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Tips from the journals of the American Society for Microbiology

August 20, 2010

New Compound May be Effective Against Chagas' Disease

A new compound may offer an effective drug candidate against the deadly tropical infection, Chagas' disease say researchers from Brazil. They report their findings in the August 2010 issue of the journal Antimicrobial Agents and Chemotherapy.

Chagas' disease is an infection caused by the parasite Trypanosoma cruzi and it affects approximately 18 million people and causes up to 50,000 deaths per year in tropical regions of the world. Human infection occurs through contact with contaminated feces or urine from infected insects, blood transfusions, contaminated food, and birth canal transmission. In areas where the disease is endemic, such as Mexico and Argentina, up to 30% of infected patients may develop cardiovascular and gastrointestinal problems.

The current drug used to treat Chagas' disease, benznidazole, is effective when treating acutely infected patients, however, it is less so when dealing with chronic infections and poses severe side effects in elderly patients.

In this study researchers identified a compound against T. cruzi and found it not only inhibited cell division, but it was also a very effective against T. cruzi even at very low doses. Additionally, it was 340 times more toxic to parasites than mammalian cells as well as more effective than benznidazole in all experiments.

"This compound was demonstrated to have a fast antiparasite effect, decreasing its viability and invasion capacity and leading to an apoptosis-like death," say the researchers. "Due to its high efficacy in vivo, it could be an alternative treatment for Chagas' disease."

(A.L. Matsuo, L.S. Silva, A.C. Torrecilhas, B.S. Pascoalino, T.C. Ramos, E.G. Rodrigues, S. Schenkman, A.C.F. Caires, L.R. Travassos. 2010. In vitro and in vivo trypanocidal effects of the cyclopalladated compound 7a, a drug candidate for treatment of Chagas' disease. Antimicrobial Agents and Chemotherapy, 54. 8: 3318-3325.)




Virus May Act as "Evolution-Proof" Biopesticide Against Malaria

A naturally occurring virus in mosquitoes may serve as a "late-life-acting" insecticide by killing older adult mosquitoes that are responsible for the bulk of malaria transmission. The researchers from Johns Hopkins University and the Johns Hopkins Malaria Research Institute, Baltimore, Maryland, detail their findings in the August 2010 issue of the Journal of Virology.

Malaria infects hundreds of thousands of people each year and is the cause of over a million deaths worldwide. Insecticides are one of the main strategies currently used to control malaria transmission, however, evolving resistance to such therapies continues to impact such efforts. "Late-life-acting" insecticides (LLAIs) are now being examined as a new approach for controlling malaria as they selectively kill older mosquitoes that spread the disease, while younger mosquitoes survive just long enough to reproduce.

"Reproduction allows for relaxation of evolutionary pressures that select for resistance to the agent," say the researchers. "If resistance alleles exert fitness costs, there are theoretical scenarios under which resistance is not expected to evolve, leading some to provocatively term LLAIs as 'evolution-proof'."

Densonucleosis viruses (or densoviruses [DNVs]) are naturally occurring parvoviruses that have been identified in multiple mosquito species. Some DNVs typically infect during the larval stage and are lethal, however, in this study researchers suggest that the Anopheles gambiae densovirus (AgDNV) may infect at low levels during early life and replicate to lethal levels at adult age. Analysis following infection showed that although AgDNV levels increased modestly during larval development they still replicated slower resulting in significantly decreased virus levels during this stage. Additionally, virus levels greatly increased in 7-to-10-day-old adults.

"Ultimately, we expect that a properly engineered LLAI AgDNV can be deployed in the field to significantly modulate malaria transmission," say the researchers.

(X. Ren, J.L. Rasgon. 2010. Potential for the Anopheles gambiae densonucleosis virus to act as an "evolution-proof" biopesticide. Journal of Virology, 84. 15: 7726-7729.)




Avian Influenza Virus May Persist on Feathers Fallen from Domestic Ducks

Highly pathogenic avian influenza virus (H5N1) may persist on feathers fallen from the bodies of infected domestic ducks and contribute to environmental contamination. Researchers from the National Institute of Animal Health, Tsukuba, Ibaraki, Japan report their findings in the August 2010 issue of the journal Applied and Environmental Microbiology.

Since the emergence of Asian avian influenza virus in 1997, it has spread to Europe, the Middle East and Africa causing significant mortality and economic loss in the poultry industry. Although the virus is mainly found in waterfowl and transmitted through fecal contamination in water, humans as well as other mammalian species have contracted the virus through close contact with infected birds.

A prior study showed that H5N1 could replicate in the skin cells of feathers and further suggested that those that drop off the body could potentially contaminate the environment. Here, researchers evaluated the environmental risk posed by contaminated feathers by inoculating domestic ducks with H5N1, collecting feathers, feces and drinking water three days following, and then storing them at 39 degrees and 68 degrees Fahrenheit for 360 days. Results showed that H5N1 persisted the longest in feathers at both temperatures.

"These results indicate that feathers detached from domestic ducks infected with highly pathogenic avian influenza virus (H5N1) can be a source of environmental contamination and may function as fomites with high viral loads in the environment," say the researchers.

(Y. Yamamoto, K. Nakamura, M. Yamada, M. Mase. 2010. Persistence of avian influenza virus (H5N1) in feathers detached from bodies of infected domestic ducks. Applied and Environmental Microbiology, 76. 16: 5496-5499.)
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American Society for Microbiology

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