Fifty nine cases of acute staphyloccocal enteritis were found during the course of therapy with broad-spectrum antibiotics against bacillary dysentery from April 1954 to October 1955. Of these cases two were fatal of which one demonstrated pathologically pseudomembranous enteritis.
The broader the spectrum of antibiotics employed was and the younger the children treated were, the higher was the incidence of staphylococcal enteritis. Initial symptoms such as pharyngeal redness, diarrhea and fever were observed in general in 4 to 5 days after the initiation of therapy. Main signs and symptoms found during the course of this disorder were as follows: Fever (96.8%), pharyngeal redness (91.5%), diarrhea (91.5%), strawberry tongue (94.7%), rash (81.4%), abdominal pain (73.6%), sore throat (58.1%), nausea (55.9%), vomiting (52.5%) and relapse with re-exanthem (18.6%). Rash and relapse accompanied with re-exanthema were characteristic of this disease. Scarlatiniform exanthema appeared on the 2nd to 3rd day of illness, continuing for 3 to 7 days in 40 cases except 9 cases without exanthema and 10 cases with erythema-like rash.
The re-exanthema, erythema-like, urticaria-like or scarlatiniform, was observed in the: 3rd to 4th week of illness in 6 cases and the relapse with enteritic syndrom such as diarrhea, vomiting and fever about the 2nd week in 4 cases, both types presenting rather mild conditions. Furthermore, one case of mixed type was noted.
Hemolytic and coagulase positive staphylococci were always isolated from the throat, vomit and feces in the acute stage, showing high resistance to the antibiotics employed. The phage patterns of the staphylococci isolated were mainly 52/155/156 in 46 cases from April 1954 to December 1955, whereas 13 cases from February to October 1956 demonstrated all 42B/29, suggesting that these cases of staphylococcal enteritis were caused by cross-infection in the hospital.

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In the previous report the alkali-labile antigen of Sh. dysenteriae 2 was described. In the following studies it was found by the authors that a similar alkali-labile antigen was present in some serotypes of Sh. flexneri. The results of the experiment were summarized as follows.
Group specific antigen 6 of Sh. flexneri present in serotypes of Sh. flexneri lb (I: 4. 6), 3a (III: 6. 7. 8), 3b (III: 4.6) and 4b (IV: 6) was serologically completely inactivated with N/10-NaOH at 37°C for 4 hrs. This is a specific character which could be recognized only in this antigen.
As shown in Tab. 1, its agglutinability was destroyed with the treatment. The anti gens of the above mentioned four serotypes treated with alkali never yielded agglutinin against group specific antigen 6 when injected into rabbits as shown in Tabs. 2, 3, 4, 5 and 6. Agglutinin-binding capacity of this antigen was also destroyed with the treatment as shown in Tab. 7. Namely, agglutinin against group specific antigen 6 was left unaffected with the absorptions of the alkali treated cells.
It was interesting to note that the alkali-stable antigens resting in the alkali treated bacterial cells closely resembled serologically the formalinized antigens of their respective non-type-specific variants dissociated naturally from their type-specific parents by loss variations.

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The fluctuation of cold hemagglutin and heterophilic antibody titer of twenty seven cases of Izumi fever were investigated during the course of illness.
The results were as follows:
1. No elevation of cold agglutinin titer.
2. The antisheep agglutinin titer demonstrated a tendency to elevate in the second week.
3. At the same time the hemolysin titer against sheep red cells elevated after the second week.
4. After the absorbtion with the mixture of human blood cells, type O, A and B, the rabbit blood cells and then the goat blood cells, the hemolysin titer of patient serum against sheep blood cells showed a higher level after the second week than that of the first week.
It was concluded that the Forssman antibody and X-antigen named by Nunome increased in Izumi fever.

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A liver biopsy was carried out on a 4 year old male patient suffering from scarlet fever with jaundice on the 17th day of illness in order to clarify the pathogenesis of scarlatinal jaundice. The clinical findings and the course of illness were reported.
The histological findings obtained were as follows:
1) Albumin-thrombi in bile capillaries.
2) Deposition of bile pigment in liver cells.
3) Neither necrosis nor fatty degeneration of liver cells.
4) Neither cholangiolitis nor stagnation of bile in the portal space.
These findings suggest that the scarlatinal jaundice represent a kind of obstructive jaundice caused by the albumin-thrombi due to the disturbance of permeability of bile capillaries which resulted from infectious liver cell impairment.

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Hundred one standard strains and 56 strains of Salmonella isolated in our hospital were cultured on the Endo medium without lactose (3.0% normal agar 100.0cc, 5.0% fuchsin ethanol sol. 0.5cc, 10.0% Na₂SO₃ 1.0cc). Twenty four red colony producing strains (red type strains) were isolated from the former and 11 from the latter. The color tone and the rate of red colonies varied from strain to strain. The red color, however, was unequivocally recognizable for the red type strains, as compared with white type strains (white colony producing strains).

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Thirteen red type strains out of Salmonella strains preserved in our hospital were morphologically studied in contrast with the white type strains.
No difference was recognized with regard to the morphological properties of colony as well as bacterial body between the two types on the normal agar medium. Regarding the white tipe strains, the Endo medium showed no difference as the normal agar medium, whereas on the former the red type ones grew worse. The latter was white at the beginning, and became gradually red with the lapse of time. The bacterial body became thickened and elongated demonstrating red granules by means of supravital staining with methyleneblue, which is the mechanism of the reddening of the colony. These granules disappeared readily by the fuchsin dissolving solution, while unchanged by the fuchsinundissolving ones, i.e. ether, sat. picric acid, Bouin, Bouin-Holland, Bouin-Allen. After the fixation with Bouin, however, they did not disappear even by the use of fuchsin-dissolving solution, decolorizing agents, acid or alkali, whereas they became invisible after the removal of R.N.A. The granules, decolorized by ethanol domonstrated affinity only to fuchsin, crystall violet, gentiana violet, acid fuchsin, eosine yellow, chrysoidine.
By HCL-Giemsa, HCL-methylenblue and Feuigen reaction, the part with the red granules and the spindle-shaped swollen part exhibited no nucleus or an irregular and complicated one. A septum was hardly recognized in the thickened and elongated bacterial body. With Unna-Pappenheim staining the nucleus was less stained. After the reaction of ribonuclease, Giemsa did not stain the nucleus. By means of peroxydase, oxydase, alkaline phosphatase staining, the part of bacterial body, corresponding to the nucleus was stained, while the part with the red granules and the spindle shaped swollen part were not stained. The bacterial body was hardly stained by the polysaccharide staining.

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