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The pathogenesis of an infection of the male genitourinary tract of mice with a human serovar of Chlamydia trachomatis has not been characterized. To establish a new model, we inoculated C3H/HeN (H-2(k)) mice in the meatus urethra with C. trachomatis serovar D. To determine the 50% infectious dose (ID(50)), male mice were inoculated with doses ranging from 10(2) to 10(6) inclusion-forming units (IFU). The mice were euthanized 10 days post infection (p.i.), and the urethra, bladder, epididimydes, and testes were cultured for Chlamydia. Positive cultures were obtained from the urethra, urinary bladder, and epididimydes, and the ID(50) was determined to be 5 x 10(4) IFU/mouse. Subsequently, to characterize the course of the infection, wild-type (WT) and C3H animals with severe combined immunodeficiency (SCID animals) were inoculated with 10(6) IFU/mouse (20 times the ID(50)). In the WT mice, the infection peaked in the second week, and by 42 days p.i., it was cleared. In contrast, most of the SCID mice continued to have positive cultures at 60 days p.i. C. trachomatis-specific antibodies were first detected in WT animals' sera at 21 days p.i. and increased until 42 days p.i. The immunoglobulin G2a (IgG2a) titers were 32-fold higher than those of IgG1, indicative of a Th1-biased immune response. A lymphoproliferative assay using splenocytes showed a significant cell-mediated immune response in the WT mice. As expected, no humoral or cell-mediated immune responses were observed in the SCID animals. In conclusion, inoculation of WT male mice in the meatus urethra with a human serovar of C. trachomatis resulted in a limited infection mainly localized to the lower genitourinary tract. On the other hand, SCID animals could not clear the infection, suggesting that in male mice, the adaptive immune response is necessary to control an infection with a C. trachomatis human serovar.

Eight male baboons inoculated intraurethrally with Neisseria gonorrhoeae failed to shed gonococci or develop serum antibody. Urethral inoculation, preceded by epididymal inoculation, elicited an anamnestic antibody response.

With slight modification of a trypsin digestion technique, Rickettsia rickettsii were demonstrated specifically by immunofluorescence staining in Formalin-fixed, paraffin-embedded tissue sections from a human, rhesus monkey, and guinea pig with Rocky Mountain spotted fever and in infected membranes from a chicken embryo. Tissues were cut at 4 micron and, using geltain as a tissue adhesive, were hydrated in a routine manner. Sections were then digested in refrigerated 0.1% trypsin for 16 h, washed, and stained specifically for R. rickettsii by direct or indirect immunofluorescence. Rickettsial organisms were localized in affected vessels of the mammalian species and within the yolk sac epithelium of the chicken embryo. Specificity was confirmed by adsorbing antibody conjugates with R. rickettsii organisms. Trypsin digestion probably decreased tissue proteins which interfered with immunochemical attachment of antibody to the rickettsiae. The technique is valuable in that a diagnosis of Rocky Mountain spotted fever can be confirmed from Formalin-fixed tissues processed in a routine manner.