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 a moderate infection of the central nervous system. 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 virus is closely related to Yellow fever virus, Dengue virus, West Nile virus, and Japanese encephalitis.[1] St. Louis encephalitis is also known as an arbovirus, or an arthropod-borne virus. St. Louis encephalitis is usually transmitted via mosquitoes to the human host. St. Louis encephalitis must be differentiated from other diseases that cause nondescript symptoms, which include fever, headache, and vomiting. Prognosis is generally poor. Approximately 5-30% of patients progress to mortality. Among patients who survive, approximately 50% suffer severe neurological, cognitive, and psychological deficits.[2] The diagnostic method of choice for St. Louis encephalitis is laboratory testing. Laboratory findings consistent with the diagnosis of leukocytosis, mild anemia, and hyponatremia. There is no treatment for St. Louis encephalitis; the mainstay of therapy is supportive care.
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.[3] The previously unknown virus that caused the epidemic was isolated by the NIH team first in monkeys and then in white mice.[4]
Classification
St. Louis encephalitis may be classified according to location of the disease into 2 subtypes: systemic or encephalitic.[5] 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.[6]
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. 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.[7]
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.[8]
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.[9]
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. St. Louis encephalitis affects men and women equally. There is no racial predilection to the development of St. Louis encephalitis. Patients of all age groups may develop St. Louis encephalitis.[10]
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.[11]
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.[13] Common complications of St. Louis encephalitis include seizures, coma, disorientation, spastic paralysis, and hemorrhage.[14] 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.
Diagnosis
History and Symptoms
If possible, a detailed and thorough history from the patient is necessary. Most patients infected with St. Louis encephalitis remain asymptomatic. Less than 1% of St. Louis encephalitis infections are clinically apparent and the vast majority of infections remain undiagnosed.[5] The incubation period for St. Louis encephalitis is usually 5-15 days. Common symptoms of St. Louis encephalitis include fever, headache, and dizziness.[15]
Physical Examination
Patients with St. Louis encephalitis are usually ill-appearing. Physical examination of patients with St. Louis encephalitis is usually remarkable for fever, convulsions, and hemorrhage.[13][15]
Laboratory Findings
The diagnostic method of choice for St. Louis encephalitis is laboratory testing. In St. Louis encephalitis, cerebrospinal fluid examination shows a moderate (typically lymphocytic) pleocytosis. 2/3 of patients with St. Louis encephalitis may have elevated concentration of CSF protein, which usually indicative of neuroinvasive disease. In the absence of a sensitive and non-invasive virus detection method, serologic testing is the primary method for diagnosing St. Louis encephalitis.[5][13][16]
Imaging Findings
Electrocardiogram
There are no electrocardiogram findings associated with St. Louis encephalitis.
X Ray
There are no x ray findings associated with St. Louis encephalitis.
CT
There are no CT findings associated with St. Louis encephalitis.[17][18]
MRI
MRI is the imaging modality of choice for St. Louis encephalitis. Findings of St. Louis encephalitis include substantia nigra edema, hemorrhage, and restricted diffusion in the basal ganglia and thalamus.[18][19][20]
Echocardiography or Ultrasound
There are no echocardiography or ultrasound findings associated with St. Louis encephalitis.[21]
EEG
On other imaging findings, St. Louis encephalitis is characterized by generalized slowing without focal activity, a persistent vegetative state, and brain death.[22]
Other Diagnostic Studies
Ultrasound-guided aspiration, via transdural insonation, has proven to show excellent abscess visualization when performed through a burr hole.
At the time of aspiration, specimens should be sent for Gram stain and routine aerobic and anaerobic cultures.[23]
Treatment
Medical Therapy
There is no treatment for St. Louis encephalitis; the mainstay of therapy for St. Louis encephalitis is supportive care.[5][13]
Surgery
Surgical intervention is not recommended for the management of St. Louis encephalitis.
Primary Prevention
There are no available vaccines against St. Louis encephalitis virus. Primary prevention strategies include the use of repellent, protective clothing, window screens, and the reduction of uncontrolled mosquito populations.[12][24]
Secondary Prevention
There are no secondary preventative measures available for St. Louis encephalitis.[12]
References
- ↑ Flavivirus. SIB Swiss Institute of Bioinformatics (2015). http://viralzone.expasy.org/viralzone/all_by_species/24.html Accessed on April 12, 2016
- ↑ Khandaker G, Zurynski Y, Buttery J, Marshall H, Richmond PC, Dale RC; et al. (2012). "Neurologic complications of influenza A(H1N1)pdm09: surveillance in 6 pediatric hospitals". Neurology. 79 (14): 1474–81. doi:10.1212/WNL.0b013e31826d5ea7. PMC 4098823. PMID 22993280.
