Publisher Summary This chapter focuses on the role of mosquitoes in the enzootic transmission of eastern equine encephalomyelitis (EEE) virus and discusses the historic and epidemiologic knowledge, structure and replication, and transmission cycles of the virus. Studies on mosquito–virus interactions and speculation on the significance of these findings have been summarized in the chapter. Early studies of EEE virus described the disease caused by this virus, identified the virus as an etiological agent, and determined arthropod and vertebrate hosts for enzootic and epidemic transmission. Subsequent studies provided important details on mosquito bionomics, vector–virus interactions, and basic virology. Because EEE virus is easy to work with in the laboratory, the virus has also been used as a model for testing concepts in entomological aspects of arbovirology. Multiple blood-feeding by mosquitoes during a single gonotrophic cycle increases the probability of virus persistence during interepidemic periods and the explosive spread of diseases during epidemics. EEE virus transmission cycles can be used to test the importance of this prediction. Moreover, the techniques that are being developed—histological examination of engorged mosquitoes and alkali metal blood markers in sentinel hosts—have broad application to hematophagous arthropods that transmit a variety of diseases.

Eastern Equine Encephalomyelitis Virus: Epidemiology and Evolution of Mosquito Transmission

West Nile virus (WNV) first appeared in the naive environment of the Western Hemisphere in 1999 in New York. Genetic analysis determined that the virus was introduced into the United States from the Mediterranean Basin. This review discusses the spread of the virus in 2001 from the initial focus in Queens, New York, to widespread activity in the eastern and midwestern United States. It concentrates on viral ecology, epizootiology, pathology, prediction, and prevention. Research questions to further our understanding of the transmission cycle of WNV are discussed, including host-preference studies, molecular confirmation of implicated mosquito vectors, and survival of WNV in the temperate environment of the United States. Comparisons are drawn with two other arboviruses enzootic in the United States, eastern equine encephalitis, and St. Louis encephalitis viruses. Although not recently introduced, these two viruses also demonstrated increased activity in the United States in 2001.

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West Nile Virus Activity in the United States, 2001

/pdf/guidelines-for-arbovirus-surveillance-programs-in-the-united-2d6h9l1kog.pdf

Guidelines for arbovirus surveillance programs in the united states

Eastern equine encephalomyelitis virus (EEEV) is perpetuated in eastern North America in a mosquito-wild bird maintenance cycle that involves Culiseta melanura (Coquillett) as the principal enzootic vector and passerine birds as the primary amplifying hosts. We examined the role of birds in the EEEV cycle at a site in southern New Jersey where EEEV cycles annually at high levels. Birds and mosquitoes were sampled during three epiornitics and one season of limited virus activity. We examined antibody prevalence in birds in relation to eight physical and natural history characteristics. Our goal was to compare EEEV cycling in C. melanura and the primary avian hosts better to understand the mechanisms that initiate annual epiornitics. Antibody prevalence was highest in the Blue Jay (62%), Wood Thrush (60%), and Tufted Titmouse (44%). Resident status of birds was the natural history characteristic most closely linked to participation in the EEEV cycle. Species spending the greatest amount of time at our study site (permanent residents, summer residents) had the highest antibody rates. We captured viremic birds as early as 25 May, 51 d before we first detected virus in C. melanura. We recaptured 10 after hatching year adults and one hatching year (HY) bird that seroconverted before we detected virus in C. melanura. We also found EEEV antibody in 15 HY birds up to 31 d before we isolated EEEV from C. melanura. We provide evidence that a cryptic cycle develops weeks before epiornitic cycling is detected in C. melanura by traditional laboratory techniques, indicating that the early season cycle is initiated by the recrudescence of latent virus in previously infected birds.

Eastern equine encephalomyelitis virus in relation to the avian community of a coastal cedar swamp.

Natural eastern equine encephalitis alphavirus (EEEV) infection was diagnosed in two adult horses with anorexia and colic, changes in sensorium, hyperexcitability, and terminal severe depression. Myo- cardium, tunica muscularis of stomach, intestine, urinary bladder, and spleen capsule had coagulative necrosis and perivascular lymphocytic infiltrate. Central nervous system (CNS) lesions were diffuse polioencephalo- myelitis with leptomeningitis characterized by perivascular T lymphocyte cuffing, marked gliosis, neuronopha- gia, and multifocal microabscesses. Lesions were more prominent within cerebral cortex, thalamus, hypothal- amus, and mesencephalon. EEEV was identified in the cytoplasm of cardiac myocytes and smooth muscle cells of spleen, stomach, intestine, urinary bladder, blood vessels, and dendritic cells. In the CNS, EEEV-positive cells included neurons, astrocytes, oligodendrocytes, microglia, and neutrophils. EEEV was isolated from the CNS of both horses. The detailed description of the encephalic and spinal EEEV localization and the findings of EEEV in extraneural tissues contribute to the understanding of this important multisystemic zoonotic disease.

https://journals.sagepub.com/doi/pdf/10.1354/vp.38-4-451

Clinical, Pathologic, Immunohistochemical, and Virologic Findings of Eastern Equine Encephalomyelitis in Two Horses

A study was undertaken to investigate an increase in reported cases of clinical encephalitis due to eastern equine encephalitis (EEE) virus in horses and to determine the natural vertebrate hosts of that virus. Horses, birds, and small mammals were sampled at sites in a contiguous area in St. Joseph and Kalamazoo counties, Michigan, from 25 August to 5 September 1980. Serum samples from four horses acutely ill with encephalitis and 16 of 39 pasture mates of ill horses had neutralizing (N) antibody against EEE virus (46.5%); no viruses were isolated from these 43 sera. None of 24 draft horses from a site in St. Joseph County 12 km southeast of the affected sites had EEE antibody. A strain of Cache Valley virus was isolated from the blood of one of the 24 draft horses. No viruses were isolated, and no antibodies to EEE virus were detected in 28 blood samples from small mammals captured at sites where equine cases of encephalitis were occurring. Six strains of EEE virus, five of Highlands J virus, and one of Flanders virus were isolated from the blood of 401 wild birds belonging to 42 species captured at eight sites in both counties. A total of 29.9% of the wild birds had EEE antibody. Five species of domestic birds, mostly chickens and ring-necked pheasants, were sampled in both counties. Six strains of EEE virus were isolated from 152 ring-necked pheasants; these included three isolates from the brains of dead birds. About 13% of 51 pheasants tested from two small flocks in backyard pens in Kalamazoo County and 9% of 103 pheasants tested from a large game farm in St. Joseph County had antibody to EEE virus. The source of the EEE virus and the factors responsible for this epizootic are unknown; however, the epizootic probably represented an explosive expansion of an enzootic level of virus transmission.

Investigations of the vertebrate hosts of eastern equine encephalitis during an epizootic in Michigan, 1980.

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Investigations of the vertebrate hosts of eastern equine encephalitis during an epizootic in Michigan, 1980.