Plasmodium ovale Malaria is endemic in the tropical Africa and a few cases are reported from the Philippines and New Guinea. We report here three Japanese cases of ovale malaria who got the infection in Africa. A 31-year-old man was infected in Congo (Brazzaville) and was seen at the first relapse 18 months after he returned to Japan. The second case was infected in Guinea and developed illness 8 days after he came back to Japan. The third case got infection somewhere in Africa as he travelled across the continent by car and sometimes on foot. He developed fever 5 months after he came home. The clinical picture was similar to vavax malaria and the first patient was successfully treated by a combination of sulfamonomethoxine-pyrimethamine and the 2nd and 3rd patients by a combination of sulformethoxine-pyrimethamine. The morphology of the parasite itself and the parasite-infected red cells was similar to that of P. vivax. But the outstanding features, as stained by the Giemsa solution at a pH of 7.2, were as follows. The parasite was smaller, compact and had less amoeboid activity than P. vivax. The average number of merozoites in the schizonts was 6 and 8 in the two patients in whom there were sufficient number of the schizonts for examination. These numbers are one half of the merozoite number of the schizonts of P. vivax. The infected cell was usually smaller than P. vivax-infected cells, and some but not all cells showed elongation and fimbriation. The Schiiffner's dots were large, distinct and were more intensely stained than the dots in P. vivax-infected cells.
A 17-year-old Japanese cook was admitted to Nakano General Hospital with nose bleeding, fever, jaundice and myalgia of several days duration. Diagnosis of “Weil's disease” was made clinically and serologically. Antibody titer of “Leptospira icterohaemorrhagiae” was found to be elevated to 320 times higher than control. No spirochaeta was found in the patient's urine nor in the blood. Streptomycin, steroid, and intravenous fluid infusion lessened the hemorrhagic tendency and jaundice. The patient, however, became agitated and made any further treatment impossible, such as hemodialysis to remove excessive blood urea and bilirubin. Sedation and tranquillization were not done in consideration of hepatic dysfunction. On the 25th day of the disease, he was expired after the abrupt onset of shock. The postmortem examination revealed a massive bleeding from a duodenal ulcer, and edema with jaundice of almost all the organs. The case was evaluated in comparison with 84 reported autopsied cases in Japan.
1) The antigen suspension, saline and formalin (0.4%) saline which were first adjusted to pH 7.4 became to pH 6.3 after two weeks stay in room temperature. These decline in pH, however, had no influence upon the agglutinability of Clostridium perfringens antigen. 2) Neither the differences of NaCl concentration in saline nor the difference of the components (agar, yeast extract, peptone, meat extract, soluble starch etc.) of the media used for the cultivation of Clostridium perfringens showed influences upon the agglutinability. 3) The differences of the intensity and the titer of agglutination reaction were observed between antigens cultured on the heart infusion agar plate and in its original broth. 4) The size of the inoculum cultures into the fluid medium for the preparation of antigen had an influence on the agglutinability. Less than 10% of the volume of medium should be inoculated for the purpose of obtaining the antigen of stable agglutinability. 5) As to the reading of tubes in the agglutination reaction, the shaking method showed more stable results than the non-shaking method.