Chapter XIV: Front Matter (14)

If on the other hand the incubation appears to have extended over one, two or three weeks; if the disease is at first equivocal, with some stiffness and firmness of the muscles, but with little or no trismus; if the patient can open the jaws an inch or more and masticate even slowly for a number of days after the onset of the first symptoms; if the haw projects only slightly over the eyeball and the excitability is not extreme the prospect for recovery is much better. Such tardy cases may seem to stand still for a week and then have a slight aggravation and this may be repeated, or a slow improvement may set in and go on gradually to complete convalescence. Improvement may be manifested by a softer or more relaxed condition of the muscles, by a slightly freer movement of the limbs and jaws, by a greater ease in swallowing, by encreasing movements of the ears and eyes, by the lessened projection of the haw, by the freer breathing and circulation and by the permanent lowering of temperature to the normal standard. Convalescence is always slow, but especially slow in severe cases in which time must be allowed for repair not only of the central nervous lesions but also of the ruptures and trophic changes in the muscles.

In _cattle_ the disease is usually slow in its progress and improvement may not set in till the close of the third week. In sheep, goats and dogs on the other hand it is habitually acute, and death may supervene from the third to the eighth day. In the horse all forms are met with and the result will vary according to the severity of the attack.

_Mortality._ Friedberger and Fröhner sets the mortality in sheep and pigs at nearly 100 per cent.: in horses at 75 to 85 per cent.: and in cows at 70 to 80 per cent. In tetanus neonatorum in lambs, the deaths reach about 100 per cent. In this case the disease usually sets in within forty-eight hours after birth, and with a very high temperature difficult deglutition becomes a marked feature, so that if the patient is not speedily killed by dyspnœa, it soon perishes from starvation and exhaustion.

The _cause of death_ is usually _asphyxia_, _hyperpyrexia_, or _exhaustion_.

_Lesions._ There are no constant or pathognomonic structural changes in tetanus. Those that are found are inconstant and as a rule secondary. A wound (entrance channel) can usually be made out, often in the region of the foot, or in connection with castration. In the new born there is the unhealed navel, and in parturient cows the catarrhal, septic or injured womb. In the seat of such wound may be found the foreign body (nail, splinter, etc.), and some pus or simple congestion or even necrosis. The nerve trunks leading from such infected wound may be hyperæmic. The presence of the bacillus in the wound may be determined by microscopic examination or inoculation on a small animal.

The changes in the nerve centres may be congestion of the horns of gray matter, and there may be slight hæmorrhage, exudation, especially shown in the encrease of the cerebro-spinal fluid, softening, cell proliferation, and granular invasion of the nervous tissue. In separate cases the myelon, the corpus striatum and the cerebellum have shown lesions. The meninges are occasionally hyperæmic. Spinal lesions have been noted especially in the bulbo-cervical and lumbar regions. Exceptionally in the horse there are blood extravasations from fractures or dislocations of the vertebræ.

In subjects dying of asphyxia the lungs and right heart are congested, and the blood may be black, only loosely coagulable and with free hæmoglobin. There is congestion of the intestinal as of the respiratory mucosa, and also of the liver, spleen and kidneys. The congested bladder usually contains urine contrary to what is the case in rabies.

_Diagnosis._ From _strychnia poisoning_ tetanus is distinguished by the gradual and progressive approach of the spasms and by the absence of the intervals of complete relaxation which separate the rapidly recurring and violent spasms of strychnia. In tetanus the spasms may be modified but never completely intermitted, and more or less stiffness, trismus and protrusion of the haw constantly persist. In strychnia too, the paroxysm is far more intense than in the early stages of tetanus. The spasms of strychnia are general, while those of tetanus are often most intense in particular groups of muscles often at first in the vicinity of the inoculation wound.

From _rabies_, tetanus is easily distinguished by the absence of any history of a bite; by the persistence of the tonic spasms especially of the masseters and abdominal muscles during the intervals between the more violent paroxysms (in rabies there is temporary complete relaxation); by the absence of clonic spasms which alone occur in rabies; by the absence of the paralysis which characterizes advanced rabies; by the mental clearness and the absence of hallucinations or mischievous disposition which are marked features of rabies; by the absence of the depraved appetite of rabies; and by the fact that the brain does not contain the infecting germ as is the case in rabies.

From _rheumatism of the neck_ (torticollis) tetanus is easily distinguished by the permanent trismus which is not shown in rheumatism, and by the fact that spasms are easily roused by any artificial excitement, indicating an extraordinary hyperæsthesia and excitability which are nearly absent in rheumatism. The steady unmistakable progress of tetanus is in itself diagnostic.

From _meningitis_ tetanus is to be diagnosed by the presence of trismus without impairment of the mental faculties or fever. In meningitis the spasms are usually confined to particular groups of muscles and do not become generalized under active excitement as in tetanus. Even if the spasms of meningitis affect the jaws and pharynx they are rarely paroxysmal or roused by excitement as in tetanus. They may even be clonic.

_Tetany_ is more commonly localized in particular groups of muscles, and shows longer and more irregular intervals between paroxysms than does tetanus. It is improved by thyroid extract, and may be roused at will to contraction by pressing on the nerve going to the affected muscles.

_Laminitis_ in its most violent form and early stages, may be confounded at first glance with tetanus, but the high fever, the standing on the heels, the advance of the hind legs under the body, the great heat and tenderness of the feet, the impossibility of standing on one fore foot when the other is lifted and the strong pulsation of the digital arteries, are sufficiently distinctive.

