Test Id : ARBOP

The following algorithms are available:

-Meningitis/Encephalitis Panel Algorithm

-Mosquito-borne Disease Laboratory Testing

This panel tests for 4 arboviruses; to test for a specific arbovirus, the following tests are individually orderable:

-CAVP / California Virus (La Crosse) IgG and IgM, Serum

-EEEP / Eastern Equine Encephalitis Antibody, IgG and IgM, Serum

-STLP / St. Louis Encephalitis Antibody, IgG and IgM, Serum

-WEEP / Western Equine Encephalitis Antibody, IgG and IgM, Serum

Supplies: Sarstedt Aliquot Tube 5 mL (T914)

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 plastic vial.

• Meningitis/Encephalitis Panel Algorithm
• Mosquito-borne Disease Laboratory Testing

If not ordering electronically, complete, print, and send Infectious Disease Serology Test Request (T916) with the specimen.

0.15 mL

Aiding the diagnosis of arboviral encephalitis (California [LaCrosse], St. Louis, Eastern equine, and Western equine encephalitis)

The following algorithms are available:

-Meningitis/Encephalitis Panel Algorithm

-Mosquito-borne Disease Laboratory Testing

California (LaCrosse) Virus:

California (LaCrosse) virus is a member of the Bunyaviridae family and is one of the arthropod-borne encephalitides. It is transmitted by various Aedes and Culex mosquitoes and is found in such intermediate hosts as the rabbit, squirrel, chipmunk, and field mouse. California meningoencephalitis is usually mild and occurs in late summer. Ninety percent of infections are seen in children less than 15 years, usually from rural areas. The incubation period is estimated to be 7 days, and acute illness lasts 10 days or less in most instances. Typically, the first symptoms are nonspecific, lasting 1 to 3 days, and are followed by the appearance of central nervous system (CNS) signs and symptoms such as stiff neck, lethargy, and seizures, which usually abate within 1 week. Symptomatic infection is almost never recognized in those over 18 years. The most important sequela of California virus encephalitis is epilepsy, which occurs in about 10% of children; almost always in patients who have had seizures during the acute illness. A few patients (estimated 2%) have persistent paresis. Learning disabilities or other objective cognitive deficits have been reported in a small proportion (no more than 2%) of patients. Learning performance and behavior of most recovered patients are not distinguishable from comparison groups in these same areas.

Eastern Equine Encephalitis:

Eastern equine encephalitis (EEE) is within the alphavirus group. It is a low prevalence cause of human disease in the eastern and Gulf Coast states. EEE is maintained by a cycle of mosquito/wild bird transmission, peaking in the summer and early fall, when humans may become an adventitious host. The most common clinically apparent manifestation is a mild undifferentiated febrile illness, usually with headache. CNS involvement is demonstrated in only a minority of infected individuals, it is more abrupt and more severe than with other arboviruses, with children being more susceptible to severe disease. Fatality rates are approximately 70%.

St. Louis Encephalitis:

Areas of outbreaks of St. Louis encephalitis (SLE) since 1933 have involved the western United States, Texas, the Ohio-Mississippi Valley, and Florida. The vector of transmission is the mosquito. Peak incidence occurs in summer and early autumn. Disease onset is characterized by generalized malaise, fever, chills, headache, drowsiness, nausea, and sore throat or cough, followed in 1 to 4 days by meningeal and neurologic signs. The severity of illness increases with advancing age; persons over 60 years have the highest frequency of encephalitis. Symptoms of irritability, sleeplessness, depression, memory loss, and headaches can last up to 3 years.

Western Equine Encephalitis:

The virus that causes Western equine encephalitis (WEE) is widely distributed throughout the United States and Canada; disease occurs almost exclusively in the western states and Canadian provinces. The relative absence of the disease in the eastern United States probably reflects a paucity of the vector mosquito species, Culex tarsalis, and possibly a lower pathogenicity of local virus strains. The disease usually begins suddenly with malaise, fever, and headache, often with nausea and vomiting. Vertigo, photophobia, sore throat, respiratory symptoms, abdominal pain, and myalgia are also common. Over a few days, the headache intensifies; drowsiness and restlessness may merge into a coma in severe cases. In infants and children, the onset may be more abrupt than for adults. WEE should be suspected in any case of febrile CNS disease from an endemic area. Infants are highly susceptible to CNS disease, with about 20% of cases under 1 year. There is an excess of males with WEE clinical encephalitis, averaging about twice the number of infections detected in females. After recovery from the acute disease, patients may require from several months to 2 years to overcome the fatigue, headache, and irritability. Infants and children are at higher risk of permanent brain damage after recovery than adults.

