The susceptibility of laboratory mice to Borrelia burgdorferi was evaluated for selected genotypes and ages. C3H/He, SWR, C57BL/6, SJL, and BALB/c mice inoculated at age 3 days developed uniformly severe polyarthritis at 30 days after intraperitoneal inoculation. Mice inoculated at age 3 weeks also developed polyarthritis, but severity was influenced by genotype, with C3H/He and SWR mice the most severely affected. Susceptible strains developed higher IgG ELISA antibody titers to B. burgdorferi than did resistant mice. Adult (12 weeks) C3H/He mice were also susceptible, but arthritis was not as severe as in those inoculated at age 3 weeks. SKH (hairless) mice developed polyarthritis but not skin disease when inoculated intradermally. Carditis occurred frequently among C3H/He, BALB/c, and hairless mice and in some SWR mice but not in C57BL/6 or SJL mice. This study demonstrates that severity of Lyme borreliosis is age- and genotype-dependent and that laboratory mice are a potentially valuable model.

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Borrelia burgdorferi infection of disease-susceptible (C3H) and -resistant (BALB) mice resulted in impaired proliferation to both T- and B-cell mitogens up to 30 days after inoculation. Interleukin-2 and -4 production was also impaired, paralleling the T-cell response to concanavalin A. Impaired lymphocyte proliferation could not be attributed to diminished numbers of T or B cells and was found to depend on the lymphoid organ (spleen or lymph node) examined. Prostaglandin production accounted for part of this immune dysfunction. Attempts to assess antigen-specific proliferation to B. burgdorferi were inconsistent, and delayed-type hypersensitivity responses were not detected. Adoptive transfer of T-enriched cells from chronically infected donors failed to prevent infection and disease development in recipient C3H mice. The current study emphasizes caution in the study of B. burgdorferi antigen-specific assays and argues against the role of a vigorous T-cell response in Lyme borreliosis in infected laboratory mice.