HIV-1 strains were isolated from three patients treated with AZT and from three patients nottreated with AZT. Progenomes of HIV-1 RT gene were amplified by PCR and cloned to M13mp18vecter. Four amino acid mutations in RT gene (Asp67, Lys70, Thr215, Lys219) associated with resistance to AZT were analysed. All of the 14 clones obtained from the three patients with AZT therapy hadmutations at codon 215 (Thr→Tyr or Phe). Some of the 14 clones also had other mutations at codon 67 (Asp→Asn or Ser), codon 70 (Lys→Arg) and codon 219 (Lys→Glu). All of 18 clones obtained from the patients not treated with AZT have no mutation at any codonmentioned above.
We investigated the immunological factors concerning the backgrouns of non-and low-responderswho could not respond well to the hepatitis B (HB) vaccine. We injected 10 μg of the recombinant HBvaccine to the medical staffs of our hospital intramuscularly three times, 199 subjects of whom couldreceive the full course of immunization with the HB surface (HBs) antigen. Wefound that 14 subjectswere non-responders whose titer of HBs antibody was under the 1.9 cut off index (C.I.) examined byradioimmunoassay (RIA) and 47 ones were low-responders whose titers were between 2.0 to 9.9 C.I. and the frequency of non-and low-responders was higher in males after the full course of HBvaccination. We chose 46 subjects and divided them into 4 groups according tothe titer of HBsantibody at 8 and 28 weeks. We compared those groups to each other according to the amounts of totalprotein, γ-globulin, Ig G, Ig A and Ig M, numbers of peripheral white blood cells and lymphocytes, andpercentages of peripheral lymphocyte and subsets of T cell including the examination by two-colorflow cytometry using monoclonal antibodies. However we could not get any significant difference inany of those immunological factors by T assay. From these findings we suggestthat the response tothe HB vaccine does not depend on the quantity of the immunological factors before vaccination but onspecific reactivity to HBs antigen after vaccination.
In Chiba Prefecture, the first patient of Tsutsugamushi disease was found in the southern part inthe 1950's, but after that no patient was detected until 1982. After 1982, patients have been noticedagain, the number of patients has been increasing year by year. The number of serologically confirmedcases was 152 and 157 in 1989 and 1990, respectively with indirect immunofluorescence assay. About 90 percent of the patients were found in November and December, prevalently in the southern part ofthe prefecture. On the other hand, a few patients were found yearly in a harf of towns and villages inthis prefecture. The number of isolated strains of Rickettsia tsutsugamushi from patients was 4, i.e., TR6030, TR6310, TR6311, and TR6324 in 1986 and 3, TR1811, TR1827 and TR1829, in 1991. Six isolates except TR6303 reacted with anti-Kawasaki monoclonal antibody but not with other strain specificmonoclonal antibodies. Therefore, these 6 isolates were determined as Kawasaki type strain. Anisolate. TR6303, reacted with anti-Kuroki monoclonal antibody at a titer of 1: 2560 and anti-Karpmonoclonal antibody at a titer of 1: 320. This result suggested that the recent Tsutsugamushi diseaseis mostly caused by Kawasaki types in this prefecture.
A study was made on the MIC distributions of chlorhexidine and benzalkonium chloride againstclinically isolated 178 strains of Pseudomonas aeruginosa to find out the existence of strains resistantto those disinfectants and also on the in vitro induction of resistance to both drugs. The MIC of chlorhexidine gluconate was found to be distributed from 78 to 625μg/ml with asingle peak at 312μg/ml. All 178 strains of clinical isolates were sensitive to chlorhexidine and nonecould be induced to become chlorhexidine resistant in vitro, suggesting that P. aeruginosa can noteasily acquire chlorhexidine resistance. On the other hand, the MIC of benzalkonium chloride was distributed in two peaks; one peak wasbenzalkonium sensitive at 625μg/ml (150 strains/178 strains: 84.3%) and the another peak wasbenzalkonium resistant at 5, 000μg/ml (28 strains/178 strains; 15.7%). Six (4.0%) of the 150benzalkonium sensitive strains acquired benzalkonium resistance by in vitro induction of resistance;the MIC of 5 strains increased from 625 μg/ml to 2, 500μg/ml and that of the residual 1 strain increasedfrom 312μg/ml to 1, 250μg/ml. However, no change of MIC was observed in 28 benzalkonium-resistantstrains of clinically isolated P. aeruginosa by in vitro resistance induction. Strains with MIC more than5, 000μg/ml could not be obtained at all. The results suggest that the benzalkonium resistance can beintroduced in P.aeruginosa whereas the resistance-acquiring rate is low. These results suggest that chlorhexidine gluconate is the first choice for prevention of Pseudomonas infection in the hospital and benzalkonium is also useful in 0.5% solution is used.
