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.
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