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PubMed2026

Frequency and characteristics of extended-spectrum beta-lactamase-producing Escherichia coli in wastewater in Dakar, Senegal.

OBJECTIVE: This study aimed to investigate the occurrence, antimicrobial resistance profiles, and genetic characteristics of extended-spectrum beta-lactamase (ESBL)-producing E. coli in wastewater collected in Dakar, Senegal. RESULTS DESCRIPTION: All samples (n = 48) carried ESBL-producing isolates. The concentrations of ESBL-producing E. coli ranged from 1.4 × 10⁴ to 3.3 × 10⁵ CFU/100 mL, whereas the ratio of ESBL-producing E. coli among the total E. coli population varied between 0.2% and 16.3%. All the 107 isolated ESBL-producing E. coli isolates were multidrug resistant (MDR), with 100% resistance to beta-lactams (ampicillin, cefalotin, cefotaxime, ceftazidime, cefepime, aztreonam) and high resistance rates to non-beta-lactam antibiotics, including ciprofloxacin (77.6%). No resistance was observed to imipenem. CTX-M-type genes were present in all isolates, with blaCTX-M-1 group (89.7%) and blaCTX-M-8 group (88.8%) being the most prevalent. The blaCTX-M-15 variant, a subgroup of blaCTX-M- group1, was detected in 96.9% of blaCTX-M-1 positive isolates. Additionally, blaTEM (31.8%) and blaOXA-1 (34.6%) were detected, while blaSHV and blaCTX-M-25 group were absent. Phylogenetic analysis of 107 isolates revealed a diverse distribution across four phylogroups: A (37.4%), D (22.4%), B1 (14.0%), and B2 (5.7%). The predominance of phylogroup A, mainly associated with intestinal commensal carriage, suggests fecal contamination as a primary source.

Senegal↗
PubMed2026

A descriptive analysis of Streptococcus suis-associated disease in Irish pigs from 2010 to 2024: serotypes, pathology, and antimicrobial resistance.

BACKGROUND: Streptococcus suis is a major cause of respiratory and systemic diseases in post-weaned pigs, leading to significant production losses and animal welfare concerns. This study provides the first long-term national level analysis of Streptococcus suis-associated disease (SSAD) in the Republic of Ireland. We examined the pig diagnostic submissions, characterised serotype distribution, antimicrobial susceptibility, and co-infection patterns from 2010 to 2024. RESULTS: The findings confirm that serotypes 9 and 2 or 1/2 were most frequently associated with disease. We observed a significant shift in recent years where serotype 9 has surpassed serotype 2 or 1/2 in number of occurrences. S. suis was frequently co-detected with viral pathogens including porcine reproductive and respiratory syndrome virus (PRRSV), porcine circovirus type 2, and swine influenza virus (SIV), as well as bacterial pathogens such as Actinobacillus pleuropneumonia and Pasteurella multocida, typically from pneumonic lungs. While resistance to tetracycline and erythromycin was high (44.4% to 65.8%), isolates remained susceptible to first-line beta-lactam antibiotics such as penicillin (7.9% resistance), ampicillin (5.5% resistance) and amoxycillin/clavulanate (0% resistance). CONCLUSION: The observed heterogeneity between and within herds challenges successful implementation of vaccination and highlights the need for ongoing disease monitoring. These findings provide the first in-depth assessment of SSAD in Ireland's pig population which will offer valuable insights for future surveillance efforts, including genomic studies and supporting evidence-based strategies and vaccine selection for controlling S. suis in Irish pig sector.

Ireland↗
PubMed2026

The antimicrobial gut resistome of the Wayampi reveals a shared background of antibiotic and metal resistance genes with industrialized populations, underscoring the "robust-yet-fragile" architecture of human gut microbiomes.

