Abstract: A major epidemic of Venezuelan equine encephalitis occurred in south Texas in the summer of 1971. More than 1500 equines died of VEE in Texas, and 110 human cases with no deaths were reported. Vector studies in south Texas and northern Tamaulipas revealed that the overall mosquito infection rates during the peak of the epidemic were about 1:100, one of the highest rates observed for a major epidemic. Mosquito infection rates of this magnitude could easily explain the intensity of VEE outbreaks in both equines and man. A total of 943 VEE virus isolations were made from mosquitoes. Eight of the 12 mosquito species found infected were implicated in the epidemic cycle of VEE for the first time. Sufficient laboratory and field evidence is available to prove that Psorophora confinnis was one of the primary vectors of VEE. The lack of laboratory evidence necessitates the use of the term "probable" primary vectors for other species apparently equally as involved on the basis of field infections; these include Aedes sollicitans, Aedes thelcter and Psorophora discolor. Eight other species from which less than 10 VEE virus isolations were made were considered auxiliary vectors. Mosquitoes of some species were tested individually; such tests showed 2-4% of the probable primary vectors to be infected. The first isolation of VEE virus of the epidemic was made from P. confinnis on June 28, 1971. Highest mosquito infection rates occurred during the week of July 5. Mosquito infection rates declined precipitously in the last 3 weeks of July 1971, signaling the end of the epidemic in the study area. One explanation for the decline was that equines, the principal epidemic hosts, were eliminated as a source of virus by death or by acquisition of natural or induced immunity. Mosquito control appeared to be effective in reducing the infected mosquito population while the immunization of equines with TC 83 VEE vaccine was accomplished. Quarantines appeared to be effective in restricting the VEE virus activity to south Texas. Undoubtedly all of the control measures contributed to stopping the epidemic. Continued VEE surveillance by various government and other agencies failed to reveal any further epidemic VEE activity in the US in 1972. Other arboviruses isolated during the VEE studies in south Texas included St. Louis encephalitis virus, and San Angelo subtype of the California Group. A virus of the Bunyamwera Group was also isolated from Palo Blanco, Tamaulipas.
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This research examines an epidemic of Venezuelan equine encephalitis (VEE) that occurred in South Texas in 1971, impacting over 1500 equines and 110 humans. The study aims to understand the mosquito vectors involved in this massive outbreak and concludes that Psorophora confinnis was one of the primary vectors.
Context of the Study
The research was centered around the VEE epidemic that occurred during the summer of 1971, mostly impacting south Texas.
The epidemic was significant – the primary victims were equines with over 1500 deaths, but there were also 110 reported human cases.
The key point of interest for this study was the mosquito infection rates which were among the highest ever observed during an epidemic, approximately 1:100.
Vector Identification
A total of 943 isolations of the VEE virus were made from mosquitoes, implicating particular species in facilitating the epidemic.
Eight out of the 12 mosquito species found infected were implicated in the epidemic cycle of VEE for the first time.
Among these, Psorophora confinnis was identified as one of the primary vectors of VEE.
Other species, including Aedes sollicitans, Aedes thelcter, and Psorophora discolor were deemed “probable” primary vectors based on field infections.
Temporal Dynamics of the Epidemic
The investigation revealed that the first isolation of the VEE virus of the epidemic was made from Psorophora confinnis on June 28, 1971.
Highest mosquito infection rates occurred during the week of July 5.
Interestingly, mosquito infection rates showed a steep decline in the last three weeks of July 1971, signalling the end of the epidemic.
Explanations for Decline and Control Measures
The authors suggest one possible explanation for the decline in the epidemic could be the result of equines (the primary hosts of this outbreak) either dying off or developing natural or induced immunity to the virus.
They also found that mosquito control efforts were effective in reducing the infected mosquito population.
Immunization of equines with a VEE vaccine (TC 83) and the implementation of quarantines contributed to controlling the epidemic effectively.
Post-Epidemic Surveillance
Despite the end of the epidemic, continued surveillance by various authorities found no more VEE activity in the US the following year.
However, during the VEE surveys in south Texas, other arboviruses were detected, including St. Louis encephalitis virus, San Angelo subtype of the California Group, and a virus from the Bunyamwera Group in Palo Blanco, Tamaulipas.
Cite This Article
APA
Sudia WD, Newhouse VF, Beadle ID, Miller DL, Johnston JG, Young R, Calisher CH, Maness K.
(1975).
Epidemic Venezuelan equine encephalitis in North America in 1971: vector studies.
Am J Epidemiol, 101(1), 17-35.
https://doi.org/10.1093/oxfordjournals.aje.a112068
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