Researchers at Virginia Commonwealth University School of Medicine have identified the "keys" and "doors" of bacteria that cause a series of tick transmitted diseases, increasing hopes of the development of a single vaccine that can protect humans, livestock and domestic animals from an entire family of disease-causing bacteria.
Survival for many bacteria is dependent on their ability to invade human or animal cells. And it needs to be done in a very precise fashion. Bacteria use a specific set of "keys" on their surfaces to unlock specific "doors", or entryways into their host cells.
By understanding how these bacteria invade cells, researchers are able to identify potential targets to block the spread of infection, and from there, develop safe and effective vaccines.
The team also identified the particular sugar residue on the surfaces of host cells to which OmpA binds.
"In other words, we identified both a key and door that together promote Anaplasma phagocytophilum infection," Jason A. Carlyon, lead investigator of the study, said.
"These findings are important because our data also establish a direction for development of a single vaccine that protects against members of an entire family of bacteria that cause disease in humans, domestic animals and livestock," he said.
According to Carlyon, the region of OmpA that mediates infection is shared among other Anaplasmataceae bacteria.
Experts have seen a steady rise in the incidence of human infections caused by tick-transmitted bacterial pathogens in the past several years.
Many tick-transmitted bacterial pathogens are considered "emerging pathogens" because it was only recently discovered that they infect humans.
Moreover, evidence suggests that many of these infections go unrecognized, signifying that the prevalence of human diseases caused by Anaplasmataceae pathogens is even higher, said Carlyon.
Livestock infections carry a significant economic burden, costing the U.S. cattle industry 100 million dollars per year, he added.
The study has been published online in journal Infection and Immunity.