_Treatment._ For fully developed tetanus no known resort of therapeutics can be relied on. In slight cases that have shown a long incubation and a slow increase and extension of spasm and in those having trismus only, a recovery may be expected. Treatment has been conducted largely on theoretic lines and may be divided into antispasmodic, eliminating and antidotal or antiseptic.

Rest, darkness and absolute quiet are the first and main considerations. A dark stall, with no straw litter, the rustling of which often excites the patient, but rather a little chaff, saw dust or even earth to prevent noise from the feet, and the exclusion of all visitors are essential. As a rule slings should be put under the patient so that he cannot lie, nor drop down, and this becomes more imperative as the disease advances. The aggravation of the spasms when down, and the danger of their extension to the respiratory muscles are far more to be dreaded than the temporary excitement caused by the application of slings. Food should be sloppy mashes, of bran, middlings, oat meal, linseed meal, gruels or milk, or green food may be allowed in moderate amount if the jaws are still movable. It must not be forgotten that digestion is impaired and food that is indigestible, especially fermentescible, or in excess, may arouse fatal colics and bloating, yet in a protracted exhausting disease like tetanus, the strength must be sustained by all means in our power. Pure water should always be accessible. Food and water should be furnished in buckets at a level which will not necessitate either raising or dropping the head to get to them (about 4 feet). The food must be given often, in small quantity to avoid fermentation and spoiling. If noise cannot be wholly excluded it may be an advantage to put cotton wool in the ears. I have seen a mare recover when completely covered with cotton wool under blanket and hoods.

_Local antiseptic treatment._ Theoretically this is of great value since the microbe is confined to the inoculation wound and by the time the first symptoms appear, the spores have developed into bacilli and are in a condition to be easily destroyed by disinfectants. We can, therefore, by caustics or active disinfectants destroy the infecting microbian colony, and prevent the further entrance of any toxins into the circulation and nerve centres. The principle has been shown experimentally successful in cases of inoculation in the tails of cats and Guinea pigs, and the amputation of these members as soon as tetanic symptoms appear (Kitasato, Babes). Unfortunately in too many cases, when first seen, too much of the marvelously potent toxin has already reached the nerve centres, and these have already undergone such changes, that the disease is likely to go on to a fatal issue in spite of the cutting off of future supplies of toxin. Yet the principle is sound and proves helpful in proportion as it is applied nearer to the time of infection. The most thorough method is the amputation of the infected member, if like the tail or ear it can be excised without ruining the animal. In 1875, Barbillon had success in again amputating the tail, in a case of tetanus after docking. Next to this comes the excision of the wounded tissues, but this can too seldom be effectually and certainly accomplished, and we must fall back on caustics and antiseptics. The actual cautery if thoroughly applied may be trusted to destroy the bacillus along with the tissues, but most of the chemical escharotics unite with the albumen to form an impermeable film, which protects the tissues in the deeper part of the wound against the antiseptic action. Of the different antiseptic applications _carbolic acid_ should be especially recommended as being not only antiseptic, but also an antidote to the toxins as shown below. It has the further advantage of acting as a local anæsthetic, and of not coagulating albumen. Creosote, creolin, lysol or other antiseptic may be used instead and should be applied thoroughly to all parts of the depth of the wound on a pledget of surgeon’s cotton or through a tube. When agents so little destructive are employed they may be continuously applied to the sores for a length of time.

Recoveries have taken place after neurectomy, and after stretching the nerve going to the wounded part, the theory being to check the afferent (sensory) nervous current, and arrest the reflex spasms. The new irritation, however, caused by the surgical wound is to be dealt with, and may itself turn the balance against recovery.

Nervous derivation appears to have been beneficial in some advanced, or partially convalescent cases. One horse after 14 days illness (Taffanel) and another after 21 days (Prud’homme), were castrated, bled freely and slowly recovered. Tisserand gives another case without mentioning the stage of the disease. A horse with advanced tetanus was taken to the seashore and shot. He fell into deep water, swam ashore and made a recovery. But whatever virtue may be in elimination of the toxins by bleeding, in nervous derivation or in the shocking of an unbalanced nervous system, these can hardly be recommended as regular methods of treatment. Yet the older veterinary records contain many instances of alleged benefit from bleeding.

_Internal treatment._ The whole list of antispasmodics have been tried, with no very satisfactory result. Opium has been extensively employed in spite of its tendency to encrease constipation, and morphia given hypodermically has checked spasm and induced sleep. Hydrocyanic acid and potassium cyanide have shown a decided reducing action on the spasms with the same drawback of favoring constipation. Potassium and other bromides are useful in mild and chronic cases, and may be given in full doses in combination with chloral hydrate. Calabar bean and eserine have been given for their physiological action on the nerve centres, and recoveries have followed their use, but they have little effect on the spasms until the system has been saturated to the point of threatening collapse. Chloroform has the advantage that it can be easily given by inhalation, but while it may be pushed to the extent of temporarily checking the spasms, yet these return at once when the action of the drug is exhausted. Chloroform is always dangerous to a weak or exhausted heart and cannot be given for any great length of time continuously. It is, therefore, very unsatisfactory. Sulphonal and trional have similarly checked the spasms. Gelsemium has given good results in certain mild cases, but it must be pushed to the extent of coming just short of poisonous doses, and the fear of an overdose, together with its failure in severe cases, have prevented its general acceptance. The same end has been sought by the use of nauseating antispasmodic agents, as tartar emetic, tobacco, apomorphia, and lobelia, but though useful in individual cases, these are on the whole no more successful than other agents. Phenacetin, antipyrin, acetanilid and cocaine have respectively received credit for some recoveries.

