1975American Journal of EpidemiologyRequires access

EPIDEMIC VENEZUELAN EQUINE ENCEPHALITIS IN NORTH AMERICA IN 1971: VERTEBRATE FIELD STUDIES1

W. D. Sudia, Robert G. McLean, V. F. Newhouse, J. Johnston, Darlene Miller, H. A. Trevino, G. Stephen Bowen, Gladys E. Sather

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Abstract

Epidemic Venezuelan equine encephalitis in North America in 1971: vertebrate field studies. Am J Epidemiol 101:36-50, 1975.-In June 1971, epidemic Venezuelan equine encephalitis (VEE) invaded the lower Rio Grande Valley in south Texas. The Boca Chica area of Cameron County was selected as a study site to investigate vertebrate involvement in the natural cycle of epidemic VEE on the basis of considerable evidence of VEE virus activity there in equines, humans, and mosquito vectors. Only one VEE virus isolation was made from 4739 wild and domestic non-equine vertebrates, although numerous equine and human VEE virus isolations were made in concurrent studies. Serologic studies indicated that VEE virus activity was far greater in large domestic animals than in wild birds, wild mammals, or reptiles. Apparently epidemic VEE virus failed to establish itself in a wild vertebrate cycle in south Texas, since VEE antibody was found only in rabbits in 1972. Eventual cessation of VEE transmission in south Texas has been attributed 1) to the elimination of equines as a source of VEE virus by death, naturally acquired antibodies, or vaccination, 2) to quarantines, 3) to mosquito control, and 4) to the failure of epidemic VEE virus to become established in the wild vertebrate population. Equines emerge as the most important vertebrate host in the amplification and spread of virus during an epidemic of VEE.

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Epidemic Venezuelan equine encephalitis in North America in 1971: vertebrate field studies. Am J Epidemiol 101:36-50, 1975.-In June 1971, epidemic Venezuelan equine encephalitis (VEE) invaded the lower Rio Grande Valley in south Texas. The Boca Chica area of Cameron County was selected as a study site to investigate vertebrate involvement in the natural cycle of epidemic VEE on the basis of considerable evidence of VEE virus activity there in equines, humans, and mosquito vectors. Only one VEE virus isolation was made from 4739 wild and domestic non-equine vertebrates, although numerous equine and human VEE virus isolations were made in concurrent studies. Serologic studies indicated that VEE virus activity was far greater in large domestic animals than in wild birds, wild mammals, or reptiles. Apparently epidemic VEE virus failed to establish itself in a wild vertebrate cycle in south Texas, since VEE antibody was found only in rabbits in 1972. Eventual cessation of VEE transmission in south Texas has been attributed 1) to the elimination of equines as a source of VEE virus by death, naturally acquired antibodies, or vaccination, 2) to quarantines, 3) to mosquito control, and 4) to the failure of epidemic VEE virus to become established in the wild vertebrate population. Equines emerge as the most important vertebrate host in the amplification and spread of virus during an epidemic of VEE.

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Available abstract

Epidemic Venezuelan equine encephalitis in North America in 1971: vertebrate field studies. Am J Epidemiol 101:36-50, 1975.-In June 1971, epidemic Venezuelan equine encephalitis (VEE) invaded the lower Rio Grande Valley in south Texas. The Boca Chica area of Cameron County was selected as a study site to investigate vertebrate involvement in the natural cycle of epidemic VEE on the basis of considerable evidence of VEE virus activity there in equines, humans, and mosquito vectors. Only one VEE virus isolation was made from 4739 wild and domestic non-equine vertebrates, although numerous equine and human VEE virus isolations were made in concurrent studies. Serologic studies indicated that VEE virus activity was far greater in large domestic animals than in wild birds, wild mammals, or reptiles. Apparently epidemic VEE virus failed to establish itself in a wild vertebrate cycle in south Texas, since VEE antibody was found only in rabbits in 1972. Eventual cessation of VEE transmission in south Texas has been attributed 1) to the elimination of equines as a source of VEE virus by death, naturally acquired antibodies, or vaccination, 2) to quarantines, 3) to mosquito control, and 4) to the failure of epidemic VEE virus to become established in the wild vertebrate population. Equines emerge as the most important vertebrate host in the amplification and spread of virus during an epidemic of VEE.

Key concepts: Encephalitis, Virology, Geography, Biology, Medicine, Virus

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