Golden hamsters were used as hosts in this work, and mice of various strains as donors of antigens. 1) There were no strain differences in immunogcnicity of erythrocytes from C57BL/6. AKR, SL and CF1 mice. 2) Primary intravenous immunization with mouse erythrocytes (MRBC) induced the production of hemolysin plaque-forming cells (PFC) in a large number, but elicited only in a negligible titer production of 2-mercaptoethanol-resistant antibody. 3) 2-Mercaptoethanol-resistant antibody was produced more efficiently in hamsters pre-sensitized with mouse lymph node (MLN) cells rather than those pre-immunized with MRBC after a booster with MRBC. 4) Numbers of PFC in pre-sensitized hamsters were three-times that of the non-sensitized hamsters after a booster with MRBC. when pre-sensitization was performed intradermally with a small number of MLN cells. 5) Average diameter of the hemolysin plaques in pre-sensitized hamsters was one and a half times larger than that in non-sensitized hamsters. Conclusions agree well with the results in our previous papers that the reversed combination of hosts and antigen donors employed support the concept that certain processes required for delased hypersensitivity contributed to antibody production under a condition suitable for antibody response.

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The gene governing ampicillin resistance and penicillinase production in Klebsiella pneumoniae was analyzed by means of a conjugation system. The gene, amp, was mapped between pyr4 and aro18 on the linkage map of K. pneumoniae. The chromosomally mediated penicillinases of K. pneumoniae were partially purified and their properties were compared with those of known species-specific penicillinases of K. pneumoniae and also those of the penicillinases of R factors haying ampicillin resistant marker. The chromosomal penicillinases were consistent with most of the species-specific penicillinases in enzymological and immunological properties and in their behavior on agar gel electrophoresis. They also showed a close relationship to type I penicillinases of R factors in enzymological and immunological properties.

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When living cells of Staphylococcus aureus were introduced into mice by various routes within a few hours before or after infection with Nocardia asteroides, a marked increase in mortality and enhanced severity of lesions were observed. This effect was presumably caused by a heat-labile substance (s) liberated from the cells of S. aureus. No increase in resistance occurred when S. aureus was given 2 to 7 days before the nocardial infection, contrary to the effect of E. coli as reported previously. An increased resistance was noted when heat-killed cells of E. coli were administered two to four days before concurrent infection with N. asteroides and S. aureus.

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³H-Serine principally labeled phosphatidylserine (PS) and phosphatidylethanolamine (PE) of lipids of chick embryo cells. ³H-Ethanolamine labeled almost entirely PE of lipids of the cells. In turnover experiment with ³H-serine incorporated into cells before infection, the pathway from PS to PE was shown to become more active by Sendai virus infection. Similar turnover experiment using ³H-ethanolamine revealed that PE synthesis directly utilizing ethanolamine was also slightly enhanced by the infection. The most marked difference of infected cells from control cells was the enhanced rate of ³H-serine incorporation into lipids- These results indicated that the Sendai virus infection enhanced the metabolic pathway serine-PS-PE.

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As described in a precious study, Sendai virus formed plaques in chick embryo (CE) cell monolaycrs with the aid of trypsin incorporated into the agar overlay medium. The virus also tormed plaques in monkey kidney (MK) cell monolaycrs without the aid of trypsin. Sendai virus grown in CE cells, as well as that grown in either of other stable cell lines tested, showed much lower plaque-forming unit (PFU) titers in MK monolayers than in CE mo nolayers. Howeycr, a mild trypsin treamnent of the virus grown in these cells enhanced its PFU titers in MK monolayers to the level obtained in CE monolayers. In spite of this marked infectivity enhancement, the enzyme treatment little affected the hemagglutinin titers of the virus. On the other hand, Sendai virus grown in embryonated eggs or MK cells showed similar PFU titers in both CE and MK monolayers and also showed no evidence of infectivty enhancement due to the enzyme treatment.

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A-decomposing enzyme prepaiation (α-N-acetylgalactosaminidase) from hog liver, liberates from the lipopolysaceharide of Salmonella riogrande, which contains O antigen 40, 15.5% of its original amount of N-aeetylgalatosamine, destroying its ability of inhibiting the agglutination of human A red cells by anti-S. riogrande rabbit serum. From the structures of blood group A-active oligosaccharides, obtained from the lipopolysaccharide by mild acid-hydrolsis, it was assumed that the antigenic determinant of A specilieity might have the following strueture, which indicated the presence of N-acetylgalactosaminlyl residue as the non-reducing end; α-N-acetylgalactosaminyl-(1→3)-mannosyl-glucosyl-(1→3)-N-acetylgalactosaminyl-glucose.

