Minimal bactericidal concentrations of the aminoglycoside antibiotics amikacin, gentamicin, and netilmicin killed intraphagolysosomal test bacteria of selected assay strains of Serratia marcescens, though not as efficiently as rifampin. The system employed consisted of 55 vol % of fresh defibrinated human blood treated with 2 mg/ml of phenylbutazone which permitted ingestion of bacteria, but selectively inhibited microbicidal activity of the peripheral blood leukocytes. Extraphagocytic bacteria were killed with the aid of group A (phage tail) bacteriocins of S. marcescens. Inhibitory and subinhibitory concentrations of amikacin, gentamicin, and netilmicin combined with 55 vol % of defibrinated blood, respectively, yielded additive effects against all test strains of S. marcescens utilized and against Escherichia coli control strain ATCC 25922.
Six strains of multiple-antibiotic resistant, DNase-positive Staph. epidermidis were found to be sensitive to chloramphenicol and gentamicin sulfate; although cephalothin alone was ineffective, the combination of chloramphenicol and cephalothin resulted in an additive effect against four of the isolates in vitro. However, two strains proved refractory to the combination of these two drugs, emphasizing the need for careful in vitro antibiotic sensitivity studies, especially so in the case of multiple-drug resistant organisms.
A strain of Listeria monocytogenes isolated from a case of early onset, generalized, fatal, perinatal listeriosis in a premature infant was found to be tolerant for ampicillin and resistant against cefotaxime. A laboratory control strain of L. monocytogenes and Staphylococcus aureus control strain ATCC 25923 proved tolerant for both β-lactam antibiotics, respectively. The combinations of ampicillin with gentamicin and cefotaxime with gentamicin resulted in additive bactericidal activity against both strains of L. monocytogenes. Based on these findings and those of the literature, it is suggested that cases of systemic listeriosis be treated with a combination of a β-lactam antibiotic, preferably ampicillin, with an appropriate aminoglycoside, such as gentamicin.
Minimal bactericidal concentrations of thienamycin revealed moderate intraphagolysosomal bactericidal activity against pseudo-(PSR) and genuinely serum-resistant (NSS) assay strains of Serratia marcescens. Combinations of inhibitory and sub-inhibitory concentrations of thienamycin with 55 vol% of defibrinated human blood resulted in additive effects against all PSR and NSS test strains of S. marcescens and against the NSS Escherichia coli control strain ATCC 25922.
Two multiple drug resistant Enterobacter cloacae isolates (Nos. 460 and 493) varied phenotypically in bacteriocin susceptibility in the absence of significant·antigen variation. Both isolates were susceptible to chloramphenicol, nitrofurantoin, polymyxin B, nalidixic acid, norfloxacin, and enoxacin only. One isolate carried a non-conjugative resistance (R) plasmid, whereas the other isolate contained a conjugative, ‘curable’ R plasmid and a cryptic plasmid. Both wild-type isolates constitutively produced a chromosomal cephalosporinase (nitrocefin hydrolysis); ‘cured’ variants of E. cloacae isolate No. 493, which had become susceptible for lamoxactam, produced a cefazolin-inducible β-lactamase. The two E. cloacae isolates, including their ‘cured’ variants, were of low-grade virulence for outbred NMRI mice. Both isolates differed somewhat in susceptibility to defibrinated human blood. Inhibitory (0.25 μg/ml), but not subinhibitory (0.125 μg/ml) concentrations of norfloxacin and enoxacin combined with human blood yielded additive effects against both E. cloacae isolates.
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