Equine Infectious Anemia

C. D. STEIN.

INFECTIOUS anemia is known also as swamp fever, malarial fever, slow fever, and mountain fever. It affects horses, mules, and donkeys. Its prevalence in the United States has been declining with the substitution of motorized equipment for horse power in industry, agriculture, and the Army, but it is still of grave concern the world over to the establishments that handle large numbers of horses.

Infectious anemia is most prevalent in poorly drained, low-lying sections, but it has been found in wooded sections and marshy pastures at high altitudes. It also appears to be more prevalent when biting insects are most numerous and in wet years more than in dry seasons.

The active form of the disease appears in May or June, reaches its height in midsummer, and usually declines late in the fall. Chronic cases may be seen in the winter.

Outbreaks in the United States have been chiefly sporadic isolated cases confined to small areas and showing little tendency to spread. Small outbreaks have been reported from time to time in parts of Idaho, Oregon, Nevada, Montana, Mississippi, Wyoming, Louisiana, and Texas.

A number of severe outbreaks have occurred at establishments where large numbers of horses are assembled, and maintained, such as Army posts, breeding farms, dude ranches, and biological institutions. A serious outbreak occurred in 1947 in a large group of Thoroughbred race horses in New England, but it was promptly controlled by destroying affected animals and applying strict sanitation.

A chronic form, formerly prevalent among mules on large cotton plantations in the Mississippi Delta, has abated because tractors have replaced many mules.

The cause is a filterable virus which under natural conditions appears to affect only horses, mules, and donkeys. The virus may persist in an infected animal for years. It is apparently present in the blood and body tissues of affected animals at all times and may be eliminated with some of the secretions or excretions, such as the milk, semen, saliva, eye and nasal secretions, urine, and manure.

The exact nature of the virus remains a matter of discussion. It has not been cultivated in vitro (outside the animal body) and cannot reproduce itself consistently in other animals.

Experiments by investigators in the Department of Agriculture with strains of virus from different areas indicated that it varies greatly in virulence. Among the factors that apparently influence the virulence are the susceptibility of the host, frequency of passage (that is, transmission of the disease from one animal to another in series at short intervals), method of exposure, source of virus, character of the inoculating substance (the inoculum), and debilitating factors affecting the host.

The virus shows considerable resistance to disinfectants, heating, freezing, and drying.

Findings of investigators as to the action of heat and chemicals on the virus have been put into practical use in formulating requirements for the treatment of antiserums prepared from horses, thus safeguarding against dissemination of the disease through the use of such biological products.

Biological supply houses operating under Government license are required to heat all antiserums prepared from horses at 58 to 59 C. (136.4 to 138.2 F.) for an hour. The heat destroys any infectious anemia virus they may contain.

In the experiments conducted in the Department of Agriculture, only horses and donkeys were found to be susceptible. Attempts to infect calves, sheep, swine, dogs, cats, rabbits, guinea pigs, rats, mice, and pigeons failed.

Although the disease can be transmitted experimentally by injecting infectious material, by insect vectors, and by ingestion of contaminated material, we do not know how it spreads naturally.

Ordinarily the disease appears to spread slowly and sporadically. Outbreaks may occur, however, when infected animals are moved into new territory and when conditions are favorable for transmission and for the exposure of large numbers of susceptible horses.

Studies made during the outbreak among race horses in New England in 1947 indicated that biting flies may have been responsible for the early spread of the disease from carriers to healthy horses and that the use of unsterilized hypodermic needles and instruments spread it further.

The disease seems to spread more rapidly among animals on pasture than among those kept in stables, especially when biting insects abound.

Experimental evidence has led to several conclusions. The disease is transmitted readily by the injection of blood or tissue emulsions from affected animals into susceptible ones. Minute doses of the virus are infective for susceptible animals. The body secretions or excretions may contain the virus.

Infected mares may transmit the disease to their offspring and therefore should not be used for breeding.

THE CLINICAL SYMPTOMS of infectious anemia are variable and depend largely on the form of the disease.

It may occur as an acute, rapidly fatal disease or more commonly as a chronic affection, characterized by intermittent attacks of fever, loss of weight, progressive weakness, marked depression, and dropsical swellings on the lower parts of the body and legs.

