Sixty-two antimicrobial agents, including several combinations, were examined for stability at 56 degrees C for 30 min and 121 degrees C for 15 min, respectively. A microtiter broth dilution MIC test and an agar disk diffusion test served to test each chemo-agent for residual antimicrobial activity. Eleven drugs were partially heat-labile (MICs raised four- to eight-fold after autoclaving) and 26 drugs were heat-labile (MICs raised > or = 16-fold following autoclaving); the remainder proved heat-stable (MICs raised < or = two-fold after autoclaving). Surprisingly, the beta-lactams, azlocillin, aztreonam, mezlocillin, and oxacillin, were remarkably heat-stable.

A total of 312 clinical β-hemolytic streptococcal isolates (Streptococcus pyogenes, group A = 63; Streptococcus agalactiae, group B = 145; group C = 50; group F = 27; group G = 27) were examined for susceptibility to 23 and 24 antimicrobial drugs with the Bauer-Kirby agar disk diffusion and the agar dilution method, respectively. Sheep blood Mueller-Hinton agar served as the reference medium. Wilkins-Chalgren agar supported optimal growth of group A and B, but not of all group C, F, and G streptococci. The group A streptococci were susceptible to all β-lactam antibiotics, clindamycin, chloramphenicol, rifampin, teicoplanin, and vancomycin, but resistant to cotrimoxazole, fusidic acid, and, except for 2 strains, to fosfomycin. Resistance (R)/intermediate susceptibility (I) rates (R/I%) to ciprofloxacin (0/2%), ofloxacin (1/2%), erythromycin (1.6 / 0%), and clarithromycin (0/1%) were low. Higher resistance rates were noted with tetracyclines (doxycycline 23.8/15.9%; tetracycline 39.7/3.2%). Among the group B streptococcal isolates, one strain was resistant against oxacillin and of intermediate susceptibility to penicillin G and cefoxitin. All isolates were susceptible to teicoplanin and rifampin. Conversely, all group B isolates were resistant to cotrimoxazole and fusidic acid; 69% and 51 % of these isolates were susceptible to fosfomycin and rifampin, respectively. R/I rates of the group B streptococcal isolates were low for ciprofloxacin and ofloxacin (0/0.7%), clindamycin (0.7/0%), erythromycin (1.4/ 3.5%), clarithromycin (1.4/0%), and chloramphenicol (0.7/0%). Resistance to tetracyclines was significant (doxycycline: 72.4/2.1%; tetracycline: 74.5/1.4%). Among the non-A, non-B β-hemolytic streptococci, 2 group C strains were resistant to oxacillin and showed intermediate susceptibility to penicillin G. All isolates were susceptible to third and fourth-generation cephalosporins, imipenem, chloramphenicol, rifampin, teicoplanin, and vancomycin. R/I rates to the other antimicrobial drugs were: ciprofloxacin (3.9/1.9%), ofloxacin (2.9/1.9%), clindamycin (2.9/1%), erythromycin (5.8/0%), clarithromycin (3.8/2.9%), and cotrimoxazole (16.4/3.9%). Resistance against tetracyclines was more frequent (doxycycline: 18.3/2.9%; tetracycline: 20.2/6.7%). On the basis of various minor discrepancies between MIC and disk diffusion test results, it is proposed that the current NCCLS inhibition zone (diameter, mm) criteria indicative of intermediate susceptibility of β-hemolytic streptococci be changed for the following antimicrobial drugs: ampicillin: 22-27 mm (only for group A and B β-hemolytic streptococci); ciprofloxacin: 16-18 mm; clindamycin: 15-18 mm; doxycycline: 17-19 mm; tetracycline: 17-19 mm, and erythromycin: 14-19 mm.

Taurolidine at ≤1,250 ug/ml killed all 37 isolates of multiple-antibiotic-resistant Staphylococcus aureus (n = 9), Enterococcus faecium (n = 17), and Enterobacteriaceae (n = 11). Time-kill experiments disclosed that bovine serum (65% v/v) only marginally retarded the bactericidal activity of 2,000 and 1,000 μg/ml of taurolidine against the various strains. Taurolidine at 2,000 μg/ml did not antagonize the bactericidal activity of 50% (v/v) fresh human serum against promptly and delayed serum-sensitive test strains of Escherichia coli and Serratia marcescens. In the presence of 65% (v/v) of fresh defibrinated human blood from two donors, however, the bactericidal activity of this antimicrobial compound was delayed, i.e., manifested only following extended (overnight) incubation, against staphylococcal and enterococcal isolates, though less so in the case of Enterobacteriaceae. Taurolidine at 2,000 μg/ml killed ingested, i.e., intraphagocytic bacteria of human-serum-resistant S. marcescens strains CDC 06 :H3 and P 016 :H-.