- ↑ "ENCEPHALITIS IN ST. LOUIS". Am J Public Health Nations Health. 23 (10): 1058–60. 1933. PMC 1558319. PMID 18013846.
- ↑ Diaz LA, Nemeth NM, Bowen RA, Almiron WR, Contigiani MS (2011). "Comparison of argentinean saint louis encephalitis virus non-epidemic and epidemic strain infections in an avian model". PLoS Negl Trop Dis. 5 (5): e1177. doi:10.1371/journal.pntd.0001177. PMC 3101189. PMID 21629729.
- ↑ 5.0 5.1 5.2 5.3 Saint Louis Encephalitis Virus (SLEV). Wisonsin Department of Health Services (2015). https://www.dhs.wisconsin.gov/arboviral/stlouisencephalitis.htm Accessed on July 28, 2016.
- ↑ May FJ, Li L, Zhang S, Guzman H, Beasley DW, Tesh RB; et al. (2008). "Genetic variation of St. Louis encephalitis virus". J Gen Virol. 89 (Pt 8): 1901–10. doi:10.1099/vir.0.2008/000190-0. PMC 2696384. PMID 18632961.
- ↑ 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.
- ↑ Rastogi M, Sharma N, Singh SK (2016). "Flavivirus NS1: a multifaceted enigmatic viral protein". Virol J. 13 (1): 131. doi:10.1186/s12985-016-0590-7. PMID 27473856.
- ↑ Burgueño A, Spinsanti L, Díaz LA, Rivarola ME, Arbiza J, Contigiani M; et al. (2013). "Seroprevalence of St. Louis encephalitis virus and West Nile virus (Flavivirus, Flaviviridae) in horses, Uruguay". Biomed Res Int. 2013: 582957. doi:10.1155/2013/582957. PMC 3891745. PMID 24490165.
- ↑ Bell RL, Christensen B, Holguin A, Smith O (1981). "St. Louis encephalitis: a comparison of two epidemics in Harris county, Texas". Am J Public Health. 71 (2): 168–70. PMC 1619618. PMID 6109458.
- ↑ ST. LOUIS ENCEPHALITIS VIRUS. Public Health Agency of Canada(2011). http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/st-louis-encephalit-eng.php Accessed on August 1, 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
- ↑ 13.0 13.1 13.2 13.3 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.
- ↑ 15.0 15.1 Carballo C, Cabana M, Ledezma F, Pascual C, Cazes C, Mistchenko A; et al. (2016). "[Saint Louis encephalitis: case report]". Arch Argent Pediatr. 114 (4): e268–71. doi:10.5546/aap.2016.e268. PMID 27399031.
- ↑ Day JF, Shaman J (2009). "Severe winter freezes enhance St. Louis encephalitis virus amplification and epidemic transmission in peninsular Florida". J Med Entomol. 46 (6): 1498–506. PMID 19960704.
- ↑ Brain Imaging. American Journal of Neuroradiology(2016). http://www.ajnr.org/content/20/7/1281.full Accessed on July 27, 2016
- ↑ 18.0 18.1 Flavivirus encephalitis. Radiopaedia.org(2015).http://radiopaedia.org/articles/flavivirus-encephalitis Accessed on July 27, 2016
- ↑ St. Louis Encephalitis and the Substantia Nigra: MR Imaging Evaluation.(1999). http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.321.6020&rep=rep1&type=pdf Accessed on July 27, 2016
- ↑ Wasay M, Diaz-Arrastia R, Suss RA, Kojan S, Haq A, Burns D; et al. (2000). "St Louis encephalitis: a review of 11 cases in a 1995 Dallas, Tex, epidemic". Arch Neurol. 57 (1): 114–8. PMID 10634457.
- ↑ Mandell, Douglas, and Bennett's Principles and Practice of Infectious Disease. (2015). Accessed on July 27, 2016
- ↑ Zhao J, Vijay R, Zhao J, Gale M, Diamond MS, Perlman S (2016). "MAVS Expressed by Hematopoietic Cells Is Critical for Control of West Nile Virus Infection and Pathogenesis". J Virol. 90 (16): 7098–108. doi:10.1128/JVI.00707-16. PMID 27226371.
- ↑ John E. Bennett, Raphael Dolin, Martin J. Blaser "Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases" (2014): 1171.
- ↑ McAuley AJ, Torres M, Plante JA, Huang CY, Bente DA, Beasley DW (2016). "Recovery of West Nile Virus Envelope Protein Domain III Chimeras with Altered Antigenicity and Mouse Virulence". J Virol. 90 (9): 4757–70. doi:10.1128/JVI.02861-15. PMC 4836310. PMID 26912625.