Germ-free swine were artificially contaminated with tetracycline (TC) sensitive strains of Escherichia coli and Klebsiella pneumoniae. One of these strains, E. coli 3306, was infected with a plasmid carrying kanamycin (KM) resistance, i.e., T-kan factor. Another strain, E. coli P-5, carried a conjugally transferable Col B factor. Among the nine strains used, onlyE. coli P-38 became TC-resistant after TC administration. Three types of TC-resistant E. coli P-38 strains were found; (a) one strain carried nontransferable TC resistance and could not produce colicin, (b) one strain carried TC resistance with a high transmission frequency which could not produce colicin, and (c) one strain carried TC resistance with a low transmission frequency that could produce colicin B. Genetic studies disclosed that the transmissible TC resistance factors, i.e., Rn_ms105 (group b) and R_ms104 (group c), were formed by recombination between Col B factor and nontransmissible TC-resistance (tet) determinant which appeared in E. coli P-38 mutants.

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An inactivated Mycoplasma pneumoniae vaccine was prepared from a culture in a liquid medium supplemented with water extract of egg yolk. Vaccinated Syrian hamsters were exposed to virulent M. pneumoniaelogical changes in the respiratory tracts. When a vaccine prepared with strain FH was administered intramuscularly or by inhalation in aerosol, no significant resistance was shown with respect to mycoplasma proliferation. An increased resistance, however, was observed when an aluminium phosphate-adsorbed vaccine, and when a plain vaccine (although to a lesser degree) prepared with hamster 24-passaged strain FH, was administered intramuscularly. Histopathologically, lung lesions were markedly suppressed in groups showing high resistance. A correlation between the serum antibody titer and the resistance to infection was observed. Hamsters which received a hyperimmune rabbit antiserum intracordally showed a high resistance to M. pneumoniae infection. The suppression of histopathological changes also coincided with high complement-fixing antibody titers of either actively or passively immunized hamster serum. The results suggest that humoral immunity plays an important role in resistance to M. pneumoniae pneumonia in hamsters.

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Properties of the receptor for influenza C virus were studied. Although the receptor for influenza C virus on chicken erythrocytes was destroyed by the homologous virion, neuraminidase activity could not be detected in any of the in fluenza C virus strains tested. The receptor activity of chicken erythrocytes for influenza C virus was diminished by formaldehyde treatment but not by periodate oxidation. There was a considerable variation in the pattern and the titer of hemagglutination of influenza C virus when human erythrocytes of different blood types were used; the virus agglutinated most type B erythrocytes but not type A erythrocytes. By using human type B erythrocytes, differences among strains of influenza C virus in the hemagglutinating activity were also demonstrated. These results showed that both the receptor for and the receptor-destroying activity of in fluenza C virus were completely different from those of influenza A or B virus and also that carbohydrates were not involved in the receptor for influenza C virus.

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The increase of PFC per spleen and the development of hemolytic foci were examined to clarify the patterns of clonal expansion of B-lymphocytes in athymic nude mice (nu/nu) and normal littermates (nu/+) subjected to the procedure for antigenic competition between horse erythrocytes (HRBC) and sheep erythrocytes (SRBC). In normal littermates without pretreatment with HRBC, a small number of PFC and hemolytic foci of small size were detected 2 days after the challenge with SRBC. The number of PFC increased progressively from day 2 to day 4, and hemolytic foci increased in the number and size during the period. In nude mice, a small number of PFC were detected on day 2 and the number increased only slightly from day 2 to day 4. No large hemolytic foci were detected during the period. In normal littermates subjected to the procedure for antigenic competition, the patterns of increase of PFC and development of hemolytic foci were similar to those in nude mice. In nude mice, the procedure for antigenic competition exerted almost no effect on the patterns.

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It was shown in our previous paper that mice primed with chemically modified bacterial α-amylase (BαA), which was neither cross-reactive with antiBαA antibody nor able to induce a humoral anti-BαA response, developed enhanced responses to a subsequent challenge with native BαA and that the magnitude of the immunological memory was closely related to the priming dose of modified BαA. This paper describes the experimental conditions for induction of delayed hypersensitivity (DH) by modified BαA in relation to the development of immunological memory for antibody response to native BαA.
Mice primed with either an intraperitoneal (i.p.) or subcutaneous (s.c.) injection of modified BαA in complete Freund's adjuvant (CFA) developed enhanced anti-BαA responses to a subsequent challenge with BαA. In contrast, when mice were immunized with an s.c. injection of the modified BαA only, a significant level of DH to native BαA could be induced, as measured by the footpad reaction (FPR). The highest degree of DH was observed in mice given 50 μg of modified BαA. DH was detectable within 5 days and persisted for 25 days after immunization. In the reciprocal combination of native BαA as the immunogen and modified BaA as the eliciting antigen, the relationship of anti-BαA responses to DH was examined. The primary anti-BαA responses induced by an i.p. injection of large doses of BaA was markedly higher than those induced by an s.c. injection, while DH was exhibited only in mice given an s.c. injection of BαA in CFA.
With respect to DH to native BαA induced by the modified BαA, it was shown that C3H/He mice were high and C57BL/6 mice were low responders.

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Mycobacterium szulgai (1) is a new species recently described. It belongs to slowly growing scotochromogens (Runyon's Group II (2)). Recently we isolated three strains of mycobacteria from sputum specimens of a patient, a 50 year-old male carpenter. The strains were isolated on the 23rd, 24th and 25th of June 1976 and formed 86, 44 and 4 colonies, respectively, on isolation media. At that time, the chest X-ray film of the patient showed a large cavity with pericavitary infiltration in his left upper lobe. After six-month-administration of a streptomycin-isoniazidrifampicin regimen, the cavity became thin-walled and the organism disappeared from sputum. In view of the above course of the disease, the organism was considered to have caused the disease in the patient.
The strains were examined according to the methods previously described (4) and identified as M. szulgai (Table 1). The strains used in the study were isolated from single colonies.
The most interesting characteristic of the strains was their temperature-dependent photochromogenicity. The strains were nonchromogenic when incubated on Ogawa egg medium at 28 C in the dark for 14 days, whereas the colonies became scotochromogenic (orange-pigmented) when incubated at 37 C in the dark. The colonies that grew at 28 C in the dark became pigmented after exposure to daylight for one day. Temperature-dependent photochromogenicity of M. szulgai in several strains was reported by Schaefer et al (3). The findings in the present study show that such strains occur and lung disease due to this organism is also present in this country.

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