St. Louis encephalitis

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]

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.

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]

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]

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]

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]

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]

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]

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]

According to the Centers for Disease Control and Prevention, there is insufficient evidence to recommend routine screening for St. Louis encephalitis.^[12]

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.

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]

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]

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]

There are no electrocardiogram findings associated with St. Louis encephalitis.

There are no x ray findings associated with St. Louis encephalitis.

There are no CT findings associated with St. Louis encephalitis.^[17][18]

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]

There are no echocardiography or ultrasound findings associated with St. Louis encephalitis.^[21]

On other imaging findings, St. Louis encephalitis is characterized by generalized slowing without focal activity, a persistent vegetative state, and brain death.^[22]

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]

There is no treatment for St. Louis encephalitis; the mainstay of therapy for St. Louis encephalitis is supportive care.^[5][13]

Surgical intervention is not recommended for the management of St. Louis encephalitis.

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]

There are no secondary preventative measures available for St. Louis encephalitis.^[12]

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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]

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]

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. The previously unknown virus that caused the epidemic was isolated by the NIH team first in monkeys and then in white mice.^[4] There have been several outbreaks of St. Louis encephalitis which are summarized below:^{[1][2][3][5][6]}

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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]

St. Louis encephalitis may be classified according to location of the disease into 2 subtypes: systemic or encephalitic.^[1][2] 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.^[3]

St. Louis encephalitis may be classified according to location of the disease into 2 subtypes: systemic or encephalitic.^[1][2] 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.^[3]

Template:WS Template:WH

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]

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.^[1] 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.^[2]

St. Louis encephalitis virus is usually transmitted via mosquitos to the human host. St. Louis encephalitis virus contains positive-sense viral RNA; this RNA has its genome directly utilized as if it were mRNA, producing a single protein which is modified by host and viral proteins to form the various proteins needed for replication. The following table is a summary of the St. Louis encephalitis virus:^[3][4]

St. Louis encephalitis is contracted by the bite of an infected mosquito, primarily Culex pipiens, Culex tarsalis, or Culex nigripalpus. St. Louis encephalitis virus circulates between a mosquito vector and birds in the United States and South America.^[5] Transmission to humans requires mosquito species capable of creating a “bridge” between infected animals and uninfected humans; this occurs when humans become part of the enzootic cycle.^[1] 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 another human. There is no evidence of St. Louis encephalitis transmission from person to person.^[2]

St. Louis encephalitis virus is transmitted in the following pattern:^[3]

1. Attachment of the viral envelope protein E to host receptors mediates internalization into the host cell by clathrin-mediated endocytosis, or by apoptotic mimicry.
2. Fusion of virus membrane with host endosomal membrane. RNA genome is released into the cytoplasm.
3. The positive-sense ssRNA virus is translated into a polyprotein, which is cleaved into all structural and non-structural proteins necessary for RNA synthesis (replication and transcription).
4. Replication takes place at the surface of endoplasmic reticulum in cytoplasmic viral factories. A dsRNA genome is synthesized from the genomic ssRNA(+).
5. The dsRNA genome is transcribed/replicated, thereby providing viral mRNAs/new ssRNA(+) genomes.
6. Virus assembly occurs at the endoplasmic reticulum. The virion buds via the host endosomal sorting complexes required for transport (ESCRT), and is sent to the Golgi apparatus.
7. The prM protein is cleaved in the Golgi, thereby maturing the virion which is fusion competent.
8. New virions are released by exocytosis.

On microscopic histopathological analysis, the enveloped, spherical, and icosahedral-like virion shape are characteristic findings of St. Louis encephalitis.

The phylogeny, genetic variation, and recombination dynamics, and envelope protein genes St. Louis encephalitis virion have been sequenced.^[6][7][8][9]

Evolutionary evidence suggests that North American strains of St. Louis encephalitis virus belonged to a single clade.^[10] Furthermore, this study found an increase in the effective population size of the St. Louis encephalitis virus around the end of the 19th century that corresponds to the split of the latest North American clade; this finding suggests a northwards colonization of St. Louis encephalitis virus in the Americas. The virus is believed to have originated northern Mexico and migrated northwards with birds.

• 
  Culex tarsalis, one of the major vectors of St. Louis encephalitis virus.
• 
  Diagram illustrates the methods by which the arbovirus, St. Louis encephalitis virus, reproduces and amplifies itself in urban avian populations, and transmitted to dead end hosts including humans and other mammals by Culex spp. mosquitos. From Public Health Image Library (PHIL). ^[11]
• 
  title = Public Health

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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]

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.^[1]

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.^[1]

Template:WS Template:WH

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]

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.

St. Louis encephalitis must be differentiated from other diseases that cause fever, headache, myalgia, and vomiting, such as:^{[1][2][3][4][5]}

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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]

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.^[1] St. Louis encephalitis affects men and women equally. There is no racial predilection to the development of St. Louis encephalitis.^[2] Patients of all age groups may develop St. Louis encephalitis.^[1]

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 neuroinvasive disease cases reported fluctuates widely, as a result of periodic epidemics. St. Louis encephalitis infection is thought to confer lifelong immunity against reinfection.^[2] From 2004-2013, an average of 7 cases were reported annually.^[2]

The case fatality rate of St. Louis encephalitis ranges between 5-30%, with higher rates among the elderly, worldwide.^[1]

St. Louis encephalitis is a rare disease that tends to affect the elderly and patients <6 months of age. Patients of all age groups may develop St. Louis encephalitis.^[1]

There is no racial predilection to the development of St. Louis encephalitis.^[2]

St. Louis encephalitis affects men and women equally.^[2]

In temperate areas of the United States, St. Louis encephalitis primarily occurs in late summer or early fall. In Southern states, where the climate is milder, cases may occur year round. Although the geographic range of the virus extends from Canada to Argentina, human cases have almost exclusively occurred in the United States. The majority of cases have occurred in Eastern and Central states, where episodic urban-centered outbreaks have recurred since the 1930s. The largest epidemic of St. Louis encephalitis occurred in the United States in 1975, with nearly 2,000 cases reported, primarily from the Central states in the Ohio-Mississippi River Basin.^[3]

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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): Vishnu Vardhan Serla M.B.B.S. [3], Irfan Dotani [4]

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.

The most potent risk factor in the development of St. Louis encephalitis is old age. Other risk factors in the development of St. Louis encephalitis are:^[1][2][3]

• Immunosuppression
• Residing or visiting woodland areas
• Mosquito contact
• Bird contact
• Outdoor recreational activities
• Low income
• Travel to Central and South America
• Children
• Summer season

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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]

According to the Centers for Disease Control and Prevention, there is insufficient evidence to recommend routine screening for St. Louis encephalitis.

According to the Centers for Disease Control and Prevention, there is insufficient evidence to recommend routine screening for St. Louis encephalitis.^[1]

Template:WS Template:WH

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]

If left untreated, approxomatly 40% of patients with St. Louis encephalitis may progress to develop fever, headache, or aseptic meningitis.^[1] Common complications of St. Louis encephalitis include seizures, coma, disorientation, spastic paralysis, and hemorrhage.^[2] 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.^[1][3]

If left untreated, approxomatly 40% of patients with St. Louis encephalitis may progress to develop fever, headache, or aseptic meningitis.^[1]

Common complications of St. Louis encephalitis include:^[2]

• Seizures
• Coma
• Disorientation
• Spastic paralysis
• Hemorrhage

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.^[3][4]

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