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This article was published in 1958
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INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Blue Tongue
N. K. GOLDING, B.V.Sc., Principal Veterinary Officer, Department of Agriculture, N.S.W.
What is Blue Tongue? Attention has been focused in recent months upon the disease Blue Tongue, and it is necessary that Departmental staff charged with the responsibility of controlling diseases in stock should be familiar with it. Blue Tongue is an acute, infectious disease, primarily of sheep, but it affects also, to a lesser extent, cattle and goats. The disease is caused by a virus which is transmitted by a biting insect of the Culicoides species.
THE WORLD SITUATION
For many years, the disease was confined to Africa. It existed in all parts of South Africa, South West Africa, both Rhodesias, as far north as the French Sudan in the west and to Abyssinia in the east. Blue Tongue was first found outside Africa in 1943-1944, when the Onderstepoort laboratories checked a strain of virus which was submitted to it. At the time of this outbreak, which was in Cyprus, the disease apparently was seen in Israel (Palestine) in milder form. The disease, identified by adequate laboratory procedures, reappeared in Palestine in 1950 in both cattle and sheep. The Turkish Ministry of Agriculture reported it in sheep in 1945, 1946 and 1947; following the probable introduction of the disease from Syria.
In the United States of America, Blue Tongue was first recognised in Texas in 1948. It reappeared three years later on a much larger scale, when about fifteen western counties were involved with altitudes ranging from 200 to 300 ft. to somewhat over 2,000 ft. above sea level. Blue Tongue first appeared in California in 1952 and spread throughout the sheep-raising areas of the interior of that State within about six months; involving flocks totalling 325,000 sheep. Since then, Blue Tongue has been diagnosed in Arizona, New Mexico, Utah and four other States of the United States of Amerca. More than one-third of the sheep population in that country is included in those States.
In 1956, Blue Tongue was diagnosed for the first time in Portugal, and also in Spain. French veterinarians writing in a reputable scientific Journal have predicted the invasion of Blue Tongue during the next European summer, when insect vectors become active.
THE IMPORTANCE OF BLUE TONGUE
It is difficult to over-emphasise the importance of Blue Tongue to Australia; a country which is so dependent on the prosperity of the sheep and wool industry for its economic well-being. If the experience of the spread and effects of the disease in the Iberian Peninsula are any indication of what might be expected in Australia should the disease become established here, then any steps which this country can take to prevent its introduction would be justified. In Portugal about one-third of the infected flocks showed symptoms, whilst there was an overall mortality rate of about twelve per cent. A few cattle showed signs of the disease. It has been reported that in one early outbreak in Spain, of 67,000 sheep which sickened, 30,000 had died and 5,000 were slaughtered. Although this death rate is unusually high, it shows what may happen to susceptible Merino sheep.
Further support is given to this prophecy by the behaviour of the two epizootics, Ephemeral Fever and Myxomatosis, both of which were spread by biting insects in a susceptible stock population. The Spanish experience is unlikely to be exaggerated, and in Australia appearance of the disease is almost certain to be associated with high mortality and morbidity.
The United States of America has spent the fantastic amount of 130,000,000 dollars to reduce the threat of Foot and Mouth disease by controlling the outbreak of that disease in Mexico. It is obvious, then, that a country like the United States of America is willing to expend enormous sums of money, even outside its own territory, to prevent the entry of a serious disease of livestock. It is reasonable to infer that a like sum, or perhaps even a greater sum, would be spent on the eradication of any serious disease if, after its introduction, the means were available to effect eradication. Therefore, the American decision to live with Blue Tongue is probably the most potent endorsement of the observation that no country ever has eradicated this disease once it has become established. It is safe to say that this situation would apply here, viz., that if the disease did become established, no steps which could be taken would enable it to be eradicated or even successfully confined to a restricted area.
Once the disease becomes established, an attempt must be made to control it to reduce the losses to the sheep industry. This can be achieved only by vaccination, which is a costly and continuous operation. Vaccination must be done annually, using a modified live virus. The production of huge quantities of the vaccine and its distribution and inoculation present grave difficulties. The vaccine itself is not innocuous and can reduce the fertility of rams for several weeks. It is a recommendation that vaccination should be performed at least three weeks prior to the breeding season, Vaccination may also result in temporary anoestrus in ewes; while undertaken in the first third of pregnancy, produces an average loss of something like five per cent. of the lamb crop. This is due to the birth of "crazy" lambs caused by damage to brain tissues. Exposure to strong sunshine after vaccination is thought also to intensify any ill-effects following vaccination.
