Host resistance to tick infestation has an immunological basis with complement-dependent, cellular and antibody-mediated effector mechanisms (Wikel, 1979; Wikel et al., 1978). Resistance to tick infestation was demonstrated by significantly fewer ticks engorging on resistant animals and by a reduced engorgement weight for those few ticks which did engorge. Host resistance to tick infestation represents a cutaneous hypersensitivity state which has a protective function. However, the effects ofho3t resistance to tick infestation on the transmission of tick-borne pathogens has been largely unexamined. Francis and Little (1964) provided evidence that host resistance to tick infestation had a protective value in the prevention of disease transmission. Transmission of Babesia argmtina and B. bigemina to cattle resistant to tick infestation was greatly reduced in comparison to transmission of these protozoa to non-resistant hosts. Recent experiments have demonstrated that host resistance to tick infestation alters the transmission of the tick-bnrne bacterium Francisella tularensis, from infected ticks to tick-resistant hosts. In order to induce host resistance to tick infestation, 11 rabbits were each infe3ted for seven days with one male and two female, pathogen-free, Dermacentor andqrsoni. After termination of the initial infestation, all rabbits were maintained tick-free for seven days. A second infestation, identical to the first, was then carried out on each rabbit. All rabbits displayed resistance to tick infestation during the second exposure. Ticks removed at the termination of the second infestation weighed significantly less (P< 0· 02) than ticks removed after the initial infestation. Fourteen days later the 11 tick-resistant and ten control rabbits (never exposed to ticks), were each infested with 25 nymphs of D. andersoni infected with F. tularensis. Infected nymphs were obtained by placing pathogen-free larvae of D. andersoni on rabbits infected with highly virulent type A organisms of F. tularensis. Engorged larvae removed from these rabbits were allowed to moult. It was determined by animal inoculation that 90% of the nymphs were infected. One organism of the type A of F. tularensis was sufficient to kill a rabbit upon inoculation. All tick-resistant and control animals were infested with infected nymphs for 14 days or until death. All rabbits in the control group d1ed and yielded F. tularensis on culture of tissue obtained at necropsy. Only 34· 4% of the tick-resistant animals died (significant at P< 0.02) and all these had done so because of F. tularensis infection (Table). None of the surviving tick-resistant animals developed an antibody titre to F. tularensis by 14 days after the termination of the infestion (haemagglutination). These animals were subsequently sacrificed and none of their tissues yeilded F. tularensis on culture