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Abstract

The lack of IgM antibodies in our case patients demonstrates that they had suffered repeated mycoplasmal infections, which has been frequently observed in adults. Such infections show a more pronounced clinical symptomatic response and a higher inflammatory response than in primary events. As Narita et al. did in their investigations [2], we detected the DNA of M. pneumoniae in our case patients, but no viable mycoplasmal cells. Therefore, one can surmise that CNS infections are not caused by the microorganisms themselves but by an immense immune reaction or an autoimmune response evoked by very high levels of antibodies to M. pneumoniae.Repeated infections with M. pneumoniae can produce interferon, TNF-a, and interleukins, which may be associated with an inflammatory infection. This theory is favored by the fact that M. pneumoniae can trigger the production of cytokines in blood cells and in rat astrocytes [3]. Another possibility is an autoimmune reaction. This is suggested by the fact that M. pneumoniae is able to stimulate an immense B-cell activation, followed by an immense induction of cytokines and autoantibodies, which may lead to the CNS-infection symptoms [4].Altogether, the pathogenesis of CNS infections with M. pneumoniae is still unclear and needs further study. ReplySIR-We agree with Baxter that screening for Chlamydia trachomatis infection in a population among whom the prevalence is low may result in a greater proportion of tests with falsepositive results. However, we do not agree that a specificity of 99% is "pretty good." In fact, the specificity of DNA amplification tests such as PCR analysis is likely to be much higher, approaching 100%. If the test specificity for our sample was indeed "only" 99%, then nearly one-half of the 22 infections diagnosed in our sample would have been expected to be falsepositive results [1]. In fact, all of the 22 infections diagnosed by PCR assay in our study were confirmed by an alternate at university of winnipeg on August 11, 2015