Sheep and Goat Pox
Sheep and goat pox (SGP) is a highly contagious disease caused by a virus in the family Poxviridae and genus Capripoxvirus. The virus is one of the largest viruses, the brick shaped 170 to 260 by 300 to 450-nm-diameter capsid contains a linear, nonsegmented, double-stranded DNA genome of approximately 150 kilobases that is surrounded by a layer of lipid that is not a true envelope (1, 3). The virus is endemic in Africa, the Middle East, India, and Asia. These photos were taken during an outbreak in Kenya. Transmission is primarily through direct contact with infectious scab material or aerosols, but insect transmission is also possible. SGP infection in goats and sheep has a similar course of disease. Signs usually begin 4 to 8 days postinfection and include fever, depression, conjunctivitis, salivation and runny nose, and enlarged lymph nodes. Within a few days lesions appear on the skin and mucous membranes. Disease usually lasts 4 to 6 weeks and recovery can take as long as 3 months. Lesions can range from mild (Fig. 1) to severe (Fig. 2, 3, and 4), and the more severe the rash, the poorer the prognosis. Viral pneumonia due to pox formation in the lungs is common and often results in mortality. Morbidity in infected flocks can reach 80%, and mortality is usually 5 to 10% but can approach 100%, particularly in young lambs. Factors such as severe weather, infection with parasites, poor diet, and stress are known to exacerbate mortality. This is considered to be the most severe pox infection of domesticated animals. Vaccines are available for the prevention of this disease (2, 4). SGP can often be misdiagnosed as bluetongue, peste des petits ruminats, or contagious ecthyma (contagious pustular dermatitis, orf) all of which have similar signs and rash. SGP is also serologically indistinguishable from lumpy skin disease of cattle which is caused by a virus in the same genus. Diagnosis is by immunofluorescence staining using antibodies that will bind to intracytoplasmic inclusion bodies (areas of scarring in the cytoplasm from viral replication), enzyme-linked immunosorbent assay, or serological methods including virus neutralization, Western blot, and agar gel.
1. Espisito J. J., and F. Fenner. 2001. Poxviruses, p. 2885–2922. InD. M. Knipe and P. M. Howley (ed.), Fields virology. Lippincott Williams and Wilkins, Philadelphia, Pa.
2. Fenner, F., P. A. Bachmann, E. P. J. Gibbs, F. A. Murphy, M. J. Studdert, and D. O. White. 1987. Veterinary virology, p. 398–399. Academic Press, Inc., Orlando, Fla.
3. Moss, B. 2001. Poxviridae: the viruses and their replication, p. 2849–2884. InD. M. Knipe and P. M. Howley (ed.), Fields virology. Lippincott Williams and Wilkins, Philadelphia, Pa.
4. Roberts, W. A., and G. A. Carter. 1976. Essentials of veterinary virology, p. 101. Michigan State University Press, East Lansing, Mich.