St. Louis Encephalitis Antibody, IgG and IgM, Serum
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Onset is characterized by generalized malaise, fever, chilliness, headache, drowsiness, nausea, and sore throat or cough followed in 1 to 4 days by the 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. Areas of outbreaks since 1933 have involved the western United States, Texas, the Ohio-Mississippi Valley, and Florida. The vector of transmission is the mosquito. Peak incidence of St. Louis encephalitis is associated with summer and early autumn.
Aiding in the diagnosis of St. Louis encephalitis
In patients with this virus, IgG antibody is generally detectable within 1 to 3 weeks of onset, peaking within 1 to 2 months, and declining slowly thereafter.
IgM class antibody is also reliably detected within 1 to 3 weeks of onset, peaking and rapidly declining within 3 months.
Single serum specimen IgG > or =1:10 indicates exposure to the virus.
Results from a single serum specimen can differentiate early (acute) infection from past infection with immunity if IgM is positive (suggests acute infection).
A 4-fold or greater rise in IgG antibody titer in acute and convalescent sera indicate recent infection.
Infections with St. Louis encephalitis can occur at any age. The age distribution depends on the degree of exposure to the particular transmitting arthropod relating to age and sex, as well as the occupational, vocational, and recreational habits of the individuals. Once humans have been infected, the severity of the host response may be influenced by age: St. Louis encephalitis tends to produce the most severe clinical infections in older persons. Infection among males is primarily due to working conditions and sports activity taking place where the vector is present.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
All results must be correlated with clinical history and other data available to the attending physician.
Specimens drawn within the first 2 weeks after onset are variably negative for IgG antibody and should not be used to exclude the diagnosis of St. Louis encephalitis (SLE). If SLE is suspected, a second specimen should be drawn and tested 10 to 21 days later.
Since cross-reactivity with dengue fever does occur with SLE 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.
Usually, when an infection with an arbovirus is suspected, it is too late to isolate the virus or draw serum specimens to detect a rise of antibody titer.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
Clinical References Provides recommendations for further in-depth reading of a clinical nature
1. Gonzalez-Scarano F, Nathanson N: Bunyaviruses. In Fields Virology. Vol. 1. 2nd edition. Edited by BN Fields, DM Knipe. New York, Raven Press, 1990, pp 1195-1228
2. Donat JF, Hable-Rhodes KH, Groover RV, Smith TF: Etiology and outcome in 42 children with acute nonbacterial meningoencephalitis. Mayo Clin Proc 1980;55:156-160
3. Tsai TF: Arboviruses. In Manual of Clinical Microbiology. 7th edition. Edited by PR Murray, EJ Baron, MA Pfaller, et al. Washington, DC, American Society for Microbiology, 1999, pp 1107-1124
4. Calisher CH: Medically important arboviruses of the United States and Canada. Clin Microbiol Rev 1994;7:89-116