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Drug-resistance (γ) determimants, γ₂₇(tet), γ₁(cml), and γ₁₁(str. sul) were obtained from R factors, and were capable of conferring resistance to tetracycline, chloramphenicol, and to both streptomycin and sulfanilamide, respectively. They were integrated into the chromosome of Escherichin coli K12 and nontransmissible by conjugation. As described previously, the recombinant T-tet factor was tormed and conjugally transmissible when E. coli K12 γ₂₁(tet)⁺ was infected with T₉₅ one of the transfer factors. Similarly, the recombinants T-tet. cml and T-tet.str. sul factors were formed by the interaction between T-tet factor and resistance determinants γ₁(cml) and γ₁₁(str. sul), respectively Subsequently, T-tet. cml. sul factor was formed bye the recombination between T-tet. cml factor and γ₁₁(str. sul) determinant, and T-tet. str. sul. cml factor was produced by the infection of E. coli K12 γ₁(cml)⁺ with T-tet. str sul factor. These recombinants were conjugally transmissible and transduced by phage PI as one unit. These results strongly suggested the origin of R factors which were capable of conferring multiple resistance and transmissible by conjugation. According to the segrcgational patterns of resistance determinants by transduction and by conjugal transmission, the genetic structure of T-tet. cml. str. sul. factors was established as being circular and the linkage order of the determinants of these factors was described.

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Ibaraki virus is an agent of epizootic cattle disease resembling bluetongue. The virus was purified from infected BHK-21 cells and bovine kidney cells. The particle negatively stained was icosahedral and had a diameter of 45-50mμ. By electron microscopy, the virus was found in the cytoplasm of cells, assembling in lysosomal or matrix-like dense bodies. In early stages of infection, 2 to 7hr, virus particles were located in vesicles, simulating a viropexis, whereas at 24 to 30hr, after infection, a large number of cores of progeny virus were scattered in matrix-like bodies or packed and crystallized in lysosomal bodies bounded by a membrane. Sometimes peculiar tubular structures were found near the matrix-like bodies. The relation-ship between these structures and vinus replication was not clear. The morphological features of the particles and virus development in cells resembled those of viruses of bluetongue, African horse-sickness. Colorado tick fever and reo.

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Response of CBA mice with γM and γG antibodies to bovine serum albumin (BSA) was studied in relation to a variety of conditions of antigen administration. The variables in the conditions were doses and physical forms of antigen, and injection routes. It was realized that γG antibody response to soluble BSA and both γM and γG antibody responses to particulate forms of BSA were augmented as the dose was increased. The γM response to soluble BSA was not elevated by an increase in the amount of antigen up to 1mg. The soluble form was not so inmunogenic as the particulate forms, in which alum-precipitated BSA was capable of inducing both γM and γG antibodies to high titers, and heat-denatured BSA elicited preferably γM antibody. Alum-precipitated BSA and the emulsified BSA were strong inducers for γG antibody response when injected subcutaneously. In any antigen form, γM response was markedly influenced by changing the injection route, the order of decreasing efficiency for γM antibody being intravenous, intraperitoneal and subcutaneous. The γG antibody response was hardly affected by the injection route. The effect of a single intravenous injection of 0.01mg of endotoxin, given 1 to 2hr after antigen injection, on γM and γG antibody production differed according to the antigen administration procedures. Generally, speaking, this agent had an enhancing effect when the antigen was given in the particulate forms, and it depressed the response when the antigen was givcn in the soluble form.

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Considerable fractions of gram-negative bacilli, Aeromonas liquefaciens, A, salmonicida, Pseudomonas, Hafnia and unidentified Enlerobacteriaceae, isolated from the intestinal tracts of cultured Amago (Oncorhyuchus rhodurus macrostomus) from 23 Amago-ponds and of Yamame (O. masou ishikawae) from one pond as well as the water of 3 ponds in Shiga, Gifu and Nagano Prefectures and Tokyo Metropolis in Japan were found to be multiple-drug-resistant. Of those drug-resistant strains, A. salmonicida and A. liquefaciens carried R factors at high frequencies and to be prevalent in many Amago ponds throughout Japan. Thcsc R factors had markers of resistance to SA, SA. TC, SA. SM.CM. All the R factors belonged to fi^-type.

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