J Med Entomol
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Historical Article
Aedes (Stegomyia) aegypti in the continental United States: a vector at the cool margin of its geographic range.
After more than a half century without recognized local dengue outbreaks in the continental United States, there were recent outbreaks of autochthonous dengue in the southern parts of Texas (2004-2005) and Florida (2009-2011). This dengue reemergence has provoked interest in the extent of the future threat posed by the yellow fever mosquito, Aedes (Stegomyia) aegypti (L.), the primary vector of dengue and yellow fever viruses in urban settings, to human health in the continental United States. Ae. aegypti is an intriguing example of a vector species that not only occurs in the southernmost portions of the eastern United States today but also is incriminated as the likely primary vector in historical outbreaks of yellow fever as far north as New York, Philadelphia, and Boston, from the 1690s to the 1820s. ⋯ This approach will require experimental studies and field surveys that focus specifically on climate conditions relevant to the continental United States. These studies also must include assessments of how the human landscape, particularly the impact of availability of larval developmental sites and the permissiveness of homes for mosquito intrusion, and the presence of other container-inhabiting mosquitoes that may compete with Ae. aegypti for larval habitat affects the ability of Ae. aegypti to establish and proliferate. Until we are armed with such knowledge, it is not possible to meaningfully assess the potential for climate warming to impact the proliferation potential for Ae. aegypti in the United States outside of the geographic areas where the mosquito already is firmly established, and even less so for dengue virus transmission and dengue disease in humans.
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The European spider Tegenaria agrestis (Walckenaer) (hobo spider) has been implicated as a spider of medical importance in the Pacific Northwest since its introduction in the late 1980s. Studies have indicated that the hobo spider causes necrotic tissue lesions through hemolytic venom or through the transfer of pathogenic bacteria introduced by its bite. Bacterial infections are often diagnosed as spider bites, in particular the pathogenic bacteria methicillin-resistant Staphylococcus aureus (MRSA). ⋯ We found 10 genera of ubiquitous bacteria on the exterior surface of the spiders. In addition, none of the spiders exposed to MRSA transferred this pathogen. Finally, the hemolytic venom assay corroborates previous studies that found hobo spider venom was not deleterious to vertebrate red blood cells.
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Sharp declines in human and animal cases of plague, caused by the bacterium Yersinia pestis (Yersin), have been observed when outbreaks coincide with hot weather. Failure of biofilm production, or blockage, to occur in the flea, as temperatures reach 30 degrees C has been suggested as an explanation for these declines. Recent work demonstrating efficient flea transmission during the first few days after fleas have taken an infectious blood meal, in the absence of blockage (e.g., early-phase transmission), however, has called this hypothesis into question. ⋯ In contrast, no transmission was observed in mice challenged by fleas held at 10 degrees C (per flea transmission efficiency estimates, 0-1.68%). These results suggest that declines in human and animal cases during hot weather are not related to changes in the abilities of X. cheopis fleas to transmit Y. pestis infections during the early-phase period. By contrast, transmission may be delayed or inhibited at low temperatures, indicating that epizootic spread of Y. pestis by X. cheopis via early-phase transmission is unlikely during colder periods of the year.