THE INSECT VECTOR
The disease is spread by biting insects known as midges, gnats or sandflies. In Texas, Culicoides variipenis has been definitely incriminated in the spread, but American authorities regard other species of Culicoides as being able to spread the disease as well. In Australia, C. variipenis is not present, but there are twenty-nine other varieties of Culicoides known to exist on this Continent. Some of these are confined to particular regions, but others are widespread over most of Australia. Some species are found even at altitudes of 4,000 to 5,000 ft.; with others at sea level. There is little doubt that several of these species would be able to transmit the disease if it were introduced here.
SYMPTOMS IN SHEEP
Blue Tongue is a disease of the warmer months and clinical manifestations are not seen after the first good frost. After artificial infection with virulent blood, the incubation period in sheep varies from two to four days, but can be as long as seventeen days. Under natural conditions it can be regarded as being of the order of one week.
The first symptom is usually a rise in body temperature; which may be gradual or which may occur very rapidly. The temperature range varies from 104 deg. F. to 106 deg. F. as a general rule, but temperatures higher than this have been recorded. The average duration of the febrile reaction is about six to seven days, although it has varied from two to eleven days. Sometimes there is irregular thermal response without any obvious disturbances of the general health. For example, in some cases there is an absence of definite fever in an animal which otherwise manifests typical symptoms of Blue Tongue. In the majority of affected animals, however, there is at least moderate fever.
The first obvious symptoms are periodic movements of the tongue and lips, a reddening of the buccal mucosa and a disinclination to feed. Marked buccal lesions do not appear sooner than about forty-eight hours after the commencement of the febrile reaction, and sometimes the sheep, showing severe hyperaemia of the mouth, keeps on feeding without any apparent signs of disturbance. In severe cases there is a frothing at the mouth; with a discharge at first catarrhal, but later muco-purulent, and even blood-stained, escaping from the nose. There is often swelling and oedema of the lips, the gums, dental pads and tongue. The buccal mucosa assumes a bluish or purplish colour, and finally there may be excoriations of the epithelium of the of the lips and cheeks, the tip of the tongue, the bars of the hard palette and the dental pad. The exposed parts are raw and often bleed so that the saliva which accumulates in the mouth becomes blood-stained. Later, putrefaction sets in and an offensive odour is given off from the mouth. The tongue becomes oedematous and swollen, dark blue in colour, with amber or yellow patches along the sides. Swallowing becomes difficult, the nasal discharge dries on the nostrils and the encrustations which are formed partly occlude the openings causing dyspnoea and snoring. Sometimes raw sores are formed on the muzzle and in the nasal chambers. These lesions may last for about three to five days.
In a proportion of cases, lesions on the feet form after about three to seven days, when the mouth lesions begin to heal. There is a coronitis; causing the claws, the coronary bands and heels to become hot, red and painful. Two or more feet may be affected at the same time.
With such clinical symptoms, it is obvious that sheep will show a marked loss of condition; with debility, muscular weakness and lameness persisting for weeks. The greatest loss sustained by the owner is an indirect one, mainly attributable to the marked loss of condition, the protracted convalescence and the break in the wool; which are the inevitable results of an attack of Blue Tongue.
LESIONS IN SHEEP
The lesions vary greatly in degree, and depend on the strain of the virus and the severity of the symptoms produced by it, the stage of evolution the symptoms have reached at the time of the animal's death, the susceptibility of the animal, the environmental conditions under which the animal is running (e.g., atmospheric conditions and solar radiation) and the condition of the animal and the length of its wool.
The most important lesions involving the skin and mucous membranes are localised or diffuse hyperaemia, multiple haemorrhages, cyanosis, oedema, swelling and excoriation of the epithelium leading to erosions and necrotic ulceration of the mucous membrane of the mouth. The hyperaemia of the skin may be patchy, leading to irregular exanthematous areas and a localised dermatitis. There are sometimes also abrasions on the exposed parts of the body.
