Prevalence of HIV transmission to female sexual partners of seropositive men is not known yet. In order to know the condition in Japan, 11 HIV-seropositive men (25-42 years old; mean±SD, 32.5±6.0) and their stable female partners (24-42 years old; mean±SD, 31.3±6.0) were analyzed. Seropositive men consisted of seven hemophiliacs including a hemophiliac with intravenous drug abuse, three men who acquired HIV infection through heterosexual contact, and a man with intravenous drug abuse. Six of them were asymptomatic carriers, two had AIDS-related complex, and three had AIDS. All of the female partners had no risk factors other than sexual contact with their stable, seropositive male partners, except one who used to inject intravenous drug.
Four of 11 female partners (36%) were found to be infected with HIV. All of the male partners of infected females had AIDS or AIDS-related complex, and had CD₄ counts fewer than 100 cells/μl. Asymptomatic carriers and men with CD₄ counts more than 200cells/μl did not transmit HIV to their partners: rate of transmission of HIV by symptomatic men was significantly higher than that by asymptomatic men (p<0.01), and the rate by men with CD₄ counts fewer than 100 cells/μl was also significantly higher than that by men with larger CD₄ counts (p<0.01). HIV-p24 antigen was measured in 10 of 11 seropositive men. The antigen was positive in four men, and negative in six. Three of four antigen-positive men transmitted HIV to their female partners, while only one of six antigen-negative men transitted HIV (p<0.05). However, there was no difference in the duration of sexual partnership between couples with transmission (5.0±1.8 years, mean±SD) and without transmission (4.1±2.0 years, mean±SD), although couples with transmission tended to have had longer partnership. The use of condom seemed to be more frequent among those who did not transmit HIV to their female partners.
In conclusion, it was found that after 4 to 5 years of sexual partnership with seropositive men, 30-40% of female partners was infected with HIV, and that men with advanced HIV disease were more likely to transmit HIV than asymptomatic carriers.

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Liposomal amphotericin B was evaluated for toxicity, pharmacokinetic properties and therapeutic efficacy in invasive pulmonary aspergillosis in Sprague-Dawley rats. The protective effect of liposomes against the toxicity induced by repeated amphotericin B infusions was observed in a survival study of rats, thereby allowing higher dosages to be administered. Pharmacokinetic studies showed that liposomes led to high levels of amphotericin B in the spleen and liver. Drug levels in the lung were higher at ten minutes after intravenous injection of liposomal amphotericin B at 20mg/kg than of free amphotericin B at 1.5mg/kg. Efficacy was assessed in rats treated with cortisone acetate, fed a low-protein diet and infected transtracheally with 8×10⁴ Aspeygillus fumigatus spores to cause fetal pneumonia and pulmonary bleeding. Dosages of 20 or 4mg/kg of liposomal amphotericin B, or 1.5mg/kg of free amphotericin B were administered intravenously to rats once daily for 8 days. Control rats received saline. Twenty mg/kg of liposomal amphotericin B was as effective on survival rate as 1.5mg/kg of free amphotericin B. However, 4mg/kg of liposomal amphotericin B was less effective than 1.5mg/kg of free amphotericin B, prolonging the mean survival time of rats treated with saline, which showed elevation of galactomannan antigen titers of Aspeygillus fumigatus in sera and invasive proliferation or mycelia with bleeding in histopathological sections of the lung. We conclude that liposomal amphotericin B reduces toxicity of the drug, thereby increasing the concentration of the drug in the lung by high-dose administration, but decreases the efficacy of the drug in experimental pulmonary aspergillosis.

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In April 1991, an outobreak of acute gastroenteritis due to group C rotavirus occurred at an elementary school in Tokyo. Fifty-one (13%) of 393 students became ill.
The main clinical symptoms were diarrhea (100%), abdominal pain (68%) and vomiting (56%). No enteropathogenic bacteria were found in the fecal specimens. However, the virus particles morphologically indistinguishable from conventional rotavirus were detected in 6 of 11 fecal specimens by electron microscopy.
Immune electron microscopy showed that these virions aggregated with antigroup C rotavirus serum. The RNA pattern of the virus particles involved in this outbreak showed a pattern similar to that of typical group C rotavirus on polyacrylamide gel electrophoresis.

