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Infection of C57BL/6J mice with Mycoplasma pulmonis (MP) enhanced NK cell function 3-7 days later, as detected by in vitro and in vivo assays. Moreover, spleen and lung cells of acutely infected C57BL/6J mice inhibited MP growth in vitro. The effectors were eliminated by treatment with anti-NK antibody in vivo and anti-asialo GM1 serum or anti-3A4 antibody plus complement in vitro. Clearance of viable and radiolabeled MP from the lungs was also enhanced in acutely infected mice. Acutely infected mice with severe combined immunodeficiency (SCID) eliminated viable MP faster than did uninfected mice. Antibodies to interferon-gamma (IFN-gamma) impaired clearance of MP from the lungs of SCID mice and decreased their survival times. Activated NK cells can function in resistance to early stages of infection with MP. NK cells directly inhibit MP with secrete IFN-gamma, which may activate macrophages or inhibit the growth of MP or both.

Fine structure and development of Encephalitozoon cuniculi from rabbits were studied in rabbit choroid plexus (CP) cell cultures and were compared to hamster and mouse microsporida. Sporoplasms had a single limiting membrane and contained a large nucleus. Proliferative forms (schizonts) had double outer membranes, the outermost being associated with the formation of the limiting membrane of vacuoles formed within the host cell cytoplasm. These organisms were often binucleate and divided to form sporonts. Sporonts divided once to form 2 sporoblasts which developed into electron-dense spores. Spores had a thick, 3-layered wall and contained a polar filament. The developmental cycle of E. cuniculi in rabbit CP cultures progressed rapidly. Sporoplasms were observed in host cells at 3 hr postinoculation (PI). By 24 hr PI proliferative forms were associated with host cell cytoplasmic vacuoles which contained developing organisms. Mature spores were present in vacuoles by 2 days PI, indicating that the life cycle in the CP system is approximately 48 hr. The fine structure and the sequential developmental cycle of the mouse and hamster isolates were observed to be identical to those of the rabbit isolate and different from those of the genus Nosema. It is proposed, therefore, that the 3 organisms represent the same species, Encephalitozoon cuniculi.

Rabbits, mice, rats and Rhesus monkeys were infected experimentally with a rabbit isolate of the mammalian microsporidan Encephalitozoon cuniculi. The lesions produced were typical of those occurring in spontaneous encephalitozoonosis in rabbits, mice, and rats, respectively. Viable E. cuniculi were recovered from tissues of injected animals with and without lesions. Titration of rabbit, mouse, and hamster isolates of E. cuniculi in mice and in rabbit choroid plexus cell cultures showed that the rabbit isolate was equally infectious for mice and cell cultures. Mouse and hamster isolates were less infectious for cell cultures than for mice. The results provide further evidence that the mouse, hamster, and rabbit isolates of E. cuniculi are identical.

Hyperimmune rabbit sera directed to the KSCN extract of 3:A Pasteurella multocida were characterized by enzyme-iinked immunosorbent assay (ELISA), presolubilized cell radioimmunoprecipitation, and immunoblotting analysis. The results showed that the hyperimmïne serum had a very high titer of immunoglobulin G ELISA antibody and a negligible immunoglobulin A ELISA antibody, precipitated 10 different outer membrane protein antigens by radioimmunoprecipitation, and reacted to 10 different membrane vesicle antigens of P. multocida by immunoblotting analysis. The hyperimmune rabbit sera were also evaluated for protective efficacy against experimental rabbit pasteurellosis by homologous challenge. Thirty-six rabbits were divided into four groups. Group 1, 2, and 3 rabbits were inoculated intranasally with hyperimmune rabbit serum, phosphate-buffered saline, or normal rabbit serpm, respectively, at 24 h prior to and 24, 48, and 72 h after iptranasal challenge with the virulent homologous P. multocida strain. Group 4 rabbits were inoculated with normal rabbit serum without challenge. Necropsies of surviving rabbits were performed 2 weeks postinfection. The mortality rates for groups 1 through 4 were 25% (3 of 12), 67% (8 of 12), 75% (6 of 8), and 0% (0 of 4), respectively. The prevalence and severity of pneumonia were significantly lower in the hyperimmune serum-treated rabbits. The prevalence of P. multocida colonization in lungs was significantly lower in group 1 rabbits, and the geometric mean CFU of P. multocida in lungs was 59,166-fold less in group 1 rabbits than in group 3 rabbits. The geometric mean CFU of P. multocida in nasal cavities of group 1 rabbits was significantly lower than that of group 3 rabbits. All challenged rabbits (groups 1, 2, and 3) had elevated nasal immunoglobulin A and pulmonary (lung lavage) immunoglobulin A antibody levels at necropsy (day 14 postinfection). Similarly, all challenged rabbits had elevated levels of ELISA immunoglobulin G antibody in serum at day 14 but not at day 7 postinfection, indicating that rabbits receiving hyperimmune serum can moVnt a specific humoral immune response against the homologous challenge P. multocida organisms. We concluded that hyperimmune serum directed to the KSCN extract of 3:A P. multocida provides significant protection against homologous challenge in rabbits.