Abstract

Abstract The most commonly recognized tick-borne coinfection in most of the eastern USA is Lyme borreliosis and babesiosis, caused by the spirochete Borrelia burgdorferi and the erythrocytic parasite Babesia microti respectively, accounting for ~80% of coinfections. Studies of clinical outcomes indicate that coinfected patients have more severe symptoms and longer duration of illness than patients with Lyme borreliosis alone. Little is known about the immune related mechanisms during tick-borne coinfections. This study used a murine model to examine whether defined disease conditions differed in severity in mice infected solely with B. burgdorferi and in mice coinfected with B. microti and B. burgdorferi. C3H.HeN and BALB/c mice cohorts were coinfected or singly infected and then monitored experimentally for 1, 7, 10, 14, 21 and 60 days after inoculation. Carditis and arthritis was determined by blinded histopathological evaluation of myocardium and tibiotarsal joints. Cytokine measurements were made on lymph node and spleen supernatants for IFN-γ, interleukin (IL-4), IL-10 and TNF-α. Coinfected C3H and BALB/c mice had a significant increase in carditis severity at day 7. In addition, a significant increase in arthritis severity was observed at day 21 and 60 for BALB/c mice. This clinical observation was correlated with a significant increase in the expression of IFN-γ and TNF-α and with a significant reduction of IL-4 and IL-10. NIH P20RR016443-04

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