Search PubMedSearch

PubMed · 646345

Diffusion disk susceptibility testing with cefaclor.

Abstract

The reliability of the standardized 30-mug cephalothin disk and that of an experimental 30-mug cefaclor disk in predicting probable clinical susceptibility to cefaclor were compared. Quantitative determinations of cefaclor susceptibility were measured by the World Health Organization International Collaborative Study agar dilution procedure; diffusion disk tests were performed by the standardized U.S. Food and Drug Administration disk test. The cephalothin disk erred in predicting probable susceptibility in 52% of isolates of Enterococcus spp. resistant to 16 mug or less of cefaclor per ml; the cefaclor disk did not. The cephalothin disk erred in correctly predicting susceptibility in only 20% of cefaclor-susceptible isolates of Enterobacter spp.; the cefaclor disk correctly predicted susceptibility for 70%. These results indicate the need for further evaluation of a separate cefaclor disk for use in susceptibility testing with this new cephalosporin.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S Shadomy, M Carver. 1978. Diffusion disk susceptibility testing with cefaclor.. https://doi.org/10.1128/aac.13.2.228

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Site-directed mutagenesis and substrate-induced inactivation of beta-lactamase I.

The substrate-induced inactivation of beta-lactamase I from Bacillus cereus 569/H has been studied. Both the wild-type enzyme and mutants have been used. The kinetics follow a branched pathway of the type recently analysed [Waley (1991) Biochem. J. 279, 87-94]. The substrate cloxacillin (a penicillin) formed an acyl-enzyme (characterized by m.s.), and it was probably the instability of this intermediate that brought about inactivation. A disulphide bond was introduced into beta-lactamase I (the wild-type enzyme lacks this bond) by site-directed mutagenesis: Ala-77 and Ala-123 were replaced by cysteine. Spontaneous oxidation yielded the disulphide. The activity of this newly cross-linked enzyme was a little diminished, but the stability towards inactivation by cloxacillin was not increased. A second mutant of beta-lactamase I was studied: this mutant lacked the first 17 residues, i.e. the first alpha-helix. The mutant had reduced activity towards ordinary (non-inactivating) substrates and no hydrolysis of cloxacillin could be detected. These mutant enzymes were expressed in Bacillus subtilis, and were purified from the extracellular medium.

Cephalosporins

In vitro activity of loracarbef and effects of susceptibility test methods.

Loracarbef is a new oral antimicrobial of the carbacephem class with in vitro activity against the common pathogens associated with skin infections, otitis media, sinusitis, bronchopulmonary infections, and urinary tract infections. A review of the literature shows the following ranges for 90% minimum inhibitory concentration (MIC90) values (microgram/mL) against the organisms that commonly cause these illnesses: Streptococcus pneumoniae, 0.25-2.0; Moraxella (Branhamella) catarrhalis (beta-lactamase positive), 0.5-8.0; M. catarrhalis (beta-lactamase negative), 0.12-0.25; Haemophilus influenzae (beta-lactamase positive), 0.5-16.0; H. influenzae (beta-lactamase negative), 0.25-8.0; Escherichia coli, 2.0-25; Klebsiella pneumoniae, 0.25-8.0; Proteus mirabilis, 1.0-8.0; Streptococcus pyogenes, less than or equal to 0.06-1.0; Staphylococcus aureus (beta-lactamase positive), 8.0; S. aureus (beta-lactamase negative), 1.0-2.0. The in vitro activity of loracarbef against these common outpatient pathogens is similar to that of other oral antimicrobials such as cefaclor, cefuroxime axetil, cefixime, amoxicillin/clavulanate, and trimethoprim/sulfamethoxazole. The results of in vitro susceptibility tests with any antimicrobial, including loracarbef, are somewhat dependent on the specific test method that is employed in the laboratory. This is particularly true with H. influenzae. Furthermore, the results of loracarbef susceptibility tests are of uncertain value in predicting therapeutic outcome.

Cephalosporins

1-Chloro-2,4-dinitrobenzene-mediated irreversible inactivation of acidic glutathione S-transferases. Inactivation mechanism--a saturation-type or simple second-order kinetic process?

A critical analysis of the inactivation kinetics exhibited by the acidic human glutathione S-transferase (GST) enzymes is presented. Data on the 1-chloro-2,4-dinitrobenzene (CDNB)-facilitated inactivation of human placental GST pi have been utilized in conjunction with published inactivation data from the literature to answer the following two questions: (a) do the inactivation kinetics deviate significantly from a simple pseudo first-order model? (b) What is the kinetic mechanism of irreversible electrophilic co-substrate-mediated inactivation of human acidic GSTs? Inactivation of human placental GST pi in the presence of 7-aminocephalosporanic acid, a non-electrophilic non-substrate ligand, is characterized and shown to occur via a process analogous to the second mechanism proposed for CDNB inactivation of the enzyme, namely: pH- and [ligand]-independent solvational inactivation.

Cephalosporins