The disease may also exist in a form the subclinical form in which no clinical symptoms are apparent though the affected animal carries virulent virus in the blood stream.

In the acute form the incubation period time elapsing between exposure and first appearance of symptoms usually is about 12 to 15 days, but it may vary from a few days to 3 months or longer.

The onset is sudden and brings a rise in temperature, which usually goes to about 105 F. but may reach 108 . The febrile attacks usually are severe and may be more or less continuous.

Respiration is accelerated and frequently is of the abdominal type. The animal is dejected, the head hangs low, leg weakness is marked, the body weight is shifted from one leg to another, and the hind feet are frequently placed well forward under the body.

The membranes of the eyes show congestion, followed by brownish to yellowish discoloration (icterus). Feed is refused. There may be a slight watery discharge from the eyes and nose and, if the weather is extremely warm, profuse sweating. Urination may be frequent, and in severe cases diarrhea may develop.

The attack usually lasts 3 to 5 days, after which the temperature returns to normal and the animal appears to be well except for a marked loss of weight. Occasionally, however, the initial attack may persist until the animal dies.

Dropsical swellings of the sheath, the legs, the chest, and the under surfaces of the body may occur at any time. Subsequent attacks usually follow. Normal periods of a few days to many weeks or months may intervene. When the intervals between the attacks of fever are short, the animal seldom lives more than 15 to 30 days. During the attacks of fever and immediately afterward, the number of red corpuscles in the blood drops. During the periods of normality between attacks, the count of red corpuscles is normal in most cases.

The subacute and chronic forms differ from the acute in that the attacks are less severe and the intervals between them are longer. The subacute cases may end in death during or following one of the attacks, or the reactions may grow less frequent and the animal may finally develop into a chronic case or a clinically recovered carrier.

The chronic form generally is manifested by unthriftiness, rough coat, underweight, sluggishness, weakness, dropsical swellings of the lower parts of the body or on the legs, muddy discoloration of the visible mucous membranes, and small hemorrhages of the third eyelid, or haw.

As the disease progresses, evidence of anemia may develop. The count of red corpuscles may be extremely low. The blood may appear thin and watery. The visible mucous membranes may become pallid in the later stages. The pulse may be slow and weak. The heart action may become irregular. A jugular pulse may be visible. The pulse may slow down quickly after exercise. Muscular weakness is manifested by a wobbly or rolling, staggering gait or by partial paralysis of the hindquarters. Animals that have the chronic form may eat constantly if they have access to feed but nevertheless lose weight steadily.

Animals with the chronic form can do some work if handled carefully but they are subject to recurring attacks, characterized by extreme weakness, knuckling, and inability to walk in a straight line. Sometimes the horse is so weak that it cannot stand by itself.

With good attention, rest, and supportive treatment (which includes abundance of good food, administration of liver extract, stimulants, and tonics), it usually overcomes the periodic attacks and may go back to routine work. Each attack takes its toll of flesh and strength, however; frequent attacks will weaken the animal, make it useless, and finally bring about death by exhaustion.

AN INACTIVE, or latent, stage may follow the first attack, but usually it is preceded by several attacks of fever. This form is observed in animals that apparently have recovered from the acute, subacute, or chronic types of the disease. Animals affected with the latent form show no clinical symptoms and are known as clinically recovered carriers. Their temperature remains normal. There is no reduction in the red corpuscles or any sign of disease over a period of months or years, and yet the infectious agent is always present in the blood stream and the tissues and may be eliminated with the body excretions.

Such animals are a menace to other horses that may be near them. The inactive form of the disease may become active at any time and present all the characteristics of the acute or subacute form. Unusually hard work or any debilitating influence may reactivate the infection. Complete recovery of carriers with a disappearance of virus from their blood rarely occurs. It has also been observed that the virulency of the blood of some carriers may diminish with time.

The Department of Agriculture had under observation two virus carriers that were good examples of the inactive form of the disease. These horses were first infected in 1935. A series of inoculation tests proved that one of the animals harbored the virus in its blood stream for more than 15 years and the other for more than 18 years.