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In fall 2017, 3 solid organ transplant (SOT) recipients from a common donor developed encephalitis within 1 week of transplantation, prompting suspicion of transplant-transmitted infection. Eastern equine encephalitis virus (EEEV) infection was identified during testing of endomyocardial tissue from the heart recipient. We reviewed medical records of the organ donor and transplant recipients and tested serum, whole blood, cerebrospinal fluid, and tissue from the donor and recipients for evidence of EEEV infection by multiple assays. We investigated blood transfusion as a possible source of organ donor infection by testing remaining components and serum specimens from blood donors. We reviewed data from the pretransplant organ donor evaluation and local EEEV surveillance. We found laboratory evidence of recent EEEV infection in all organ recipients and the common donor. Serum collected from the organ donor upon hospital admission tested negative, but subsequent samples obtained prior to organ recovery were positive for EEEV RNA. There was no evidence of EEEV infection among donors of the 8 blood products transfused into the organ donor or in products derived from these donations. Veterinary and mosquito surveillance showed recent EEEV activity in counties nearby the organ donor's county of residence. Neuroinvasive EEEV infection directly contributed to the death of 1 organ recipient and likely contributed to death in another. Our investigation demonstrated EEEV transmission through SOT. Mosquito-borne transmission of EEEV to the organ donor was the likely source of infection. Clinicians should be aware of EEEV as a cause of transplant-associated encephalitis.

The Alphavirus genus of the family Togaviridae contains mosquito-vectored viruses that primarily cause either arthritogenic disease or acute encephalitis. North American eastern equine encephalitis virus (NA-EEEV) is uniquely neurovirulent among encephalitic alphaviruses, causing mortality in a majority of symptomatic cases and neurological sequelae in many survivors. Unlike many alphaviruses, NA-EEEV infection of mice yields limited signs of febrile illness typically associated with lymphoid tissue replication. Rather, signs of brain infection, including seizures, are prominent. Use of heparan sulfate (HS) as an attachment receptor increases the neurovirulence of cell culture-adapted strains of Sindbis virus, an arthritogenic alphavirus. However, this receptor is not known to be used by naturally circulating alphaviruses. We demonstrate that wild-type NA-EEEV strain FL91-4679 uses HS as an attachment receptor and that the amino acid sequence of its E2 attachment protein is identical to those of natural isolates sequenced by RT-PCR amplification of field samples. This finding unequivocally confirms the use of HS receptors by naturally circulating NA-EEEV strains. Inactivation of the major HS binding domain in NA-EEEV E2 demonstrated that the HS binding increased brain replication and neurologic disease but reduced lymphoid tissue replication, febrile illness signs, and cytokine/chemokine induction in mice. We propose that HS binding by natural NA-EEEV strains alters tropism in vivo to antagonize/evade immune responses, and the extreme neurovirulence of wild-type NA-EEEV may be a consequence. Therefore, reinvestigation of HS binding by this and other arboviruses is warranted.

Table 1 Case 1 2 3 Normal Serum Sodium (mmol/L) 135 138 135 133-145 Calcium (mg/dL) 8.5 8.8 9.1 8.8-10.2 Phosphorous (mg/dL) 4.9 2.0 - 2.7-4.5 Magnesium (meq/L) 2.5 2.2 1.8 1.8-2.4 Aspartate aminotransferase (u/L) 42 46 17 5-40 Creatinine 1.5 1.1 1.2 0.6-1.4 Total protein 7.0 6.8 7.8 5.9-8.3 Urine Colour Yellow Yellow Yellow Yellow Clarity Clear Clear Cloudy Clear Specific gravity 1.024 1.030 1.020 1.002-1.035 pH (units) 6 5 5 5-8 Protein (mg/dL) '3+' 30 0 0-10 Haemoglobin '2+' 0 0 0 Mucus '1+' '1+' 'Trace' 0 Bacteria (per high power field) '1+' 'Few' '1+' 0 White blood cells (per high power field) 0-2 0 3-5 0-2 Red blood cells (per high power field) 3-5 0 75-80 0-3 Epithelial cells (per high power field) '1+' 0 3-5 0 Coarse granular casts (per high power field) 0-2 0 0 0 Creatine kinase brain-type isoenzyme elevation was apparently due to the well-described extensive destruction of brain tissue caused by this viral encephalitis. 3 The only published distinguishing clinical features of Eastern equine encephalitis have been greater severity 3 and a more rapid rate of progression 4 compared with other viral causes of encephalitis, such as West Nile virus neuroinvasive infection 5 and Herpes simplex encephalitis. 6 In one case of Coxsackie virus B4 encephalitis, serum creatine kinase increased to 6215 IU transiently. 7 In one case of subacute sclerosing panencephalitis, creatine kinase was thought to reflect the extent of lesions. 8 The level of serum creatine kinase may be useful to distinguish encephalitis from meningitis for timely diagnosis and prompt reporting to public health services. [...]retrospective or prospective study of the level, rate of change and area under the curve of total creatine kinase and brain isoenzyme in viral encephalitis could prove useful for measuring the extent of brain destruction, monitoring the standard or experimental treatment and correlation with clinical or anatomic outcome.

Thirteen cases of a disease with a low morbidity and very high mortality in horses in Nigeria are described; the disease is characterised by fever (rectal temperature ≥40°C), generalised muscle spasms, ataxia, increased respiratory and heart rates and terminal lateral recumbency. The illness generally lasts three to five days but durations of 12 to 30 hours have been observed. Laboratory investigations, including histopathology and serology suggest a viral aetiology, possibly an alphavirus of the equine encephalitis group.