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Cases of enterohaemorrhagic Escherichia coli (EHEC) are being increasingly reported in Japan. Bacteriological isolation of EHEC has been a constant problem because the organism is shed for a short duration after onset on illness and generally during the prodromal stages. In order to ease the diagnosis of EHEC infections in this country, we have developed a LPS-based solid phase enzyme linked immunosorbent assay for serological diagnosis of the infection. Adequate knowledge on the prevalence of EHEC serogroups in Japan is mandatory for the success of such a diagnostic test. O157 is currently the prominent serogroup associated with EHEC infections in Japan followed by O111, O26 and O128 in that order of prevalence.
In February 1992, a 1 year-old infant developed hemolytic uremic syndrome (HUS) 15 days later the prodrome of watery diarrhoea. Stool sample obtained on day 15 was cultured for detection of EHEC. Ten colonies of E. coli picked from MacConkey agar plate were examined by the polymerase chain reaction (PCR) using primers specific for both verotoxins (VT1 and VT2). Of the 10 colonies, only one was positive for the VT2 gene. The strain was confirmed to be cytotoxic on cultured Vero cells. The strain agglutinated with antisera of E. coli O2, Ki and with 117 serogroups. As of date, none of such strains of O2: K1: H7 EHEC has been reported in Japan. The patient's sera was found to be positive for antibodies against LPS from the homologous isolate as well as against VT2. The patient recovered uneventfully from HUS 40 days after the onset of the disease and was discharged from the hospital.

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We tried to isolate verotoxin-producing Escherichia coli (VTEC) from 323 sporadic pediatric enteritis patients who came to three clinics in the Fukuoka area. We used the sorbitol-MacConkey medium for the isolation of VTECO157: H7. For non-0157 VTEC strains we used the V1/PECS method. VT/PECS method was applied. VTEC strains were isolated from three patients (0.9%). None of the patients were seriously, ill or developed the hemolytic uremic syndrome. The three patients were all seen in the summer season, July and August. O157: 117 strains were isolated from two patients, and O145: NM from one. This study showed that sporadic enteritis cases due to VTEC exist in the Fukuoka area. In the future a rapid and easy method for the detection of VT or VTEC should be developed and commercialized to proceed with epidemiological studies of VTEC infections throughout Japan.

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Biological characters of enterohemorrhagic Escherichia coli (EHEC) strains isolated from food poisoning cases in Canada, 1987-1988 were examined in comparison with that isolated in Saitama, 1990. The Saitama strain was found to belong to biotype I, and biotypes I and II were found in Canada. Most of the strains including the Saitama strain were found to have siderophilins suggesting their advantagous growth in vivo. An enteroinvasive strain with 140 megadalton (Md) plasmid and two colicinogenic strains with 4.8 Md plasmids were detected. All strains were found to have 60 Md plasmids. This plasmid might be specific for this serotype. A few strains were resistant to streptomycin (SM) and/or tetracycline (TC), and a strain transferred its SM-TC resistances by conjugation.
Many strains including the Saitama strain were found to produce vero cytotoxin (VT) types 1 and 2 (VT1 and VT2). A few type 2 and untypable toxin producing strains were also detected. VT titers produced by untypable toxin producing strains were over 10 times lower than those by other strains. High annealing temperature for PCR amplification of VT1 gene and a variety of annealing temperatures of VT2 gene suggested that the nucleotide sequences for VT1 gene were well preserved, but that those for VT2 might have some mutations.

