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The mechanisms of immunity to Mycoplasma pneumoniae were investigated by evaluating different vaccination procedures in an experimental animal model. Hamsters were immunized by intranasal inoculation of broth cultures or by parenteral injections of saline-suspended organisms. All vaccinees received a standardized intranasal challenge which produced pneumonia in 94% of controls. Intranasal immunization with virulent organisms produced a 71 % reduction in pneumonia. Subcutaneous and intraperitoneal inoculation of the same organisms yielded 56 and 61% reductions, respectively. Animals similarly immunized with an attenuated strain developed resistance to pneumonia only after intranasal infection. Serum antibody levels did not correlate with protection. Growth-inhibiting activity was demonstrated in bronchial washings of challenged animals, suggesting the development of local antibody in response to infection with M. pneumoniae. Crosschallenge studies were performed in animals vaccinated intranasally with virulent and avirulent variants of the same strain. The avirulent vaccine prevented pneumonia in animals challenged with homologous virulent organisms but not in those receiving an unrelated strain; the virulent vaccine provided protection to both homologous and heterologous challenge. These studies indicate that organism strain variation as well as vaccination technique are important determinants of the immune response to M. pneumoniae.on July 15, 2020 by guest http://iai.asm.org/ Downloaded from

PLATE XI1THE pathogenesis of pneumonia in man caused by Mycoplasma pnewnoniae is poorly understood. However, the M. pneumoniae-infected Syrian hamster is a useful model, not only because this is one of the few small animals that can be successfully infected, but also because the histological characteristics of the pneumonia and the temporal development of antibody are similar to these features in man (Dajani, Clyde and Denny, 1965;Fernald, 1969).Pneumonia in hamsters infected with M. pneumoniae consists of peribronchial and perivascular cuffing by lymphocytes, and this suggests that it is the result of a delayed hypersensitivity response in the lung. However, immunoglobulin is associated with many of the cells (Fernald, Clyde and Bienenstock, 1972), indicating that the response may not be a pure delayed hypersensitivity reaction. Nevertheless, other observations suggest that delayed hypersensitivity develops during M. pneumoniae infection. Thus, guinea-pigs and man develop skin hypersensitivity (Fernald, 1971 ;Mizutani et al., 1971). Furthermore, lymphocytes from previously infected human subjects and guinea-pigs can be stimulated in vitro by M. pneumoniae antigens to undergo blast transformation (Leventhal et al., 1969;Fernald, 1971; Biberfeld, 1972;Fernald, 1972), and the migration of macrophages can be inhibited by M. pneumoniae antigen (Arai et al., 1971). Nevertheless, these in-vitro demonstrations of delayed hypersensitivity may not be relevant in vivo. However, with regard to the latter situation, Denny, Taylor-Robinson and Allison (1972) demonstrated that mice, immunosuppressed by thymectomy and X-irradiation and infected intranasally with M. pulmonis, developed lung lesions that were much less severe than those observed in infected but immunologically normal mice. Although the lung lesions in these mice and in M. pneumoniae-infected hamsters appear similar, this does not necessarily mean that thymusdependent mechanisms are also important in the development of hamster lung lesions.Because we are particularly interested in the hamster as a model for the human disease, the effect of thymus-dependent lymphocyte depletion on the development of M. pneumoniae-induced lung lesions in hamsters was investigated. Immunosuppression was effected by the use of anti-thymocyte serum. The present report records findings obtained with this model in two laboratories. MATERIALS AND METHODSMycoplasma pneumoniae strains. Virulent M. pneumoniae strains P1-104166, B8-Ml29 and P5-427AY known to produce pneumonia in hamsters were used. The mycoplasmas

Infections with Herpesvirus hominis type 1 were associated with 11.5% of acute respiratory illnesses of university students who were admitted to the student infirmary over a 6-year period. Over three-quarters of these infections were detected in students with pharyngitis or tonsillitis; 42% had ulcerated lesions on tonsils or posterior pharynx but only 11% had lesions in the anterior portion of the mouth or lips. Almost all of the H. hominis infections were accompanied by significant rises in neutralizing antibodies and few students had detectable antibodies in the initial serum collected during the acute phase of illness. Special studies revealed herpes-specific IgM antibodies in the early convalescent sera of some of these patients. The data demonstrate that 80% of the infections detected were primary infections with H. hominis. Only 30% of university students possessed neutralizing antibodies to H. hominis and about 10% of those without antibodies acquired antibodies each year. These data suggest that the majority of persons from middle income families reach young adulthood without acquiring infections of H. hominis and the spread of the virus requires close and intimate contact.

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