Comment; The perfect storm, Babesiosis with Lyme co-infection; Lyme is accelerated by the Babesia. Next we’ll need to see the mechanism of action and look for a defense against this synergistic attack.
Vitomir Djokic1†, Lavoisier Akoolo1†, Shekerah Primus1,
Samantha Schlachter1‡, Kathleen Kelly2,
Purnima Bhanot1 and Nikhat Parveen1*
- 1Department of Microbiology, Biochemistry and Molecular Genetics, Rutgers New Jersey Medical School, Newark, NJ, United States
- 2Biomedical Sciences, Cornell University College of Veterinary Medicine, Ithaca, NY, United States
Lyme disease is the most prominent tick-borne disease in the United States. Co-infections with the tick-transmitted pathogens Babesia microti and Borrelia burgdorferi sensu stricto are becoming a serious health problem. B. burgdorferi is an extracellular spirochete that causes Lyme disease while B. microti is a protozoan that infects erythrocytes and causes babesiosis. Testing of donated blood for Babesiaspecies is not currently mandatory due to unavailability of an FDA approved test. Transmission of this protozoan by blood transfusion often results in high morbidity and mortality in recipients. Infection of C3H/HeJ mice with B. burgdorferi and B. microti individually results in inflammatory Lyme disease and display of human babesiosis-like symptoms, respectively. Here we use this mouse model to provide a detailed investigation of the reciprocal influence of the two pathogens on each other during co-infection. We show that B. burgdorferi infection attenuates parasitemia in mice while B. microti subverts the splenic immune response, such that a marked decrease in splenic B and T cells, reduction in antibody levels and diminished functional humoral immunity, as determined by spirochete opsonophagocytosis, are observed in co-infected mice compared to only B. burgdorferi infected mice. Furthermore, immunosuppression by B. microti in co-infected mice showed an association with enhanced Lyme disease manifestations. This study demonstrates the effect of only simultaneous infection by B. burgdorferi and B. microti on each pathogen, immune response and on disease manifestations with respect to infection by the spirochete and the parasite. In our future studies, we will examine the overall effects of sequential infection by these pathogens on host immune responses and disease outcomes.
Conclusion
Our studies indicated that during co-infection of susceptible C3H mice with tick-borne pathogens, potential stimulation of the innate immune response by B. burgdorferi attenuate B. microti parasitemia while changes in symptoms of babesiosis were not discernible. However, in our model, B. microti suppressed adaptive immune response triggered by B. burgdorferiinfection such that diminished splenic B and T cells populations were reflected by overall reduction in the specific functional humoral immunity against both pathogens. As a consequence, B. burgdorferi persists at higher levels in tissues causing more severe Lyme disease in the susceptible C3H mice.
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