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Biomedical subjects

H Kawabe

Publications and source records attributed to H Kawabe.

At least 109 records · Page 6Linked to original sources
PubMed1981

Synergistic activities of fortimicin A and beta-lactam antibiotics against Pseudomonas aeruginosa.

The inhibitory and bactericidal activities of fortimicin A (FTM-A) alone against Pseudomonas aeruginosa were compared with those of FTM-A in combination with beta-lactam antibiotics. As tested by the checkerboard method, most beta-lactam antibiotics tested had synergistic effects on the inhibitory activity of FTM-A against one strain of P. aeruginosa. Addition of a sublethal concentration of carbenicillin resulted in a significant increase in the rate of bacterial killing of FTM-A against P. aeruginosa. The antibacterial activity of FTM-A against 50 gentamicin-susceptible and 50 gentamicin-resistant clinical isolates of P. aeruginosa was clearly enhanced by addition of a subinhibitory concentration of carbenicillin or piperacillin.

Aminoglycosides↗
PubMed1980

In vitro and in vivo antibacterial activity of KW1070, a new aminoglycoside antibiotic.

KW1070, a new aminoglycoside antibiotic with the novel aminocyclitol, fortamine, has a broad spectrum of activity in vitro and in vivo against gram-positive and gram-negative bacteria. The minimum inhibitory concentrations of KW1070 are similar to those of kanamycin against aminoglycoside-susceptible strains, slightly less than those of gentamicin or 3',4'-dideoxykanamycin B. Minimal bactericidal concentrations were found to be near minimal inhibitory concentrations. KW1070 was active in vitro against many aminoglycoside-resistant bacterial strains that possess aminoglycoside-inactivating enzymes, particularly AAC(6'), AAC(2'), AAD(2''), and APH(3'). The activities of KW1070 in mice infected with Staphylococcus aureus, Escherichia coli, Proteus sp., and Serratia marcescens compared favorably with the activities of amikacin and kanamycin; KW1070 was also singificantly active in mice infected with resistant strains bearing the aminoglycoside-inactivating enzymes listed above.

Acetylation↗
PubMed1978

Studies on the outbreak of hepatitis A in an institute for mentally retarded children.

The authors encountered an outbreak of acute hepatitis in a public institute for mentally retarded children in Aomori Prefecture, Japan. Studies revealed that the probable vehicles of transmission of infection were contaminated water, contaminated meals, and close contact. From the clinical manifestations and epidemiological investigations of 41 affected children and staff members, an outbreak of hepatitis A was strongly suspected. Immune electron microscopy disclosed hepatitis A virus antigen particles in the stool specimens collected during the few days before and after peak transaminase elevation. Hepatitis A antigen was further extracted and purified. The antigen was the first reported recovery of the virus from a natural outbreak of hapatitis A in Asia. Subsequently, with the immune adherence hemagglutination test, using this extracted antigen, an increase in titer of antibody to hepatitis A antigen was demonstrated. Thus, this epidemic was serologically established as an outbreak of hepatitis A. Human immune serum globulin for the protection against hepatitis A was administrated to the 80 individuals concerned, and it was effective in preventing the clinical manifestation of hepatitis.

Adolescent↗
PubMed1978

Streptomycin and Spectinomycin resistance mediated by plasmids.

Resistance to tetracycline (Tc), chloramphenicol (Cm), streptomycin (Sm), and sulfanilamide (Sa) was surveyed in clinical isolates of Escherichia coli and Shigella strains. Among the Sm Sa-resistant strains, the frequency of nonconjugative r (Sm Sa) plasmids was much higher than that of conjugative R plasmids encoding double resistance. The biochemical mechanism of Sm resistance mediated by the conjugative plasmids R(Tc Cm Sm Sa) and R(Cm Sm Sa) and about half the numbers of conjugative R(Tc Sm Sa) and R(Sm Sa) plasmids tested were found to be due to adenylylation of the drug. The remaining conjugative R(Tc Sm Sa) and R(Sm Sa) plasmids and all nonconjugative (Sm Sa) plasmids tested inactivated Sm by phosphorylation.

Conjugation, Genetic↗
PubMed1975

Acetylation of amikacin, a new semisynthetic antibiotic, by Pseudomonas aeruginosa carrying an R factor.

A clinical isolate Pseudomonas aeruginosa GN315 resistant to amikacin (AK), a new semisynthetic antibiotic, inactivated AK by acetylation. The acetylating enzyme was purified approximately 146-fold from a crude extract of GN315 by affinity chromatography. Fractionated samples obtained by affinity chromatography showed almost the same inactivation curves toward 3',4'-dideoxykanamycin B (DKB) and AK. Partially purified AK-acetylating enzyme inactivated DKB and kanamycin A but could not inactivate gentamicin C(1). The optimal pH for their inactivation was 6.0 to 7.0, and the pH curves for the inactivation of both drugs were almost the same. These facts indicate that AK and DKB are inactivated by the same aminoglycoside-acetylating enzyme. Through elemental analysis, the inactivated AK was found to be a monoacetylated product of AK. A sample of inactivated AK was purified and compared with a synthetic 6'-N-acetyl AK by thin-layer chromatography, and the results indicated that AK was inactivated by acetylation of the 6'-NH(2) group. The ultraviolet, infrared, and nuclear magnetic resonance spectra of the inactivated AK showed that AK was inactivated by the enzyme through acetylation of the amino group of 6'-amino-6'-deoxy-d-glucose moiety of AK. This enzyme, mediated by R factor, is capable of conferring resistance to AK, DKB, kanamycin, gentamicin, and sulfanilamide.

Aminoglycosides↗