St. Louis encephalitis overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Anthony Gallo, B.S. [2]; Contributor(s): Irfan Dotani [3], Vishnu Vardhan Serla M.B.B.S. [4]
Overview
St. Louis encephalitis is one of the most common mosquito-transmitted human pathogens in the United States. St. Louis encephalitis virus is a flavivirus that was first identified in St. Louis, Missouri in 1933. St. Louis encephalitis is diagnosed based on symptoms, physical findings, laboratory testing, and the possibility of exposure to infected mosquitoes. There is no specific treatment for St. Louis encephalitis; care is based on symptoms. Steps to prevent infection with St. Louis encephalitis virus include use of insect repellent, protective clothing, and staying indoors while mosquitoes are most active. While periodic St. Louis encephalitis epidemics have occurred only in the Midwest and Southeast, St. Louis encephalitis virus is distributed throughout the lower 48 states.
Historical Perspective
St. Louis encephalitis was first discovered by Dr. Joseph F. Bredeck, an American Director of Public Health for the City of St. Louis, in 1933 following a major outbreak in the city. During Autumn of 1933, over 1,000 cases were reported to local health departments and the National Institute of Health.[1][2][3] The previously unknown virus that caused the epidemic was isolated by the NIH team first in monkeys and then in white mice.[4][5][6]
Classification
St. Louis encephalitis may be classified according to location of the disease into 2 subtypes: systemic or encephalitic.[6][7] St. Louis encephalitis may also be classified according to neuroinvasiveness of the disease into two subtypes: neuroinvasive and non-neuroinvasive. St. Louis encephalitis virus is a Group IV positive-sense ssRNA virus within the Flaviviridae family of viruses, and the genus Flavivirus. St. Louis encephalitis is also known as an arbovirus, or an arthopod-borne virus.[8]
Pathophysiology
St. Louis encephalitis virus is usually transmitted via mosquitos (generally from the genus Culex) to the human host. St. Louis encephalitis virus contains positive-sense viral RNA. Transmission to humans requires mosquito species capable of creating a "bridge" between infected animals and uninfected humans. The incubation period is 5-15 days.[9] Humans are dead-end hosts for the virus, meaning there is an insufficient amount of St. Louis encephalitis virus in the blood stream to infect a mosquito; there is also no evidence of person to person spread.[10][11][12][13][14][15][16][17][18]
Causes
St. Louis encephalitis virus is a member of the genus Flavivirus, family Flaviviridae. Other similar diseases are West Nile virus, eastern equine encephalitis, western equine encephalitis, and La Crosse encephalitis. SLEV has a single-stranded, positive-sense RNA genome. The virus particles are spherical and have a diameter of 40 nm.
Differentiating St. Louis encephalitis from other Diseases
St. Louis encephalitis virus is a member of the genus Flavivirus, family Flaviviridae. Other similar diseases are West Nile virus, eastern equine encephalitis, western equine encephalitis, and La Crosse encephalitis.
Epidemiology and Demographics
4,651 cases have been reported throughout the United States from 1964 to 2005. Over this time period, the central and eastern states have reported the largest number of cases. In temperate areas of the United States, St. Louis encephalitis cases occur primarily in the late summer or early fall. In the southern states, where the climate is milder, St. Louis encephalitis can occur year round.
Risk Factors
All residents of and visitors to areas where SLEV activity has been identified are at risk of SLEV infection, particularly persons who engage in outdoor work and recreational activities and those living in low-income areas. SLEV infection is thought to confer life-long immunity against re-infection with SLEV. The elderly are at highest risk for severe disease and death.
Screening
Natural History, Complications and Prognosis
Mortality rate ranges from 5% to 30%, with higher rates among the elderly.
Diagnosis
In acute SLEV neuroinvasive disease cases, cerebrospinal fluid (CSF) examination shows a moderate (typically lymphocytic) pleocytosis. CSF protein is elevated in about a half to two-thirds of cases. Computed tomography (CT) brain scans are usually normal; electroencephalographic (EEG) results often show generalized slowing without focal activity.
SLEV is difficult to isolate from clinical samples and almost all isolates have come from brain tissue or CSF. In the absence of a sensitive and non-invasive virus detection method, serologic testing is the primary method for diagnosing SLEV infection. Combined with a consistent clinico-epidemiologic presentation, a rapid and accurate diagnosis of acute neuroinvasive SLEV disease can be made by the detection of SLEV-specific IgM antibody in serum or CSF. SLEV IgM tests are available commercially, in some state health department laboratories, and at CDC. A positive SLEV IgM test result should be confirmed by neutralizing antibody testing of acute- and convalescent-phase serum specimens at a state public health laboratory or CDC. To submit specimens for testing at CDC, contact your state health department. All SLEV disease cases should be reported to local public health authorities.