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Minimum inhibitory concentrations (MICs) of penicillin G, cefazolin, tetracycline, chioramphenicol, four aminoglycosides, and seven macrolides against Helicobacter pylori strains were determined on Brucella agar supplemented with bovine serum albumin fraction V (albumin agar) and compared with those on blood agar. MICs of the macrolides against H. pylori determined on albumin agar were markedly lower than those found with blood agar. The susceptibilities of 26 H. pylori strains to the macrolides were estimated from the MIC₅₀ values determined on blood agar and albumin agar, which were 0.39 and ≤ 0.05μg/ml for erythromycin, midecamycin and rokitamycin, 3.13 and 0.10μ g/ml for clindamycin, 1.56 and ≤0.05μg/ml for josamycin, 1.56 and 0.10μg/ml for kitasamycin, and 0.10 and ≤0.05μg/ml for roxithromycin, respectively. However, the MICs of other antibiotics against H. pylori and of all antibiotics against two reference Campylobacter strains differed minimally between values obtained on blood agar and albumin agar.

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Experimental ascending urinary tract infection was induced by transurethral instillation of Pseudomonas aeruginosa in mice whose neutrophilic chemotactic activity was suppressed by administration of colchicine, and we investigated the time course fluctuationof local immune response at the infected sites in terms of immune response cells as compared with thatin normal mice.
In comparison with that in normal mice, a significant suppression was noted in the chemotactic activity of the peritoneal exudating neutrophils when colchicine at a dose of 0.02mg/mouse was administrated a total of 4 times, namely, 1, 3 and 5 days, and 6 hours beforeinfection (the day of assessment). When experimental ascending urinary tract infection was induced by P. aeruginosa, markedly increased susceptibility to bacterial infection was noted in mice with an impaired chemotaxis of neutrophils (impaired neutrophilic chemotaxis group) as compared with that in normal mice (control group). Apparent infiltration of neutrophils was recognized oneday after infection in the control group by the time course observation of the immune response cells at the sites of infection while hardly any infiltration was observed in the impaired neutrophilic chemotaxis group one day after infection. In other words, the cellular infiltration into an infected site was conceivably obstructed when the chemotactic activity was impaired. On the other hand, macrophages inthe impaired neutrophilic chemotaxis group demonstrated marked infiltration as compared with that in the control group one day after infection, and such infiltration remained on the same higher level thereafter. As for T and B cells, an increased ratio was noted in helper T cells and early infiltration in IgG positive B cells 3 days after infection and onward when compared with the control group.
It was therefore suggested that other immune response cells compensated for the infiltration of neutrophils when their chemotactic activity was obstructed, and that these cells on the whole possibly responded toward the preservation of their protective mechanism against infection.

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A 41-year-old Japanese male with uncontrolled diabetes mellitus and alcoholicliver dysfunction developed melioidosis after his business trip to Indonesia and Singapore in 1988. His disease started with spiked fever on the following day after extraction of a tooth, and a liver abscess developed, followed by abscesses in the spleen and in the subphrenic space. In spite of splenectomy and intensive antimicrobial treatments for three months, he developed parotitis, prostatitis, and abscessof the right submandibular gland at 5 to 16-month interval. Pseudomonas pseudomallei was isolated from the blood and pus from each abscess. The lung was not involved. At present, he has returned to work, withcontinued intravenous instillation of imipenem/cilastatin.

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We report a case of fulminant pneumonia that was due to aspiration of contaminated hot spring water and was not affected by β-lactam antibiotics. We suspected that the patient had Legionnaires' disease and treated the clinical symptoms with erythromycin. Legionellaceae could not be isolated from sputum or lung biopsy material, but an elevated titer to Legionella pneumophila serogroup 4 was found by indirect immunofluorecence test. We diagnosed the patent as having Legionnaires' disease with improved clinical symptoms. Furthermore, we went to the hot spring that he visited and tried to isolate Legionellaceae. Hot spring water was collected from the bathroom and water, hot water, and shower water from the guestroom. After using a low-pH method, samples were cultured on BCYE α medium. Serogroups are classified by agglutination method with immune rabbit serum. As a result, we successfully isolated Legionella pneumophila serogroup 4 from hot spring water (42°C) from the bath. No bacteria could be isolated from the other samples. Therefore, we believe that this case of Legionnaires' disease was caused by aspiration of contaminated hot spring water. The infection route of Legionnaires' disease is unclear. There are no previous reports of isolation of Legionellaceae from Japanese hot springs. This case would provide important information when considering the infection route of Legionnaires' disease in Japan.

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