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Arie van der Ende, PhD
Department of Medical Microbiology
Academic Medical Center
University of Amsterdam
1105 AZ, Amsterdam, Netherlands
We thank Tozzi et al for their response to our article. They agree with our idea that finding risk factors is an important step in prevention of infectious diseases by pointing at the unique immune status during pregnancy. As stated in our report, our study design knows some limitations that should be taken into account when interpreting our data. Although information on other environmental risk factors such as low economic status and contact with a patient with a meningococcal infection, as suggested by Tozzi et al, would be interesting to analyze, we believe that the nature of these data and reliability of the information would be insufficient and not very useful because of the retrospective design of the study.
As Tozzi et al suggest, we do not think that host risk factors for invasive bacterial disease (complement or deficiency, asplenia, immunodeficiency, variants of mannose-binding lectin [MBL]) are associated with pregnancy. Concerning their remark about the risk of confounding, these factors were excluded as relevant factors in our cohort of meningococcal patients. Of course, we do not have data on these matters in our control patients. Although we can never totally exclude contact with cases that were treated before becoming clinically evident, none of these cases were part of a small endemic cluster of meningococcal infection. Moreover, the presence of clustered pregnancy as a correlate seems rather odd to us. Finally, MBL variants may play a role in meningococcal disease, although this has been disputed by others.1,2 With respect to MBL variants, a separate analysis is currently being performed in pedigrees of our affected patient cohort. These data will be described extensively elsewhere.
Table 1 in our article gives an overview of reasons for hospitalization of controls. Eleven (13%) control patients were admitted because of infectious problems such as viral upper respiratory tract infection or pneumonia. We very much doubt that an increased risk of bacterial invasive disease in children of pregnant mothers transmitted by healthy carriers could be extrapolated to other bacteria (eg, Haemophilus influenzae type b or Streptococcus pneumoniae), considering the differences in carrier state, virulence, and mechanisms of invasion.
We agree with the authors that additional research on this topic is certainly relevant from a public health perspective. Confirmation of the assumption on carriage in mothers requires prospective studies. Despite the limitations of our study design, we think that our finding of an increased risk of meningococcal disease in children of pregnant mothers is interesting and therefore warrants additional research. Introduction of the meningococcal group C conjugate (MenC) vaccine in the Netherlands in September 2002 coincided with a strong reduction in the annual incidence of meningococcal disease and will make a study in mothers of affected children difficult to perform. At this moment, we are finishing a study on meningococcal carriage in pregnant and nonpregnant women. Analysis by serologic and multilocus sequence typing of the meningococcal strains obtained by pharyngeal swabs may give additional clues about hormonal influences on carriage rates.3,4
REFERENCES
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