Arbovirus Infections of Laboratory Workers

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

“…Unlike vector-borne infections, where virus is deposited subcutaneously, the process of neuroinvasion by aerosolized alphaviruses is more direct, via the olfactory tract, and causes increased severity and incidence of encephalitis [50]. For example, a laboratory accident resulting in aerosolization and exposure to WEEV resulted in encephalitis with a mortality of 40 % [51]. Similar to VEEV and EEEV, neurologic sequelae of WEEV encephalitis may persist for months to years or be permanent, and postmortem brain specimens of fatal cases exhibit perivascular cuffs of lymphocytes and neutrophils, multifocal necrosis, and gliosis throughout the basal ganglia, thalamus, and brainstem [48].…”

Encephalitic Development in Alphaviral Infection

“…Strains of WEE virus have been isolated from humans, horses, wild birds, and vertebrates from western Canada to Argentina (Calisher, et al, 1985;Reisen, 1988). Specifically, infection of bobwhite quails, house finches, sparrows, and domestic chickens has been demonstrated (Hardy, 1987;O'Brien, et al,;Watts & Williams, 1972;Williams, et al, 1971). The virus can also infect some small mammals including opossum, squirrels, bats, rabbits, and hares.…”

“…Peripheral routes of infection result in approximately 50% mortality with intracerebral (IC) or intranasal (IN) challenge resulting in more uniform, dose-dependent mortality depending on strain of virus and background of murine model (Hardy, et al, 1997;Julander, et al, 2007;Liu, et al, 1970). In suckling mice, subcutaneous (SC) inoculation results in rapid, acute disease with uniform mortality by 48 hours post-infection (PI).…”

“…The virus can also infect some small mammals including opossum, squirrels, bats, rabbits, and hares. Like horses and humans, a number of these species exhibit a tangential infection and do not act as amplifying hosts (CFSPH, 2008;Fastier, 1952;Hardy, 1987;Kiorpes & Yuill, 1975;Reisen, et al, 2004;Ubico & McLean, 1995;Yuill & Hanson, 1964) Isolations of WEE viruses have been reported in the Veracruz region of Mexico and South America and the genetic analyses of isolates from Brazil and northern Argentina revealed a level of nucleotide identity >90% in the E2/6K/E1 coding region when compared to isolates from the US. This data suggests a monophyletic nature of the WEEV lineage, with an overall slow evolution (Weaver, 2005;Weaver & Barrett, 2004;Zacks & Paessler, 2010) WEE is maintained in an enzootic cycle between a number of passerine birds and its most common mosquito vector, Culex; however, the virus has also been isolated from mites (Hammon & Reeves, 1946;Hammon, et al, 1941;Hammon, et al, 1943;Reeves, et al, 1947;Zacks & Paessler, 2010).…”

“…Overall case fatality rates are estimated at 3-7%, but mortality rates depend on both age and other factors such as virus strain, dose, and route of infection (Calisher, 1994;CFSPH, 2008;Hanson, et al, 1967;Ryzhikov, et al, 1991;Steele, et al, 1998;Steele & Twenhafel, 2010;Zacks & Paessler, 2010). Accidental, artificial exposure of aerosolized virus in laboratory settings has been documented with the few cases demonstrating a 40% fatality rate (Fothergill, et al, 1939;Gold & Hampil, 1942;Hanson, et al, 1967;Helwig, 1940). As with all the encephalitic alphaviruses, higher mortality rates and incidence of neurological complications are associated with pediatric patients.…”