When mice infected with the Venezuelan equine encephalomyelitis (VEE) virus were exposed to 2500 lux with a 12 h light: 12 h dark photoperiod, the serum levels of melatonin (MLT) remained constantly elevated. In mice exposed to 400 lux low levels of serum MLT were detected during the day and high levels during the night. An increase in the survival rate of the infected mice from 6 to 13 days after virus inoculation was also observed. The significant increment in the concentration of serum MLT produced by the high intensity light could be responsible for the longer survival rate of mice infected with the VEE virus.

In 2010, an increase in human encephalitis occurred in Panama that was associated with eastern and Venezuelan equine encephalitis viruses. This report establishes linkages with concomitant equine infections, suggesting a change in human pathogenicity. Eastern equine encephalitis (EEE) and Venezuelan equine encephalitis (VEE) viruses, alphaviruses that are members of the Togaviridae family, are important causes of febrile illness and encephalitis in the Americas. 1 The VEE virus occupies sylvatic, rodent–mosquito enzootic cycles that spill over to infect people; equine-adaptive or mosquito-adaptive mutations result in amplification, causing cause major epidemics. 2 On average, only 5 to 6 cases of human infection with the EEE virus are reported each year in North America. More cases occur in equids and other domesticated animals by means of spillover from avian–mosquito swamp cycles, with case fatality rates of more than 50% . . .

We screened 1,972 febrile patients from the Peruvian Amazon in 2020-2021 for Venezuelan equine encephalitis virus (VEEV). Neutralizing antibody detection rate was 3.9%; 2 patients were PCR positive. Genome identity compared to Peru VEEV subtype ID strains was 97.6%-98.1%. Evidence for purifying selection and ancestry ≈54 years ago corroborated VEEV endemicity.

Eastern equine encephalitis (EEE) virus (Togaviridae, Alphavirus) is a highly pathogenic mosquito-borne zoonosis that is responsible for occasional outbreaks of severe disease in humans and equines, resulting in high mortality and neurological impairment in most survivors. In the past, human disease outbreaks in the northeastern U.S. have occurred intermittently with no apparent pattern; however, during the last decade we have witnessed recurring annual emergence where EEE virus activity had been historically rare, and expansion into northern New England where the virus had been previously unknown. In the northeastern U.S., EEE virus is maintained in an enzootic cycle involving the ornithophagic mosquito, Culiseta melanura, and wild passerine (perching) birds in freshwater hardwood swamps. However, the identity of key avian species that serve as principal virus reservoir and amplification hosts has not been established. The efficiency with which pathogen transmission occurs within an avian community is largely determined by the relative reservoir competence of each species and by ecological factors that influence contact rates between these avian hosts and mosquito vectors. Contacts between vector mosquitoes and potential avian hosts may be directly quantified by analyzing the blood meal contents of field-collected specimens. We used PCR-based molecular methods and direct sequencing of the mitochondrial cytochrome b gene for profiling of blood meals in Cs. melanura, in an effort to quantify its feeding behavior on specific vertebrate hosts, and to infer epidemiologic implications in four historic EEE virus foci in the northeastern U.S. Avian point count surveys were conducted to determine spatiotemporal host community composition. Of 1,127 blood meals successfully identified to species level, >99% of blood meals were from 65 avian hosts in 27 families and 11 orders, and only seven were from mammalian hosts representing three species. We developed an empirically informed mathematical model for EEE virus transmission using Cs. melanura abundance and preferred and non-preferred avian hosts. To our knowledge this is the first mathematical model for EEE virus, a pathogen with many potential hosts, in the northeastern U.S. We measured strong feeding preferences for a number of avian species based on the proportion of mosquito blood meals identified from these bird species in relation to their observed frequencies. These included: American Robin, Tufted Titmouse, Common Grackle, Wood Thrush, Chipping Sparrow, Black-capped Chickadee, Northern Cardinal, and Warbling Vireo. We found that these bird species, most notably Wood Thrush, play a dominant role in supporting EEE virus amplification. It is also noteworthy that the competence of some of the aforementioned avian species for EEE virus has not been established. Our findings indicate that heterogeneity induced by mosquito host preference, is a key mediator of the epizootic transmission of vector-borne pathogens. Detailed knowledge of the vector-host interactions of mosquito populations in nature is essential for evaluating their vectorial capacity and for assessing the role of individual vertebrates as reservoir hosts involved in the maintenance and amplification of zoonotic agents of human diseases. Our study clarifies the host associations of Cs. melanura in four EEE virus foci in the northeastern U.S., identifies vector host preferences as the most important transmission parameter, and quantifies the contribution of preference-induced contact heterogeneity to enzootic transmission. Our study identifies Wood Thrush, American Robin and a few avian species that may serve as superspreaders of EEE virus. Our study elucidates spatiotemporal host species utilization by Cs. melanura in relation to avian host community. This research provides a basis to better understand the involvement of Cs. melanura and avian hosts in the transmission and ecology of EEE virus and the risk of human infection in virus foci.

Powassan virus (POWV) and Eastern equine encephalitis virus (EEEV) are regionally endemic arboviruses in the United States that can cause neuroinvasive disease and death. Recent identification of EEEV transmission through organ transplantation and POWV transmission through blood transfusion have increased concerns about infection risk. After historically high numbers of cases of both viruses were reported in 2019, we conducted a seroprevalence survey using blood donation samples from selected endemic counties. Specimens were screened for virus-specific neutralizing antibodies, and population seroprevalence was estimated using weights calibrated to county population census data. For POWV, median county seroprevalence in 4 states was 0.84%, ranging from 0% (95% CI 0%-2.28%) to 11.5% (95% CI 0.82%-40.9%). EEEV infection was identified in a single county (estimated seroprevalence 1.62% [95% CI 0.04%-8.75%]). Although seroprevalence estimates in sampled areas were generally low, additional investigation of higher-prevalence areas could inform risk for transmission from asymptomatic blood and organ donors.