In order to investigate how long the antibody to hepatitis surface antigen (anti-HBs) remains in the blood stream after a hepatitis B vaccine (HB vaccine) is given, a total number of 525 vaccinees were followed up from 19 to 36 months after the first injection. 261 infants (137 males and 124 females) and 264 adults (61 male and 203 females), who were negative for HBV markers such as HBsAg, antii-HBs and anti-HBc were immunized with 10 mcg for infants and 20 mcg for adults. Four kinds of vaccine were used in the study. Thirty-four infants who either had no anti-HBs response or who had an anti-HBs response which later disappeared were given one or two more doses of 10 mcg. The following results were obtained. 1) The anti-HBs seroconversion rate after three vaccinations was 83.5% in 9 (after the first vaccination), 76.2% in 19 months and 60.9% in 36 months. 2) The anti-HBs seroconversion rate was higher in females than in males.3) The anti-HBs seroconversion rate was higher in the age groups 4-5 years, 20-29 years and 30-39 years than in above 50 years. 4) The anti-HBs seroconversion rate after 4 or 5 vaccinations was 44% in 36 months. 5) The titer of anti-HBs was 27.2 in 9 months, 25.6 in 19 months and 25 in 36 months. 6) The main side effects were soreness at the injection site (15.0%) and general fatigue or malaise (17.7%). But most of the side effects were mild and disappered soon without any treatment. We think that HB vaccine is safe and effective for the prevention of hepatitis B infection.
We studied an experimental urinary tract infection in mice with 30 strains of Escherichia coli to know whether the strains isolated from urine of patients with urinary tract infections are more vilulent on the urinary tract than the strains isolated from feces. Mice were transurethrally inoculated with 1×107bacteria, and given no additional treatment. The bacteria were recovered from 50% of the kidneys. Common O serogroups in the infection caused inflammatory responses not more severely than the other serogroups did. Pathogenecity of these bacteria may be too weak to be detected by the experimental infection in animals with normal condition. On the other hand, the strains isolated from urine of patients, however, were recovered more frequently and densely from the kidneys of mice than the strains from feces (p<0.01). Thus, we concluded that the strains causing urinary tract infections are not mere opportunistsbut have some affinity for the tracts.
A foodborn outbreak of beta hemolitic streptococcal sore throat occurred in Tokyo, in an early July, 1983, among people who had attended at a lecture meeting sponsored by a company. Questionnaire information was obtained on 890 persons or 97.6% of the attendees, 583 (65.5%) of whom became ill with a sore throat. Other major symptomes and signs of the patients were fever (85.4%), malaise (83.2%), headache (65.4%) and tender cervical adenopathy (61.1%). Ninety-eight or 18.1% had diarrhoea, 52 or 9.4% had abdominal pain, and 2.7% experienced vomiting. Skin rash was reported by 13 or 2.3%. There were no fetal cases. The median incubation time was estimated to be 37 hours. Twenty-seven of 74 (36.5%) throat culture, 24 of 49 (49.0%) from ill persons and 3 of 25 (12%) from healthy persons, were positive for group A beta hemolitic streptococci. All of the isolates were classified as T type 13 and M untypable. Among ill persons, significant rise of serum anti-streptolysin 0, anty-hyaluronidase and anti-NADase titers was observed in convalescence. Food preferences and illness rates incriminated the egg-sandwich catered at the meeting as the vehicle of the infection. Further support for this incrimination was provided by the following facts;(1) throat cultures of two food handlers who cooked the sandwiches were positive for the outbreak strain, and (2) some attendees and family members who ate the left-over sandwiches also had become ill with a short incubation period, and the outbreak strain was recovered from their throat.
A study of bile acid composition and bacteriological and histological findings ofgallbladder from patients with biliary tract infection has been done. Gallbladder bile was examined by high performance liquid chromatography (HPLC) for the presence of free bile acids. The results were as follows. 1) The concentration of total free bile acids and free deoxycholic acid was significantly higher in case of anaerobic infection than in those of aerobic infection or without infection. 2) The concentration of total free bile acids and free deoxycholic acid was higher in case of acute inflammatory changes of gallbladder than in those of chronic inflammatory changes. To determine the etiological significance of free bile acids on the pathogenesis of acute inflammation of gallbladder, further investigation is necessary.
Vibrio vulnificus infection has gained increasing attention because it often causes serious septicemia with skin lesion and has a high mortality rate. That this infection is found in connection with basic disease, especially hepatic disease, is of great interest. Recently, we have experienced a case of vibrio vulnificus sepsis and succeeded in saving it. As of April, 1985, in Japan, 16 vibrio vulnificus caused cases were reported, including ours; the majority of the more cases ended in death. A 54-year-old male was admitted, on August 16, 1984, to a neighborhood hospital because of swelling and pain in the left leg. Despite treatment, he fell in shock state and was transferred to our hospital on the next day. Liver dysfunction was pointed out for the patient in 1974. Vibrio vulnificus was isolated from blood culture although he had no history of wound infection following exposure to seawater or eating seafood. The final diagnosis we made was septicemia, septic shock, disseminated intravascular coagulation and necrotizing fascitis, caused by vibrio vulnificus. Antibiotics and anticoagulant agents were administered, and necrotomy was done for the skin lesion. The patient was discharged on November 8, 1984 following remission.
A 16-year-old female infected with Mycoplasma pneumoniae developed pneumonia withautoimmune hemolytic anemia. During the acute phase of the illness, the patient developed Raynaud's symptom and acrocyanosis of the finger by cold exposure. A cold agglutinin titer of 131, 072 was found on the 12th day of hospitalization; the agglutinin was polyclonal IgM and predominantly blood group I-specific. The diagnosis of autoimmune hemolytic anemia, associated with Mycoplasma pneumoniae was made due to the marked elevation of cold agglutinin titers and anti-mycoplasma antibody titers. Both conditions responded promptly to erythromycin.
A 34-year-old male became ill after returning to Japan from Guinea, where he already had contracted malarial fever. He was admitted to the Infectious Disease Center, FukuokaMunicipal Hospital, complaining of fever, jaundice and general fatigue. An examination of peripheral blood smear showed severe malarial parasitaemia with P. falciparum. The parasitic count was calculated as greater than 240, 000/mm3. He was orally given only 500 mg of quinine and 4 tablets of MP-tablet (sulfamonomethoxine250 mg & pyrimethamine 12.5 mg). After several hours he became confused andpassed dark urine. The next morning the parasitic count had decreased to 6, 300/m3, but he lost consciousness and showed hemoglobinuria, severe jaundice and slight renal dysfunction. Acute intravascular hemolysis was suggested by the marked decrease in hemoglobin, increase in serum lactate dehydrogenase, hyperbilirubinemia and hemoglobinuria. He was administered quinine intravenously because of frequent vomiting. The following day he regained consciousness, and passed clear urine, and the parasites had disappeared from the peripheral blood. There have been many reports of acute intravascular hemolysis following the use of quinine to treat Falciparum Malaria. Based on the time relationship between the use of quinine and the acute manifestation, it was strongly suggested that the use ofquinine was the cause of this Black Water fever. However, the continuous injection of quinine fortunately brought about cure without progressive hemolysis.