"For some reason, bacteria lacking the BptA protein either can't utilize the blood meal in the way the wild-type bacteria do, or something about the blood becomes hostile to them," said Dr. Norgard, who holds the B.B. Owen Distinguished Chair in Molecular Research. "Instead of helping the bacteria, the blood harms them. Ultimately, as the tick feeds on blood and begins to go through its molting process, the levels of the knockout Bb bacteria in the tick drop by about 90 percent, which is a very dramatic decrease." In the study, each time infected ticks fed, bacteria levels within them dropped until they eventually were zero.
"We're not sure whether the lack of the BptA protein ultimately kills the bacteria or inactivates them," Dr. Norgard said. "But certainly it prevents them from replicating in the manner that they should to sustain the numbers needed to move from the midgut to the salivary glands. We don't understand the mechanism for that yet, and that will be the next step in our research."
Further study of the function of the BptA protein could give researchers additional clues as to how the organism has evolved to survive in ticks and why it has chosen a tick environment to be its natural vector in nature.
"It potentially could give us a target for eradicating the bacterium, because if you understand what it needs to sustain itself, then in theory you could disrupt that cycle by blocking whatever that mechanism is," Dr. Norgard said.
Traditionally, scientists studying pathogens have looked at genes that affect how the infecting organisms behave once inside a human host. What tends to get ignored, Dr. Norgard said, is the other side of the coin.
"This organism has to live half of its life cycle in a tick," he said. "There must be subsets of genes important to its survival there. If it
Source:University of Texas Southwestern Medical Center at Dallas