Chloral hydrate commends itself as being at once a most potent antispasmodic and hypnotic, and an antiseptic. It can, moreover, be conveniently given as a rectal injection, thus avoiding the irritation and excitement of administration by the mouth. Given in this way too, it tends to relaxation of the bowels, instead of constipation. Carbolic acid which can be conveniently given by enemata has an anæsthetic action.

_Antiseptic and Antidotal_ or _Antitoxin treatment_ is more promising, yet it has failed to come up to the full measure of expectation, mainly because the nervous changes have already reached a stage which cannot be undone speedily or at all. Under this heading would come phenic acid (½ oz.) and probably chloral hydrate (1 oz.), already referred to, and the various compounds of iodine which may be here noted.

_Iodine Terchloride._ _Iodine._ Behring and Kitasato secured immunity of two months duration, by injecting the animal with a filtrate of a culture of tetanus bacillus, and then injecting at the same point 3cc. daily, for five days, of a 1 per cent solution of iodine terchloride. Roux and Chamberland had similar results by using iodine instead of the iodine terchloride, and maintained the full measure of immunity by repeating the inoculation every fortnight. Here it is evident that the action of the iodine is directly antitoxic or antidotal, when introduced along with the toxins and before they can reach the nerve centres.

_Iodide of Potassium._ In an experimental case of general tetanus in the dog, Babes had a recovery in ten days, by injecting subcutem 5cc. of Lugol’s solution and thereafter for eight days 10 to 30cc. daily. This suggests the use of this agent along with phenic acid, or as an alternate, in any case in which phenol appears to be losing its effect by use. It may be used hypodermically, or in the drinking water or by rectal injection. It has an advantage over phenic acid in being actively diuretic and eliminating, while phenic acid has the recommendation that it tends to lower nervous excitability and moderate the reflex spasm. Theoretically the combination of the two agents, which do not mutually decompose each other, should give the best results.

These experiments have been often repeated showing clearly the antidotal action of the iodine compounds when mixed with the virus before inoculation, or injected with the virus into the seat of the wound. When employed later when the symptoms have developed, everything depends on the changes already accomplished in the nerve centres, and the severity and generalization of the spasms.

_Serum Antitoxin Orrotherapy._ Babes appears to have been the first (1889) to use the serum of animals (rat) recovered from tetanus in mitigating and curing tetanus in experimental cases. An attempt on a well developed case in man failed. His method of preparing the serum is as follows: A horse of 900 lbs. (461 kgm.), is inoculated with a mixture composed of 0.5cc. toxin (of which 0.001 mgm. kills a mouse) and 0.5cc. iodo-potassium iodide, and then at intervals of four or five days of 2.5cc., 4, 5 and 10cc. of the iodine mixture. Then stronger mixtures are used: first 2 parts of toxin to 1 part of the iodine mixture; dose 10cc.; then 3:1 dose 10cc.; then 4:1 dose 5cc.; then 15:1 dose 10cc.; then 30:1 dose 25cc.; and finally virulent cultures in progressively encreasing doses 10, 20, 30 and 50cc. One week after the last injection 1cc. of the blood serum will antidote 50cc. of toxin. Injection of toxin is however continued and the dose is gradually raised to 200cc. Eight or fourteen days after the last injection the blood serum may be taken for protective purposes. He has prepared antitoxin from cows in the same way, and Brieger and Ehrlich have prepared it from the goat. Chickens being naturally refractory to tetanus toxin can bear large doses and a potent antitoxin is more speedily secured from them. In the case of the cow the milk is rich in antitoxin.

Other methods of preparing an animal for producing the antitoxin have been resorted to as injecting it with a mixture of toxin and antitoxin in increasing doses, or again injecting with a mixture of toxin and thyroid extract in increasing doses. The extract of the normal thyroid contains a natural antitoxin.

It may be fairly inferred that the antitoxin is not formed in the nerve cells alone in their resistance to the toxin, but also in the thyroid, the liver (bile having an antitoxic action), and perhaps in other organs or liquids.

The blood of the immunized animal drawn through the sterilized cannula and aspirating syringe is coagulated in vessels set on ice, and the serum when separated is mixed with 0.5 per cent. carbolic acid and 1 per cent. chloroform, and kept in the dark in well closed bottles. It will usually keep for years.

Early experiments with antitoxins showed that when mixed with the toxin before injection it could be trusted to neutralize it. Ehrlich, Tizzoni and Cattani even claimed success in all experimental subjects if employed as soon as the slightest symptoms of tetanus were shown. They found, however, that it required 1000 to 2000 times the amount of antitoxin in such cases than was required when it was mixed with the toxin prior to injection. They found, moreover, that when the disease is fully developed the dose must be 150 times more than is required when the first symptoms are shown. It should be added that when the disease has developed rapidly, after a short incubation, and is well advanced the antitoxin treatment is usually of little avail. The changes in the nerve centres are already too great to allow hope of recovery. In man the ratio of recoveries are about as follows: After incubation of 10 days or under, 3 to 4.5 per cent. recover. After an incubation of 11 to 15 days 50 per cent. recover (Woodhead). Lambert claims 46 per cent. recoveries in 114 cases, and 38.71 per cent. recoveries in acute cases with an incubation of 8 days and under.

On the whole the ratio of recoveries is greater under the antitoxin treatment than before, though far from sustaining the optimistic views of Behring and other early experimenters. Babes draws attention to the fact that spore laden splinters of wood, in the wound render the antitoxin useless as a continuous succession of fresh spores, bacilli and toxins are thereby supplied. As this is one of the most common forms of casual infection it interferes seriously with the success of antitoxin treatment.

