The first C. pneumoniae strain was obtained in the 1960s in chick embryo yolk sac culture. After the development of cell culture methods, this initial strain was thought to be a member of the species C. psittaci. Subsequently, C. pneumoniae was firmly established as a new species that causes respiratory disease in humans and nonhuman species.

Properties of the Agent

 C. pneumoniae produces round, dense, glycogen-negative inclusions that are sulfonamide resistant, similar to C. psittaci (see Table 1). The EBs sometimes have a pear-shaped appearance. The genetic relatedness of C. pneumoniae isolates is greater than 95%. Only one serovar has been demonstrated.

Table1. Characteristics of the Chlamydiae

Clinical Findings

 Most infections with C. pneumoniae are asymptomatic or associated with mild illness, but severe disease has been reported.

There are no signs or symptoms that specifically differentiate C. pneumoniae infections from those caused by many other agents. Both upper and lower airway diseases occur. Pharyngitis is common. Sinusitis and otitis media may occur and be accompanied by lower airway disease. An atypical pneumonia similar to that caused by Mycoplasma pneumoniae is the primary recognized illness. The proportion of cases of community-acquired pneumonia caused by C. pneumoniae varies in the literature from 0% to 40%, but seems to be lower in more recent series (<5%).

Laboratory Diagnosis

 A. Smears

 Direct detection of EBs in clinical specimens using fluorescent antibody techniques is insensitive. Other stains do not effectively demonstrate the organism.

B. Culture Swab specimens of the pharynx should be put into a chlamydiae transport medium and placed at 4°C; C. pneumoniae is rapidly inactivated at room temperature. It grows poorly in cell culture, forming inclusions smaller than those formed by the other chlamydiae. C. pneumoniae grows better in HL and HEp-2 cells than in HeLa 229 or McCoy cells; the McCoy cells are widely used to culture C. trachomatis. The sensitivity of the culture is increased by incorporation of cycloheximide into the cell culture medium to inhibit the eukaryotic cell metabolism and by centrifugation of the inoculum onto the cell layer. Growth is better at 35°C than 37°C. After 3 days’ incubation, the cells are fixed and inclusions detected by fluorescent antibody staining with genus- or species-specific antibody or, preferably, with a C. pneumoniae–specific monoclonal antibody conjugated with fluorescein. Giemsa staining is insensitive, and the glycogen-negative inclusions do not stain with iodine. It is moderately difficult to grow C. pneumoniae—as evidenced by the number of isolates described compared with the incidence of infection.

C. Serology

 Serology using the MIF test is the most sensitive method for diagnosis of C. pneumoniae infection. The test is species specific and can detect IgG or IgM antibodies by using the appropriate reagents. Primary infection yields IgM antibody after about 3 weeks followed by IgG antibody at 6–8 weeks. In reinfection, the IgM response may be absent or minimal, and the IgG response occurs in 1–2 weeks. The following criteria have been suggested for the serologic diagnosis of C. pneumoniae infection: a single IgM titer of 1:16 or greater, a single IgG titer of 1:512 or greater, and a fourfold rise in either the IgM or IgG titers.

The CF test can be used, but it is group reacting, does not differentiate C. pneumoniae infection from psittacosis or LGV, and is less sensitive than the MIF test.

D. Nucleic Acid Amplification Methods

Many research and reference laboratories have attempted to develop molecular assays targeting genes such as the 16SrRNA gene and the ompA gene butprogress has been hampered by the lack of a reliable gold standard. However, BioFire Diagnostics, Inc. (Salt Lake City, UT) offers a nested multiplex PCR in a closed “lab-in-a-pouch” format for testing nasopharyngeal specimens. Such tests are needed so that the true contribution of C. pneumoniae to clinical disease can be fully determined.

Immunity

Little is known about active or potentially protective immunity. Prolonged infections can occur with C. pneumoniae, and asymptomatic carriage may be common.

Treatment

 C. pneumoniae is susceptible to the macrolides and tetracyclines and to some fluoroquinolones. Treatment with doxycycline, azithromycin, or clarithromycin, levofloxacin or moxifloxacin, appears to significantly benefit patients with C. pneumoniae infection, but there are only limited data on the efficacy of antibiotic treatment. Reports indicate that the symptoms may continue or recur after routine courses of therapy with erythromycin, doxycycline, or tetracycline, and these drugs should be given for 10- to 14-day courses.

Epidemiology

 Infection with C. pneumoniae is common. Worldwide, 30–50% of people have antibody to C. pneumoniae. Few young children have antibody, but after the age of 6–8 years, the prevalence of antibody increases through young adult hood. Infection is both endemic and epidemic, with multiple outbreaks attributed to C. pneumoniae. There is no known animal reservoir, and transmission is presumed to be from person to person, predominantly by the airborne route.

Lines of evidence suggesting that C. pneumoniae is associated with atherosclerotic coronary artery and cerebrovascular disease consist of seroepidemiologic studies, detection of C. pneumoniae in atherosclerotic tissues, cell culture studies, animal models, and trials of prevention using anti biotic agents. However, other studies have shown no association. The possible link between C. pneumoniae infection and coronary artery disease remains controversial.

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مواضيع ذات صلة

Chlamydia psittaci and Psittacosis

Chlamydia trachomatis Genital Infections and Inclusion Conjunctivitis

Trachoma

Coxiella burnetii

Ehrlichia and Anaplasma

Rickettsia and Orientia

Cultivation of Mycoplasma and Ureaplasma

Laboratory Diagnosis of Mycoplasma and Ureaplasma

Epidemiology and Pathogenesis of Mycoplasma and Ureaplasma

Tropheryma whipplei

Mycoplasma Pneumonia and Atypical Pneumonias

Leptospira and Leptospirosis