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HelpTest Code WNMS West Nile Virus Antibody, IgM, Serum
Reporting Name
West Nile Virus Ab, IgM, SUseful For
Detection of IgM antibodies in West Nile virus infections
Method Name
Only orderable as part of a profile. For more information see WNS / West Nile Virus Antibody, IgG and IgM, Serum.
Enzyme-Linked Immunosorbent Assay (ELISA)
Performing Laboratory
Mayo Clinic Laboratories in Rochester
Specimen Type
SerumSpecimen Required
Only orderable as part of a profile. For more information see WNS / West Nile Virus Antibody, IgG and IgM, Serum.
Collection Container/Tube:
Preferred: Serum gel
Acceptable: Red top
Submission Container/Tube: Plastic vial
Specimen Volume: 0.5 mL
Collection Instructions: Centrifuge and aliquot serum into a plastic vial.
Specimen Minimum Volume
0.4 mL
Specimen Stability Information
| Specimen Type | Temperature | Time | Special Container |
|---|---|---|---|
| Serum | Refrigerated (preferred) | 14 days | |
| Frozen | 14 days |
Reject Due To
| Gross hemolysis | Reject |
| Gross lipemia | Reject |
| Gross icterus | Reject |
| Heat inactivated specimen | Reject |
Reference Values
Only orderable as part of a profile. For more information see WNS / West Nile Virus Antibody, IgG and IgM, Serum.
Negative
Reference values apply to all ages
Day(s) Performed
Monday, Wednesday, Friday
CPT Code Information
86788
LOINC Code Information
| Test ID | Test Order Name | Order LOINC Value |
|---|---|---|
| WNMS | West Nile Virus Ab, IgM, S | 29567-5 |
| Result ID | Test Result Name | Result LOINC Value |
|---|---|---|
| WNMS | West Nile Virus Ab, IgM, S | 29567-5 |
Test Classification
This test has been cleared, approved, or is exempt by the US Food and Drug Administration and is used per manufacturer's instructions. Performance characteristics were verified by Mayo Clinic in a manner consistent with CLIA requirements.Clinical Information
West Nile virus (WNV) is a mosquito-borne flavivirus (single-stranded RNA) that primarily infects birds and can also infect humans and horses. WNV was first isolated in 1937 from an infected person in the West Nile district of Uganda. Until the viral infection was recognized in 1999 in birds in New York City, WNV was found only in the Eastern Hemisphere, with wide distribution in Africa, Asia, the Middle East, and Europe.(1-3) Most recently, in 2012, a total of 5674 cases of WNV were reported to the Centers for Disease Control and Prevention, among which 2873 (51%) were classified as neuroinvasive disease (eg, meningitis or encephalitis) and 286 (5%) cases resulted in death.(2)
Most people who are infected with WNV will not develop clinical signs of illness. It is estimated that about 20% of those who become infected will develop West Nile fever with mild symptoms, including fever, headache, myalgia, and occasionally a skin rash on the trunk of the body. Case fatality rates among patients hospitalized during recent outbreaks have ranged from 4% to 14%. Advanced age is the most important risk factor for death, and patients older than 70 years of age are at particularly high risk.(1)
Laboratory diagnosis is best achieved by demonstration of specific IgG and IgM class antibodies in serum specimens. Polymerase chain reaction (PCR) tests (WNVS / West Nile Virus, RNA, PCR, Molecular Detection, PCR, Serum) can detect WNV RNA in serum specimens from patients with recent WNV infection (ie, 3-5 days following infection) when specific antibodies to the virus are not yet present. However, the likelihood of detection is relatively low as the sensitivity of PCR detection is approximately 55% in cerebrospinal fluid and approximately 10% in blood from patients with known WNV infection.
Interpretation
Presence of specific IgM-class antibodies in a serum specimen is consistent with acute-phase infection with West Nile virus (WNV). By the 8th day of illness, most infected persons will have detectable serum IgM antibody to WNV; in most cases it will be detectable for at least 1 to 2 months following disease resolution and, in some cases, will be detectable for 12 months or longer.
The absence of IgM antibodies to WNV is consistent with lack of acute-phase infection with this virus. Specimens collected too early in the acute phase (eg, before 8-10 days postinfection) may be negative for IgM-specific antibodies to WNV. If WNV is suspected, a second specimen collected approximately 14 days postinfection should be tested.
In the very early stages of WNV infection, IgM may be detectable in cerebrospinal fluid before it becomes detectable in serum.
Cautions
Test results should be used in conjunction with a clinical evaluation and other available diagnostic procedures.
The significance of negative test results in immunosuppressed patients is uncertain.
Positive test results may not be valid in persons who have received blood transfusions or other blood products within the past several months.
False-negative results due to competition by high levels of IgG, while theoretically possible, have not been observed.
False-positive results may occur in persons vaccinated for flaviviruses (eg, yellow fever, Japanese encephalitis, dengue).
False-positive results may occur in patients infected with other arboviruses, including flaviviruses (eg, dengue virus) and alphaviruses (eg, LaCrosse [California] Encephalitis virus, Eastern or Western Equine Encephalitis virus, St. Louis virus) and in persons previously infected with West Nile virus (WNV). Because closely related arboviruses exhibit serologic cross-reactivity, it sometimes may be epidemiologically important to attempt to pinpoint the infecting virus by conducting cross-neutralization tests using an appropriate battery of closely related viruses.
WNV antibody results for cerebrospinal fluid (CSF) should be interpreted with caution. Complicating factors include low antibody levels found in CSF, passive transfer of antibody from blood, and contamination via a traumatic lumbar puncture.
Clinical Reference
1. Petersen LR, Marfin AA. West Nile Virus: a primer for the clinician. Ann Intern Med. 2002;137(3):173-179
2. Centers for Disease Control and Prevention (CDC). West Nile virus and other arboviral diseases--United States, 2012. MMWR Morb Mortal Wkly Rep. 2013;62(25):513-517
3. Brinton MA. The molecular biology of West Nile Virus. a new invader of the western hemisphere. Ann Rev Microbiol. 2002;56:371-402
4. Centers for Disease Control and Prevention (CDC). Provisional surveillance summary of the West Nile virus epidemic--United States, January-November 2002. MMWR Morb Mortal Wkly Rep. 2002;51(50):1129-1133
5. Centers for Disease Control and Prevention (CDC). Investigations of West Nile virus infections in recipients of blood transfusions. MMWR Morb Mortal Wkly Rep. 2002;51(43):973-974
Method Description
Polystyrene microwells are coated with the antihuman antibody specific for IgM (mu-chain). Diluted serum specimens and controls are incubated in the wells. The IgM present in the specimen binds to the antihuman antibody (IgM specific) in the wells. Nonspecific reactants are removed by washing. WNV antigen is then added to the wells and incubated. If anti-WNV IgM is present in the specimen, the WNV antigen binds to the anti-WNV in the well. Unbound WNV antigen is then removed by washing the well. Mouse anti-flavivirus conjugated with horseradish peroxidase (HRPO) is then added to the wells and incubated. If WNV antigen has been retained in the well by the anti-flavivirus in the specimen, the mouse anti-flavivirus:HRPO binds to WNV antigen in the wells. Excess conjugate is removed by washing. Enzyme substrate and chromogen are added, and the color is allowed to develop. After adding the Stop reagent, the resultant color change is quantified by a spectrophotometric reading of optical density (OD) that is directly proportional to the amount of antigen-specific IgM present in the specimen. Specimen OD readings are compared with reference cutoff OD readings to determine results.(Package insert: West Nile Virus IgM Capture DxSelect. Focus Diagnostics; 05/08/2018)