Roux and Borrel found that in animals, intracranial injection of the antitoxin was the most effective method. Recovery also followed its injection into the cerebrum of a tetanic boy. Babes had recoveries in two cases out of three with cerebral or intracranial injections. As the reflex spasms depend on the spinal centres these would seem to be the ideal points of injection.

Babes who has done a large amount of subcutaneous and intraperitoneal injection of antitoxin, employed for man doses of 300 to 500cc., which would represent 8 to 10 ozs. as the dose for an ordinary horse. As the antitoxin is rapidly eliminated from the body, these should be repeated daily or every other day. Nor should this supercede other curative measures. The leading principles may be thus stated: 1st. Antitoxin should be used at the earliest possible moment. 2nd. The infected wound area must be thoroughly disinfected or destroyed by caustics, and that at once. 3rd. The antidotal treatment by phenol and iodine must not be omitted. 4th. Palliative treatment by antispasmodics, narcotics or soporifics must go hand in hand with antitoxic treatment. 5th. Measures should be taken to secure elimination of the toxins present in the blood.

_Treatment by brain emulsion._ Wassermann and Takaki (Berlin Klin. Woch. Jan. 3d, 1898) have in a number of cases, mixed 1cc. of brain substance of a warm-blooded animal with ten times the lethal dose of tetanus toxin and injected without producing any symptoms of tetanus. They obtained a similar immunity by injecting the brain emulsion 24 hours after the injection of three times, and in other cases of five times the lethal dose of tetanus toxin. Control cases uniformly died of tetanus. The brain matter was obtained from Guinea pigs, pigeons, rabbits, horses, and men. They accordingly advanced the theory that brain matter is a direct antidote to the tetanus toxin, uniting with it chemically and rendering it innocuous. The liver, spleen, kidney, bone marrow and blood serum gave no such protection.

Marie, in a series of experiments, injected the brain emulsion and tetanus poison at different parts of the body of Guinea pigs and found that fatal tetanus ensued. It would appear, therefore, that the brain emulsion acts by direct contact, and that it is only by its meeting and combining with the toxin before the latter reaches the spinal cord that tetanus can be prevented.

Roux and Borrel (Ann. de l’Instit. Pasteur, 1898) demonstrated this union between the poison and brain matter, by making an emulsion of the two, and putting in a centrifuge, which will separate the brain substance from the clear liquid. The fluid obtained in this way was shown by injection on the living animal to contain almost no toxin. Knorr and Blumenthal reached the same conclusion as to a chemical union with the brain matter which robbed the toxin of its toxicity.

Knorr, and Tizzoni, and Cattani and Morax showed indeed, that if the tetanus toxin is injected subdurally or into the surface layers of the cerebrum, it produces not tetanus, but a characteristic cerebral disease. A dose of ¹⁄₂₀th or ⅒th cc. of tetanus toxin produces in the rabbit, in 10 to 12 hours, restlessness, constant change of place, and signs of great fear like hiding the head, turning rapidly round, attempting to escape, polyuria, grinding the teeth, epileptoid convulsions. The toxin in this case had manifestly united with the brain substance while the cord suffered little.

Metchnikoff (Ann. de l’Inst. Past., April, 1898) holds that the brain matter is only valuable in holding the toxin until it can be destroyed by the leucocytes. He showed that the injection of the tetanus toxin in chickens or Guinea pigs greatly encreased the production of leucocytes. He injected tetanus toxin into the aqueous humor of the rabbit without producing much effect, but when the same agent mixed with cerebral substance was injected, the result was a great accumulation of leucocytes, and hypopion. If the mixture of brain substance and tetanus toxins were injected on the brain, little encrease of leucocytes occurred, but if thrown into the peritoneum, a most remarkable leucocytosis took place. In twenty minutes after the injection the fluid withdrawn from the abdomen showed large numbers of leucocytes filled with brain substance, but no free cerebral matter.

The present status of the treatment by brain substance is therefore somewhat uncertain. The value of that agent in holding the toxin is allowed, but like the antitoxin it must be employed before the toxin has reached the nerve centres and united with the living ganglion cells. Its use would be called for therefore at the earliest possible moment and it should be continued so long as there is reason to suspect the production of fresh toxin in the wound. Its direct action on the toxin would suggest its injection around an infected wound, or even as a dressing for the wound in connection with antiseptics. When tetanus has already set in it cannot be expected to undo the evil already accomplished by the union of the toxin with the cells of the cord, though it might in part arrest and hold new supplies of this poison coming from the wound to the nerve centres.

_Prevention._ In a disease so deadly as tetanus and so refractory to treatment even by antitoxin when it is once developed, prophylactic measures are of the greatest importance. With the extensive adoption of antiseptic surgery there has already been a material diminution in the number of cases, yet a greater attention is demanded to the prevention of casual cases which result from ordinary wounds. Dirty, grimy wounds filled with the dust of stable yard or garden soil, and such as contain splinters of wood, stones, thorns, straw and the like can only be considered quite safe after thorough disinfection. It has been shown that the toxin is easily neutralized at the time of infection, whereas, after the disease is developed it will require 1,000 or 100,000 times as much antitoxin to produce the same effect. In the case of soiled wounds, therefore, in a valuable animal, a harmless injection of antitoxin or of phenic acid or iodine solution before the development of tetanic symptoms is not an unwise precaution. A succession of such injections might be given to ward off the disease until after a lapse of time exceeding the short and dangerous incubation.

