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American Journal of Epidemiology Advance Access originally published online on August 19, 2008
American Journal of Epidemiology 2008 168(8):976; doi:10.1093/aje/kwn226
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American Journal of Epidemiology © The Author 2008. Published by the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org.

LETTERS TO THE EDITOR

THE AUTHORS REPLY

Thomas Hjuler1, Gry Poulsen1, Jan Wohlfahrt1, Margit Kaltoft2, Robert J. Biggar1,3 and Mads Melbye1

1 Department of Epidemiological Research, Statens Serum Institut, 2300 Copenhagen S, Denmark
2 Department of Bacteriology, Mycology and Parasitology, Statens Serum Institut, 2300 Copenhagen S, Denmark
3 Viral Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892

(e-mail: tta{at}ssi.dk)

We thank Dr. Davis (1) for his interest in our study (2). Dr. Davis questions our interpretation of the results and states that genetics may well be critical, but only given exposure.

We previously reported that exposure to Streptococcus pneumoniae appears to be almost ubiquitous in Denmark (3). Most children appear to become infected in the first year of life, and those who escape infection will most likely acquire it soon thereafter (e.g., at a day-care center). Since everyone in Denmark is exposed early in life, one would suppose that invasive pneumococcal disease (IPD) would cluster within families if genetics were of great importance.

As we stressed in our article (2), analysis of national population-based data is not appropriate to determine whether genetic factors can be important within particular families. Elsewhere, we and others have reported strong associations between IPD and specific genetic conditions that result in structural or immunologic abnormalities (4–8). However, we feel confident that these genetic predispositions are too infrequent to play a major role in determining the risk of IPD at the population level. Thus, IPD risk in populations appears to be dominated by environmental exposures. For example, concurrent infections with other respiratory agents may establish a milieu in which S. pneumoniae infection can become established as an invasive condition (9).


   ACKNOWLEDGMENTS
 
Conflict of interest: none declared.


   References
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 References
 

  1. Davis R. Re: "Genetic susceptibility to severe infection in families with invasive pneumococcal disease." (Letter). Am J Epidemiol. (2008) 168(8):976.[Free Full Text]
  2. Hjuler T, Poulsen G, Wohlfahrt J, et al. Genetic susceptibility to severe infection in families with invasive pneumococcal disease. Am J Epidemiol. (2008) 167((7)):814–819.[Abstract/Free Full Text]
  3. Hjuler T, Wohlfahrt J, Simonsen J, et al. Perinatal and crowding-related risk factors for invasive pneumococcal disease in infants and young children: a population-based case control study. Clin Infect Dis. (2007) 44((8)):1051–1056.[CrossRef][Web of Science][Medline]
  4. Hjuler T, Wohlfahrt J, Staum Kaltoft M, et al. Risks of invasive pneumococcal disease in children with underlying chronic diseases. Pediatrics (2008) 122((1)):e26–e32.[Abstract/Free Full Text]
  5. Tamouza R, Neonato MG, Busson M, et al. Infectious complications in sickle cell disease are influenced by HLA class II alleles. Hum Immunol. (2002) 63((3)):194–199.[CrossRef][Web of Science][Medline]
  6. Kronborg G, Weis N, Madsen HO, et al. Variant mannose-binding lectin alleles are not associated with susceptibility to or outcome of invasive pneumococcal infection in randomly included patients. J Infect Dis. (2002) 185((10)):1517–1520.[CrossRef][Web of Science][Medline]
  7. Roy S, Knox K, Segal S, et al. MBL genotype and risk of invasive pneumococcal disease: a case-control study. Lancet (2002) 359((9317)):1569–1573.[CrossRef][Web of Science][Medline]
  8. Yee AM, Phan HM, Zuniga R, et al. Association between Fc{gamma}RIIa-R131 allotype and bacteremic pneumococcal pneumonia. Clin Infect Dis. (2000) 30((1)):25–28.[CrossRef][Web of Science][Medline]
  9. Stensballe L, Hjuler T, Andersen A, et al. Hospitalization for respiratory syncytial virus infection and invasive pneumococcal disease in Danish children aged <2 years: a population-based cohort study. Clin Infect Dis. (2008) 46((8)):1165–1171.[CrossRef][Web of Science][Medline]

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This Article
Right arrow Extract Freely available
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Right arrow All Versions of this Article:
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kwn226v1
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