CALIFORNIA VIRUS (La CROSSE) ENCEPHALITIS ANTIBODY

IgG: <1:10

IgM: <1:10 

Reference values apply to all ages.

EASTERN EQUINE ENCEPHALITIS ANTIBODY

IgG: <1:10

IgM: <1:10 

Reference values apply to all ages.

ST. LOUIS ENCEPHALITIS ANTIBODY

IgG: <1:10

IgM: <1:10 

Reference values apply to all ages.

WESTERN EQUINE ENCEPHALITIS

IgG: <1:10

IgM: <1:10 

Reference values apply to all ages.

In patients infected with these or related viruses, IgM class antibody is reliably detected within 1 to 3 weeks of onset, peaking and rapidly declining within 3 months. Results from a single serum specimen can differentiate early (acute) infection from past infection with immunity if IgM is positive (suggests acute infection).

IgG antibody is generally detectable within 1 to 3 weeks of onset, peaking within 1 to 2 months, and declining slowly thereafter. A single serum specimen IgG of 1:10 or greater indicates exposure to the virus. A 4-fold or greater rise in IgG antibody titer in acute and convalescent sera indicates recent infection.

In the United States, it is unusual for any patient to show positive reactions to more than 1 of the arboviral antigens, although Western equine encephalitis and Eastern equine encephalitis antigens will show a noticeable cross-reactivity.

All results must be correlated with clinical history and other data available to the attending physician.

Specimens collected within the first 2 weeks after onset are variably negative for IgG antibody and should not be used to exclude the diagnosis of arboviral disease. If arboviral infection is suspected, a second specimen should be collected and tested 10 to 21 days later.

Since cross-reactivity with dengue fever virus does occur with St. Louis encephalitis antigens and, therefore, cannot be differentiated further. The specific virus responsible for such a titer may be deduced by the travel history of the patient, along with available medical and epidemiological data, unless the virus can be isolated.

Eastern and Western equine encephalitis viruses show some cross-reactivity; however, antibody response to the infecting virus is typically at least 8-fold higher.

1. Gonzalez-Scarano F, Nathanson N. Bunyaviruses. In: Fields BN, Knipe DM, eds. Fields Virology. Vol 1. 2nd ed. Raven Press; 1990:1195-1228

2. Donat JF, Rhodes KH, Groover RV, Smith TF. Etiology and outcome in 42 children with acute nonbacterial meningoencephalitis. Mayo Clin Proc. 1980;55(3):156-160

3. Tsai TF. Arboviruses. In: Murray PR, Baron EJ, Pfaller MA, et al, eds. Manual of Clinical Microbiology. 7th ed. American Society for Microbiology; 1999:1107-1124

4. Calisher CH. Medically important arboviruses of the United States and Canada. Clin Microbiol Rev. 1994;7(1):89-116

5. Dolin R. California encephalitis, hantavirus pulmonary syndrome, hantavirus hemorrhagic fever with renal syndrome, and bunyavirus hemorrhagic fevers. In: Bennett JE, Dolin R, Blaser MJ, eds. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 9th ed. Elsevier; 2020:2169-2176

The indirect immunofluorescent antibody (IFA) assay is a 2-stage "sandwich" procedure. In the first stage, the patient serum is diluted in Pretreatment Diluent for IgM and phosphate buffered saline (PBS) for IgG, added to appropriate slide wells in contact with the substrate, and incubated. Following incubation, the slide is washed in PBS, which removes unbound serum antibodies. In the second stage, each antigen well is overlaid with fluorescein-labeled antibody to IgM and IgG. The slide is incubated allowing antigen-antibody complexes to react with the fluorescein-labeled anti-IgM and anti-IgG. After the slide is washed, dried, and mounted, it is examined using fluorescence microscopy. Positive reactions appear as cells exhibiting bright apple-green cytoplasmic fluorescence against a background of red negative control cells. Semi-quantitative endpoint titers are obtained by testing serial dilutions of positive specimens.(Package inserts: Arbovirus IFA IgM and Arbovirus IFA IgG Instructions for Use; Focus Diagnostics; Rev. 03, 02/17/2023)

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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.

86651 x 2-California virus (La Crosse) encephalitis antibody, IgG and IgM

86652 x 2-Eastern equine encephalitis antibody, IgG and IgM

86653 x 2-St. Louis encephalitis antibody, IgG and IgM

86654 x 2-Western equine encephalitis antibody, IgG and IgM