Much more important is the disinfection of the wound itself. All foreign bodies must be removed, but especially those that like splinters of wood and straws are likely to harbor the spores of the bacillus. Then the wound may be thoroughly cauterized thermically or chemically, or it may be irrigated with a strong antiseptic solution and then dressed with some agent that will prove destructive to the spores, and antidotal to the toxin. Strong carbolic acid may be applied to the whole raw surface including the uttermost recesses of the wound, and after a few seconds or half a minute this may be neutralized by filling the wound with dilute acetic acid or alcohol, after which a dressing of Lugol’s solution may be applied. Lambert advises a combination of hydrochloric and carbolic acids.

Weaker antiseptics, like a 5 per cent. solution of carbolic acid, do more harm than good, as they destroy the pus and saprophytic microbes and even the tetanus bacillus in the wound, without affecting the tetanus spores, which finding no other microbes to contest with them the possession of the field may find themselves in a better position than before to develop into bacilli and cause tetanus.

Tetanus neonatorum may be certainly prevented by the application of a disinfectant plaster on the navel at birth. Over 50 years ago in Scotland this desideratum was met by applying on the navel of the new-born child a soft and immaculately clean piece of cotton cloth which had just been flamed over a light. On the island of St. Kilda the former mortality of 67.2 per cent. of new-born infants, was promptly abolished by dressing the navel daily with iodoform. For new-born animals a cheap and convenient application may be made by incorporating 1 oz. powdered iodine and 2 lbs. wood tar, and smearing this on the navel.

Much may be done by disinfection of stables and yards where the victims of tetanus have been. The anærobic germ soon loses its virulence in free air and sunshine, and one has to dread especially, filthy stables, collections of manure, contaminated litter, wood, combs, brushes and buckets. In unpaved yards remove the infected surface soil and replace by fresh disinfected earth, or still better, well burned brick.

For horses which are necessarily exposed to manure or contaminated soil, it is commendable to wash the hoofs and pasterns on returning from work and then sponge with a weak solution (5 per cent.) of phenic acid. Another resort is to smear the hoofs daily with an ointment of tar and lard, equal parts. This cannot protect from infection by splinters of wood containing the spores, but is to a large extent preventive in the case of bacilli that might have been otherwise lodged on the surface and which could have been carried into the wounds inflicted by nails and other noninfected bodies. Careful shoeing is all important, to avoid the bruises, suppurating corns and _gravelling_ which make openings for the ready entrance of the spore.

Roux and Nocard recommend immunization by protective inoculation. This is not only possible, but would be justified economically in the case of valuable animals, or in all animals in a district where the bacillus tetani is universally spread. The method is the same as advised above for the immunization of animals, for the production of antitoxin.

In districts where tetanus is rare, the cost of universal immunization against the disease would very far exceed the losses front casual cases. Under such conditions it would be an economical blunder.

FOOT AND MOUTH DISEASE.

Synonyms. Definition. Susceptible animals: cloven footed, all warm
blooded animals. Historic notes; Geographical distribution; English
invasions in 18th and 19th centuries; North and South American
invasions in 1870; In Asia from immemorial times. Causes: infection in
liquid of vesicles, saliva on pastures, roads, feeding and drinking
places, halters, etc.; from feet on pastures, buildings, yards, roads,
cars, boats, etc.; from teats through milk. Microbe not certainly
known, micrococci, streptococci and bacilli found. Virus inert when
dried 24 hours at 88° F.; survived 9 months at 32° F., attack
immunizes for 5 months; injection of 1 lymph and 2 of blood of immune
renders refractory; filtered lymph still virulent; microbe probably
infinitesimal; accessory causes: movement, mingling of cattle, sheep,
swine, etc., war, trade, common pasturage, infected roads, ships,
yards, halters, etc. Symptoms: incubation 36 hours to 6 days; slight
fever; redness, tenderness of buccal mucosa and teats, grinding teeth,
smacking tongue, tender feet, shaking them backward, bullæ on mouth
and teats, not nodular, nor chambered as in variola, salivation,
bloody, circular or irregular raw sores, vesicles and erosions in
interdigital space, shedding hoofs, sheep walk on knees, gangrenous
mammitis; intestinal eruption and diarrhœa in sucklings. Mortality.
Prognosis; recovery in 15 days, deaths rare if cared for. Losses from
destruction of product and emaciation—occasional abortion. Diagnosis:
based on infection of all exposed bisulcates, localization on mouth,
teats and feet, inoculability on other warm blooded animals,
unchambered vesicles, slight fever, and prompt recovery. Notes of
affection in man. Symptoms in man. Prevention and treatment in man.
Prevention in animals: exclusion of contagion, immediate and mediate;
close infected pastures and roads, stop all movement of bisulcates,
disinfect all boats, cars, places and things exposed, exclude
visitors, guarantees with strange animals, quarantine and disinfect
arrivals, exclude fresh animal products, fodder and litter, wash,
disinfect soiled clothes. Inoculation undesirable. Treatment in
animals: cleanliness, dryness, disinfection, segregate sick and well,
gaseous antiseptics, liquid ointments. Gruels, mashes, sliced, boiled,
or pulped roots. Local dressings for mouth, teats and feet. Evulsion
of hoof. Mammitis.

_Synonyms._ Aphthous fever: Aphtha Epizoötica, Eczema Epizoötica.

_Definition._ An acute infectious disease of the lower animals but especially of ruminants, characterized by a slight fever and the eruption of vesicles, or ballæ on the skin and mucosæ, and usually those of the mouth, feet and teats.

