Epidemiological significance of Venezuelan equine encephalomyelitis virus in vitro markers.

One hundred and fifty-eight strains of Venezuelan equine encephalomyelitis virus were typed antigenically and classified epidemiologically as either epizootic or enzootic. Plaque sizes for 148 of these strains were determined, and the pH requirements for hemagglutination (HA) of goose erythrocytes of 131 were studied. Only antigenic variant group IABC strains could be classified epidemiologically as epizootic. In vitro these strains were characterized by the formation of small plaques in Vero cells and a relatively narrow pH range for optimum HA reactivity. Experimental studies in horses confirmed the fact that only IABC strains have epizootic potential. We concluded that plaque size in Vero cell monolayers would be a useful method of screening VEE viruses for equine virulent strains. Indirect evidence suggested that small plaques resulted from sensitivity to an anionic substance present in the agar overlay medium.

Eastern equine encephalomyelitis in Panama: the epidemiology of the 1973 epizootic.

In late June 1973, a small outbreak of equine encephalitis caused by eastern equine encephalomyelitis (EEE) virus occurred in the Republic of Panama. At least 100 horses were affected by the disease and 40 died. More than 1,700 human sera were obtained from areas of virus activity but no serological evidence for infection was found. Four isolates of EEE virus were recovered, one of which was from a small pool of Culex taeniopus mosquitoes. Serologic studies of infected horses and classification by the short incubation hemagglutination-inhibition tests revealed that these isolates were South American strains. Our evidence suggests that another agent virulent for horses was active during this outbreak.

Ten clinical cases of human infection with venezuelan equine encephalomyelitis virus, subtype I-D.

The clinical and laboratory findings in ten humans infected with Venezuelan equine encephalitis virus, subtype I-D, are described in this report. Clinical and laboratory data indicate that, in contrast to equine infections, human infection with these enzootic virus strains (I-D) is similar to human infection with epizootic strains (I-ABC). In most cases there was an abrupt onset of fever, muscle pain, and vomiting. Virus was recovered from sera obtained during the first 3 days of illness. Lymphopenia occurred in all patients, and neutropenia occurred in three. No sequelae of these infections were apparent.

Enzootic and epizootic Venezuelan equine encephalomyelitis virus in horses infected by peripheral and intrathecal routes.

Forty-five horses were infected peripherally or intrathecally with enzootic or epizootic strains of Venezuelan equine encephalomyelitis (VEE) virus. Low titers of virus appeared in cerebrospinal fluid (CSF) after peripheral inoculation of enzootic or epizootic VEE virus strains. Intrathecal infection with either epizootic or enzootic VEE virus produced higher titers of virus in CSF than did peripheral infection. In contrast to peripheral infections with enzootic strains, intrathecal infections with these strains caused death. The animals that died had widespread histopathologic changes and large amounts of virus in brain tissue. The attenuated VEE virus vaccine strain, TC-83, also multiplied in the brain of horses inoculated intrathecally but caused no clinical disease and little histopathologic damage.

Experimental infection of horses with an attenuated Venezuelan equine encephalomyelitis vaccine (strain TC-83).

Ten horses (Equus caballus) were vaccinated with strain TC-83 Venezuelan equine encephalomyelitis (VEE) virus vaccine. Febrile responses and leukopenia due to a reduction of lymphocytes and neutrophils were observed in all animals. Viremias were demonstrable in eight horses, with a maximum of 10(3.5) median tissue culture infectious dose units per ml of serum in two horses. Clinical illness with depression and anorexia were observed in five horses. Neutralizing (N), hemagglutination-inhibiting, and complement-fixing antibodies to the vaccine virus were demonstrable by 5, 6.5, and 7 days, respectively, after vaccination. Differential titrations of serum to six VEE strains revealed high titers of N antibody to vaccine virus, moderate titers to the epizootic Trinidad donkey no. 1 strain (VEE antigenic subtype I, variant A) from which TC-83 was derived, and low titers to two other epizootic strains (subtype I, variants B and C) in all horses at 1 month after vaccination; some animals responded with low levels of N antibody to the enzootic viruses (subtype I, variants D and E). Fourteen months after vaccination, six animals with detectable N antibody were challenged with MF-8 (subtype I, variant B), an epidemic-epizootic strain isolated in 1969 from a man in Honduras. All horses resisted challenge with the equine pathogenic strain of VEE. Marked increases of N antibody in most horses were demonstrable to some VEE strains when tested 1 month after challenge.

Experimental Venezuelan equine encephalomyelitis virus infection of the bovine.

Two groups of four dairy cows (Bos taurus) were infected subcutaneously with the epizootic Venezuelan equine encephalomyelitis virus (VEE) strains MF-8 and San Pelayo, respectively. Animals experienced no clinical illness, but all developed significant neutropenia. Virus was recovered once each from the blood of three animals but did not exceed 10(2.2) SMICLD(50) (Suckling mouse intracerebral lethal dose(50))/ml. Specific neutralizing antibodies appeared in the serum of all animals, but there were no significant differences in titers against different naturally occurring VEE subtypes. Dairy cattle thus appear to play no role in virus transmission during VEE epizootics but may serve as retrospective immunological sentinels of virus activity.

Field studies of an attenuated Venezuelan equine encephalomyelitis vaccine (strain TC-83).

A series of field studies using strain TC-83 attenuated Venezuelan equine encephalomyelitis vaccine in horses was made to determine the rate of seroconversions, the postvaccination viremia, and the possibility of adverse reactions to the vaccine. The rate of seroconversions varied from 50% in one study to 91 and 100% in two others. The highest level of viremia measured was 7 x 10(3) to 8 x 10(3) plaqueforming units per ml. No adverse reactions to the vaccine were observed in any horses, including 42 pregnant mares and their resulting foals.