Eastern equine encephalomyelitis virus in experimentally infected bats.

Colonial bats (Myotis supp. and Eptesicus sp.) were infected with eastern equine encephalomyelitis virus by subcutaneous inoculation or by the bite of infected mosquitoes. Bats were maintained in an environment simulating conditions encountered in hibernacula or in summer maternal colonies. Virus was detected in the blood of hibernating bats at irregular intervals over a 42-day observation period; viremia perhaps was influenced by the amount of disturbance (arousal) involved in the blood sampling process. Target organs included brown fat, spleen, lung, kidneys, pancreas, and liver. Neutralizing antibody was not detected in sera collected from these bats between days 4 and 42 post-inoculation. In nonhibernating bats, virus was recovered from mammary glands, brown fat, pancreas, lungs, kidneys, and liver, in addition to blood. Attempts to infect bats orally or to transmit virus to suckling mice by the bite of viremic bats were unsuccessful. Virus was transmitted from viremic chickens to E. fuscus by the bite of Culiseta melanura and Aedes aegypti.     

Infection of the western treehole mosquito,Aedes sierrensis (Diptera: Culicidae), with Lambornella clarki (Ciliophora: Tetrahymenidae)

Lambornella clarki was a common parasite of Aedes sierrensis immatures collected from treeholes in Mendocino County, California, in 1982–1983. The ciliate was not found in mosquitoes from treeholes with water having the most extreme values of electrical conductivity (<0.23 and >1.74 mmhos/cm) and pH (<6.5 and >7.7). Infection rates for individual monthly samples from L. clarki-positive treeholes ranged from 1 to 75%; 67% of all infections were observed in 4th-instar larvae. Infection with pathogens and parasites such as L. clarki, Ascogregarina clarki, Octomyomermis troglodytis, and unidentified bacteria and fungi, appeared responsible for high mortality rates (21–76%). Parasitism with L. clarki did not always result in death of the mosquito host; 7% of adults emerging from samples held in the laboratory were found to be infected. Ciliates were restricted to the host hemocoel except in older females where they invaded the ovaries, resulting in parasitic castration. This phenomenon may be associated with parasite dispersal.     

Enhanced esterase activity in salivary gland and midgut of Aedes aegypti mosquito infected with dengue-2 virus

Mosquitoes were infected by intrathoracic inoculation. About 95% head squashes were positive for dengue virus antigen on the 15th post infection day (PID). Esterase activity was determined in the homogenates prepared from the salivary glands and midguts on different PIDs of dengue virus inoculated and control mosquitoes showed that it was consistently higher in the virus-infected batches.     

Dissemination of western equine encephalomyelitis virus in the potential vector,Culex pipiens pallens

Two western equine encephalomyelitis virus (WEEV) strains have been isolated in China. Our previous studies have verified that the mosquito Culex pipiens pallens Coquillett (Diptera: Culicidae) infected with WEEV was capable of transmitting this arbovirus, but it was not clear how the sequential multiplication and spread of virus occurred within the mosquito. In this study, we observed the distribution of WEEV antigen in orally‐infected Cx. p. pallens by immunohistochemistry in order to better understand the initial infection, dissemination, and transmission of WEEV in the potential vector. Orally‐infected WEEV dissemination varied within the different tissues of Cx. p. pallens, with virus antigen consistently observed in the salivary glands, foregut, midgut epithelial cells, Malpighian tubules, hindgut, and ovarian follicles of some individuals after various days of extrinsic incubation. We suggest that Cx. p. pallens, the potential vector of WEEV, has the ability to harbor the virus through the alimentary system, and the midgut epithelial cell may be the initial site of WEEV replication after ingestion of a viremic blood meal.     

Fetal mortality and malformations associated with experimental infections of western equine encephalomyelitis vaccine virus in rhesus monkeys (Macaca mulatta).

Pregnant Rhesus monkeys were infected via installation of Western Equine Encephalomyelitis (WEE) vaccine virus into the amniotic sacs at 50 and 80 days gestation to determine if the resulting infections would produce fetal mortality or fetal malformations, particularly within the central nervous system. Of those receiving virus at 50 days gestation, 13 of 18 fetuses were aborted or dead in utero at time of Caesarean section; 2 of 18 were malformed (hydrocephalus and polyarthrosis); and 3 of 18 were anatomically normal. Of those receiving virus at 80 days gestation four of eight fetuses were aborted or dead in utero at time of Caesarean section, one of eight was malformed (hydrocephalus) and three of eight were anatomically normal. Three of three controls receiving neutralized virus at each gestational age were anatomically normal. Fetal WEE vaccine virus infection significantly increased fetal mortality and resulted in a significant incidence of fetal malformations.