_Susceptible Animals._ The animals that prove the most obnoxious to the disease are the bisulcates—large and small ruminants and swine. Man however is susceptible as are also horses, dogs, cats and fowls, when they are inoculated or fed upon the infected milk or other products. It is doubtful if any warm-blooded animal enjoys an immunity.

_History, Geographical Distribution._ Toward the middle of the eighteenth century this disease prevailed in Central Europe and England. The latter country stamped out both this and the Rinderpest, but it continued to prevail on the Continent and was re-imported into England in 1839. It reached America through an importation from England to Montreal in 1870, but owing to more or less effective quarantine, to the absence of cattle traffic from east to west, and above all to the prolonged confinement in yards and stables during our northern winter, it burnt itself out in the course of the year. In Asia it has prevailed from time immemorial, and it was imported into South America in 1870.

_Etiology._ This disease has long been known as caused by infection alone. Excluded from England in the middle of the eighteenth century it did not appear again until re-imported in the middle of the nineteenth, and then speedily overran the whole island except the breeding districts into which strange stock were never taken. In South America it was unknown until imported from the Old World into the Argentine Republic and then it made a wide extension and maintained itself where the stock was kept on unfenced ranches. In our fenced Northeastern states it died out and has not reappeared.

The infection is especially resident in the vesicles or aphthæ. From the mouth this is distributed, with the abundant drivelling saliva, on pastures, roads, feeding and drinking troughs, ponds, streams and halters, and readily communicates the disease to healthy stock following in the same places. From the feet and especially the interdigital space, it is left on the vegetation, buildings, yards, cars, boats and all other possible media to infect other stock in turn. From the teats it mingles with the milk so as to infect the young suckling and all animals and men to whom the milk may be given. It may become dried on litter and other light objects and carried by the winds, or it may be carried on the feet of men or animals including birds, but apart from this it is not readily diffused and oftentimes a broad highway may set a limit to its propagation.

The infecting microbe is not definitely known. Nosotti found a micrococcus in the lymph of the vesicle, which stained readily in aniline colors, was easily cultivated and pathogenic. Klein found a streptococcus which, similarly tested, presented an equal claim to be the causative factor. Bassianus and Siegel found in the blood and tissues of a person who died of foot and mouth disease a small oval bacillus, which they later obtained from the vesicles of three children who were suffering from the disease, and from animals attacked in two successive epizoötics. With this they first successfully inoculated a calf and from the pure cultures obtained from its blood, inoculated three calves and a young pig.

Löffler and Frosch, the recent commission on foot and mouth disease in Germany, report that no organisms could be seen nor cultivated from the lymph found in recent bullæ of the buccal mucosa, though this lymph proved virulent when inoculated on calves.

They found that the lymph became inert when dried for 24 hours at 31° C. (88° F.), while it retained its vitality and virulence after exposure for 9 months to a temperature of 0° C. They concluded that it could not penetrate through the unbroken skin nor mucosa, and that it was most effective when injected into the blood or peritoneal cavity. One attack conferred immunity for 5 months. Blood from immune animals, injected into susceptible ones, does not confer immunity, but 75 per cent. could be rendered immune if injected with a mixture of the lymph from the vesicle and double the same amount of the blood from the immune animal. Animals so treated become immune to 100 times the infecting dose. Filtered lymph was still virulent and the commission suggests that the microbe may be so small as to pass through the filter, and escape discovery by the most powerful lenses. An object one fifth the size of the smallest known bacillus—that of influenza—would be invisible under our best microscope.

By actual experiment the virus has been found in the nose, larynx, bronchia, stomach and intestines, but into all these the virulent lymph of the bullæ can find its way. In the intestines, indeed, in cases caused by feeding, bullæ have been found on the mucosa.

A most important question would be that of the virulence of the milk, but inasmuch as the vesicles appear on the teats and even on the openings of the milk ducts, and in bursting discharge their contents with the milk into the pail, the milk becomes per force infecting. The experiment of Hertwig and his students who infected themselves by drinking the warm milk by way of experiment, has been often repeated unwittingly by unwilling victims, and the many cases of calves, pigs and chickens contracting the disease by consuming the otherwise discarded milk leaves no room for doubt that this product is often infecting.

Among conditions contributing to a spread of infection, nothing is more potent than a free movement of ruminants, and swine whether determined by war, trade, or the intermingling of different herds on commons or unfenced ranges. In infected countries, in which cattle are distributed through large central markets there is always a wide extension after one of these fairs, the infection being narrowly circumscribed to herds receiving cattle from the fair, or those that have travelled on the same roads or fields after the market cattle. It has repeatedly happened that cattle shipped from the United States, where this disease has long been unknown, have been found diseased on their arrival at a British port, simply because they have been tied upon the passage with halters formerly used on infected Irish or Continental stock.

_Symptoms in animals._ There is first a period of incubation shorter in hot than in cold weather and varying from 36 hours to 6 days (exceptionally 15 days). It is altogether probable that prolonged incubation is really delayed infection, the virus having been attached to the feet for some time before it entered the tissues. Cattle usually show the disease two days after exposure in a public market, building or conveyance.

There is first moderate hyperthermia (102° to 103° F.), indicated by the clinical thermometer before there is any outward sign of ill health. There may be erection of the hair, tremors or distinct shivering, dryness and heat of the muzzle, redness and even tenderness of the buccal mucosa and teats, saliva drivels from the mouth or may show as a frothy mass at the commissures or margins of the lips, and there may be grinding of the teeth and a peculiar smacking of the tongue and hard palate which may be heard at a considerable distance. There are greatly impaired appetite and rumination. Tenderness of the feet is shown by halting or lameness and by the extension backward and shaking of the hind feet in turn.