There are a few diffuse red areas in the subcutis which cannot be attributed to bruising. They are dark red, gelatinous and may extend into the muscles of the back, the shoulder and the neck. The intramuscular connective tissues are infiltrated with a clear, reddish, gelatinous fluid. There are small, but sometimes extensive, haemorrhages in the muscles. These are either in the form of spots or streaks which may be missed unless looked for especially, The haemorrhages can be seen readily when a thin strip of muscle is held up to the light. Microscopically, there is extensive capillary haemorrhage. Most of the lesions occur in localised portions of muscle or in small groups of muscle fibre. A diffuse opacity, cloudiness or greyish mottling of the muscle may be present. This can be attributed to the degenerative processes obscured by the haemorrhagic effusions.
In addition to affecting the buccal mucosa and skin, the hyperaemia affects the mucous membranes of the rumen, the folds of the abomasum and of the intestine; and such organs as the liver, heart and kidneys. The coronet also is affected. Multiple haemorrhages of varying size may involve also the intestine, the myocardium, the epi and endo-cardium, and, less frequently, the respiratory mucosa, the bladder and urethra. There are usually circumscribed haemorrhages around the roots of the hairs within skin follicles. In more advanced cases, there are excoriations of the epithelium followed by necrotic ulceration of the inner aspects of the lips, dental pad, tongue, rumen, pylorus and the external nares. Sometimes there is gangrene of the tongue as a result of secondary infection.
SYMPTOMS AND LESIONS IN CATTLE
In cattle, the lesions in the mouth are much less marked and, in fact, the majority of cattle do not show symptoms although they carry the disease. They may remain infected for upwards of three months as carriers. There may be hyperaemia of the skin in the region of the accessory digits and necrosis of the epidermis of the skin of the udder and teats, followed by scab formation. Sometimes a thermal reaction is the only symptom in bovines. In goats, the lesions are similar to cattle.
DIAGNOSIS
In Australia, the diagnosis of Blue Tongue might be attended with some difficulty because of its similarity to photosensitisation and the feeling that the disease is not present in the country. For this reason, early cases are likely to be missed. The disease is likely to make its appearance in serious proportions in the spring and summer, a period in which photosensitisation also occurs. Any connection with imported stock at this stage is likely to have been remote and, indeed, there may be no indication of contact with imported stock at all.
The most important clinical symptoms are the superficial localised inflammation and necrosis of the buccal mucosa, muzzle and external nares. The temperature reaction is not of much value at the stage when mouth lesions are developed sufficiently to draw attention to the presence of the disease. When coronitis is present, it usually appears at the time when the mouth lesions are healing: some days, that is, after the onset of fever.
If cattle are present on the property, an inspection may reveal minor lesions in a few of them, and this may assist in the diagnosis.
The disease bears a slight similarity to Foot and Mouth Disease, but can be differentiated from it by the absence of vesicle formation and possibly by its failure to spread by contact within a mob to the same extent as would be expected with Foot and Mouth; and particularly by its failure to spread to cattle to any marked degree. Diagnosis is confirmed by the inoculation of blood from clinical cases into susceptible sheep, with the production of characteristic symptoms. Absolute confirmation depends on further passage into susceptible sheep after the initial inoculation.
CONTROL MEASURES FOR AUSTRALIA
Naturally, the first aim of the authorities is to prevent the disease gaining entrance into Australia. There is no indication that it is present and consequently the policy of prohibiting the importation of ruminant animals from overseas, recently adopted by the Commonwealth, is the only sensible one. Action which might be taken in Australia will depend primarily upon the speed with which the presence of the disease is recognised. If it is localised, it is possible that an all-out policy of destruction would be attempted in the first instance. If not, then the only action left is to minimise the effects of instituting a programme of control by vaccination. A heavy responsibility, therefore, rests upon the veterinary profession in this country, and it is essential that the utmost vigilance be exerted at all times. The establishment of the disease here would be the most serious threat to which the sheep and wool industry of Australia could be exposed.
In this article, information collated by Dr. T. S. Gregory and Mr. R. N. Wardle has been freely incorporated. Fortunately, no one has had any firsthand experience with Blue Tongue here and all information must be culled from the experience of others.