American Journal of Epidemiology Vol. 154, No. 6 : 590
Copyright © 2001 by The Johns Hopkins University School of Hygiene and Public Health
LETTERS TO THE EDITOR |
RE: "INCIDENCE OF GUILLAIN-BARRÉ SYNDROME FOLLOWING INFECTION WITH CAMPYLOBACTER JEJUNI"
Department of Biology and Program in Medical Sciences, Indiana University, Bloomington, IN 47405-6801
In their well-controlled study of Campylobacter jejuni-induced Guillain-Barré syndrome (GBS), McCarthy and Giesecke (1
) examined a Swedish cohort of 29,567 individuals with laboratory-confirmed C. jejuni infection. The authors noted that of 6,293 persons below age 20 years, no cases of GBS were found. Among 20,856 adults aged 20–59 years, the rate of GBS was 14 per 100,000, while in the set of 2,417 people over age 59 years, the rate was 248 per 100,000 (1).
A host factor in addition to age that might contribute to the risk of developing GBS as a complication of C. jejuni infection is gender. In a British group of 27 persons with C. jejuni-induced GBS, the ratio of men to women was 3.5:l, whereas in 76 GBS patients with no evidence of C. jejuni infection, the ratio was 1.5:1 (2).
Among persons of European descent, the rate of homozygosity for the iron-loading mutated gene of hereditary hemochromatosis is 300–500 per 100,000 (3). Iron loading begins in men in early adulthood; in women, because of menstruation and childbearing, it is delayed by a decade or two (4). The virulence and invasiveness of nearly all microbial pathogens are enhanced by excessive host levels of iron (5), and C. jejuni is no exception. For instance, in one study, iron-injected mice inoculated with C. jejuni developed severe mucoid diarrhea, while iron-normal mice remained healthy (6). Severe septicemic C. jejuni infections have been reported among iron-loaded humans because of thalassemia (7). Thus, it might be useful to compare levels of transferrin iron saturation and/or serum ferritin among C. jejuni patients who develop GBS with levels among persons who remain free of the neurologic complication.
References
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McCarthy N, Giesecke J. Incidence of Guillain-Barré syndrome following infection with Campylobacter jejuni. Am J Epidemiol 2001;153:610–14.
[Abstract/Free Full Text] -
Rees JH, Soudain SE, Gregson NA, et al. Campylobacter jejuni and Guillain-Barré syndrome. N Engl J Med 1995;333:1374–9.
[Abstract/Free Full Text] - Halliday JW. Hemochromatosis and iron needs. Nutr Rev 1998;56(suppl):S30–7.
- Edwards CQ, Griffen LM, Goldgar D, et al. Prevalence of hemochromatosis among 11,065 presumably healthy blood donors. N Engl J Med 1988;318:1355–62.[Abstract]
- Weinberg ED. Iron loading and disease surveillance. Emerg Infect Dis 1999;5:346–52.[Web of Science][Medline]
- Stanfield JT, McCardell BA, Madden JM. Campylobacter diarrhea in an adult mouse model. Microb Pathog 1987;3:155–65.[Web of Science][Medline]
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Jackson N, Zaki M, Rahman AR, et al. Fatal Campylobacter jejuni infection in a patient splenectomized for thalassemia. J Clin Pathol 1997;50:436–7.
[Abstract/Free Full Text]
THE AUTHORS REPLY
Department of Public Health Medicine, Oxfordshire Health Authority, Headington OX3 7LG, United Kingdom
Swedish Institute for Infectious Disease Control, SE-171 82 Solna, Sweden
We thank Dr. Weinberg for his observations (1) on our study (2). Weinberg highlights the possibility that host factors additional to those we mentioned may be important in determining the likelihood of Guillain-Barré syndrome (GBS) following Campylobacter jejuni infection. This is undoubtedly true. In addition to age and human lymphocyte antigen type, as mentioned in the article, many other host factors may be important.
Weinberg hypothesizes that increased severity of infection due to high iron loading may be one such factor, and he shows how this is compatible with the age distribution of cases in our study and the sex distribution in other published work. However, it is important that in considering this hypothesis, we do not assume that severe infection leads to GBS while subclinical infection does not. Although there are theoretical arguments that invasive infection may be more likely to result in GBS (3), empirical evidence on this issue is lacking. Our study was confined to reported cases and so undoubtedly represented a more severe spectrum of infection than average, but it did not show a high incidence of subsequent GBS. We do not have information with which to assess whether infection was more severe among persons who subsequently developed GBS. Other investigators have detected evidence for recent C. jejuni infection among GBS cases with no recent history of gastroenteritis (4), which indicates that GBS can follow asymptomatic infection.
Thus, the more basic question of whether the severity of C. jejuni infection is associated with risk of GBS remains, in addition to the more detailed issues concerning the mechanisms, such as iron loading, by which this putative association might be mediated.
References
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Weinberg ED. Re: "Incidence of Guillain-Barré syndrome following infection with Campylobacter jejuni." (Letter). Am J Epidemiol 2001;154:590.
[Free Full Text] - McCarthy N, Giesecke J. Incidence of Guillain-Barré syndrome following infection with Campylobacter jejuni. Am J Epidemiol 2001;153:610–14.
- Blaser MJ. Epidemiologic and clinical features of Campylo-bacter jejuni infections. J Infect Dis 1997;176(suppl 2):S103–5.
- Rees JH, Soudain SE, Gregson NA, et al. Campylobacter jejuni infection and Guillain-Barré syndrome. N Engl J Med 1995;333:1374–9.
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  E. D. Weinberg, N. McCarthy, and J. Giesecke RE: "INCIDENCE OF GUILLAIN-BARRE SYNDROME FOLLOWING INFECTION WITH CAMPYLOBACTER JEJUNI" Am. J. Epidemiol., September 15, 2001; 154(6): 590 - 590. [Full Text] [PDF]
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