Delayed-type
hypersensitivity responses of inbred mice during the course of lethal and
chronic infections with strains of Rickettsia tsutsugamushi were evaluated by using the influx of radiolabeled cells into
antigen-injected ears. Congenic strains of C3H mice, which previously have been shown to be resistant (C3H/RV) or sensitive (C3H/HeDub) to lethal intraperitoneal
infection with the Gilliam strain of rickettsiae, both expressed delayed-type
hypersensitivity early in the course of
infection (5 to 7 days). The sensitive C3H/HeDub mice, however, exhibited a marked decline in reactivity just before death. In contrast, reactivity of C3H/RV mice remained high through day 9 and declined slowly through day 15 after
infection. Similar results were obtained when BALB/c mice were infected with either the Karp or the Gilliam strain of rickettsiae, which produce a lethal or nonlethal
infection, respectively, in this strain of mice. Rechallenge of C3H/RV mice elicited a rapid increase in reactivity, suggesting a secondary memory response. To analyze delayed-type
hypersensitivity during
chronic infection, C3H/HeDub mice were immunized by subcutaneous
infection with the Gilliam strain of R. tsutsugamushi, and both delayed-type
hypersensitivity reactivity and resistance to intraperitoneal challenge were examined. Delayed-type
hypersensitivity reactivity developed slowly and peaked at 21 days postimmunization, which correlated with resistance to intraperitoneal challenge. Delayed-type
hypersensitivity reactivity declined thereafter, but resistance to intraperitoneal challenge remained through 28 days postimmunization. Delayed-type
hypersensitivity reactivity increased after secondary challenge at 28 days, again suggesting
antigen memory generated by primary immunization. Transfer of delayed-type
hypersensitivity reactivity was accomplished by using immune thymus-derived splenic lymphocytes isolated with
nylon-wool columns. Abrogation of the ability of immune spleen cells to transfer delayed-type
hypersensitivity reactivity
after treatment with anti-Thy 1.2 alloantiserum and
complement further supported the view that delayed-type
hypersensitivity responses to
scrub typhus rickettsiae were mediated by thymus-derived lymphocytes.