Lumpy Skin Disease

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Also known as: LSD

Introduction

Lumpy Skin disease (LSD) is a condition caused by a capripox virus of the family Poxiviridae, which is diagnostically indistinguishable from sheep pox virus. It affects cattle only and sheep and goats do not become infected during outbreaks of LSD even when held in close contact with infected cattle. The capripox virus strains are identical in every way in the laboratory, differing only in their ability to produce LSD in one host and sheep and goat pox in the other. No sheep pox has ever occurred in southern Africa during the LSD epizootics there, despite the presence of 40 million sheep.

The clinical syndrome of lumpy skin disease was first described in Zambia in 1929. It was at first, considered to be the result of hypersensitivity to insect bites or poisoning. Then, in the mid 1940's cases occurred in a much wider region of Southern Africa and concerns were raised over the infectious nature of the disease. Over eight million cattle were affected in Southern Africa at this time and this caused a devastating effect on the economy there. The disease is now widespread across Africa and is enzootic in sub-Saharan Africa.

Transmission is mostly via insect vectors, although direct contact can transmit the virus. Pox viruses are highly resistant and may remain viable in infected tissue for at least four months, and probably longer. Virus is also present in blood, nasal and lachrymal secretions, semen and saliva, which may be sources for transmission. It is not known if a particular insect is the main vector, as the virus has been found in the Stomoxys spp., and the Biomyia fasciata mosquito species. Tabanidae, Glossina and Culicoides spp. have all been found in situations where there has been ongoing LSD transmission and have been suspected to be involved. Considerable research into the transmission of the disease still needs to be undertaken in order to fully understand the condition and devise control measures for it.

Mortality rates in this condition can reach around 40% and morbidity rates are considerably higher. Skin lesions result in severe and permanent damage to hides, which is a cause of economic loss, while lesions in the mouth, pharynx and respiratory tract cause a rapid decrease in body condition, which may persist for several months.

Signalment

Cattle of all ages can be infected by the virus. There is no sex predilection. Channel Island breeds are much more susceptible to the virus.

Clinical Signs

Signs include pyrexia of 40 - 42oC, anorexia, depression, lethargy and excess lacrimation. Soon after this onset, dermatological signs begin to develop which appear as round circumscribed areas of erect hair measuring between 5 to 50mm in diameter. These lesions are raised and firm and they may be surrounded by a ring of haemorrhage. The regional superficial lymph nodes are enlarged and oedematous.

Other signs include nasal discharge and ptyalism, which is thought to be due to lesions in the nose and mouth. Lesions can be found in the respiratory tract and alimentary tract and so can cause coughing, increased respiratory noises and diarrhoea. The lesions are often secondarily infected by bacteria causing any discharge to be purulent and pneumonia is a common sequelae of the disease. Lesions may eventually slough away to leave a hole of full skin thickness, known as "sitfast".

Diagnosis

In countries where the disease is endemic, diagnosis based on clinical signs is generally all that is required as veterinarians here are experienced at detecting the lesions. In countries where the disease is exotic, signs may be confused with other diseases such as bovine herpes virus 2, foot and mouth disease, insect bite hypersensitivity or demodicosis.

Samples should be taken from the lesions and can be viewed under electron microscope to identify pox-virus particles.

Samples of skin also show characteristic histopathological changes which include vasculitis and perivascular infiltration with white cells causing a thrombosis of the vessel in the dermis and subcutis. Cells infiltrating the lesion are epithelial cells, known as celles clavelauses, which are also described in sheep pox.

Virus isolation by culture can also be carried out, but this takes many days and is not useful diagnostically for this reason.

Treatment and Control

Treatment is supportive, in the form of wound dressing to prevent fly strike and secondary infections. If secondary infections have already occurred, systemic antibiotics can be given to treat these accordingly.

In countries where the disease is exotic, measures to control the disease would include immediate slaughter of all infected animals and in-contact animals and the carcasses destroyed. A vaccination cover with a 25 to 50 km radius around the focus may then be established and all cattle movements stopped within that zone, however, this vaccination policy may allow the virus to persist in some cattle. Where an epizootic infection occurs in an already enzootic area, slaughter policies are inappropriate and vaccination campaigns are recommended instead. Vaccination will greatly reduce the morbidity and economic effects of an epizootic infection. Follow-up vaccination of calves and re-vaccination programmes over a period-of two to three years will greatly reduce the incidence of clinical disease. No country in sub-Saharan Africa, however, has succeeded in eradicating LSD once it has occurred. Movement should be restricted to prevent new spread of the disease in these situations also.

Two different vaccines have been widely and successfully used for the prevention of LSD in cattle populations in Africa. The Neethling strain vaccine has been used in Southern Africa and has proven effective in reducing the clinical signs of disease in cattle. Some local reactions do occur in many animals following inoculation, but these are not severe. In Kenya, an effective vaccine has been produced, which does not cause localised reactions.

References

Ali, A.A., Esmet, M., Attia, H., Selim, A. & Abdel Hamid, Y.M. 1990. Clinical and pathological studies on lumpy skin disease in Egypt. Vet. Rec., 127: 549-550.
Bridger, J and Russell, P (2007) Virology Study Guide, Royal Veterinary College.
Diesel, A.M. 1949. The epizootiology of lumpy skin disease in South Africa. Proc. 14th Int. Vet. Cong., London, 2: 492-500.
Green, H.F. 1959. Lumpy skin disease; its effect on hides and leather and a comparison in this respect with some other skin diseases. Bull. Epizootic Dis. of Africa, 7: 63-79.
Kitching, P.R. & Mellor, P.S. 1986. Insect transmission of Capripox viruses. Res. Vet. Sci., 40: 255-258.
MacOwan, K.D.S. 1959. Observations on the epizootiology of lumpy skin disease during the first year of its occurrence in Kenya. Bull. Epizootic Dis. of Africa, 7: 7-20.




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