Groups of chickens which were surgically thymectomized or bursectomized immediately after hatching, or hormonally bursectomized by testosterone injection at an early embryonic stage, or thymo-bursectomized were used in an attempt to elucidate the immunobiologic roles of the bursa of Fabricius and the thymus of the chicken in the initial development of immunologic competence, particularly the ability to produce serum antibody. There were no significant differences in the rate of elimination of an injected antigen (¹³¹ I-human serum albumin) from the blood of all the groups. However, a significant difference was observed in antibody production; no antibody was produced in the sera of hormonally bursectomized birds after the primary and secondary injections, while there was recognizable production of antibody in the sera of surgically thymectomized or bursectomized birds. Further, no antibody production was observed in tissue cultures of spleen cells derived from hormonally bursectomized chickens after immunization with human serum albumin or sheep erythrocytes. The injection of viable cells of the bursa restored to a significant degree the impaired capacity to produce antibody in hormonally bursectomized and surgically thymectomized birds as well as surgically thymo-bursectomized birds, while cell-free extracts of the bursa could restore the capacity only in the latter group of birds. These results suggest that in the chicken, only the bursa is concerned in the development of immunologic competence as measured by the ability to produce serum antibodies. The main role of the bursa seems to be to provide the initial supply of lymphoid cells and, in addition, the production of a humoral factor which promotes the proliferation of lymphoid cells and their immunological maturity.

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Transfer of flagellar characters from a motile strain of E. coli K12 Hfr to non-motile strains of E. coli F-by sexual conjugation and transduction tests was done. Motile recombinants were obtained from eight out of ten non-motile strains tested. Non-motile strains of E. coli tested were classified into three genetic groups according to their flagellar characters: (1) Motile recombinants of the first group possessed H antigens other than that of the donor (E. coli K12), or possessed the same H antigens as that of the donor, inheriting their latent H locus intact. (2) The H antigens of the motile recombinants from the second group were always the same as that of donors. Attempts to prove existence of latent H locus in strains in this group by recombination and transduction were unsuccessful. (3) No motile recombinants were obtainable from the third group of non-motile E. coli strains. In addition to the above, some of our experimental data on the motility of E. coli are described.

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Vibrio cholerae produces indole in the presence of nitrite even though the formen cannot always be demonstrated as such by standard test procedures. The results of present experiments indicate that the inhibition of a positive indole reaction by nitrite may be due to the interaction of nitrite with the para-dimethyl-amino-benzaldehyde in the indole reagent. Several factors, such as strain differences, pH change of culture medium, nature of fermentable carbohydrates, are also associated with the inhibition of indole production in the presence of fermentable substrates. The way in which these factors, singly or in combination, affect this inhibition is not known.

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Experimental infection of an inbred strain of DK1 mice was carried out with a mouse adenovirus strain K87, isolated from the feces of apparently healthy DK1 mice. Strain K87 was orally administered to four-week-old mice and the virus was recovered from their feces for at least 3 weeks. The highest virus titers in the feces were observed between 1 and 2 weeks after inoculation. In 7-week-old mice the period of virus excretion was about one week shorter. When neonatal or 2-week-old mice were administered virus orally, somewhat irregular results but similar to those from the 4 or 7-week-old mice were obtained. In these infected mice, virus growth was detected in the intestinal tract but not in oropharyngeal washings, nasal tissue, lung, spleen or urine. After inocu-lation through several parenteral routes, the virus was also detected in the feces and virus growth seemed to be limited mainly to the intestinal tract. No clinical manifestations were observed in any infected mice. When the virus was almost undetectable in the mice infected either orally or parenterally, the virus was readministered orally, but no further virus was recovered in the feces. Neutralizing antibody in the serum was detected 3 weeks after primary inoculation. Induction of immunological tolerance was examined by inoculating mice in utero 2-4 days before birth, but no evidence of induced tolerance was obtained. The use of the adenovirus strain K87-mouse system as a model system for the study of the infectious process and immune mechanisms is suggested because strain K87 has tissue tropism analogous to many human adenoviruses.

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A new species of Mycobacterium was described. Four strains of rapidly growing and non-pathogenic mycobacteria were isolated from soil by chicken passage, and were found to form one cluster by numerical classification based on similarity value. They were named Mycobacterium chitae (sp. nov.) and are deposited in the American Type Culture Collection (holotype; ATCC 19627).

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Surveys of staphylococcal strains, isolated from clinical sources in geographically scattered hospitals in Japan, disclosed the following facts: 1) Triple (TC•SM•SA, TC•PC•SA, PC•SM•SA) and quadruple (TC•SM•PC•SA) resistant strains with reference to TC, SM, PC and SA, were manifest and they were restricted to specific phage group. 2) There is a maximum population of resistant strains (M.P.R.) in a restricted area, which is governed by the amount and period of use of a drug and by genetic characters of the bacteria such as the mutation rate to resistance, and character which governs infectivity and ability for successful parasitism. 3) There are two types of resistant strains: the first becomes resistant easily and consequently multiple resistant when a new drug is introduced, and consists largely of strains in phage group I containing phage type 80/81. The second type remains single (SA) or double (PC•SA; SM•SA) resistant, and consists primarily of strains in group II and III. From the facts that all of the tested staphylococcal strains from clinical sources carry prophages and their drug resistance can be transduced to other strains by their prophages, the present author presents the hypothesis that transduction of drug resistance by prophage is mainly responsible for the acquisition of multiple resistance and wide distribution of multiple resistant strains in phage type or phage group.
Genetic studies of drug resistance in staphylococci have disclosed the following facts: 1) Resistance to TC is easily transduced at high frequencies by prophages obtained from multiple resistant strains, and in various combinations of donors and recipients. Resistance to SA and SM is jointly transduced with TC, and vice donors and recipients. Resistance to SA and SM is jointly transduced with TC, and vice versa. Resistance to PC, the ability to form penicillinase (PCase), and chloramphenicol (CM) resistance is not transduced jointly with resistance to TC, SM, and SA. 2) Resistance to macrolide (Mac) antibiotics (EM, OM, LM, SP) is eliminated jointly and irreversibly by acriflavine treatment or by ultraviolet irradiation, and is transduced jointly by phages obtained from donor strains. From these results it can be concluded that Mac resistance is located on an extrachromosomal plasmid. 3) Because of the genetic character of PCase formation (PCase⁺) and irreversible elimination of PCase⁺ it was concluded that the gene which governs PCase formation is located on a plasmid. And there are two types of plasmid; one which carries the genetic characters of resistanceto macrolide antibiotics (Mac^r) and of the penicillinase formation (PCase⁺) and the other carries only PCase⁺. A genetic model for the genes which govern resistance to TC, SM, SA and for the plasmids is presented. 4) The genetic character which governs resistance to CM is irreversibly eliminated during storage of stock culture or by treatment with acriflavine. This fact and results from transductional analysis suggest that the gene responsible for CM resistance may be located on α plasmid, probably different from the plasmids which govern (Mac^r. PCase⁺) or (PCase⁺). The findings that CM resistant strains of S. aureus inactivated CM in the presence of acetylcoenzyme A strongly suggest that CM resistance in strains from clinical sources is accounted for by inactivation of CM through acetylation of the drug molecule.

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