Chlamydia pneumonia
المؤلف:
Patricia M. Tille, PhD, MLS(ASCP)
المصدر:
Bailey & Scotts Diagnostic Microbiology
الجزء والصفحة:
13th Edition , p519-520
2025-09-15
315
The TWAR strain of C. pneumoniae was first isolated from the conjunctiva of a child in Taiwan in 1965. It was initially considered to be a psittacosis strain, because the inclusions produced in cell culture resembled those of C. psittaci. The Taiwan isolate (TW-183) is serologically related to a pharyngeal isolate (AR-39) isolated from a college student in the United States, and thus the new strain was called “TWAR,” an acronym for TW and AR (acute respiratory). Only one serotype of C. pneumoniae has been identified.
General Characteristics
C. pneumoniae is considered more homogeneous than either C. trachomatis or C. psittaci, because all isolates tested are immunologically similar because of the homogeneity of the MOMP. One significant difference between C. pneumoniae and the other chlamydiae is the pear-shaped appearance of its EB (Figure 1).
Fig1. Electron micrograph of C. pneumoniae (A) and C. trachomatis (B) (bar = 50.5 µm). E, Elementary body; om, outer membrane; R, reticulate body; arrowhead, small electron-dense bodies of undetermined function. (From Grayston JT, Kuo C-C, Campbell LA, and Wang S-P: Chlamydia pneumonia sp. nov. for Chlamydia sp. Strain TWAR. Int J Syst Bacteriol 39:88, 1989.)
Epidemiology and Pathogenesis
C. pneumoniae appears to solely be a human pathogen; no bird or animal reservoirs have been identified. It is transmitted from person to person by aerosolized drop lets via the respiratory route. The spread of infection is low. Antibody prevalence to C. pneumoniae starts to rise in school-aged children and reaches 30% to 45% in adolescents; more than half of adults in the United States and in other countries have C. pneumoniae antibody. Of interest, C. pneumoniae infections are both endemic and epidemic. Unfortunately, little is known about the pathogenesis of C. pneumoniae infections, but it is similar to C. trachomatis in inducing inflammation that contributes to tissue damage.
Spectrum of Disease
C. pneumoniae has been associated with pneumonia, bronchitis, pharyngitis, sinusitis, and a flulike illness. It causes 5% to 10% of cases of community-acquired pneumonia. Infection in young adults is usually mild to moderate; the microbiologic differential diagnosis primarily includes Mycoplasma pneumoniae. Severe pneumonia may occur in older or respiratory-compromised patients. Of note, asymptomatic infection or unrecognized, mildly symptomatic illnesses caused by C. pneumoniae are common. In addition, an association exists between C. pneumoniae infection and the development of asthmatic symptoms. Finally, an association between coronary artery disease and other atherosclerotic syndromes and C. pneumoniae infection has been suggested by seroepidemiologic studies and the demonstration of the organism in atheromatous plaques (yellow deposits within arteries containing cholesterol and other lipid material). Such an etiologic role by this organism is still under intense scrutiny. An excellent and comprehensive review of the literature related to whether C. pneumoniae is a cause of atherosclerosis was published in 2008 by Watson and Alp. Their research indicated that “it is difficult to attribute causality to a common infectious agent in a highly prevalent multifactorial disease.” They also stated that “C. pneumoniae is neither alone sufficient nor is it necessary to cause atherosclerosis or its clinical consequences in humans,” but they allowed for the possibility that treatment of C. pneumoniae may reduce the risk of atherosclerosis development.
Laboratory Diagnosis
In the laboratory, C. pneumoniae infections are diagnosed by cell culture, serology, or NAATs.
Direct Detection Methods. To date, assays to directly detect C. pneumoniae antigens have poor sensitivity. A variety of NAAT, including conventional and real-time PCR assays, have been developed to detect C. pneumoniae nucleic acid sequences in clinical specimens. Several of these amplification assays are commercially available. Using these methods, the organism has been detected in throat swabs and other specimens, such as nasopharyngeal, bronchoalveolar lavage fluids, and sputum.
Cultivation. Specimens for isolation are usually swabs of the oropharynx; techniques for isolation of the organism from sputum are unsatisfactory. Swabs should be placed into chlamydial transport media, transported on ice, and stored at 4° C; organisms are rapidly inactivated at room temperature or by rapid freezing or thawing. A cell culture procedure similar to that used for C. trachomatis but using the more sensitive HL or Hep-2 cell lines must be substituted for McCoy cells. Multiple blind passages might be necessary to improve recovery rates. C. pneumoniae species-specific monoclonal antibodies can detect the organism in cell culture.
Serodiagnosis. C. pneumoniae infection can also be diagnosed via serology. However, serologic testing has had variable success and questionable validity. Complement fixation using a genus-specific antigen has been used, but it is not specific for C. pneumoniae. A microimmunofluorescence test using C. pneumoniae elementary bodies as antigen is more reliable. However, availability is limited to specialized laboratories. A fourfold rise in either IgG or IgM is diagnostic, and a single IgM titer of 16 or greater or an IgG titer of 512 or greater suggests recent infection.
Antibiotic Susceptibility Testing and Therapy
Methods for susceptibility testing of C. pneumoniae have been largely adapted from those used for C. trachomatis. Similar to C. trachomatis, susceptibility testing is not practical for the clinical microbiology laboratory and, because methods are not yet standardized, the results can be influenced by several variables. Treatment with tetracycline, doxycycline, macrolides, fluroquinolones, and erythromycin has been successful.
Prevention
Little is known regarding effective ways to prevent C. pneumoniae infections beyond avoiding aerosolized drop lets from infected people.
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