Posted 8/10/2015 6:11 PM (GMT 0)
Babesiosis
American Society of Microbiology
2000
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC88943/pdf/cm000451.pdf
**i know this is 15 years old**
"Immunosuppression is a common characteristic among various parasitic infections (71, 144, 220). There are several lines of evidence that demonstrate the immunosuppressive effects of B. microti infections on the maintenance of coinfecting agents. B. microti infections can impair the ability of host mice to reject Trichuris muris (nematode) infections (163), prolong and en- hance Trypanosoma musculi infections in mice (144), result in decreased Trypanosoma-specific antibody production (144), and decrease the ability of mice to mount an immune response to sheep erythrocytes (2, 175).
In the case of coinfection with the agent for Lyme disease, infections with B. microti may elicit an immune response that results in establishment of higher numbers of Lyme disease spirochetes (160). Borrelia burgdorferi establishment and pathogenesis are favored in a Th1-dominant environment, whereas the infection can be effectively controlled by a Th2- dominant CD4 T-cell response (124, 160). Studies with C3H mice (respond to B. burgdorferi with a Th1-dominant response) and BALB/c mice (Th2-dominant response to B. burgdorferi) have shown that C3H mice maintain higher numbers of spiro- chetes than BALB/c mice when infected with B. burgdorferi. It is possible that coinfection with B. microti could skew T-cell development towards a Th1 response, thereby facilitating a more established infection of B. burgdorferi. The alternative situation is also possible, in which B. burgdorferi could enhance babesial infection; this could be consistent with recent field survey results in mice, in which B. microti was primarily found in mice that were also infected with B. burgdorferi (5)."