BOSTON – The spirochete that causes Lyme disease in humans may be lending a helping hand to the weaker protozoan that causes babesiosis, escalating the rate of human babesiosis cases in regions where both are endemic.
Peter Krause, MD, a research scientist in epidemiology, medicine, and pediatrics at Yale University School of Public Health, New Haven, Conn., reviewed what’s known about babesiosis–Lyme disease coinfections at the annual meeting of the American Society for Microbiology.
Dr. Peter Krause
Understanding the entire cycle is necessary, he said, because the effects of coinfection will be different depending on the stage of the cycle, and upon the coinfection pathogens.
Over the course of many years, Dr. Krause and his collaborators have used an interdisciplinary, multi-modal approach to try to understand the interplay between these pathogens, their hosts, and environmental, demographic, and ecologic factors.
One arm of their research has taken them to the lab, where they have modeled coinfection and transmission of Borrelia burgdorferi and Babesia microti from their reservoir host, the white-footed mouse (Peromyscus leucopus), to the vector, the deer tick (Ixodes scapularis), which can transmit both diseases to humans.
In an experimental design that mimicked the natural reservoir-vector ecology, Dr. Krause and his collaborators first infected mice with 5 to 10 nymphal ticks, to approximate the average number of ticks that feed on an individual mouse in the wild. The researchers then tracked the effect of coinfection on transmission of each pathogen to ticks during the larval feeds, finding that B. burgdorferi increased B. microti parasitemia in mice who were coinfected. Coinfection also increases B. microti transmission from mice to ticks. This effect happens at least partly because of the increased parasitemia, Dr. Krause said.
The downstream effect on humans is to increase the risk of babesiosis for those who live in regions where both B. microti and B. burgdorferi are endemic, Dr. Krause said.
B. microti is less “ecologically fit” than B. burgdorferi, Dr. Krause said, noting that there are more ticks and humans infected with the latter, as well as more reservoir mice carrying B. burgdorferi. Also, the rate of geographic expansion is more rapid for B. burgdorferi. “B. microti is only endemic in areas where B. burgdorferi is already endemic; it may not be ‘fit’ enough to establish endemic sites on its own,” Dr. Krause said.
The increased rate of B. microti transmission via ticks from mice, if the mice are coinfected with B. burgdorferi, may help explain the greater-than-expected rate of babesiosis in humans in areas of New England where coinfection is common. “This paradox might be explained by the enhancement of B. microti survival and spread by the coinfecting presence of Borrelia burgdorferi,” Dr. Krause said.
This naturalistic experiment has ecological implications in terms of the human impact as well: “Coinfection may help enhance geographic spread of B. microti to new areas,” Dr. Krause said.
Clinicians in geographic areas where both pathogens are endemic should maintain a high level of suspicion for coinfection, especially for the most ill patients. “Anaplasmosis and/or babesiosis coinfection increases the severity of Lyme disease,” Dr. Krause said. “Health care workers should consider anaplasmosis and/or babesiosis coinfection in Lyme disease patients who have more severe illness or who do not respond to antibiotic therapy.”
Understanding the complex interspecies interplay will be increasingly important as more cases of tick-borne illness are seen, Dr. Krause concluded. “Research on coinfections acquired from Ixodes scapularis has just begun.”
Dr. Krause reported no relevant conflicts of interest.
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