Measles virus suppressed cellular DNA synthesis two hours after infection but did not inhibit RNA or protein syntheses. The suppression of DNA synthesis was not dependent on the cellular growth phase but was dependent on the multiplicity of infection. This activity of measles virus was inactivated neither by ultraviolet-irradiation nor by heating at 56C for two hours, but was lost after treatment with a convalescent antiserum of a measles patient or with proteolytic enzymes (pronase and trypsin).

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1. Changes in virulence of Shigella and Shigella-like enteropathogenic Escherichia coli, which occurred during their acquiring resistance to rifampicin were examined, Virulence was evaluated in vitro by their cell-invasive activity, infectivity to the eye of guinea pigs, and LD₅₀ values in intraperitoneally infected mice. 2. The mutants obtained in vivo and those obtained in vitro somewhat varied in cell invasiveness. Ability to produce keratoconjunctivitis in guinea pigs was lacking or diminished in all mutants though the parent strains constantly showed high abilities to invade cultured cells or produce keratoconjuctivitis in guinea pigs. 3. Mutations to resistant strains were not accompanied by any changes in LD₅₀ values in mice.

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In vitro-developed resistant mutants were obtained by inoculating a clinical isolate of Aerobacter cloacae on plates containing various concentrations of ampicillin (APC). This resistance was paralleled by an increase in the formation of β-lactamase. When A. cloacae carrying the nontransmissible APC resistance-determinant (amp) was infected with a T-tet factor, a recombinant T-tet.amp factor was formed; the recombinant being conjugally transmissible and capable of conferring APC resistance on their host. This fact implies the origin of the R factor; the R factor being formed by the recombination of sex factors with nontransmissible drug resistance-determinants.

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The relationship between antistreptolysin-O (ASLO) titers and β-lipoprotein were examined The following results were obtained. 1. Fifty-three children with unmeasurably low ASLO titers had variable β-lipoprotein concentrations which were within normal ranges. 2. Streptococcal infections in the children correlated well with the elevation of ASLO titers, but β-lipoprotein concentration in these sera did not show any correlation with the behavior of ASLO titers. 3. From the Sephadex G 200 gel filtration chromatographical study, no ASLO activities were found in the fraction containing β-lipoprotein except in some special cases that had the IgM ASLO antibody. 4. The inhibitory effect of β-lipoprotein upon hemolysis by streptolysin-O was incomplete and its effect decreased with a pro longed incubation time. 5. The partially purified β-lipoprotein had no effect upon the hemolytic activity of streptolysin-O, when the ASLO titers were measured by the method of 100% inhibition cf hemolysis. From these observations, it was concluded that the ASLO antibody titers were truly relate to streptococcal infection and not influenced by the presence of β-lipoprotein if the ASLO titers wer measured by the 100% inhibition of hemolysis.

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Spontaneous mutants possessing quantitative differences in enterotoxin B production were isolated from the parent strain of Staphylococcus aureus S6 by using NZ-amine agar plate which contained antienterotoxin B antiserum. A shake-flask culture of S. aureus S6 715H, a high enterotoxin B-producing strain, extracellularly produced 370μg/ml of enterotoxin B after 16hr of incubation at 37C. A shake- flask culture of S. aureus S6 715NH. a low enterotoxin B-producing strain, produced 22μg/ml of enterotoxin B under the same conditions. The difference in the ability to produce enterotoxin B among the strains resulted from differences in their activities of de novo enterotoxin B synthesis. A quantitative difference in the production of individual extracellular proteins existed in the strains. S. aureus S6 715H produced higher levels of α-and δ-hemolysins, alkaline phosphatase, ribonuclease and staphylokinase (fibrinolysin) than S. aureus S6 715NH. These results suggest that the production of enterotoxin B and most of the other extracellular proteins, at least the above five toxins or enzymes, may be dependent upon some coordinated control mechanisms in S. aureus S6.

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Two samples of slime obtained from Pseudomonas aeruginosa strains, IFO 3445 and No. 24, the latter which produced mucoid colonies on brain heart infusion agar as well as on the synthetic agar medium, were investigated for their physicochemical properties, primarily for their viscosities. Results obtained indicated that the principal component of the slime from strain IFO 3445 might be a deoxyribonucleic acid-like substance, while the slime from the mucoid strain No. 24 might be an alginic acid-like substance.

