BALB/c mice infected with Coxiella burnetii phase I developed a state of acquired resistance which could be detected during week 2 postinfection. Immune serum, administered to normal mice 24 h before challenge with C. burnetii, appeared to accelerate the development of resistance. An increased clearance rate could be measured in these serum recipients 1 week postinfection. Simultaneous administration of immune serum and C. burnetii did not affect the normal clearance rate of rickettsiae from the spleens of infected mice during week 1, but enhanced clearance of the organism by 14 days postchallenge. Passive transfer of immune serum 24 h after challenge of normal mice with viable C. burnetii had no effect on rickettsial growth within the spleens of animals treated in this fashion. Treatment of athymic mice with immune serum 24 h before challenge with C. burnetii had no effect on rickettsial multiplication within the spleens of these T-cell-deficient animals.

Studies were carried out to determine the effects of treatment with killed suspensions of Propionibacterium acnes (formerly designated Corynebacterium parvum) on the course of Mycobacterium leprae infection in mice. Systemic (intravenous or intraperitoneal) treatment with P. acnes failed to significantly alter the growth of M. leprae in the mouse footpad. In contrast, injections of P. acnes directly into the infected footpad markedly inhibited the growth of the leprosy bacilli regardless of whether the local treatments were administered before infection or 3 months after infection with M. leprae. The effects of local treatment with P. acnes appeared to be bactericidal and not merely bacteriostatic. Clearance of the organism from the tissues was not enhanced by P. acnes treatment. A large body of evidence attests to the immunopotentiating effects of treatment with suspensions of killed Propionibacterium acnes (formerly designated Corynebacterium parvum [5]). In mice, treatment with P. acnes markedly enhances the function of the reticuloendothelial system (2, 11), increases host resistance to tumors (11, 14, 17, 20-22), and enhances their capacity to resist infection with a variety of pathogenic organisms including Salmonella enteritidis (3), Bordetella pertusis (1), Brucella abortus (1), Plasmodium berghei (18), Toxoplasma gondii (28), and Listeria monocytogenes (28). The present studies were carried out to determine the effects of systemic and local treatment with P. acnes on the growth of Mycobacterium leprae in the mouse footpad. MATERIALS AND METHODS Mce. Locally bred BALB/c mice were used. All of the mice were females and weighed 18 to 22 g at the start of each experiment. P. acnes. A killed suspension of P. acnes (C. parvum, lot no. CA749, 7 mg/ml dry weight) was kindly provided by Richard Tuttle (Burroughs-Wellcome Co., Research Triangle Park, N.C.). P. acnes treatments were administered intravenously (i.v.), intraperitoneally (i.p.), or subcutaneously (s.c.) in the groin area or s.c. into the hind footpad. M. kprae infection. Mice were inoculated in the right or both hind footpads (RHF and BHF, respectively [LHF = left hind footpad]) with 5 x 103 M. leprae, and the course of infection was followed at intervals by harvest and enumeration of acid-fast

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Studies were carried out to determine whether treatment of mice with the synthetic adjuvant muramyl dipeptide (MDP) afforded any resistance to infection with Listeria monocytogenes. Regardless of the timing, dose, or route of administration, there was no evidence that treatment with either MDP or two of its analogs (des-MDP or MDP-D-D) induced any resistance to listeria infection in BALB/c, CBA/J, or C57BL/6J mice. In contrast, pretreatment with MDP induced marked protection to infection with Streptococcus pneumoniae (type III).