Abstract
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
Babesia
species 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.