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A novel ultramicro microbioassay was developed. The present method, referred to as amplified cultivation, is composed of two successive kinds of culture. The first culture is performed until a maximum difference is obtained in the ratio of numbers of viable cells appearing in a basal medium and that contained in a nutrient. The second culture is continued after adding a complete medium to the cultures and stopped just after the growth of microorganisms in the blank reaches a certain detectable limit, e. g., by optical density or acid production. Lactose was analyzed by this amplified cultivation method with an extremely low concentration of viable cells of Bifidobacteriumz bifidum N4 as the inoculum. The detectable limits of lactose were 0.05μg and 1μg by the test tube method and by the pulp disc method respectively, with an increase in sensitivity by a factor of more than 10³ compared with the corresponding conventional microbioassays. Moreover, a relationship between the diameters of the growth zones and the logarithm of the amount of lactose was achieved in a range of 50-1000μg of lactose in the pulp disc method.

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Shigella strains isolated in Japan from 1968 through 1970 were surveyed for drug resistance and distribution of R factors. Of the 2688 strains, 93.4% were resistant to either one or various combinations of four drugs, tetracycline (TC), chloramphenicol (CM), streptomycin (SM) and sulfanilamide (SA). Among these resistant strains, 74.2, 10.7, 1.48, and 13.6% were quadruply, triply, doubly, and singly resistant, respectively. Fifty-eight per cent of these resistant strains were found to carry R factors when judged by transferability of the resistance. The isolation frequencies of R (TC. CM. SM. SA), R (CM. SM. SA), R (SM. SA), and R (TC. SM. SA) factors were 73.2, 13.0, 11.5, and 1.3%, respectively. The strains resistant to drugs other than the aforementioned four were very few; 4.3, 3.4, and 0.7% being resistant to ampicillin (APC), nalidixic acid (NA), and kanamycin (KM), respectively. Among 117 APC-resistant strains, 97.4% could transfer their APC resistance together with other resistance markers. Seventeen out of 18 KM-resistant strains could transfer KM resistance by mixed culture. But none of the NA-resistant strains could transfer their NA resistance. The authors could demonstrate strains carrying two different R factors in a cell and one of them was consistently an R (SM. SA) factor. These results were very similar to those obtained in surveys of strains isolated from 1965 through 1967.

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A surface antigen(s) was detected in adenovirus type 12 (Ad12)-transformed cells by fluorescent antibody technique. The antigen was revealed by antisera of mice and rabbits immunized with the virus, and by those of rabbits immunized with conditioned medium from cell cultures carrying the surface antigen. The antigen was specific for the Ad12-transformed cells, since it was found only in the Ad12-transformed cells regardless of the animal species and not in any other cells, including SV40-and polyoma virus-ransformed cells. The antigen was distinct from the Ad12-specific viral and T antigens, since the sera of rabbits immunized with the conditioned medium contained little or no detectable antibodies to the latter two antigens. On the contrary, the surface antigen was not detected in any tumor cells induced by Ad12 by the above antisera, and no detectable antibody to the surface antigen was produced in mice immunized with the tumor cells.

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Alternate changes of specific surface antigen(s) (S antigen) were examined in transformed and tumor cells induced by human adenovirus type 12. All of the hamster and mouse cells transformed in vitro showed ring-form membrane fluorescence staining by anti-S antigen rabbit sera, whereas tumor cells, either induced by the virus in vivo or produced by inoculation with the S(+)-transformed cells, did not show any fluorescence. When the S(-) tumor cells were serially subcultured in vitro, all of them converted to S(+) cells, although more than ten subcultures were necessary. For the S(+) cells to form tumors in hamsters about ten times as many cells were necessary as the S(-) cells. This difference became greater when tumor formation was tested in preimmunized hamsters, while little, if any, when tested in X-irradiated hamsters. In addition, immunogenicity of the S(+) cells was sug-gested to be higher than that of the S(-) cells. These findings indicate that the S(+) cells are more immunosensitive and immunogenic than the S(-) cells, and that in vivo conversion from S(+) to S(-) may be due to selection of S(-)-mutant cells. In vitro conversion from S(-) to S(+) was also suggested to be due to the appearance of S(+)-mutant cells.

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