According to the study, the Enterobacter bacterium is part of the naturally occurring microbial flora of the mosquito’s gut and kills the parasite by producing reactive oxygen species (or free radical molecules). The study is published in the May 13 edition of Science.
“We’ve previously shown that the mosquito’s midgut bacteria can activate its immune system and thereby indirectly limit the development of the malaria parasite. In this study we show that certain bacteria can directly block the malaria parasite’s development through the production of free radicals that are detrimental to Plasmodium in the mosquito gut,” said George Dimopoulos, PhD, senior author of the study and associate professor at theW. Harry Feinstone Department of Molecular Microbiology and Immunology, and the Johns Hopkins Malaria Research Institute. “We are particularly excited about this discovery because it may explain why mosquitoes of the same species and strain sometimes differ in their resistance to the parasite, and we may also use this knowledge to develop novel methods to stop the spread of malaria. One biocontrol strategy may, for example, rely on the exposure of mosquitoes in the field to this natural bacterium, resulting in resistance to the malaria parasite. ”
Like humans, mosquitoes have a variety of bacteria in their digestive systems. For the study, the researchers isolated the Enterobacter bacterium from the midgut of Anopheles mosquitoes collected near the Johns Hopkins Malaria Research Institute at Macha, which is located in southern Zambia. About 25 percent of the mosquitoes collected contained the specific bacteria strain. Laboratory studies showed the bacterium inhibited the growth of Plasmodium up to 99 percent, both in the mosquito gut and in a test tube culture of the human malaria parasite. Higher doses of bacteria had a greater impact on Plasmodium growth.
Worldwide, malaria afflicts more than 225 million people. Each year, the disease kills nearly 800,000, many of whom are children living in Africa.
Authors of “Natural microbe-mediated refractorieness to Plasmodium infection in Anopheles gambiae” include Chris M. Cirmotich, Yuemei Dong, April M. Clayton, Simone L. Sandiford, and Jayme A. Souza-Neto of the Johns Hopkins Bloomberg School of Public Health and Musapa Mulenga of the Malaria Institute at Macha in Zambia.
The research was supported by the National Institutes of Health/National Institute of Allergy and Infectious Disease, and the Johns Hopkins Malaria Research Institute.
Tim Parsons | Newswise Science News
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