Posted by Vector and Vector-borne Disease Committee
August 10, 2022
Mary E. Danforth1, Robert E. Snyder1, Tina Feiszli1, Teal Bullick2, Sharon Messenger2, Carl Hanson2, Kerry Padgett1, Lark L. Coffey3, ChristopherM. Barker3, William K. Reisen3, Vicki L. Kramer1
1 California Department of Public Health, Vector-Borne Disease Section, Richmond and Sacramento, California, 2 California Department of Public Health, Viral and Rickettsial Disease Laboratory, Richmond, California, 3 Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, California, United States of America
PLoS Negl Trop Dis 16(8): e0010664. https://doi.org/10.1371/journal.pntd.0010664
Author summary. St. Louis encephalitis virus is a mosquito-borne virus that can cause human disease and is found in California, where it was detected every year from 1938 to 2003. However, after
West Nile virus arrived in 2003, St. Louis encephalitis virus was not detected again until 2015, when it re-emerged in Riverside County. From 2015 through 2020, St. Louis encephalitis virus has been detected in mosquito pools and sentinel chicken sera samples in 16 counties and a total of 24 human disease cases have been reported. However, during that same time-period, West Nile virus has been detected in 10 times as many mosquito pools and 60 times as many chicken sera samples across 58 counties and over 2,400 human disease cases have been reported. Although mosquitoes are tested routinely for both viruses, surveillance is not uniform throughout the state, and there has been a steady decline in the use of sentinel chickens. Since St. Louis encephalitis virus patient screening is dependent upon environmental detection, California may be underestimating the incidence of human disease due to this virus.
Note: Although WNV and SLEV cycle enzootically in basically the same vectors and avian hosts, historically SLEV in California never amplified to the levels documented for WNV. This may be because SLEV does not elicit elevated viremias in a wide diversity of avian hosts which limit transmission efficiency and therefore amplification. In addition, recently widespread WNV activity may have ‘immunized’ avian populations against SLEV as well as WNV, because previous infection with WNV produces sterilizing immunity against subsequent infection with SLEV.