Published online December 31, 2007
PEDIATRICS Vol. 121 No. 1 January 2008, pp. 224 (doi:10.1542/peds.2007-2675)
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LETTER TO THE EDITOR

Mycoplasma pneumoniae Encephalitis and Cytokines

Mitsuo Narita, MD
Department of Pediatrics
Sapporo Tetsudo Hospital
Sapporo 060-0033, Japan

To the Editor.—

I read with great interest the article by Christie et al,1 which concisely described the clinical aspects of Mycoplasma pneumoniae encephalitis, and I have some opinions concerning pathogenesis. Biologically, M pneumoniae is not active in nature in the central nervous system (CNS) and has been believed to have no ability to directly damage neural cells. On the other hand, the organism has an ability to induce various kinds of cytokines to cause inflammation.2 In this context, I and co-workers have reported that interleukins 6 and 8, but not interferon {gamma} or tumor necrosis factor {alpha}, were frequently detected in the cerebrospinal fluid samples from patients with M pneumoniae encephalitis, and the former cytokines could be involved in the pathogenesis.3 A very small amount of the organism in the CNS is sufficient to induce the cytokines, and failure to detect the organism in the CNS does not necessarily lead to the hypothesis of autoantibodies as a principal cause of encephalitis. It may well be that the polymerase chain reaction sometimes fails to detect the small amount of organism, possibly delivered from the respiratory tract to the CNS by hematogenous dissemination.4 Moreover, M pneumoniae is not a virus and must be located unevenly within the CNS. Therefore, special attention must be paid to the sample processing for the polymerase chain reaction to achieve sufficient sensitivity.5 In addition, because the organism per se does not actively propagate in the CNS, macrolide antibiotics are necessary to eradicate the organism from the respiratory tract, but to or not to cross the blood-brain barrier may not be a significant problem. This must also be true for the autoantibodies theory. In this context, one of the future directions of research should be to investigate a therapeutic role of steroids as an immunomodulator.

REFERENCES

  1. Christie LJ, Honarmand S, Talkington DF, et al. Pediatric encephalitis: what is the role of Mycoplasma pneumoniae? Pediatrics. 2007;120 :305 –313[Abstract/Free Full Text]
  2. Yang J, Hooper WC, Phillips DJ, Talkington DF. Cytokines in Mycoplasma pneumoniae infections. Cytokine Growth Factor Rev. 2004;15 :157 –168[CrossRef][Web of Science][Medline]
  3. Narita M, Tanaka H, Togashi T, Abe S. Cytokines involved in CNS manifestations caused by Mycoplasma pneumoniae. Pediatr Neurol. 2005;33 :105 –109[CrossRef][Web of Science][Medline]
  4. Narita M, Matsuzono Y, Itakura O, Togashi T, Kikuta H. Survey of mycoplasmal bacteremia detected in children by polymerase chain reaction. Clin Infect Dis. 1996;23 :522 –525[Web of Science][Medline]
  5. Narita M, Matsuzono Y, Togashi T, Kajii N. DNA diagnosis of central nervous system infection by Mycoplasma pneumoniae. Pediatrics. 1992;90 :250 –253[Abstract/Free Full Text]
PEDIATRICS (ISSN 1098-4275). ©2008 by the American Academy of Pediatrics

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This Article
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