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Tips from the Journals of the American Society for Microbiology

Peer-Reviewed Publication

American Society for Microbiology

New Approach May Lead to Effective H5N1 Influenza A Virus Vaccine

Manipulating a previously identified protein may be the key to developing an effective H5N1 influenza A virus vaccine say researchers from the University of Wisconsin-Madison and the University of Tokyo. They report their findings in the March 2008 issue of the Journal of Virology.

Since its emergence in 1997, the highly pathogenic avian influenza virus (H5N1) has affected wild birds and poultry in more than 10 Asian countries as well as Europe and Africa. A total of 321 confirmed human cases have occurred since late 2003 resulting in 194 deaths and a fatality rate of approximately 60%. Although there are currently some antiviral drugs available for treatment of influenza virus infection, H5N1 has proven resistant to most, therefore emphasizing the need for an effective vaccine.

The influenza A virus M2 protein consists of three structural domains, one of which is a 54-amino acid cytoplasmic tail domain. In a previous study the researchers demonstrated that deleting the M2 cytoplasmic tail caused a growth defect in the H1N1 influenza virus, indicating that the M2 cytoplasmic tail plays a vital role in virus replication. In the current study they created an M2 tail mutant H5N1 virus, vaccinated mice with it and challenged the mice with a lethal dose of influenza virus. Results showed that the mice were protected from death suggesting that the virus could not replicate and could therefore be used as a vaccine.

“Here, we demonstrate that an M2 cytoplasmic tail deletion mutant protects mice from lethal challenge with a highly pathogenic H5N1 virus, suggesting the potential of M2 tail mutants as live attenuated vaccines against H5N1 influenza virus infection,” say the researchers.

(T. Watanabe, S. Watanabe, J. Hyun Kim, M. Hatta, Y. Kawaoka. 2008. Novel approach to the development of effective H5N1 influenza A virus vaccines: use of M2 cytoplasmic tail mutants. Journal of Virology, 82. 5: 2486-2492.)


Salmonella Strains in Humans Distinct from Animals

A new study suggests salmonella strains collected from human salamonellosis patients to be distinct from those of animal origin, a finding that could significantly impact the development of treatment methods for foodborne illnesses. The researchers report their findings in the March 2008 journal Applied and Environmental Microbiology.

Salmonella enterica, one of the most infectious foodborne pathogens inflicting humans today, is commonly transmitted through consumption of meat and food products that have been contaminated with animal waste. Currently over 2,300 types of S. enterica have been identified, and although useful epidemiologically, they provide limited information concerning bacterial diversity, evolutionary relatedness and pathogenicity. Virulence determinants and degree of pathogenicity in a particular animal host are not yet well understood.

In the study researchers tested the virulence capacities of 184 human and animal S. enterica isolates in mice. Results showed that all 21 serovar typhimurium isolates derived from animals were virulent in mice, while only 16 of 41 serovar typhimurium isolates collected from human salmonellosis patients were virulent. In contrast to all animal and human bacteremia samples tested, only 10 of 29 serovar typhimurium isolates from gastroenteritis patients were virulent. Lastly, among the serovar typhimurium isolates harboring virulent Salmonella, 6 of 31 from human salmonellosis patients were avirulent in mice, in direct contrast to the virulence exhibited by all the animal isolates studied.

“These studies suggest that Salmonella isolates derived from human salmonellosis patients are distinct from those of animal origin,” say the researchers. “The characterization of these bacterial strain variants may provide insight into their relative pathogenicities as well as into the development of treatment and prophylactic strategies for salmonellosis.”

(D.M. Heithoff, W.R. Shimp, P.W. Lau, G.Badie, E.Y. Enioutina, R.A. Daynes, B.A. Byrne, J.K. House, M.J. Mahan. 2008. Human Salmonella clinical isolates distinct from those of animal origin. Applied and Environmental Microbiology, 74. 6: 1757-1766.)


New Study Compares Antibiotic Resistance in Wild American Bison and Farm Cattle

The first ever study of antibiotic-resistant bacteria in free-living American bison finds resistance rates, while relatively low, are still higher than expected. The researchers from Kansas State University report their findings in the March 2008 issue of the journal Applied and Environmental Microbiology.

Currently, over 50% of antibiotic use in the United States is attributed to the animal industry. As antibiotic resistance continues to rise researchers have extensively studied the link between humans and farm animals, however little is known about the spread of antibiotic resistance in wild animal populations.

Enterococci are one of the most common organisms associated with nosocomial infections worldwide and are also considered a reservoir for acquisition and distribution of antibiotic resistant genes. In the study enterococci isolates were collected from an American bison (Bison bison) population on a native tall-grass prairie preserve in Kansas. Bison showed resistance to tetracycline and erythromycin at rates of 8% and 4% which while higher than expected, still relatively low when compared to resistance rates of 42.9% and 12.7% in domestic cattle.

“This is the first study of antibiotic resistance in enterococci associated with American bison,” say the researchers. “The results provide us with an opportunity to gain insight into the origin of antibiotic resistance and the flow of genetic elements between environments.”

(J.F. Anderson, T.D. Parrish, M. Akhtar, L. Zurek, H. Hirt. 2008. Antibiotic resistance of enterococci in American bison (Bison bison) from a nature preserve compared to that of enterococci in pastured cattle. Applied and Environmental Microbiology, 74. 6: 1726-1730.)

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