Ninety-six clinical isolates of Stenotrophomonas maltophilia were examined with the agar dilution method for susceptibility to 19 antimicrobial drugs. Doxycycline, cotrimoxazole, timentin, ofloxacin, fosfomycin, and piperacillin + tazobactam, in that order, inhibited the majority of strains. All isolates were resistant to nitrofurantoin. Concurrent disk susceptibility (Bauer-Kirby method) testing, using currently valid NCCLS interpretative criteria for Pseudomonas aeruginosa, uncovered a significant incidence of very major (category I), major (category II), and minor (categories III and IV) discrepancies for aminoglycosides, cephalosporins, chloramphenicol, and piperacillin + tazobactam and ticarcillin + clavulanic acid. Therefore, new interpretative criteria indicative of intermediate (I) susceptibility of S. maltophilia to these various antibiotics were proposed. In addition, new intermediate susceptibility criteria were proposed for the two β-lactam-β-lactamase inhibitor combinations. It was recommended to exclude ciprofloxacin from test batteries against this microorganism due to the wide scatter of minimal inhibitory concentration values and diameters of inhibition zones; the same was true for polymyxin B. It is hoped that the proposed modified, species- specific criteria will improve the clinical utility of laboratory-generated disk antibiograms with respect to the inherently multiple antibiotic-resistant, opportunistic pathogen S. maltophilia.

Serogrouping (determination of O antigens) and bacteriocin typing (based on susceptibility to one or more of 18 bacteriocins) were employed to survey 210 isolates of Pseudomonas aeruginosa from 201 patients in 8 intensive care units (ICU) during an observation period of 18 months. Eighty-eight isolates (41.9%) were nonserogroupable (NT); most common were serogroups O1, O9, O11, and O3. All except 5 isolates (97.6%) were bacteriocin-typable. However, phenotypic variation of bacteriocin susceptibility, in particular the receptor for bacteriocin No. 13, rendered this typing method presumptive as well. Bacteriocin susceptibility profiles were not predictive of serogroup and vice versa. Workup of 19 isolates from 9 patients disclosed phenotypic variation of antibiotic susceptibility in 3 patients, superinfection by a different strain in 4 patients, and persistence (3 months) of the same strain in 2 patients, respectively. Serotyping and bacteriocin susceptibility test data revealed 15 clusters of putative cross-infection of 2 patients each, 8 clusters involving 3 patients each, one outbreak (serogroup NT, bacteriocin profile 777736) involving 4 patients in the pediatric ICU, one outbreak due to a multiple-antibiotic resistant (MAR) strain in the surgical ICU (4 patients, serogroup O12, bacteriocin profile 30400), and two putative outbreaks in the pneumonology ICU involving 6 patients (serogroup NT, bacteriocin profile 777726) and 9 patients (serogroup NT, bacteriocin profile 777736). Pulsed-field gel electrophoresis (PFGE) macrorestriction analysis (SpeI, XbaI) confirmed the pediatric and surgical ICU strains as singular strains. However, the two putative outbreaks in the pneumonology ICU were due to one particular strain which had infected 13 of the 15 patients as determined with the PFGE genotypic method. Isolates comprising the MAR strain of P. aeruginosa were susceptible only to amikacin, fosfomycin, and polymyxin B; the isolates varied in susceptibility to aztreonam and ceftazidime. This MAR strain was susceptible to the bactericidal activity of 65 vol% of fresh defibrinated human blood from donors B, L, and T. Either amikacin (16 µg/ml) or fosfomycin (8 µg/ml) plus blood and amikacin (8 µg/ml) combined with fosfomycin (8 µg/ml) with and without blood consistently killed isolates of the MAR strain, which thus was amenable to antibiotic therapy.