Inactivation of NDV and Vaccinia virus by isopropanol (IP) in organic materials was investigated. Virucidal activity of IP on viruses was inhibited markedly by organic materials which denoted different extent of inhibition by the sort and the state of them. In a liquid phase, such as in urine or defibrinated blood, the inhibitory effect of the organic materials increased more and more, as the concentration of IP became lower, just as like in the case of disinfection by ethanol. In a rabbit blood clot, however, 50-80% IP was found to be the most effective against NDV. Viruses in dry smear of calfserum were inactivated by relatively lower concentration of IP, more effectively than by the higher one. NDV and Vaccinia virus were inactivated by IP at 40% and 30-60% respectively in one minute, whereas 90% IP didn't inactivate both viruses in 10 minutes.
Previously, Pollack et al., Bjorn et al. and Sanai et al. reported that an incidence of the exotoxin producing P. aeruginosa was 87, 89 and 87 % among clinical isolates, respectively. In the present study, the exotoxin production of clinical and environmental isolates of P. aeruginosa was tested by an intradermal inoculation of their culture filtrates into any guinea pig and correlation between the exotoxin producibility of isolates and their isolating sources or serotypes was investigated. Exotoxin production was observed to be 79% among clinical isolates from patients with underlying diseases, while it was 22% positive from the environmental isolates of P. aeruginosa. Difference was significant at P<0.05. Actually, number of the exotoxin positive strains from different clinical source tested were 8 out of 12 isolates from urine, 12 out of 15 isolates from sputum, 9 out of 10 isolates from pus and 3 out of 5 isolates from others (bile, ear discharge and tonsil), suggesting not significant dependency upon the isolating sources. So far as the present results were concerned, as difinite relation of the exotoxin producibility to any serotype of the isolates was not observable, that is, there were 7 exotoxin positive strain out of 9 A type isolates (78%), 12 out of 13 B type isolates (92%), 1 out of 1 D type isolates, 2 out of 6 E type isolates (50%), 1 out of 2 F type isolates (50%), 6 out of 8 G type isolates (75%) and 3 out of 3 I type isolates (100%). However, a higher frequency of the exotoxin producing strains among both B and I serotypes of isolates was remained for further investigation.
Inactivation of PCG and CER in sputum was studied using sputum samples obtained from 15 cases with chronic respiratory tract infections. As a result, it was found that in 8 of the 15 cases, both substrates were inactivated, whereas in 7 of these 8 cases inactivation was prevented when clavulanic acid was added to the sputum. In almost all of these cases the fact that the addition of clavulanic acid had inhibited the inactivation suggested the involvement of β-lactamase in the inactivation of the antibiotics. Therefore, whether the inactivation was due to the cleavage of the β-lactam ring or not was examined. The cleavage of the β-lactam ring was consequently found in inactivated PCG. On the basis of these findings, itwas considered that the inactivation of the antibiotics observed in the sputum samples was caused by β-lactamase contained in the sputum samples. In view of this, the relationship between the maximum level of AMPC-Na transferred into the sputa of patients and the activity of β-lactamase in their sputa after AMPC-Na which was given in a dose of 40 mg/Kg by drip infusion was studied (Fig. 3). The lesser activity of β-lactamase inthe sputum, the higher sputum level of AMPC was noted. Also the higher activity of β-lactamase in the sputum, the lower sputum level of AMPC was found. This finding suggested that AMPC which had been transferred into the sputum was inactivated by β-lactamase presented in the sputum. Next, sputum levels of AMPC were determined after a dose of AMPC (500 mg) given alone or simultaneously combined with each of various doses ofclavulanic acid (125 mg, 250 mg or 375 mg) was administered to two patients having β-Iactamase activity previously demonstrated in their sputa (Fig. 5). When AMPC alone was administered, the sputum levels of AMPC of the two patients were less than 0.03μg/ml, but when AMPC was given in combination with clavulanic acid, the AMPC levels in the sputum were increased depending on the doses of clavulanic acid contained. These results of both in vitro and in vivo study indicated that AMPC was inactivated there when β-lactamase-producing strain was present in the sputum. As in the case of the in vitro study, the inactivation could be inhibited to some extent by the concomitant administration of clavulanic acid in vivo.
This paper reports a case of neonatal meningitis caused by Flavobacterium meningosepticum, recovered without hydrocephalus. Five day old boy with apneic episodes was transfered to our hospital from a obsteric hospital. Pathogens were isolated from blood on admission and hospital day 4, and from cerebrospinal fluid on hospital day 5. The chemotherapy to Fravobacterum meningitis was started on hospital day 5. Minocycline (MINO), erythromycin (EM) and piperacillin (PIPC) were administered intravenously.The next day, antibiotics were changed for cefmetazole (CMZ) and lincomycin (LCM) considered possible side effects of MINO in neonate and the sensitivity of isolated pathogen to EM and PIPC, though the cerebrospinal fluid became sterile and the general condition of the patient improved. On hospital day 9, the administration of LCM was discontinued, and CMZ alone continued for 13 days. After the discontinuance of the chemotherapy, the patient was still in good condition. The enlargement of the ventricles was not ofserved in the computed tomography of the brain performed in series. At 3 month old, the patient showed normal development without abnormal neurological signs. MINO and CMZ were considered to be effective in this case from the clinical course and the minimum inhibitory concentration of these antibiotics to the isolated Fravobacterium.
From February to June, 1980, four children with bilateral calf muscle pain were found. The muscle pain followed one to 4 days after upper respiratory symptoms and was so marked as to be unable to walk. But it subsided to walk on tiptoe within a few days and they recovered 7 to 10 days later without sequellae. Elevations of GOT, CPK and LDH were demonstrated in the acute phase and returned to the normal ranges within 10 days according to clinical improvement. No myoglobinuria observed. Pair sera revealed significant rises of influenza type B CF titer in two of 4 cases, and a type B influenza virus was isolated from the throat in one case. In the other 2 cases, CF titers of influenza B did not show a significant increase or decrease in their two point sera. But their titers were enough to explain the recent infection of influenza B virus and were compatible to the association of transient calf muscle pain. The HA antigenicity of the virus derived from our case was moderately (4 to 8 folds) drifted from current vaccine strain B/Kanagawa/3/76 on cross HI. B type influenza virus was not predominantly isolated in that season but association with calf muscle pain were not observed on H3N2 or H1N1 type A influenza that year.
A family of four developed acute viral hepatitis A beginning with the father, 33 years old. He complained of general malaise, nausea, vomiting, loss of appetite, high fever and showed jaundice and elevation of transaminases level. Chemical recovery was made in 99 days. His wife, 28 yrs., showed almost the same symptoms 31 days after the onset of her husband's hepatitis. Transaminases returned in 27 days. In a 5-year-old boy, 10 days after the onset of his mother's illness he complained of anorexia, nausea and vomiting but showed no pyrexia and jaundice. He recovered in 20 days. In a 4-year-old boy, he showed loss of appetite, dark urine and slight jaundice 3 days earlier than his brother. Chemical recovery was delayed and returned in 56 days. Symptoms were more severe in adults than in children but there was no remarkable difference as to clinical course between them. Serum antibody to hepatitis A antigen was determined with radioimmunoassay (HAVAB-M kit, DAINABO'IT) and all patients showed high titers. The determination of IgM revealed: husband, 272 mg/dl; wife, 318 mg/di; elder brother, 302 mg/dl; younger one, 180 mg/dl. IgM level of children declined gradually. In all cases, examination of the blood disclosed 2-5 per cent atypical lymphocytes (type 2) in differential count and it lasted the first 20-30 days of illness.