Bluetongue of Sheep

D. G. McKERCHER, B. R. McCRORY, AND J. L. HOURRIGAN.

BLUETONGUE, or catarrhal fever, is a virus disease of sheep. Typical symptoms are fever, depression, and lack of appetite. Inflammation and ulceration of the mucous membranes of the nasal cavity, mouth, and the tongue may occur. The tongue may sometimes be swollen and cyanotic (bluish).

The acute phase is relatively short, but recovery may take a long time and may be marked by lameness, debility, and extreme emaciation. A "break" in the staple lowers the value of the wool. The fleece is sometimes shed. The mortality occasionally is high but usually does not exceed 15 percent of the affected animals in an outbreak. Because of loss of condition, long convalescence, interruption of breeding schedules, and lower value of the wool, however, the indirect economic losses from bluetongue are considerably greater than those suffered directly in terms of actual deaths.

Bluetongue has been serious in some countries for many years but is relatively new to the United States. For a long time it apparently was confined to the Union of South Africa and other parts of Africa. It has been studied extensively in the Government Veterinary Research Laboratories at Onderstepoort, Union of South Africa. The disease was reported on Cyprus in 1943 and later in Israel. It has been reported, without confirmation, in Palestine, Turkey, and Syria.

The presence of bluetongue in the United States was suspected in 1948 and confirmed in 1952 on the basis of studies by American and South African investigators, who could not find out, however, how it was introduced or when. Its presence in Arizona, California, Colorado, Kansas, Missouri, and Texas has been verified,and it was diagnosed clinically in Montana, Nebraska, New Mexico,. Oklahoma, and Utah. Suspected outbreaks were reported in Idaho, Indiana, Oregon, and Wyoming in 1954 and 1955.

ALL BREEDS of sheep are susceptible to bluetongue, but severity of infection depends on several factors.

Certain breeds are less susceptible than others. In South Africa the native Afrikander and Persian breeds are considered quite resistant; the Merino is less so; and the Dorset Horn and other British breeds display but little natural resistance. The susceptibility of individuals in each breed also seems to vary.

Another factor is the strain of the virus. Some strains produce relatively mild infections, irrespective of breed; others regularly give rise to a severe form of the disease.

Age is a factor. Sheep about 1 year old are most susceptible. Lambs of susceptible ewes suffer a much milder form of the disease, possibly because of the natural resistance of youth. Lambs of dams that have recovered from the disease have a passive immunity, which gives a measure of protection for 2 months or more after birth.

Environmental circumstances also. have a part: Sheep born and bred in, an area where bluetongue exists are more resistant than those introduced from a place where the disease is less prevalent or absent.

Bluetongue is seasonal. (Very likely insects transmit it.) It is more prevalent during wet years and occurs mainly in low-lying localities, although: conditions suitable for the vector,. rather than the absolute elevation, may be the critical factor. The disease. usually begins in early June and ends abruptly with the first severe frosts. Its onset and duration, therefore, vary for different areas of the country. The peak of the disease coincides generally with the period of greatest insect activity in any particular area.

THE FILTERABLE VIRUS that causes bluetongue is present in the blood, blood serum, organs of circulation, and tissue fluids of the infected sheep. Sheep are regarded as the natural hosts. The virus is also found in cattle, but in cattle the clinical manifestations of disease are negligible or absent.

Infant mice, hamsters, and chicken embryos can be infected by experimental inoculation.

The bluetongue virus can remain viable in decomposed blood and tissues for long periods. In suitable storage it retains its viability for years.

A number of strains of bluetongue virus exist. Most of them differ in virulence. Thus, in fully susceptible sheep, some strains the virulent strains regularly produce a severe form of bluetongue, whereas others of low virulence give rise to a relatively mild infection.

When a strain of low virulence is passed from sheep to sheep by injection, the virus tends to become weaker and eventually loses its capacity to produce a recognizable clinical infection. The virulent strains retain full power to cause disease when they are passed in this way. When passed through a succession of chicken embryos, however, strains of high and low virulence alike lose their ability to cause bluetongue in susceptible sheep. The weakened virus is then said to be "modified" or "attenuated." Such viruses are used to protect or immunize against their fully virulent counterparts.

Of utmost importance in vaccinating and immunizing against blue-tongue is that all known strains of the virus are divisible into four distinct groups, or types. Recovery from an attack of bluetongue caused by a strain of one particular type fails to protect the individual against subsequent exposure to a strain of virus belonging to any of the other three types. Type and virulence are unrelated, however, because a mild strain of virus protects against infection with a fully virulent strain of the same type, and vice versa. The significance of this point is referred to later.

