Knowing the natural hiding place of a disease-causing pathogen is the first step to defeating it. It has taken 60 years of trying, but scientists have finally found the home environment of the microbe that causes Buruli ulcer, a devastating skin disease.
Researchers now report isolating the culprit, Mycobacterium ulcerans, from insects nabbed in a stagnant pond in West Africa.
Earlier epidemiological reports showed that Buruli ulcer outbreaks often occur near such still waters in the tropics. “This study confirms what other investigations have suggested, that M. ulcerans is present in viable form in aquatic insects,” says Mark Wansbrough-Jones, a physician not involved in the study who is at St. George’s, University of London.
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The researchers, led by biologist Françoise Portaels at the Institute of Tropical Medicine in Antwerp, Belgium, took water and wildlife samples from ponds and swamps in areas of Benin and Togo where Buruli ulcer is epidemic. They ground up the bugs and cultured the tissues in the lab.
But in lab dishes, other faster-growing bacteria crowded out the slow-growing mycobacterium. So the researchers took the unusual step of injecting the bug tissues directly into mice and letting the microbes grow there. After 9 months, the mice began forming skin lesions that contained a strain of M. ulcerans virtually identical to the kind already known to cause Buruli ulcers in people. The microbes even harbored the same DNA and manufactured the same toxin that causes the skin ulceration that defines the disease. The report appears in the March PLoS Neglected Tropical Diseases.
“This is a major accomplishment,” says Pamela Small, a microbiologist at the University of Tennessee–Knoxville. “We know that people don’t spread this disease between each other. It’s an environmental pathogen that has its own life. People get it accidentally.”
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Buruli skin ulcers are oddly painless, apparently because the bacterium’s toxin dulls nerves. The toxin might also exert an anti-inflammatory effect that sidetracks an immune response and prevents wounds from healing. If ulcers get too big, doctors typically remove them surgically and apply skin grafts. An antibiotic combination of streptomycin and rifampicin can knock out smaller ulcers, but treatment takes months. Also, streptomycin must be injected and has side effects.
Buruli ulcer is becoming more common in some wet areas of West Africa than its better-known mycobacterial cousins, tuberculosis and leprosy.
Meanwhile, it remains unclear just how M. ulcerans infects people. The long-legged water bugs found to harbor M. ulcerans in this study—called water striders—probably don’t transmit the disease to humans, says study coauthor Pieter Stragier, a microbiologist on the Belgian team. Since most water bugs seldom bite people, they are more likely to be temporary hosts for the microbe.
While some Australian researchers suspect mosquito bites transmit the disease, other scientists speculate that small cuts or abrasions allow M. ulcerans to penetrate and infect the skin through water contact. The microbe might even exist as part of a biofilm, an aggregate of adhesive microorganisms, on water-based plants with sharp leaves, Small says. The hunt for a mode of transmission continues.