Physiological saline solutions, each adjusted to p H 1.0, p H 2.0 and p H 7.2, and added urea andurease inhibitor (Acetohydroxamic acid), were inoculated with a culture solution of Helicobacter pyloriNCTC11637 strain derived from man, and allowed to react for 10, 30, 60 and 120 minutes. After fivedays of incubation on a blood agar medium, remaining viable H. pylori was counted. Survival of H.pylori was inadequate under the conditions of p H 1.0 and p H 2.0, but survival up to 120 min wasobserved on addition of urea. Further, on addition of urease inhibitor the survival time was reduced. H. pylori survived under the condition of p H 7.2 independent of addition of urea and urease inhibitor. Ureais essential for survival of H. pylori under strongly acidic conditions, and utility of urease inhibitor wasobserved for inhibition of survival of H. pylori.
One hundred and seventy one neonates were treated with flomoxef (FMOX) and the clinical efficacy and safety were evaluated. The ages of the patients ranged from 0 to 28 days, and their body weights from 450 to 4300g. Dose levels were 12.4 to 24.9mg/kg every 8 or 12 hours for 1 to 10 days. Fifty two patients who responded to the FMOX treatment included 5 neonates with sepsis, 17 with suspected sepsis, 9 with urinary tract infections, 12 with pneumonia, 8 with intrauterine infections, and 1 with omphalitis. The other neonates could not be retrospectively diagnosed as bacteral infections. Of 52 patients, clinical results were excellent in 15, good in 34, fair in 1, and poor in 2. And the FMOX treatment was effective in 13 out of 14 patients in which causative bacteria were identified. The drug was well tolerated, but 6 neonates out of 33 over 5 days old had diarrhea. From these results, empiric treatment with FMOX against neonatal bacterial infection was as clinically useful as that of combination with ampicillin and gentamicin or cefotaxime and ampicillin in our neonatal intensive care unit. But, as this study did not include neonate with meningitis, efficacy to meningitis was not evaluated.
In this paper, we report two successful cases of empyema treated by pleural washing with povidone-iodine solution. In these two cases, empyema was caused by secondary infection of multidrug resistant Pseudomanas aeruginosa. First, we replaced intrathoracic drainarge tube and washed intrathoracic space with 500-1000 ml saline containing antibiotics (tobramycin, aztreonam) every 8 hours for 10-14 days. But, cultural studies of pleural effusion were positive even after this treatment. So, we tried pleural washing with warm povidone-iodine solution 1: 20 diluted with saline every 8 hours. Surprisingly, after 3 days treatment, cultural studies of the pleural effusion became negative. This pleural washing method with povidone-indine was very effective for treatment of empyema patients.
Drug susceptibility of 430 Staphylococcus aureus strains isolated in 1991 from clinical specimens at all of the Japanese national university hospitals was evaluated in relationship with the epidemiological markers, namely, coagulase typing, and staphylococcal enterotoxins (SE) and toxic shock syndrome toxin 1 (TSST-1) production. There were five major methicillin-resistant Staphylococcus aureus (MRSA) groups in all the 252 MRSA strains: coagulase-type II-SEC + TSST-1-producing strains (II-SEC + TSST-1): 34.5%; coagulase-type II-no toxin-producing strains (II-): 15.4%; coagulase-type N-SEA-producing strains (IV-SEA): 10.3%; coagulase-type II-SEA + SEC + TSST-1-producing strains (II-SEA + SEC + TSST-1): 8.7%; and coagulase-type III-no toxin-producing strains (III-): 7.1%. II-SEA+SEC+TSST-1 group was highly resistant to OFLX, whereas half of the other strain groups were sensitive to OFLX. Seventy-eight percent of the IV-SEA group was sensitive to FMOX, but there was no sensitive strain to FMOX in the II-SEA + SEC + TSST-1 group. More than 50% of the IV-SEA, III and II-groups were sensitive to IPM, while the II-SEC + TSST-1 and II-SEA+SEC+TSST-1 groups were highly resistant to IPM. The III-and II-groups showed very good sensitivity to MINO, but the sensitivity to it of the II-SEA + SEC + TSST-1 group was very low. All of the strain groups were sensitive to ST except for the IV-SEA group. These results may provide useful information in the choice of antibacterial agents for MRSA infection.
A case of streptococcal toxic shock like syndrome occurring in a 44-year-old previousluy healthy Japanese male is reported. He initially had a sore thoat, low grade fever, diarrhea and mild pains in a lower extremities. Shortly thereafter, he rapidly developed a high fever, profound hypotension, multifocal epidermal necrosis, and sever purulent fascitis and myositis in both lower etremities, which required above knee amputation of both legs. He later developed disseminated intravascular coagulapathy, adult respiratory distress syndrome, acute renal failure, coma and necrotizing inflamation of both arms and external genitalia despite treatment. He died on the 13th hospital day. Streptococcus pyogenes was isolated from the necrotic muscles and right knee joint. The organism was typed as M3, T3, was sensitive to penicillins, and was found to be producting streptococcal pyogenic exotoxin A in vitro. This is the first case report of streptococcal toxic shock like syndrome in Japan.