MYCOPLASMA IGG IGM

Code
900.2800
Name
MYCOPLASMA IGG IGM
Category
None
Department
Send-Out
Start Date
Expiration Date
Synonyms
CPT Codes
86738 X2
Site
SBMF
Reference Test
44043
ATLAS Test Code

Specimen Information

Type

Gold, SST

Volume

0.5 ml

Transport Info

Centrifuge and immediately transfer serum to separate plastic tube
Refrigerated

Fasting Required?
False
Patient Instructions

Reference Range

See report

Methodology

Enzyme-Linked Immunosorbent Assay (ELISA)

Clinical Significance

Aid in the diagnosis of atypical pneumonia, which is a cause of community-acquired pneumonia.

Mycoplasma pneumoniae (Mp) (along with Chlamydia pneumoniae) is a common cause of community-acquired pneumonia in school-aged children and young adults, accounting for 10-15% of cases. A wide variety of additional etiologic agents can cause community-acquired pneumonia, including Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, influenza virus, the parainfluenza viruses, respiratory syncytial virus, adenovirus, Legionella pneumophila, and Mycobacterium tuberculosis. It is usually not possible to define the etiologic agent from epidemiologic and clinical features, and initial management in the ambulatory patient is empiric antimicrobial therapy without diagnostic evaluation. However, Mp, C. pneumoniae, the respiratory viruses, L. pneumophila, and M. tuberculosis do not respond to penicillin or cephalosporin therapy. It is appropriate, therefore, to initiate diagnostic evaluation on patients ill enough to require hospitalization or who worsen on initial empiric outpatient therapy. Mp, C. pneumoniae, and L. pneumophila all respond to treatment with erythromycin, clarithromycin, or azithromycin. A variety of complications from Mp infection can occur. These include erythema multiforme major, meningoencephalitis, anemia, thrombocytopenia, leukopenia, and myocarditis. Although it is not clear whether antimicrobial therapy will reduce the severity or shorten the duration of these complications; establishment of Mp as the etiologic agent can decrease unnecessary additional diagnostic studies. M. pneumoniae infections can be diagnosed by: • Presence of specific IgM antibody in a single specimen will lend support to the diagnosis of M. pneumoniae. A significant rise or fall in specific IgM values between acute and convalescent sera may confirm the diagnosis. • In the absence of specific IgM antibody and persistence of symptoms, it is recommended that testing for specific IgG antibody to M. pneumoniae on both acute and convalescent samples be performed. As there is no protective or immune level of IgG antibody, testing of a single sample is of little value. • Detection of the organism in infected respiratory secretions by culture. • Detection of the organism in infected respiratory secretions by PCR. Due to the difficulty in culturing mycoplasma, serological tests are often used to diagnose M. pneumoniae. Four types of antibody tests are commercially available: • Cold agglutinin titers, • Complement fixation (CF), • Indirect fluorescent antibody (IFA) for IgG and IgM antibodies, • Enzyme immunoassay (EIA) for IgG and IgM antibodies. The cold agglutinin assay measures nonspecific IgM antibodies produced against the red cell "I" antigen during the course of M. pneumoniae infection. Although convenient and adapted to a bedside test, cold agglutinin antibodies are only approximately 75% sensitive and 75% specific for the diagnosis of acute M. pneumoniae infection. CF antibodies are the gold standard of comparison, but may require 3-4 weeks for significant rises to occur and cannot differentiate between specific IgG and IgM antibodies. Significant levels of CF antibodies to mycoplasma are found in the majority of culture-proven infections. However, many healthy individuals also have titers, so it becomes important that acute/convalescent samples be tested in parallel to confirm a diagnosis by the presence of the classical 4-fold titers. The IFA assay is adapted for both IgG and IgM antibodies and detects seroconversions earlier than the CF test. Species-specific antibodies to surface antigens are readily detected by immunofluorescence, even in the early stages of the disease. The EIA test is also adapted for both IgG and IgM antibodies. These assays are more objective and in most cases have a higher sensitivity and specificity than other methods. All antibody tests, however, have the major disadvantage of a 2-4 week delay from the onset of illness for a reliable diagnostic seroconversion. The presence of IgM antibodies in a single serum sample provides evidence of a current infection. A single determination is not diagnostic by itself, however. A negative result does not rule out current infection, since the specimen may have been collected before demonstrable antibody is present or after the antibody has decreased below detectable levels. Appearance of an IgM antibody response normally occurs 7-14 days after the onset of disease. Testing immediately post- exposure is of no value without a later convalescent specimen. While the presence of IgM antibodies suggests current or recurrent infection, low levels of IgM antibodies may occasionally persist for more than 12 months post-infection. Such a residual IgM response may be distinguished from early IgM response to infection by testing sera from patients 2-3 weeks later for changing levels of specific IgM antibodies. As there is no protective or immune level of IgG antibody, there are no established reference intervals for a single sample. If either the acute or convalescent sample is classified as IgM positive, IgG evaluation is not required. If neither sample is IgM positive and symptomatology is consistent with M. pneumoniae infection, acute and convalescent samples should be tested at the same time for IgG levels.

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