||1. A 21-day whole body x-irradiation LD50 was determined for guinea pigs, white mice and deer mice. As measured by post-exposure deaths, guinea pigs were most susceptible (LD50: 163 r), white mice less susceptible (LD50: 431 r) and deer mice least susceptible (LD50: 588 r) to the irradiation. 2. In a pilot rickettsiae study, Coxiella burnetii was shown to persist for over 12 weeks in kidneys of guinea pigs and reproductive tract and kidneys of white mice. Fecal material and urine in guinea pigs, white mice and deer mice were infectious for three weeks. The organism persisted a total of six week in deer mouse spleen, kidneys and liver. 3. Whole body x-irradiation in dosages slightly less than or greater than the 21-day LD50 caused a reactivation of C. burnetii infection in guinea pigs, white mice, and deer mice infected three months previously. This reactivation was determined by demonstrating infectious quantities of rickettsiae in various tissues and in urine and feces in these animals, as compared to the detection of little or no rickettsiae in the same tissues from non-irradiated similarly infected control animals. 4. The Q fever antibody response in the irradiated and control animals in (3) were shown to vary markedly in titer with animal species, dosage of irradiation and type of antibody. The Phase I and II CF antibody from irradiated guinea pigs was depressed at one week after irradiation, but increased significantly by four weeks in the animals receiving high irradiation dose. A negative antibody phase occurred in the animals receiving the low dose within four weeks. Phase 1 CTA antibody, by contrast, increased in titer by one wee, but was depressed subsequently only in the low dosage irradiated animals. White mice reacted to a lesser extent than guinea pigs, but the same general trends in antibody depression and enhancement were noted. Few variations of significance could be demonstrated n sera from deer mice, although one to tow weeks after irradiation a slight depression of CF antibody occurred in the irradiated animals. 5. A definite transmission of C. burnetii to control guinea pigs and white mice in relation to reactivation of the Q fever infections in irradiated animals was demonstrated. This was shown by the infection of normal control animals placed as cage mates with the infected and irradiated animals. No transmission could be observed in deer mice and non-irradiated control animals. 6. An injection of cortisone give daily for seven days induced a reactivation of Q fever infection in guinea pigs and white mice but not in deer mice infected three months previously. This reactivation was indicated by the presence of C. burnetii in various tissue, urine and feces which were usually uninfected in untreated animals infected at the same time. 7. The multiple cortisone injections described in (6) had only a moderate effect upon the Q fever antibody response in the three species tested. A slight depression in titer occurred in most animals at varying time intervals following the cortisone injections. This was usually preceded by a sudden increase in CF titer during the treatments. 8. Normal control animals placed as cage mates with cortisone-treated guinea pigs and white mice became infected with C burnetii. This indicated that a reactivation of Q fever infection by cortisone treatment can result in spread of the disease agent. No transmission was observed in deer mice at the cortisone concentrations employed, and all normal cage mates of untreated control animals remained uninfected. 9. a reactivation of Q fever infection occasionally occurred following parturition in guinea pigs and white mice previously infected with C. burnetii. Various viscera and frequently blood, urine and feces from these animals were shown to contain C burnetii as early as 8 days and a long as 20 days after birth of offspring. Partus, primarily guinea pigs, from these infection-reactivated parents often were also infected. Little change in Q fever antibody titer was noted in parents or progeny. 10. A secondary Q fever antibody response was studied in guinea pigs reinfected with C. burnetii three months after a primary infection. Fluctuations in titer were slight, although many animals exhibited a slight decrease in serum antibody titer to all three antigens employed. This was succeeded by a moderate increase of titer above the original amount by one to two weeks. The titers gradually dropped to, or slightly below, the original titer. Intraperitoneal, subcutaneous and intravenous routes of secondary injection were employed in separate experiments, with litter difference noted in induced antibody titers.