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(Stroke. 2006;37:756.)
© 2006 American Heart Association, Inc.
Editorial |
From the Department of Clinical Microbiology, Institute of Hygiene and Medical Microbiology, National Reference Laboratory for Chlamydia pneumoniae, Vienna General Hospital, Vienna, Austria.
Correspondence to Petra Apfalter, MD, DTMH (Lond), Department of Clinical Microbiology, Institute of Hygiene and Medical Microbiol-ogy, National Reference Laboratory for Chlamydia pneumoniae, Vienna General Hospital, Waehringer Guertel 18-20/5P, 1090 Vienna-AUSTRIA. E-mail petra.apfalter@meduniwien.ac.at
Key Words: Chlamydia pneumoniae serology stroke
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
There are now more arguments against than for a causal relationship between C. pneumoniae and atherosclerosis. Seroepidemiologic results are largely technique-dependent; PCR results show intra- and interlaboratory variability; methodological factors contribute to bias; and detection of C. pneumoniae fails when the specificity of the reaction is optimized. Immunohistochemical staining detects nonspecific compounds in atherosclerotic lesions, and secondary prevention trials are unsuccessful. The evidence for an association between a pathogen and a chronic disease should be based on concordance of evidence arising from different approaches applied by different groups, at different times, in different places, and under different circumstances. None of these conditions have been fulfilled in the case of C. pneumoniae and atherosclerosis.1
Citing the concluding paragraph of Margareta Ievens excellent review on Chlamydia pneumoniae and atherosclerosis, published in 2005 by the American Society of Micobiology (ASM) in their flagship journal for clinical microbiologists, the Journal of Clinical Microbiology, probably best summarizes the problems arising from diagnostic shortcomings of C pneumoniae, a microorganism that has been associated with well over 30 various diseases of markedly different pathologies and pathogenic mechanisms. Even though there is now "more evidence of no evidence" of the particular association on "C pneumoniae and atherosclerosis" than ever, every month articles continue to be published based on methods for which there is evidence that they are inadequate at various levels to define a patients C pneumoniae status. C pneumoniae serology is one of these methods.
In this issue of Stroke, Elkind et al2
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