Mycoplasma Pneumoniae

In 1898, Nocard and Roux (62) identified Mycoplasma as a cause of respiratory tract illness when they isolated a slowly growing organism from contagious bovine pleuropneumonia specimens. Later investigators referred to similar clinical isolates as pleuropneu-monia-like organisms. Some investigators thought these organisms should be considered viruses because the organisms were smaller than any known bacteria. The fact that the organisms could replicate extracellularly led to the correct conclusion that they were somewhat similar to bacterial L forms.Mycoplasma species belong to the class Mollicutes (soft skin), which comprises the smallest free-living microorganisms. M. pneumoniae is the most widely recognized pathogen of the 12 species of Mycoplasma found in humans (63). A receptor on the cell membrane allows the organism to attach to diverse cell types, such as respiratory tract epithelia and red blood cells. In high concentrations the organisms inhibit the ciliary action of the respiratory epithelia and cause cell necrosis. The resulting morbidity is the combined direct effect of cytotoxins produced by the organisms and the indirect effect of inflammatory responses to the presence of the organisms. Although antimicrobial agents influence the course of illness, they do not eliminate the nasopharyngeal carriage stage and, therefore, many persons are susceptible to a chronic form of the illness (64).

Horne et al. (65) first described a serological association betweenM. pneumoniae infection and atherosclerosis in a case-control study of498 patients undergoing coronary arteriography, of which 307 patients had diseased and 191 had healthy coronary arteries. The prevalence of CAD was significantly greater among patients with elevated IgA antibody titers toM. pneumoniae (OR: 2.2;p = 0.005) although not among those with elevated IgG titers. This association was further strengthened by an analysis of1517 patients with angio-graphically defined CAD who were followed clinically for 2.4 yr (66). The incidence of death or MI was significantly higher among patients with elevated IgA antibody titers to M. pneumoniae (26 vs 16%; adjustedp = 0.04; HR: 1.5; 95% CI: 1.1, 2.1). IgG titers to M. pneumoniae did not have any predictive value.

Although the evidence is not nearly so convincing as with C. pneumoniae, some studies have also reported the presence ofM. pneumoniae organisms within atherosclerotic plaque (67,68).

Year after transplant

Fig. 5. Graph of survival curves of patients undergoing cardiac transplant who are seropositive vs seronegative to CMV. (Adapted from ref. 164.)

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