4.7 Article

Pubertal development predicts resistance to infection and reinfection with Schistosoma japonicum

Journal

CLINICAL INFECTIOUS DISEASES
Volume 42, Issue 12, Pages 1692-1698

Publisher

UNIV CHICAGO PRESS
DOI: 10.1086/504326

Keywords

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Funding

  1. NIAID NIH HHS [K23AI52125, R01AI48123] Funding Source: Medline

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Background. In communities where Schistosoma species are endemic, the prevalence and intensity of schistosomiasis is disproportionately high among children, compared with adults. This epidemiologic pattern is consistent with either the slow development of resistance or the requirement of host developmental changes for the expression of resistance. Methods. We enrolled 87 individuals aged 7-18 years who did not have Schistosoma japonicum infection and 641 individuals aged 7-30 years with S. japonicum infection, all of whom reside in 3 villages in Leyte, Philippines. At baseline, S. japonicum infection was assessed by Kato-Katz thick-smear stool examination, and the levels of the pubertal hormone dehydroepiandrosterone sulfate (DHEA-S) in serum were determined. Individuals with S. japonicum infection were treated with praziquantel, after which stool examination and DHEA-S level measurement were performed every 3 months for 18 months. Results. In cross-sectional analyses, the intensity of infection among individuals with high DHEA-S levels was 43% lower (28 eggs per g, n=243), compared with individuals with low DHEA-S levels (50 eggs per g, n=243), even after adjusting for age, sex, and village (p=.01). Following praziquantel treatment, increased DHEA-S levels were associated with resistance to reinfection (p=.006). The intensity of reinfection among individuals with high DHEA-S levels was 42% lower, compared with individuals with low DHEA-S levels, even after adjusting for age, baseline intensity of S. japonicum infection, village, sex and water contact (P <.001). Conclusions. Increased DHEA-S levels in serum, a marker for adrenal development, is associated with reduced S. japonicum infection and reinfection, even after adjusting for age and, by proxy, cumulative exposure. These data suggest that an intrinsic property of host pubertal development mediates, in part, the resistance to infection observed in older individuals.

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