This is a non-contagious viral disease spread by biting midges (Culicoides sp), and that can infect sheep, goats, deer and cattle. Sheep are the most seriously affected species.
There are 25 serotypes of Bluetongue virus (BTV) worldwide. Some (but not all) strains are found in northern Australia (Northern Territory and northern parts of Queensland and Western Australia). Under conditions favouring southern spread of the vector, the virus may be found further south.
Infection of cattle with strains of BTV present in Australia has not been reported to cause any clinical symptoms. Clinical disease from BTV infection has also never been reported in sheep, goats or deer in Australia.
Clinical disease in livestock (particularly sheep) has been reported in other countries as a result of infection with virulent strains of BTV. Pathogenic strains damage blood vessels throughout the body causing them to leak or become blocked. This leads to oedema and haemorrhage which if mild can result in full recovery and immunity, and if severe can cause rapid death and long term debilitation in survivors.
Pathogenic strains of virus are not present in the sheep producing areas of Australia and exposure to infected midges is unlikely to occur at sea. The virus and the midge vectors are present in many countries to which Australia exports sheep. Clinical disease due to Bluetongue infection is therefore more likely to be seen in destination feedlots during periods of high insect activity, which is usually after rain in equatorial regions. Earliest cases occur about one week after being bitten.
Bluetongue should be suspected if multiple animals are affected. Symptoms may be mild to severe and if severe there are usually some deaths.
Clinical signs include depression, fever and inappetence, and swelling of the head and lameness.
The head, including the eyelids and ears, will be swollen with oedema. The inside of the mouth and tongue may be congested, and erosions, ulceration and haemorrhages may be present on the gums. There may be nasal discharge and crusting around the nostrils. Lameness will be in all feet similar to laminitis, and the coronary band may be purple red colour.
At necropsy there will be oedema and haemorrhage in organs and tissues, especially under the skin and in muscle. There may be haemorrhage at the base of the pulmonary artery and focal necrosis of the papillary muscle of the left ventricle which if present should raise strong suspicions. There will be excess fluid in the pericardium, thorax and abdomen.
Differential diagnoses include photosensitisation, big head and possibly bottle jaw. However, these are likely to occur at the beginning of the export process rather than at destination.
Laboratory confirmation requires whole blood (10-20 ml) collected as early as possible from febrile animals into an anticoagulant and submitted chilled for virus isolation. Specimens from dead animals should include sections of spleen, lymph nodes, and red bone marrow collected as soon as possible after death and submitted chilled. Sections of heart, lung, liver, kidney, spleen, lymph nodes and red bone marrow should be submitted in buffered formalin for histology. In long standing cases or survivors, submit chilled serum for serology.
There is no specific treatment other than nursing and provision of antibiotics (procaine penicillin, oxytetracycline, or trimethoprim sulpha) for prevention or treatment of secondary infections such as pneumonia. Animals that are unable to stand, eat or drink should be euthanased.
Principles of control include controlling midges with insecticides, moving animals into sheltered areas during the evening to reduce the number of bites, and vaccination to increase resistance of animals.