Interrupting the Lyme Disease Life Cycle
Blocking a tick protein that protects the Lyme disease bacteria as it moves from mice back to the tick that infected them might reduce incidences of the illness among humans, a Yale School of Medicine researcher reports in Cell Host & Microbe.
Lyme disease, which is transmitted to people by deer ticks, is the most common tick-borne illness in the United States. The primary reservoirs for its bacteria, known as Borrelia burgdorferi, are mice, chipmunks, and other small rodents. Symptoms include a skin rash, abnormal heart rhythms, arthritis, and meningitis.
In this study on mice, Erol Fikrig, professor of internal medicine, first blocked the protein Salp25D in the tick’s salivary gland to see if it would interrupt transmission of the bacteria, but it did not affect the bacteria.
The ticks engorge on humans and other vertebrates for several days, penetrating the skin, damaging vessels, and obtaining blood from the resulting bruise. In response, neutrophils and other inflammatory cells are recruited to the bite site to disrupt tick feeding. Ticks counteract these forces with an assortment of immunomodulators, anticoagulants, and other biologically active proteins in saliva.
Fikrig then found that the tick must secrete the protective Salp25D into the bite site in order for the Lyme disease agent to successfully migrate from mice to ticks. The tick acquires the pathogen from the host it infected—in this case, mice.
“Developing Salp25D-based strategies to interrupt the Borrelia burgdorferi life cycle may lead to new methods of reducing the incidence of Lyme disease,” he said.
Fikrig said the control and prevention of many insect-borne diseases has been primarily focused on trying to produce antibodies to fight the infection. The emphasis is now shifting to disrupting the insects’ life cycle.
The research was supported by grants from the National Institutes of Health.
Cell Host & Microbe 2: 7-18 (July 12, 2007)