Two Distinct Patterns of Central Nervous System Complications Due toMycoplasma pneumoniaeInfection

Sir—We read with great interest the article by Sočan et al. [1] that appeared in a recent issue of the journal (electronic edition only). The authors described 13 patients with CNS complications due to Mycoplasma pneumoniae infection. Of these 13 patients, 9 had CSF samples that were positive for M. pneumoniae by culture and all 13 had CSF samples positive for M. pneumoniae by PCR. Most strikingly, the CSF samples from the 8 patients who had acute-onset CNS infection soon after respiratory symptoms appeared were all positive by culture, which was in sharp contrast to the finding that culture results were positive for only 1 of the 5 patients whose neurological symptoms began gradually and lasted longer. (However, the authors did not mention the exact number of days from the onset of respiratory symptoms to the onset of CNS infection.) This finding is quite important with respect to the etiology of CNS complications due to M. pneumoniae infection and is fairly consistent with our previous PCR findings [2], to which, unfortunately, Sočan and colleagues did not refer. In our study, using PCR, we detected M. pneumoniae DNA in CSF samples at a significantly higher rate for patients with early-onset encephalitis (defined as onset of CNS disease ⩽7 days after the onset of fever) than for patients with late-onset encephalitis (defined as onset of CNS disease ⩽8 days after the onset of fever) [2]. Recent reports from institutions other than ours have also supported this finding—describing both early-onset, PCRpositive cases [3–5] and late-onset, PCRnegative cases [6]. On the basis of these findings and those of Sočan et al. [1], it seems clear that there are 2 distinct patterns of CNS complications due to M. pneumoniae infection: early-onset encephalitis, in which the presence of the organism (which must be viable?) in the CNS is a prerequisite for the development of disease, and late-onset encephalitis, in which the presence of the organism in the CNS might not be essential when the disease occurs. We believe that Sočan and colleagues should have discussed this matter. In this context, it is rather unexpected that the CSF samples from the 4 patients with possible late-onset encephalitis were negative for M. pneumoniae by culture but still were positive by PCR. The authors also should have mentioned the sensitivity of the PCR system they used. In addition, the route of invasion of the CNS by M. pneumoniae is a matter of concern. We have also reported that, when using PCR, hematogenous dissemination is possible [7]. It would be interesting to know whether Sočan and colleagues tested or will test serum samples from patients with CNS complications.