American Journal of Epidemiology Advance Access originally published online on November 9, 2006
American Journal of Epidemiology 2006 164(12):1253; doi:10.1093/aje/kwk081
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LETTERS TO THE EDITOR |
RE: "ANTIBIOTIC USE AND RISK OF MULTIPLE SCLEROSIS"
1 Department of Neurology, University of Sydney, Sydney, New South Wales 2006, Australia
2 Department of Medical Microbiology, University of Dundee, Dundee, Scotland DD1 4HN, United Kingdom
3 Department of Neurology, Tayside University Teaching Hospitals, Dundee, Scotland DD1 9SY, United Kingdom
(e-mail: jparratt{at}med.usyd.edu.au)
Alonso et al. (1) demonstrated that premorbid antibiotic treatment of patients with multiple sclerosis, active against the respiratory pathogen Chlamydophila (previously Chlamydia) pneumoniae, did not alter the risk of developing the disease. Although noted by the authors, it should be emphasized that lack of an association may reflect unaccounted pathologic factors.
The duration of appropriate antibiotic therapy was short (less than 21 days). Such treatment is unlikely to have an effect on chronic chlamydial infection, a postulated mode by which persistent inflammation induces central nervous system demyelination (2). In studies of respiratory disease, therapy of up to 12 months' duration did not alter conventional, serologic parameters of C. pneumoniae infection (3). Moreover, in vitro studies demonstrate that partial or short-term antibiotic therapy may induce chlamydial persistence (4). It therefore seems unlikely that brief courses of premorbid antibiotics would alter the risk of multiple sclerosis, if C. pneumoniae is a pathogen that induces demyelination.
In theory, a single exposure to C. pneumoniae could induce demyelination, the so-called "hit-run" hypothesis (5, p. 265). This would, however, be difficult to detect and consequently treat, as most infections present with nonspecific respiratory symptoms (6) and diagnostic testing is not usually undertaken, reducing the possibility of practitioners' prescribing the appropriate antibiotic during the salient time period.
C. pneumoniae is an atypical pathogen, and epidemiologic studies should account for this. Infection may be asymptomatic, not easily diagnosed, resistant to treatment, and prone to persistence. After a series of discrepant studies, it would appear that the only method by which to effectively investigate C. pneumoniae infection in multiple sclerosis is via prospective, antibiotic trials using bacterium-specific outcome measures.
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ACKNOWLEDGMENTS |
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Conflict of interest: none declared.
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References |
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 TOP References |
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- Alonso A, Jick SS, Jick H, et al. (2006) Antibiotic use and risk of multiple sclerosis. Am J Epidemiol 163:997–1002.
[Abstract/Free Full Text] - Sriram S, Stratton CW, Yao S, et al. (1999) Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis. Ann Neurol 46:6–14.[CrossRef][Web of Science][Medline]
- Branden E, Koyi H, Gnarpe J, et al. (2004) Intermittent azithromycin treatment for respiratory symptoms in patients with chronic Chlamydia pneumoniae infection. Scand J Infect Dis 36:811–16.[CrossRef][Web of Science][Medline]
- Hogan RJ, Mathews SA, Mukhopadhyay S, et al. (2004) Chlamydial persistence: beyond the biphasic paradigm. Infect Immun 72:1843–55.
[Free Full Text] - Scarisbrick IA and Rodriguez M. (2003) Hit-hit and hit-run: viruses in the playing field of multiple sclerosis. Curr Neurol Neurosci Rep 3:265–71.[Medline]
- Kuo CC, Jackson LA, Campbell LA, et al. (1995) Chlamydia pneumoniae (TWAR). Clin Microbiol Rev 8:451–61.[Abstract]
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