News Release

Tips from the Journals of the American Society for Microbiology

Peer-Reviewed Publication

American Society for Microbiology

Harmless bacteria may contribute to production of deadly toxin

The virulent E. coli O157:H7 bacteria could be enlisting the help of formerly harmless intestinal bacteria to cause some lethal side effects say researchers from the University of Cincinnati and Cincinnati Children's Hospital Medical Center. Their findings appear in the June 2003 issue of the journal Infection and Immunity.

E. coli O157:H7 bacteria are a common cause of gastrointestinal disease which in some cases can lead to hemolytic uremic syndrome (HUS), which results in acute kidney failure in children. Antibiotic treatment of the infection can trigger progression to HUS in some cases but not in others. The reason for this is not known, but the production of shiga toxin by the bacteria is believed to be involved.

In the study, the researchers found that E. coli O157:H7 bacteria, when killed by antibiotics, not only released shiga toxin, but also a bacteriophage, a virus that infects other bacteria, that contained the genetic code for production of the toxin. The phage would then infect the harmless E. coli bacteria that normally inhabit the intestines, causing them to produce more shiga toxin and more phage, which would infect more bacteria and continue the cycle.

(S. D. Gamage, J. E. Strasser, C. L. Chalk, A. A. Weiss. 2003. Nonpathogenic Escherichia coli can contribute to the production of Shiga toxin. Infection and Immunity, 71. 6: 3107-3115.)


Herpesvirus may cause lung disease

A herpesvirus may contribute to the development of a fatal lung disease say researchers from Vanderbilt University, Meharry Medical College, Duke University Medical Center, National Institutes of Health, and Emory University School of Medicine. Their findings appear in the June 2003 issue of the Journal of Clinical Microbiology.

Idiopathic Pulmonary Fibrosis (IPF) is a disease of inflammation that results in scarring, or fibrosis, of the lungs. In time, this fibrosis can build up to the point where the lungs are unable to provide oxygen to the tissues of the body. In studies of patients with IPF, the average survival rate has been found to be 4 to 6 years after diagnosis. The cause of IPF is currently unknown.

In the study, lung specimens from patients with IPF were tested against samples with other diseases for signs of infection with the herpesvirus. Researchers detected up to four different strains of the herpesvirus in thirty-two out of thirty-three subjects with IPF. Of the twenty-five controls, only nine showed positive signs of the virus.

"We have detected the DNA of four herpesviruses in the lungs of all but 1 of 33 unselected patients with familial or sporadic IPF, a frequency much greater than that for the lungs of the controls with other diseases," say the researchers. "Establishment of chronic pulmonary herpesvirus infection as the cause of IPF will require detection of a herpesvirus in the lungs before or at the beginning of the time of appearance of clinical manifestations in a large sample of untreated patients early in the course of their disease and demonstration that eradication of the viral infections stops the progression of lung fibrosis."

(Y. W. Tang, J. E. Johnson, P. J. Browning, R. A. Cruz-Gervis, A. Davis, B. S. Graham, K. L. Brigham, J. A. Oates Jr., J. E. Loyd, A. A. Stecenko. 2003. Herpesvirus DNA is consistently detected in lungs of patients with Idiopathic Pulmonary Fibrosis. Journal of Clinical Microbiology, 41. 6: 2633-2640.)

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