Epidemic Venezuelan Equine Encephalitis in North America in 1971: Vector Studies1

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.

Venezuelan equine encephalitis emergence: Enhanced vector infection from a single amino acid substitution in the envelope glycoprotein

“…Human serosurveys also indicate that many human infections probably occurred (J.G.E.-F. and S.C.W., unpublished work). The classical epidemiological paradigm for epizootic VEEV is efficient equine replication to produce high titer viremia (2,6,7,9), resulting in efficient amplification via infection of mammalophilic mosquitoes, which also bite humans (34). Epizootic mosquito vectors can be only marginally susceptible to infection, but because of the high equine viremia and exposure to large mosquito populations, they are capable of transmitting VEEV.…”

Virulence and viremia characteristics of 1992 epizootic subtype IC Venezuelan equine encephalitis viruses and closely related enzootic subtype ID strains.

“…Because many mosquito vectors implicated in epizootics are relatively insusceptible to systemic infection leading to transmission, 31,32 high levels of equine viremia are believed to be required for efficient amplification during outbreaks. This limited vector susceptibility, combined with little or no equine viremia following enzootic infections, explains the inability of enzootic VEE virus strains to generate epidemics and epizootics like serotypes IAB and IC.…”

Addressing theFertility needs of HIV-Seropositive Males

“…Through a combination of observations made during field studies and through experimental infections, the infection of horses, donkeys and mules with epizootic VEEV varieties are known to typically result in high rates of overt illness, with animals developing viremia levels that are sufficient for infection of susceptible mosquitoes [4,8]. Several species have been incriminated as vectors of epizootic VEEV IAB and IC, including Psorophora columbia e , Psorophora confinnis, Aedes sollicitans , Aedes taeniorhynchus, Mansonia indubitans and Deinocerites pseudes [9–12]. …”