BLUETONGUE is not a contagious disease. It can be transmitted only by the injection of infectious blood and other virus-containing tissues. The evidence we have strongly suggests that under natural conditions transmission is by a nocturnal bloodsucking insect, or insects, which transfer the blood from diseased to susceptible sheep.

Circumstantial evidence originally implicated the mosquito as the vector, but investigations have not proved that to be true.

Limited experiments later demonstrated that a night-feeding gnat of the genus Culicoides could possibly transmit the infection. It has not been possible to raise these gnats in captivity, however, and research men have been unable to determine whether this gnat might be a biological vector (that is, one in which the virus undergoes multiplication) or merely a mechanical vector of the virus. In any event, we think it is highly significant that these gnats are found wherever bluetongue occurs in the United States, although bluetongue does not necessarily occur where these gnats abound.

Of equal importance is the manner in which the virus is maintained from one bluetongue season to the next. The disease does not occur in late fall, winter, and early spring, a period of about 6 months; yet, as far as we know, the virus does not persist for longer than 4 months in recovered sheep. These two points can be reconciled only on the premise that the virus is maintained from year to year in a host other than sheep.

Although species of the Culicoides gnat can harbor the virus, that the gnats normally maintain the virus is considered highly improbable. Much more likely is that some vertebrate species is involved from which the insect obtains the virus before the beginning of each bluetongue season. The fact that cattle harbor the virus for variable periods while showing little or no evidence of clinical infection might therefore be significant.

IN SHEEP into which the virus is injected experimentally the disease appears usually 6 to 9 days after the injection. The time required for the disease to develop naturally has not been determined but is believed also to be about 6 to 9 days.

Rarely will all the signs of the disease be observed in any one sheep or even in any one outbreak. A definite pattern of symptoms may predominate in one flock, but another set of symptoms may be found in an outbreak nearby. Likewise the morbidity and mortality vary greatly. Sheep may occasionally contract the disease and experience only a febrile reaction. Others may display the typical clinical symptoms and have no fever.

The early stage of the disease is characterized in most cases only by a temperature, which ranges from 104 to 106 F. or even higher. The fever begins to subside after 3 or 4 days, and clinical symptoms appear.

The first symptoms consist of a flushing of the skin over the sternum, inside the thighs and forelimbs, and sometimes over the shoulders, ribs, and flanks; swelling of the lips and tongue; and reddening of the mucous membranes of the mouth and nasal cavity. A watery discharge and an excessive amount of salivary secretion, often stringy, also are observed. The nasal discharge soon becomes quite thick, dries on the nostrils, and forms encrustations, which leave a raw, bleeding, underlying surface when removed.

In many cases the swelling of the lips extends to the ears, muzzle, and inter-mandibular space and less frequently to the neck and sternum. The ears become hot and pendulous. The lower part of the head looks swollen. Affected animals show variable degrees of depression. The appetite is diminished or absent. Breathing and the pulse rate speed up. The animals lie down much the time.

Parts of the mucous membranes of the mouth and tongue may slough,' leaving bleeding areas on the margin, inner surfaces of the lips, at the corners of the mouth, on the upper surface and tip of the tongue, and on the dental pad and gums.

The tongue may be greatly swollen and bluish and protrude from the mouth, so that breathing is difficult. Necrotic ulcers often are observed in severe cases on the sides of the fixed part of the tongue. Sometimes raw sores develop on the muzzle and in the nasal passages. Animals that develop pneumonia as a sequel to the febrile reaction breathe with great difficulty, and the saliva becomes frothy and sometimes tinged with blood. These cases usually die.

The flushing of the skin results ultimately in the formation of localized areas of dermatitis and is associated with the development of a bluish-red or purplish band at the coronet (skin-margin of the hoof), which moves down with the growth of horn. This inflammatory process is believed to account for the lameness that often occurs. This band is not observed in all naturally occurring cases of the disease, however, and is seldom observed in animals that are infected experimentally.

Most deaths occur during or shortly after the acute stage. A few deaths occur just afterwards; they usually are due to secondary pneumonia. Most of the other animals recover in a relatively short time, but some develop emaciation, weakness, stiffness, and lameness. Sometimes the fleece is shed. In some cases the head is held to one side a condition that is known as torticollis or wryneck. It is caused by a muscular weakness resulting from the degeneration (wasting) of the neck muscles. Such animals, which survive a long period of convalescence, rarely if ever regain their former condition and are of little economic value.