Drug resistance in river blindness


A new study by McGill parasitologist Roger Prichard has found that ivermectin, the only drug available to treat onchocerciasis, or river blindness, is triggering the very genetic changes that are building drug resistance in the parasite that causes the disease. The study, to be published in the inaugural edition of the new journal PLoS Neglected Tropical Diseases, was previewed online Aug. 30.

Dr. Prichard, who is James McGill Professor at the University's Institute of Parasitology, published a study in The Lancet in June documenting the growing rate of ivermectin resistance in onchocerca volvulus in the West African nation of Ghana. The current study, conducted in Cameroon, proves the genetic basis of this resistance. Samples of the parasite were taken from people in an area where ivermectin treatments had never been administered. Three years later, samples were taken from the same people after intensive treatment.

"We were then able to compare the parasites obtained after treatment with those obtained before," explained Prichard. "And we found significant changes in one of the genes that is involved in drug resistance in other species of parasites."

River blindness, which is the second-leading infectious cause of blindness worldwide after trachoma, is caused by the filarial nematode parasite onchocerca volvulus, a worm transmitted by blackfly bite. It leads to visual impairment, blindness and, in some cases, pathological changes in the skin. Adult worms can survive as long as 10 to 15 years in a human host, releasing millions of tiny worms (microfilariae) each year. An estimated 37 million people are infected worldwide, primarily in sub-Saharan Africa but also in parts of Central and South America and, to a lesser extent, the Middle East.

Ivermectin — originally developed as a veterinary drug for cattle — has been used for the treatment of river blindness for nearly two decades, and is currently the only safe drug available for mass treatment of the millions of people infected with the parasite. Prichard's latest study identifies the process that leads to this resistance, and also provides researchers with a recognizable genetic marker to monitor the spread of resistance from one population to another.

Prichard cautions that ivermectin is unlikely to become completely ineffective in the short term, and emphasized existing, albeit less satisfactory alternatives such as surgery or spraying. He underscored the need for new research and new treatments, either drugs or a vaccine.

"Unfortunately, there is no economic incentive for the drug companies to do more research, so we're far from having a new drug available," he said.

In the accompanying commentary article, Sara Lustigman of the New York Blood Center and James McCarter of Washington University School of Medicine said that the study is "a wake-up call for onchocerciasis control programs to select their treatment regimens carefully and to develop plans for detecting ivermectin resistance and the associated genetic markers."

These two articles are the first to be released by the Public Library of Science's newest journal, PLoS Neglected Tropical Diseases.

Please note: The study is available online.

Contact Information

Mark Shainblum
McGill University
mark.shainblum [at] mcgill.ca
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