West Nile Virus. By Frank Riusech

Transcription

1 West Nile Virus By Frank Riusech Disease Etiology: West Nile virus(wnv), genus, flavivirus is positive- stranded RNA arbovirus (arthropod- borne), belonging to the Flaviviridae family. Included in this family are other globally important mosquito borne pathogens; such as, dengue virus, yellow fever virus, Japanese encephalitis virus, and tick- borne encephalitis virus. [1],[2]. Disease Transmission: WNV is transmitted primarily by Culex mosquitoes, but other genera may also be vectors. In North America, WNV has been found in 59 different mosquito species with diverse ecology and behavior. However, less than 10 of these mosquito species are considered vectors. In 2001, 57% of mosquitoes that tested positive for WNV in the Northeast were Cx. pipiens, the common northern house mosquito. Culex pipiens is an efficient vector that feeds on birds and mammals. Cx. quinquefasciatus, the southern house mosquito, is the predominant vector in the South, and west of the Mississippi River, Cx. tarsalis, was the predominant vector.[1],[2],[3] Reservoirs : Mosquitoes become infected with WNV primarily through taking blood meals from infected birds. However, WNV may be passed from infected female mosquitoes to their eggs, resulting in infected offspring, often referred as vertical transmission. Vertical transmission is likely responsible for maintaining the virus over the winter in northern parts of the country. Birds are the most important amplifying hosts of WNV. Laboratory studies have demonstrated that song birds, shorebirds, owls, and hawks developed viremia levels that are sufficient to infect most feeding mosquitoes; however, pigeons, woodpeckers and ducks did not [2]. Field studies during and after WNV outbreaks in several areas of the United States have confirmed that house sparrows were abundant and frequently infected with WNV, characteristics that would allow them to serve as important amplifying hosts [2]. Besides birds, other vertebrates in the wild appear to be incompetent as amplifying hosts and thus don t seem to contribute to transmission of WNV.[2] Specific Microbial Characteristics: WNV is a small spherical icosahedral virus with a 50 nm diameter and a lipid envelope surrounding an icosahedral nucleocapsid. The capsid proteins are associated with the RNA genome (Figure 1).[5]

2 Specific Tests for Identification: DNA based tests: In humans the virus is present at very low levels in blood and tissue, so the only way to test for the presence of the virus is to amplify the genetic material (PCR). These nucleic acid based tests are much more sensitive than serological tests that detect antibodies, but take longer. [5]. Serological based tests: Following exposure to WNV, both IgM and IgG antibodies are produced. In most cases, IgM antibodies can be detected within 4 to 7 days after the initial exposure and may persist more than one year In comparison, anti- WNV IgG are reliably detected ~ 8 days after the onset of symptoms and they have a limited use in the initial diagnosis of WNV infection [71]. The plaque reduction neutralization test (PRNT) is still used as the reference assay for specific diagnosis of WNV infection.however, PRNT is a laborious test and must be carried out in a biosafety level 3 (BSL-3) facility as viable WNVviruses are used in this assay. For high-throughput screening, different ELISA methods (e.g. indirect IgG, IgM antibody-capture and blocking ELISA) have been developed over the last years. ELISAs have the advantage of being rapid, reproducible and less expensive than other methods. [4]. Diagnosis in humans: Diagnosis is generally accomplished by testing of serum or cerebrospinal fluid (CSF) to detect WNVspecific IgM antibodies. Immunoassays for WNV-specific IgM are available commercially and through state public health laboratories. Specific IgM antibodies are usually detectable 3 to 8 days after onset of illness and persist for as long as 90 days. Antibodies may not be detectable after the onset of symptoms so it s recommended to test after the 8 days. The presence of WNV-specific IgM in blood or CSF provides good evidence of recent infection but may also result from cross-reactive antibodies after infection with other flaviviruses. To avoid false positives, it s recommended to confirm by a neutralizing antibody test with a known acute and convalescent serum at a state public health laboratory or CDC.[6] Signs and symptoms of disease in humans: Most people (70-80%) are asymptomatic and about 1 in 5 people who are infected will develop a fever. Other symptoms include headache, body aches, joint pains, vomiting, diarrhea, or rash. Recovery from West Nile virus disease is usually complete, but fatigue and weakness can last for weeks or months. Less than 1% of people who are infected however will develop a serious neurologic illness such as encephalitis or meningitis.[6]

3 The symptoms of neurologic illness can include headache, high fever, neck stiffness, disorientation, coma, tremors, seizures, or paralysis. People with certain medical conditions, such as cancer, diabetes, hypertension and kidney disease are also at greater risk for serious illness. Recovery from severe disease may take several weeks or months. Some of the neurologic effects may be permanent. About 10 percent of people who develop neurologic infection due to West Nile virus will die. Historical information: WNV was first isolated from a patient from the West Nile district of Northern Uganda in 1937(index patient). In 1957, an outbreak of WNV occurred in Israel. This outbreak had neurologic manifestations and the first reports of such neurologic events among humans. Prior to this, neurologic illness had rarely been reported; however, during subsequent outbreaks, including France in 1962 and South Africa in 1974, patients developing meningitis or encephalitis was recognized. In 1999, the first cases in the Western Hemisphere were detected in New York City. Within a 3-year period, the virus expanded its range in North America from a 6-county area around metropolitan New York City to the West Coast of the United States, establishing itself in 44 states and the District of Columbia, as well as in five Canadian provinces.[4] Virulence factors: Differences that determine pathogenicity of WNV are mutations that lead to loss of envelope (E) protein glycosylation together with mutations in the nonstructural (NS) protein genes.[5] Control/Treatment: Unfortunately, no vaccine or specific antiviral treatments for West Nile virus infection are available. Overthe-counter pain relievers can be used to reduce fever and symptoms. In severe cases, patients often need to be hospitalized to receive supportive treatment, such as intravenous fluids, pain medication, and nursing care.[6] Prevention/ Vaccine info: Using insect repellents when you go outdoors is the best preventative for infection. Repellents containing DEET, picaridin, IR3535, and some oil of lemon eucalyptus and para-menthane-diol products provide longer-lasting protection. Current outbreaks / cases locally (with prevalence/incidence) : West Nile Virus Neuroinvasive Disease Incidence by State United States, 2013 (as of January 7, 2014)

4 This map shows the incidence of human West Nile virus neuroinvasive disease (e.g., meningitis, encephalitis, or acute flaccid paralysis) by state for 2013 with shading ranging from , , , and greater than 1.00 per 100,000 population.[1] Human West Nile Virus (West Nile Virus, WNV, WestNile) ICD ; ICD- 10 G93.3 Human West Nile Virus Cases in Texas, Year WN Fever WNND Fatalities Case Fatality Rate % % % % % % % % 2004 * NR % 2003 * NR % 2002 * NR % Total: % [7] References: [1] Centers for Disease Control and Prevention. West Nile Virus Homepage. Last updated, January 7, /1/2014 [2] Recent progress in West Nile virus diagnosis and vaccination Vet Res. 2012; 43(1): 16. Published online Mar 1, /2/2012 [3] Experimental Infection of North American Birds with the New York 1999 Strain of West Nile Virus. Emerg Infect Dis. Mar 2003; 9(3): [4] West Nile Virus: An Historical Overview 3/1/2014 [5]Genetic Determinants of Virulence in Pathogenic Lineage 2 West Nile Virus Strains. Last updated, January 7, /1/2014

5 [6] Prevention and Control. Last updated, January 7, /2/2014 [7] Texas Department of State Health Services. Last updated December 31, /1/2014