, goats and pigs, attacking all cloven-footed animals virtually without exception. The cowpox patient, on the contrary, does not necessarily attack the cow in the next stall unless milked by the same hands, and spares heifers, bulls, steers, sheep, goats and pigs.

From the _rinderpest_ cutaneous eruption it is easily distinguished by the presence of lymph in the lesion, that of rinderpest being a mere epidermic concretion; by the absence of the intense fever, anorexia and general constitutional disturbance, and of the early and high mortality which characterize that disease; by the absence of rapid and uniform infection of other cattle irrespective of a common milker; by the immunity of heifers, steers and bulls, which are speedily prostrated by rinderpest, and by the absence of the congestions and epithelial concretions of the mucosæ which characterize rinderpest.

From the _leg irruption_ found in animals feeding on distiller’s swill and grains, or on the mast of beet sugar factories, by the history of the outbreak, of the dietary, of the seat and nature of the disease, and by the escape of animals living on a different aliment.

From the _false cowpox_ (varicella) it is distinguished by the unilocular lesion of the latter, its absence of areola, and its rapid pustulation and drying, in five or six days into a thin papery crust instead of a thick, firm, umbilicated scab, as in cowpox. Varicella is further liable to appear in successive crops and thus last for several weeks.

The _streptococcus eruption_ on teats and udder, is marked by the formation of abscesses of various sizes from a simple pustule upward, by the unilocular condition of the pus sac, by its tendency to invade the deeper tissues, and by its rupture and granulation without the formation of the thick umbilicated scab of cowpox.

The _hard warty growths_ on the teats which last for weeks or months should never be mistaken for cowpox.

_Cowpox_ usually lasts for some weeks in a herd, the duration depending on the number of susceptible animals and, whether these are habitually milked by the same person.

_Course. Prognosis._ It is a mild affection, which does not endanger life, yet it causes considerable loss through diminution of the milk secretion and, it may be, altered character of the milk, through the persistent sores and ulcers of the teats, through inflammation of the mammæ, and through an acquired habit of kicking.

_Treatment_ is rarely needed. Any costiveness should be corrected by a cooling saline laxative (½ to 1 lb. Epsom salts) or by soft food, and milking should be done with great care to prevent rupture of the vesicles and the formation of sores. A teat tube may be used if necessary. Sores may be dressed with bland ointment. An ounce each of spermacetti and sweet almond oil with half a dram of gum myrrh. Or the vesicles or sores may be washed after each milking with a solution of 2 drams hyposulphite of soda in 1 quart water.

SHEEPPOX. VARIOLA OVINA.

_Synonyms._ Pocks; Peltrot; Clavelee, Picotte, (Fr.).

_Definition._ An acute febrile affection, eminently contagious, prevailing epizoötically in sheep and goats, characterized by early and marked hyperthermia, and general constitutional disorder, followed by the appearance on the bare or merely hairy portions of the skin, of diffuse redness becoming intensified in points, a rounded papular eruption, passing into vesicles, pustules and scabs, which latter dry up and drop off in 15 to 20 days.

_Pathogenesis._ Beside sheep and goats which contract the disease by exposure, the following genera have been successfully inoculated: ox, dog, pig, horse.

_Forms._ Two typical forms are recognized: (_a_) the _discrete_, _regular_ or _benign_, in which the vesicles remain relatively few, and well isolated from each other, and (_b_) the _confluent_, _irregular_ or _malignant_ in which the vesicles are generally diffused over the body, even on the parts covered by wool, and set so close together that they merge into each other forming extensive continuous lesions. Other forms are the _hæmorrhagic_, _purple_ or _black sheeppox_, the volante or intermittent kind, etc.

_Geographical Distribution._ Formerly common in Central and Western Europe, it still prevails continuously in the Balkans, the Danubian Principalities, Italy, Spain, the South of France and Algiers. Like other forms of variola, its permanent home is in Asia.

_Causes._ Long before the advent of modern bacteriology, sheeppox was held to be always and everywhere the result of contagion alone. Whenever it entered a new locality it was as the result of the importation of an affected sheep or one of its products; insular places like England maintained a permanent immunity, though the disease prevailed on the other side of the narrow straits or channel; yet when imported (1847 and 1862) it demonstrated a general susceptibility of the flocks on exposure or inoculation; more distant lands (America, Australia, Tasmania, South Africa, etc.) in the absence of imported infection remain clear to the present day.

The infection is more intense and diffusible than that of cowpox and horsepox following in this the smallpox of man. Absolute contact is not necessary, in either case the infection is carried in the air either on dust or otherwise, and above all in a confined building, a crowded sheep fold or a dusty highway.

In all forms of variola the virulence is concentrated in the lymph of the vesicle, and in horsepox and cowpox it is largely confined to this, whilst in sheeppox in severe cases it must also at times infect the blood, as lambs are occasionally born with sheeppox. On this basis the infection of the secretions generally has been advocated, but it is to be supposed that in moderate cases these are contaminated after secretion. Nocard and Roux produced immunity by the transfusion of blood from the sick to the healthy, but in no case a variolous eruption. Even the serosity from the swollen lymph glands failed to convey the disease.

In view of the diffusible nature of the germ, however, we must recognize that all secretions may be quickly contaminated as soon as they are exposed, and therefore no product of a sick or suspected sheep can be held to be safe, and all should be treated as presumably infected. The most dangerous products and those most liable to convey the disease are wool, hides, litter, buildings, yards, covers, parks, railway cars, boats, manure, urine and milk.

Living creatures like men, dogs, cats, birds, vermin, flies and other predacious insects are occasional bearers of infection.