Penicillin

About: Penicillin is a research topic. Over the lifetime, 17916 publications have been published within this topic receiving 368480 citations. The topic is also known as: penicillin antibiotic & PCN.

Penicillin-binding proteins in a Staphylococcus aureus strain resistant to specific beta-lactam antibiotics.

Abstract: The penicillin-binding proteins (PBPs) of a clinical isolate of Staphylococcus aureus specifically resistant to oral cephalosporins were compared with those of a susceptible strain. In the resistant strain, PBP3 (75,000 molecular weight) was missing or had substantially (greater than 100-fold) reduced affinity for penicillin; PBP2 (80,000 molecular weight) was increased in amount and contained a satellite band, PBP2'; PBPs 1 and 4 were unchanged. Oral cephalosporins bound poorly to PBP2 in both susceptible and resistant strains, but only in the latter did binding correlate with antibiotic activity. The results are consistent with the suggestion that PBP2 is essential in S. aureus. PBP2 might in addition compensate for PBP3 when the latter is missing. In the susceptible strain the lack of correlation between binding to PBP2 and beta-lactam antibiotic activity is due to the very high affinity of the also essential PBP3 for beta-lactam antibiotics.

β-Lactamase Activity in Human Pus

Abstract: Pus was obtained from patients with polymicrobial intraabdominal abscesses or polymicrobial empyema. Physical and chemical characteristics of 12 specimens were examined, and bacterial isolates were enumerated. Pus supernatant of six specimens rapidly inactivated penicillin, cephalothin, and cefazolin. Carbenicillin and ticarcillin were similarly degraded by supernatant of certain pus specimens. Cefoxitin, chloramphenicol, and clindamycin were not appreciably inactivated by pus supernatant. Degradation of penicillin and cephalosporin congeners in pus was due to the presence of beta-lactamase, as shown by chemical interaction with nitrocefin, chromatography, and inhibition by the beta-lactamase inhibitor clavulanic acid. Pus supernatant containing beta-lactamase activity reduced the bactericidal activity of carbenicillin against Bacteroides fragilis in whole pus in an abscess model in vitro. Bactericidal activity of clindamycin or cefoxitin was not impaired in pus containing beta-lactamase.

Penicillin Combined with Gentamicin or Streptomycin: Synergism against Enterococci

Abstract: The action of penicillin in combination with gentamicin against enterococci was studied. One hundred strains of enterococci, 14 of which were recovered from blood cultures of patients with endocarditis, were studied for susceptibility to penicillin, gentamicin, and streptomycin. All strains were inhibited by ^50 ^g of gentamicin/ml. The majority were inhibited by ^78 pg of streptomycin/ml, but 13 strains were not inhibited by 50,000 pg/ml. Thirty-three strains were studied for synergism of combinations of antibiotics. A combination of 20 pg of penicillin and 4 pg of gentamicin/ml was synergistic against all 33 strains, while 20 pg of penicillin combined with 20 pg of streptomycin/ml was synergistic against only 20 of the 33 strains. The minimal inhibitory concentration of streptomycin for four of these 20 strains was more than 50,000 pg/ml. The combination of penicillin and gentamicin may be considered an alternative for the treatment of enterococcal endocarditis, especially when penicillin and streptomycin are not synergistic.

Tolerant Response of Streptococcus sanguis to Beta-Lactams and Other Cell Wall Inhibitors

Abstract: In contrast to group A streptococci or Streptococcus pneumoniae, cells of Streptococcus sanguis (group H) do not exhibit the irreversible effects of penicillin treatment, such as loss of viability or lysis. On the other hand, the same bacteria show typical effects of penicillin, such as morphological alterations, reduction in the rate of cell wall synthesis, and secretion of murein and lipoteichoic acid polymers into the medium. A novel effect of cell wall inhibitors was also noted: treatment with beta-lactams or with fosfomycin, d-cycloserine, or beta-halogeno-d-alanine caused the release of substantial amounts of glycerol lipids into the growth medium. The antibiotic “tolerance” of S. sanguis is interpreted in terms of the hypothesis that the activity of bacterial murein hydrolases is essential for the irreversible effects of cell wall inhibitors.