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Subcutaneous inoculation of 34 Texas tortoises (Gopherus berlandieri) with either of two strains of Western Equine Encephalitis (WEE) virus resulted in prolonged viremia of up to 105 days' duration. Peak viremia titers exceeded 10(6) suckling mouse intracranial lethal doses per milliliter. The length of the previremic period, the maximum viremia level attained, and the duration of viremia were markedly affected by environmental temperature. Higher temperatures (30 degrees C) shortened the previremic period and the duration of viremia and elevated the maximum viremia level. Lower temperatures had the opposite effect. Mechanisms are suggested whereby Texas tortoises could serve as an overwintering reservoir for WEE virus at any temperature. Neutralizing antibody was detectable following viremia in only 11 of 16 (69%) of surviving tortoises.

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Eighty-three wild mammals of ten species were inoculated with a first mouse passage level Venezuelan encephalitis (VE) virus isolated from south Texas in 1971 during the VE outbreak. Rodents were highly susceptible to VE infection and circulated VE virus at levels ranging from 10(7.7) to 10(11.5) suckling mouse intracranial lethal doses per ml for 2 to 4 days. These levels of virus could easily infect vector mosquitoes. Mortality was high in all species of rodents except Sigmodon hispidus, adult Neotoma micropus, and adult Peromyscus leucopus. Lagomorphs were susceptible to VE infection but circulated VE virus at or near mosquito threshold levels for 1 day only. Raccoons and opossums were relatively resistant to VE infection or circulated low levels of virus in the blood. Juvenile animals of four species were more susceptible and experienced higher viremias than did adults. In two of the four, mortality was higher in the juveniles than in adults. A consideration of results obtained during this study and those of other investigators led to the conclusion that equines were of major importance, that canines, lagomorphs and rodents were of minor importance, and that other species tested were of no importance as virus amplifiers in VE epizootics.

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In August-October 1980, a sudden increase occurred in the number of cases of jaundice reported among residents of a rural, agricultural section of Lancaster County, Pennsylvania. Investigation confirmed the cases as hepatitis A and showed that the outbreak was associated with consumption of water from a water fountain in a hardware store and water from the adjacent family home, both of which came from a well contaminated with feces. A total of 49 cases occurred from August 11 to October 21 in store customers, employees, family members, and persons visiting the family residence. Unusual features of the outbreak included an epidemic curve with two peaks, a very high attack rate in susceptibles at highest risk (greater than 90%), a high proportion of cases with jaundice (85%), absence of asymptomatic cases, and a high male to female ratio due to the makeup of the group at risk.