Diagnostic criteria
History and Symptoms
Less than 1% of St. Louis encephalitis virus (SLEV) infections are clinically apparent and the vast majority of infections remain undiagnosed. The incubation period for SLEV disease (the time from infected mosquito bite to onset of illness) ranges from 5 to 15 days. Onset of illness is usually abrupt, with fever, headache, dizziness, nausea, and malaise. Signs and symptoms intensify over a period of several days to a week. Some patients spontaneously recover after this period; others develop signs of central nervous system infections, including stiff neck, confusion, disorientation, dizziness, tremors and unsteadiness. Coma can develop in severe cases. The disease is generally milder in children than in older adults. About 40% of children and young adults with SLEV disease develop only fever and headache or aseptic meningitis; almost 90% of elderly persons with SLEV disease develop encephalitis. The overall case-fatality ratio is 5 to 15%. The risk of fatal disease also increases with age.
Physical Examination
Laboratory Findings
In acute SLEV neuroinvasive disease cases, cerebrospinal fluid (CSF) examination shows a moderate (typically lymphocytic) pleocytosis. CSF protein is elevated in about a half to two-thirds of cases.
Imaging Findings
CT
Computed tomography (CT) brain scans are usually normal.
Treatment
No vaccine against SLEV infection or specific antiviral treatment for clinical SLEV infections is available. Patients with suspected SLE should be evaluated by a healthcare provider, appropriate serologic and other diagnostic tests ordered, and supportive treatment provided.
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
References
- ↑ "ENCEPHALITIS IN ST. LOUIS". Am J Public Health Nations Health. 23 (10): 1058–60. 1933. PMC 1558319. PMID 18013846.
- ↑ Bredeck JF (1933). "The Story of the Epidemic of Encephalitis in St. Louis". Am J Public Health Nations Health. 23 (11): 1135–40. PMC 1558406. PMID 18013860.
- ↑ Epidemiologic Notes and Reports St. Louis Encephalitis -- Baytown and Houston, Texas. Centers for Disease Control and Prevention (1998). http://www.cdc.gov/mmwr/preview/mmwrhtml/00000817.htm Accessed July 28, 2016.
- ↑ Edward A. Beeman: Charles Armstrong, M.D.: A Biography; 2007; p. 305; also online here (PDF).
- ↑ SAINT LOUIS ENCEPHALITIS: A FLORIDA PROBLEM. Florida Medical Entomology Laboratory. http://mosquito.ifas.ufl.edu/SLE.htm Accessed on May 3, 2016.
- ↑ 6.0 6.1 Current Trends Update: St. Louis Encephalitis -- Florida and Texas, 1990. Centers for Disease Control and Prevention (1998). http://www.cdc.gov/mmwr/preview/mmwrhtml/00001813.htm Accessed on July 28, 2016.
- ↑ Saint Louis Encephalitis Virus (SLEV). Wisonsin Department of Health Services (2015). https://www.dhs.wisconsin.gov/arboviral/stlouisencephalitis.htm Accessed on July 28, 2016.
- ↑ Genetic variation of St. Louis encephalitis virus. Journal of General Virology (2008). http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696384/ Accessed on July 28, 2016.
- ↑ Saint Louis Encephalitis. Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Division of Vector-Borne Diseases. (2010) http://www.cdc.gov/sle/general/qa.html Accessed on May 3, 2016.
- ↑ Saint Louis Encephalitis Transmission. Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Division of Vector-Borne Diseases. (2010) http://www.cdc.gov/sle/technical/transmission.html Accessed on May 3, 2016.
- ↑ Flavivirus. SIB Swiss Institute of Bioinformatics. (2015) http://viralzone.expasy.org/viralzone/all_by_species/24.html Accessed on April 12, 2016
- ↑ Japanese encephalitis - Frequently Asked Questions. CDC Centers for Disease Control and Prevention. (2015) http://www.cdc.gov/japaneseencephalitis/qa/index.html Accessed on April 12, 2016
- ↑ The Management of Encephalitis: Clinical Practice Guidelines by the Infectious Diseases Society of America. http://www.idsociety.org/uploadedFiles/IDSA/Guidelines-Patient_Care/PDF_Library/Encephalitis.pdf Accessed on May 3, 2016.
- ↑ Kramer LD, Presser SB, Hardy JL, Jackson AO. (1997) Genotypic and phenotypic variation of selected Saint Louis encephalitis viral strains isolated in California. American Journal of Tropical Medicine and Hygiene 57(2):222–229. Abstract
- ↑ Kramer LD, Chandler LJ. (2001) Phylogenetic analysis of the envelope gene of St. Louis encephalitis virus. Archives of Virology 146(12):2341–2355. doi:10.1007/s007050170007.
- ↑ Twiddy SS, Holmes EC. (2003) The extent of homologous recombination in members of the genus Flavivirus. Journal of General Virology 84:429-440. doi:10.1099/vir.0.18660-0.
- ↑ May FJ, Li L, Zhang S, Guzman H, Beasley DW, Tesh RB, Higgs S, Raj P, Bueno R Jr, Randle Y, Chandler L, Barrett AD. (2008) Genetic variation of St. Louis encephalitis virus. Journal of General Virology 89(8):1901-1910. doi:10.1099/vir.0.2008/000190-0.
- ↑ Baillie GJ, Kolokotronis SO, Waltari E, Maffei JG, Kramer LD, Perkins SL. (2008) Phylogenetic and evolutionary analyses of St. Louis encephalitis virus genomes. Molecular Phylogenetics and Evolution 47(2):717-728. doi:10.1016/j.ympev.2008.02.015.