It may be making a leap to connect frogs with tuberculosis in humans, but California researchers contend that their research on the amphibians may soon lead to a way to arrest the spread of the human form of the disease.

When the researchers from Stanford University in Palo Alto decided to study human tuberculosis (TB), they had little patience for the 30 days the bacterium takes to grow, and were not properly equipped to contain the human pathogen that is known to spread rapidly through the air, according to Dr. Stanley Falkow, a co-author of the report published in the May 26th issue of Science.

Instead, they isolated a close relative of the TB microbe known as Myobacterium marinum from lesions on frogs, explained Falkow. Within 5 days, the researchers grew M. marinum in the macrophages (an immune cell also found in humans) of frogs.

Using fluorescent molecules to identify the bacterial genes in these immune cells, the investigators isolated genes turned on when the pathogen M. marinum is present. The fluorescent gene is only expressed within the frog. These genes are always present in bacteria but are typically not expressed under ordinary conditions of growth in the laboratory, Falkow said. About a dozen genes were identified in the tuberculosis chromosome, he noted.

"When we sequenced this chromosome, we a found a family of genes with the unusual structure PE-PGRS,'' he told Reuters. This family of genes comprises up to 10% of the genes implicated in the human form of the disease. "No one knew what they did before,'' he added.

Two of those genes were particularly interesting because they were found to be essential to the progression of tuberculosis. When the two genes were inactivated, they either stopped functioning or functioned poorly in macrophages and granulomas, a collection of immune cells characteristic of TB. The frogs who had these genes mutated did not develop the amphibian form of tuberculosis.

If the similar genes in the human form of tuberculosis are identified and inactivated, it is likely the bacterium in humans will no longer be virulent, meaning that it cannot cause disease, Falkow said.

Aside from stating that this finding "is very interesting,'' Falkow believes that other researchers will jump on the results of their research to find and inactivate the gene in human tuberculosis patients. The time to the development of a way to stop the spread of the disease in humans could be very short indeed, he said.