The serendipitous pursuit of a rapid outbreak of virulent tuberculosis shows how the disease can be stopped in its tracks, according to a report in tomorrow's New England Journal of Medicine. The study of the new strain's genetic structure might also lead researchers to a better understanding of how the microbe adapts itself to human hosts.
Mycobacterium tuberculosis, the organism that causes TB, infects up to one-third of the world's population. The World Health Organization estimates there are 8 million new TB cases and 3 million deaths each year, making it the biggest killer among infectious diseases. Yet TB travels discreetly; only 10% of those infected ever display symptoms, making it hard for medical scientists to predict how rapidly an outbreak will spread or who will become infected.
Such uncertainties may point to subtle, as-yet-undiscovered genetic differences among TB strains. With that in mind, Sarah Valway and colleagues at the Centers for Disease Control and Prevention in Atlanta and at several other institutions were called to examine a suspected TB outbreak in rural Tennessee in May 1995. The team had been summoned after routine screenings of a boy, his family, and their immediate contacts in neighboring counties showed that nearly half of the people tested had been infected--five times the rate for a typical TB outbreak.
"It's the first time we've seen an outbreak like this," Valway says. The team eventually located 21 TB cases in the sparsely populated region, which normally averages less than one case per year. Hundreds of others in the area were also infected with the mycobacterium, even though many had only brief contact with any of the patients showing symptoms, Valway says. Despite the presumed virulence of the strain--experiments with mouse lungs showed it produces 1000 times more bacteria in infected cells than do standard varieties--Valway says the number of TB cases that developed were kept in line with other typical outbreaks, which "shows that doing good contact investigations is important and preventative therapy works." The team administered the drug isoniazid to those who were infected, which killed the myobacterium and put the brakes on the outbreak.
The CDC team's work combines "superb conventional epidemiology with a well-characterized animal model," epidemiologists Barry Bloom and Peter Small write in an accompanying editorial. Bloom, of Albert Einstein College of Medicine in New York City, and Small, of Stanford Medical Center in Palo Alto, California, also express hope that more studies could reveal a gene in the myobacterium for virulence or transmissibility. Valway and colleagues say they have already found a stretch of DNA that distinguishes this strain of TB from others--a first step toward finding such genes.