With the appearance of the eruption, usually on the second day of illness, the fever as a rule moderates, and on examination of the mouth bullæ of ⅓d. to 1 inch in diameter may be found on the inside of the lips, and cheeks, or on the palate and tongue, with, in many cases, a congested areola, but showing no nodule as in variola. These bullæ may extend to the muzzle, pituitary membrane or pharynx. They burst very soon after their formation, exposing a red base of inflamed corium, with a clearly rounded margin, or, at first, with shreds of the torn epithelial covering. The salivation now becomes more profuse, glairy and even bloody, and there is more active movement of the tongue. When the bullæ have been confluent there are formed extensive red patches denuded of epithelium, and the suffering causes a complete but temporary dysphagia. The renewal of the epithelium, however, takes place promptly and may be well advanced in four or five days. Upon the teats the bullæ appear at about the same time but are usually smaller than the buccal, and do not show the thickened base of cow pox. They burst in 36 to 48 hours unless broken earlier by the hands of the milker, forming sores comparable to those of the mouth, which are liable to be kept up by the necessary manipulations in milking.

Upon the feet the eruption shows especially in the interdigital space, at first as vesicles smaller than those of the mouth and teats, leaving erosions and ulcers which extend under the adjacent horn, and upward on the front and back of the pastern. From exposure to mud and filth these are liable to be kept up even longer than those of the mouth and teats, and under neglect the entire hoof is often shed. In sheep and swine the disease may be localized almost exclusively in the feet. Sheep will even walk on the knees.

In young animals and those fed on the milk, the eruption may take place on the intestinal mucosa with violent congestion, diarrhœa and a fatal issue. Aggravated cases may show gangrenous mammitis or abortions.

_Mortality and Prognosis._ While there are seasons of special pathogenic severity, yet as a rule, the foot and mouth disease is a mild affection and unless neglected, the patients entirely recover in about fifteen days. The pecuniary loss in dairy and feeding cattle has been found to average in Great Britain about $10 per head, and as few animals escape, the consequences are usually very serious. In England the losses from this disease in 1883 reached $5,000,000, in France, those of 1871 were $7,500,000 and in Switzerland, $2,500,000. In Germany, over 7,000,000 animals suffered from 1889–94.

_Differential Diagnosis._ While a mistake might be made in an isolated case, such a thing should be absolutely impossible where cattle and other animals are collected in herds. The rapid infection of the whole herd, the implication of sheep and swine along with the cattle, and the eruption of the characteristic bullæ on the mouth, feet and udder or on two of these locations to the exclusion of the rest of the body, is not likely to be counterfeited by another disease. An outbreak of gangrenous ergotism in Kansas, Missouri and Illinois in the spring of 1884, was pronounced to be foot and mouth disease by a number of veterinarians, including an expert sent by the Government of Canada. On behalf of the U. S. Treasury I investigated the disease, which caused in many cases sores on the mouths and feet, but it spared all sheep and swine, could not be conveyed to them nor to new born calves by inoculation, and in many cases it caused gangrene of all the tissues, soft and hard, and separation of the limb at a given point, often near the tarsus. The quarantines were raised, the disease made no further extension, and the existing panic subsided.

_Infection of Man._ The first authentic record of this affection in man we owe to Valentin, who records that during the outbreak in Hesse in 1695 men suffered from inflammation of the gums, tongue and mouth. Michel Sagar says, that in 1764 men who drank the milk were affected with aphtha. In 1828 it was conveyed from animals to men in Bohemia (Nadberny), in Styria (Levitsky) and Wurtemberg (Kolb). In 1834, three veterinarians, Hertwig, Mann and Villain, voluntarily drank a quart each of the warm milk of a cow suffering from this affection. On the second day Hertwig suffered from fever, headache and itching of the hands and fingers. Five days later bullæ formed on the hands and fingers, the tongue, cheeks and lips. In the two others the eruption was confined to the buccal mucosa. Since that time records of the infection of human beings have been very numerous. During the American epizoötic of 1870 I met with the case of a farmer at South Dover, N. Y., who suffered from sore mouth and blisters along the margin of the tongue from drinking the milk. The danger is greatest in children on an exclusive milk diet and who drink it warm. Kolb in 1828, noticed acid vomiting and diarrhœa in such subjects, Hübner observed that beside the buccal eruption such children often suffered from inflammation of the stomach and bowels and that very young children fed on the milk of the diseased cows died. Balfour, Watson and others have noticed similar results in Scotland.

Allbutt saw the buccal eruption in three children in Yorkshire, England, during the local prevalence of the English epizoötic in 1883, and secured information of a number of other cases in the same district.

A number of cases were recorded during 1893 in Germany. A shepherd infected himself by holding in his mouth the knife with which he had pared the diseased feet of sheep, and another workman and a veterinarian had extensive eruptions on the hands after dressing the affected feet. A number of milk-maids were infected by milking, the eruption appearing on the hands, and in one case on the breast. A child fed on the milk of diseased cows, had chill and fever with gastric disturbance, and later an eruption of vesicles on the lips and tongue and between the fingers and toes.

Again, in 1895, during the prevalence of foot and mouth disease in the southern part of Berlin, a considerable number of the milk consumers suffered from fever with the eruption of bullæ on the tongue and buccal mucosa generally, which on early bursting left very painful ulcerations. The acute disease did not last more than five days, but left a sense of great weakness for a time. Virchow, who made an investigation, unhesitatingly pronounced it to be foot and mouth disease.

