Brown University News Bureau

The Brown University News Bureau

1998-1999 index

Distributed January 27, 1999
Contact: Scott Turner

Experimental antibiotic promptly kills drug-resistant bacteria in studies

New findings by Dr. Stephen Zinner and colleagues at Brown University suggest that the compound moxifloxacin is a potential treatment against a range of drug-resistant infectious organisms that produce serious, even deadly illnesses.

PROVIDENCE, R.I. -- Brown University studies show that an experimental antibiotic promptly kills six strains of drug-resistant bacteria that cause respiratory tract infections, and that, at an equal dose, the antibiotic is more effective than an antibiotic now in use against different breeds of drug-resistant bacteria that cause staph infections, gastrointestinal illnesses or pneumonia.

The experimental drug is called moxifloxacin. The findings suggest it is a potential treatment against a range of drug-resistant infectious organisms that produce serious, even deadly illnesses. Resistance to penicillin and other antibiotics is increasing worldwide among bacterial strains.

A research team used lab tests to show that a single 400-mg moxifloxacin dose is enough to quickly kill six strains of Streptococcus pneumoniae, with no regrowth. The strains killed included those resistant to the antibiotics penicillin and erythromycin. Respiratory tract illnesses caused by Streptococcus pneumoniae are among the leading types of bacterial infections in many countries.

"The findings suggest that moxifloxacin should be useful in treating infections caused by Streptococcus pneumoniae bacteria, which are susceptible to treatment with, yet resistant to, penicillin and erythromycin," said Stephen Zinner, M.D., professor of medicine. Clinical trials are needed to confirm these findings, he said.

Zinner presented the results last October at the Interscience Conference on Antimicrobial Agents and Chemotherapy.

In November, at the Sixth International Symposium on New Quinolones and Related Antibiotics, Zinner reported that moxifloxacin, at equal doses, was more effective against different strains of resistant bacteria that cause staph infections, gastrointestinal illnesses or pneumonia than the antibiotic levofloxacin, currently used to treat a range of infections.

These new findings about moxifloxacin are not necessary for it to become licensed but are used to determine optimal dose and may help in clinical-trial design, said Zinner, head of the Division of Infectious Diseases at Roger Williams Medical Center and Rhode Island Hospital.

The research employed a two-section lab model created in collaboration with Alexander Firsov and colleagues at the Centre of Science and Technology (LekBioTech) in Moscow. The model's external compartment features a series of tubing-linked chambers that house bacteria. This peripheral structure communicates with a central compartment into which antibiotic is infused.

The design allows researchers to periodically vary the concentration of antibiotics in contact with the bacteria, simulating the half-life of a drug being absorbed, distributed and eliminated in the human body.

"Changing the concentrations mimics the pharmacokinetic profile in patients," Zinner said. "Comparing activities of new drugs against old drugs based on pharmacokinetic considerations allows us to end up with a better idea of the dose of the new drug that gives the same effect as that of the old drug."

In November, the model was described in two papers in the journal Antimicrobial Agents and Chemotherapy.