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 may be caused by St. Louis encephalitis virus. St. Louis encephalitis virus is closely related to the West Nile virus, Dengue virus, Murray Valley encephalitis virus, and Japanese encephalitis virus.[11]
Differentiating St. Louis encephalitis from other Diseases
St. Louis encephalitis must be differentiated from other diseases that cause nondescript symptoms, which include fever, headache, myalgia, and vomiting, such as meningitis, brain abscess, and demyelinating diseases.[19][20][21][22][23]
Epidemiology and Demographics
The incidence of St. Louis encephalitis is approximately 192 per 100,000 individuals worldwide. The majority of St. Louis encephalitis cases are reported in the United States. In the United States, the annual number of reported St. Louis encephalitis cases reported fluctuate widely, as a result of periodic epidemics. St. Louis encephalitis infection is thought to confer lifelong immunity against reinfection. The case fatality rate of St. Louis encephalitis ranges between 5-30%, with higher rates among the elderly, worldwide.[7] St. Louis encephalitis affects men and women equally. There is no racial predilection to the development of St. Louis encephalitis.[3] St. Louis encephalitis is a rare disease that tends to affect increased age and decreased age. Patients of all age groups may develop St. Louis encephalitis.[7][24]
Risk Factors
The most potent risk factor in the development of St. Louis encephalitis is old age. Common risk factors include immunosuppression, mosquito contact, and visits to Central and South America.[12][25][26]
Screening
According to the Centers for Disease Control and Prevention, there is insufficient evidence to recommend routine screening for St. Louis encephalitis.[12]
Natural History, Complications and Prognosis
If left untreated, approxomatly 40% of patients with St. Louis encephalitis may progress to develop fever, headache, or aseptic meningitis.[27] Common complications of St. Louis encephalitis include seizures, coma, disorientation, spastic paralysis, and hemorrhage.[28] Prognosis is generally poor. Approximately 5-15% of patients progress to mortality. Among patients who survive, approximately 50% suffer severe neurological, cognitive, or psychological deficits.[27][29][30]
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.
- ↑ 3.0 3.1 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.
- ↑ 7.0 7.1 7.2 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.
- ↑ 11.0 11.1 Flavivirus. SIB Swiss Institute of Bioinformatics. (2015) http://viralzone.expasy.org/viralzone/all_by_species/24.html Accessed on April 12, 2016
- ↑ 12.0 12.1 12.2 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.
- ↑ M.D. JE, Dolin R, Blaser MJ. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, Expert Consult Premium Edition. Saunders; 2014.
- ↑ Kennedy PG (2004). "Viral encephalitis: causes, differential diagnosis, and management". J Neurol Neurosurg Psychiatry. 75 Suppl 1: i10–5. PMC 1765650. PMID 14978145.
- ↑ Arboviral Infections (arthropod-borne encephalitis, eastern equine encephalitis, St. Louis encephalitis, California encephalitis, Powassan encephalitis, West Nile encephalitis). New York State Department of Health (2006). https://www.health.ny.gov/diseases/communicable/arboviral/fact_sheet.htm Accessed on February 23, 2016
- ↑ Eckstein C, Saidha S, Levy M (2012). "A differential diagnosis of central nervous system demyelination: beyond multiple sclerosis". J Neurol. 259 (5): 801–16. doi:10.1007/s00415-011-6240-5. PMID 21932127.
- ↑ De Kruijk JR, Twijnstra A, Leffers P (2001). "Diagnostic criteria and differential diagnosis of mild traumatic brain injury". Brain Inj. 15 (2): 99–106. doi:10.1080/026990501458335. PMID 11260760.
- ↑ Impact of the West Nile virus on the Natural History of St. Louis Encephalitis. (2008). http://scholarcommons.usf.edu/cgi/viewcontent.cgi?article=1437&context=etd Accessed on July 28, 2016.
- ↑ Bagdure D, Custer JW, Rao S, Messacar K, Dominguez S, Beam BW; et al. (2016). "Hospitalized Children With Encephalitis in the United States: A Pediatric Health Information System Database Study". Pediatr Neurol. doi:10.1016/j.pediatrneurol.2016.04.014. PMID 27353693.
- ↑ Day JF, Tabachnick WJ, Smartt CT (2015). "Factors That Influence the Transmission of West Nile Virus in Florida". J Med Entomol. 52 (5): 743–54. doi:10.1093/jme/tjv076. PMID 26336216.
- ↑ 27.0 27.1 Saint Louis Encephalitis. Centers for Disease Control, and Prevention (2010). https://www.cdc.gov/sle/technical/symptoms.html Accessed on July 29, 2016.
- ↑ Flavivirus encephalitis. Radiopaedia.org (2015). http://radiopaedia.org/articles/flavivirus-encephalitis Accessed on July 29, 2016.
- ↑ Yellow Fever. MedlinePlus (2015). https://medlineplus.gov/ency/article/001365.htm Accessed on July 29, 2016.
- ↑ Meningitis and Encephalitis Fact Sheet. National Institute of Neurological Disorders and Stroke (2016). http://www.ninds.nih.gov/disorders/encephalitis_meningitis/detail_encephalitis_meningitis.htm#3083_9 Accessed on July 29, 2016.