Cutaneous leishmaniasis occurs in cycles that are related to temperature and the El Niņo Southern Oscillation. Luis Chaves and Mercedes Pascual from the University of Michigan studied monthly data, between 1991 and 2001, of the incidence of cutaneous leishmaniasis in Costa Rica.
Using mathematical models they were able to show that this disease has cycles of approximately 3 y that are related to temperature and indices of the El Niņo Southern Oscillation, including the sea surface temperature. Using such a model they could predict the incidence of cutaneous leishmaniasis up to 12 months ahead, with an accuracy of between 72% and 77%.
Cutaneous leishmaniasis is one of the main emerging diseases in the Americas. As in other vector-transmitted diseases, its transmission is sensitive to the environment, but this is the first study to look at the interannual patterns of cycling of the disease.
Citation: Chaves LF, Pascual M (2006) Climate cycles and forecasts of cutaneous leishmaniasis, a nonstationary vector-borne disease. PLoS Med 3(8): e295.
PLEASE ADD THE LINK TO THE PUBLISHED ARTICLE IN ONLINE VERSIONS OF YOUR REPORT: http://dx.doi.org/10.1371/journal.pmed.0030295
PRESS-ONLY PREVIEW OF THE ARTICLE: http://www.plos.org/press/plme-03-08-chaves.pdf
Related image for press use: http://www.plos.org/press/plme-03-08-chaves.jpg
· Caption: Cross-wavelet analysis for temperature and cases
University of Michigan
Ecology and Evolutionary Biology
830 North University
Natural Science (Kraus) Building
Ann Arbor, MI 48109 United States of America
THE FOLLOWING RESEARCH ARTICLE WILL ALSO BE PUBLISHED ONLINE:
Mycobacterium tuberculosis Induces Interleukin-32 Production through a Caspase- 1/IL-18/Interferon-γ-Dependent Mechanism
Synthesis of IL-32, a cell-associated proinflammatory cytokine, was promoted by Mycobacterium tuberculosis and M. bovis, suggesting a role in a role in inflammation and host defense against tuberculosis.
Citation: Netea MG, Azam T, Lewis EC, Joosten LAB, Wang M, et al. (2006) Mycobacterium tuberculosis induces interleukin-32 production through a caspase-1/IL-18/interferon-γ-dependent mechanism. PLoS Med 3(8): e277.
PLEASE ADD THE LINK TO THE PUBLISHED ARTICLE IN ONLINE VERSIONS OF YOUR REPORT: http://dx.doi.org/10.1371/journal.pmed.0030277
PRESS-ONLY PREVIEW OF THE ARTICLE: http://www.plos.org/press/plme-03-08-netea.pdf
Radboud University Nijmegen Medical Center
Department of Medicine
Geert Grooteplein 8
Nijmegen, 6500 HB Netherlands
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PLoS Medicine is an open access, freely available international medical journal. It publishes original research that enhances our understanding of human health and disease, together with commentary and analysis of important global health issues. For more information, visit http://www.plosmedicine.org
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