Doctoral student produces model of waterborne pathogen
Published March 28, 2014
A recent NDSU graduate has made a breakthrough that could help save the lives of millions of children in underdeveloped countries.
Ebot Tabe produced a first-of-its-kind model of waterborne parasite Cryptosporidium parvum’s motility that eventually could play a role in ending an alarming global rate of sickness and death from diarrheal disease. Tabe, who earned a doctorate in molecular pathogenesis in August, recently began NIH Biodefense and Emerging Disease infection training at the New York State Department of Health’s Wadsworth Center.
“Cryptosporidium has been one of those pathogens classified as a neglected tropical parasite,” Tabe said. “Not a lot of attention has been put on studying the mechanisms. But this is a serious problem that needs a remedy.”
A majority of water-related deaths occur in underdeveloped countries and are largely due to lack of safe drinking water and sanitation, and poorer overall health, hygiene and nutrition, according to a recent UNICEF study. In the United States, the parasite is found mostly in tainted swimming pools.
Cryptosporidium is one of the leading causes of child death from severe diarrheal disease in developing countries. Diarrheal disease is responsible for more deaths each year worldwide than malaria and AIDS combined.
And there is no consistently effective treatment.
The effects of Cryptosporidium are generally non-lethal to people who have strong immune systems. People who have compromised immune systems, such as cancer and AIDS patients, are at a much greater risk of death when they come into contact with the parasite.
“A very recent study that looked at the causes of severe diarrheal disease in children in South Asia and sub-Saharan Africa found that Cryptosporidium was second only to Rotavirus,” said John McEvoy, NDSU associate professor of veterinary science and microbiology. “It’s the major cause of death in toddlers in those countries from diarrheal disease.”
Attacking the parasite
Working in conjunction with McEvoy and Sinisa Urban, associate professor of microbiology and genetics at Johns Hopkins School of Medicine, Tabe looked at Cryptosporidium at a molecular level.
Tabe studied the mechanics of the parasite’s motility in the early stage of its lifecycle. Cryptosporidium is most vulnerable in its early stages, McEvoy said. Slowing down the parasite’s replication process in the early stages would greatly reduce the impact of the disease.
Tabe’s research resulted in a new model that shows how proteins in Cryptosporidium react and work together to achieve motility at the time of invasion.
“The goal is that this eventually helps identify new weak points and targets for new medications or maybe vaccines,” Tabe said. “There is still much more work to be done. But it’s only when you understand how these things interact that you can understand how you can build inhibitors to block the action.”
McEvoy said Tabe’s study created an important new marker that will help researchers better understand Cryptosporidium’s vulnerabilities.
“Most studies to date have focused on individual proteins during invasion,” McEvoy said. “Ebot’s research provides the framework to understand how these proteins work together.”
Tabe’s research was supported by National Institutes of Health grant P20 RR015566 from the National Center for Research Resources, and National Institute of Food and Agriculture grant 2008-35102-19260.