Cases of infection through butter made from infected milk are on record. A Berlin veterinary student suffered from the buccal eruption and erysipelatoid swelling of the ear, and a German clergyman had in addition a period of chilliness, fever, diarrhœa and pruritus. Similarly Schneider quotes cases determined by infected cheese, and Friedberger and Fröhner, cases caused by virulent buttermilk.

_Symptoms in Man._ In man there is observed the tendency to localization on the same points as in animals. As the hands are naturally exposed to infection by milking or treating the diseased animals, they are especially obnoxious to the eruption, and the same is true of the mouth when the infected milk or other dairy products are consumed. The bullæ on the buccal mucosa are generally confluent, and often extend to the fauces and pharynx, rendering speech difficult and swallowing painful, and leaving extensive and painful sores which, however, soon heal up. In women the bullæ have been seen around the congested nipples, and in exceptional cases they have been generally diffused over the body.

In cases due to drinking the milk, the early febrile symptoms are liable to be accompanied or followed by nausea, anorexia, abdominal pain and diarrhœa, and still later by the cutaneous and buccal eruption.

The duration of the disease is from 10 to 15 days and as a rule no permanent scars are left on the skin or mucous membranes.

The _diagnosis_ is assisted by the knowledge of the prevalence of the disease in herds in the district, and that the patient has handled the diseased animals, or drunk their milk, or eaten their butter or cheese products. The predilection of the eruption for the fingers, the roots of the nails and the mouth is very significant. The disease follows an acute course and convalescence is complete in ten or fifteen days, which serves to differentiate it from most skin eruptions. From variola which pursues an equally rapid course it is distinguished by the absence of the primary nodular swelling, and of the septa or pillars that divide the mature pock into independent chambers.

_Prophylactics._ The best prevention for man is to exclude the disease from the country and its herds as is now the case in the United States. When the disease does exist in herds the attendants should cauterize any sores on the hands, and wash the hands with an antiseptic, such as a 10 per cent. carbolic acid solution, after handling the diseased. The milk and its manufactured products—butter and cheese—should be withheld from consumption until after the herd has recovered. Infection can be obviated by boiling the milk.

_Treatment._ The disease follows a rapid course and is self-limiting, and usually benign so that active treatment is not urgently demanded. The local lesions are best met by non-poisonous antiseptics, such as: borax in powder or strong solution; boric acid (4:100); sodium hyposulphite (½ oz. 1 qt.); chlorate of potash (½ oz. to 1 quart); salicylic acid (1:100); or salicylate of soda. Pounded ice may be used as a soothing agent. The cutaneous lesions may be wrapped in cloth wet with one or other of the antiseptic lotions. Any disposition to ulcerate may be met by the stick of silver nitrate.

Slightly laxative or diuretic agents may be employed for their febrifuge and eliminating properties and the food should be light, easily digestible and given cold.

_Prevention in Animals._ When the disease exists in a country or district this includes all measures preventive of immediate or mediate contagion. Arrest of all movement of cloven footed animals in infected districts, disinfection of cars, boats and other conveyances, of markets, yards, highways, seclusion of infected herds and pastures, exclusion of visitors, disinfection of products, certificates of soundness of origin, thorough disinfection after recovery of the herd, such are the leading points to attend to. Inspection or closure of fairs and markets is desirable and any exposure of diseased or infected animals should be visited with heavy penalty, in addition to the cost of detention and supervision. For a noninfected country a certificate and guarantee of non-exposure with each cloven-footed animal imported, and of thorough disinfection of the cars, boats, halters or other objects used upon them, and of the places, fodder and litter supplied, together with a quarantine (1 week) and surface disinfection should be required under penalty. Exclusion of fresh hides, bones, guts, hair, bristles, wool, horn, as well as of fodder and litter is essential. Cattle attendants, drivers and others whose clothes are soiled with the products of the barn, should have the same washed and disinfected.

Inoculation has been proposed, and even practiced to pass a whole herd promptly through the malady, but as immunity lasts but three months, and the attendant risks to other herds are greatly encreased it is at once an economic blunder, and a great injury to adjoining owners. Any resulting extension to other herds should be an occasion for a verdict for damages at common law.

_Treatment in Animals._ Provision is first made against extension of the infection. The floor should be kept clean, dry and covered with sawdust, tan bark, gypsum or litter sprinkled with these or with phenic acid. The herd should be divided into two lots—the apparently sound, and unsound kept strictly apart under separate attendants, above all separate milkers. As soon as any symptoms are shown by an animal in the sound enclosure it must be instantly transferred to the other and its stall disinfected. Antiseptics such as gaseous iodine (two tablespoonful of tincture of iodine, thrown into a quart of boiling water twice daily), sulphurous acid, salicylic acid, creolin, lysol or other ointment on the feet and teats, may also be used. In this way it may be possible to save a number from an attack, yet most commonly the exposure is common and universal and the malady develops in all simultaneously. For those already attacked, gruels, mashes, and cool pulped, finely sliced or boiled roots may be all that is required, the disease runs its course and recovery ensues in 15 days. As local dressings the following may serve as examples: for the mouth, borax, chlorate of potash, salicylate or sulphite of soda 2 drs. to 1 quart water; phenic acid, creolin, or lysol, one or two teaspoonfuls to a quart; for the foot, clean the interdigital space and apply tar and carbolic acid with bandage, or use solutions of creolin, lysol, pyoktanin or blue-stone; in aggravated cases strong mineral acids with tar; for the teats, ointments of boric or salicylic acid, creolin, lysol, naphthalin or napthol. Separation of the hoof or mammitis will require treatment according to indications.

MILK SICKNESS. “THE TREMBLES.”