Between January 1992 and June 1993, serotype identification was carried out against Pseudomonas aeruginosa isolated in the microbiology laboratory of Osaka University Hospital, and the isolation rate of serotypes was evaluated according to materials and department clinics. The MICs of fifteen antibiotics, piperacillin (PIPC), cefsulodin (CFS). ceftazidime (CAZ), cefoperazone (CPZ), cefclidin (CFCL), aztreonam (AZT), carumonam (CRMN), imipenem (IPM), tobramycin (TOB), amikacin (AMK), gentamicin (GM), minocycline (MINO), ofloxacin (OFLX), ciprofloxacin (CPFX) and fosfomycin (FOM), were measured by the micro-broth dilution method in about 100 strains that indicated a high incidence of serotype, and we evaluated the MIC80, materials, clinics and serotypes individually. 1. Isolation rates of serotypes were in the order of G, E, B, I, A, non-type, M, F, H, D, C and K. P. aeruginosa was isolated most often from sputum and throat samples of inpatients, and from pus, secretion and wound of outpatients. Among department clinics, P.aeruginosa was most often isolated from inpatients of the department of abdominal surgery, and from outpatients of the department of otorhinolaryngology. 2. MIC80 s of antibiotics against P. aeruginosa 100 strains were in the order of CPFX > CFCL, IPM, TOB>GM, OFLX, CAZ>CFS>CRMN, MINO, AZT, PIPC, AMK>CPZ > FOM, The MIC80 of CPFX was 2μg/ml, and that of CFCL, IPM and TOB was 4μg/ml. 3. Susceptibility rate of each antibiotic that based on interpretative standards by NCCLS was in the order of CFCL 97.0%, IPM 91.0%, TOB 90.0%, followed by PIPC, CAZ, CPFX, GM, AMK, CPZ, CRMN, AZT, OFLX, CFS, MINO and FOM.
This report concerns the fact that the postmortem level of histamine in blood was unchanged in guinea pigs (GP) that they died of antibody reaction the cefaclor (CCL)-human serum albumin (HSA) conjugates or cephalexin (CEX)-HSA during anaphylactic shock. In order to analyze this result, we studied how antibiotics affect platelets activated by platelet activating factor (PAF), as platelets are major source of histamine in GP blood. When PAF (1.5×10-7M) reacts to platelets histamine is released and platelet aggregation is induced, CCL and CEX (1mM or 10mM) blocked histamine release but did not block platelet aggregation. From these results, it was suggested that the release of histamine from platelets was blocked by CCL and CEX, and therefore, the level of histamine did not increase during anaphylactic shock.