BACKGROUND: Metagenomics enables detailed profiling of genes encoding antimicrobial resistance. However, most studies focus exclusively on antibiotic resistance genes (ARGs), excluding those associated with non-antibiotic antimicrobials (metals, biocides), and often rely on methods with low-sensitivity and low-specificity. Furthermore, they rarely examine populations exposed to minimal anthropogenic pollution. We analyzed fecal resistomes of 95 Wayampi individuals, an Indigenous community in remote French Guiana, using a targeted metagenomic capture platform covering 8667 genes, including ARGs, metal resistance genes (MRGs) and biocide resistance genes (BRGs) (PMID: 29335005). Resistome profiles were compared with those of Europeans to assess population-level differences. RESULTS: ARG richness was similar between groups (259 in Wayampi vs. 264 in Europeans, 159 shared), but MRGs&#x2009;+&#x2009;BRGs gene richness was significantly higher in Wayampi (11,930 vs. 7419). Most genes appeared in a minority of individuals (mean 5% for ARGs, 2% for MRGs&#x2009;+&#x2009;BRGs), but several ARGs for tetracyclines [tet(32), tet(40), tet(O), tet(Q), tet(W), tet(X), tetAB(P)], aminoglycosides (ant6'-I, aph3-III), macrolides (ermB, ermF, mefA), and sulfonamides (sul2) were present in all individuals. Tetracycline resistance genes predominated overall, while beta-lactam resistance genes were more common in Wayampi, and genes conferring resistance to aminoglycosides, amphenicols, and folate inhibitors were more frequent in Europeans. Among MRGs, copper and arsenic resistance genes prevailed in both groups, followed by those for zinc, iron, cobalt, and nickel. Up to 76% of Wayampiis carried acquired MRGs for copper (pcoABCDRS and tcrB), silver (silACFPRS), arsenic (ars), and mercury (mer) detoxification. Shannon diversity indices were similar for ARGs, MRGs, and BRGs, but composition and evenness differed significantly. UMAP and ADONIS analyses distinguished cohorts based on ARG profiles (p&#x2009;<&#x2009;0.001), but not on MRGs or BRGs. Correlation analysis revealed conserved gene-sharing networks and introgression of acquired ARGs and MRGs within both gut microbiomes. CONCLUSIONS: The diverse and balanced Wayampi resistome reflects a less perturbed microbiome compared to industrialized populations, and reveals a background of "core" and "shell" acquired ARGs and MRGs, consistent with the "robust-yet-fragile" architecture of scale-free networks. The patchy yet resilient gene distribution suggests varying levels of conserved gene sharing highways among populations, likely shaped by long-term microbial-human evolution, and supports a broader view on acquired antimicrobial resistance. Video Abstract.

Humans↗
PubMed2025

Global genomic and antimicrobial resistance profiling of Neisseria gonorrhoeae: Insights from whole genome sequencing and minimum inhibitory concentration analysis.

BACKGROUND: The rising antimicrobial resistance (AMR) of Neisseria gonorrhoeae is a major global health concern that limits treatment options and complicates disease management. Efflux pump systems and resistance genes are key to bacteria's ability to evade antibiotics. This study examined the genetic and phenotypic resistance landscape using a large dataset of whole-genome sequences to identify key resistance mechanisms, assess efflux pump gene prevalence, and analyze regional variations in Minimum Inhibitory Concentration (MIC) values to inform treatment strategies and public health interventions. METHODS: A total of 38,585 whole-genome sequences of N. gonorrhoeae were analyzed to identify AMR determinants. This study focused on the presence and distribution of efflux pump genes (mtrC, farB, norM, and mtrA) and specific resistance genes, including tet(C) (tetracycline resistance) and aph(3')-Ia (aminoglycoside resistance). The MIC values were assessed for multiple antibiotics to evaluate resistance trends and regional variations, including penicillin, spectinomycin, zoliflodacin, gentamicin, and fluoroquinolones. RESULTS: This analysis revealed widespread resistance to multiple antibiotics. Efflux pump genes (mtrC, farB, norM, and mtrA) were found in nearly all isolates, highlighting their essential roles in resistance and adaptation. The presence of tet(C) and aph (3')-Ia varied across different Gene Presence Patterns, suggesting that regional or therapeutic factors may influence tetracycline and aminoglycoside resistance. High MIC values for penicillin were observed, likely because of blaTEM, a beta-lactamase gene responsible for beta-lactam resistance. Resistance to spectinomycin is also widespread, raising concerns about the diminishing efficacy of this antibiotic. In contrast, zoliflodacin, gentamicin, and fluoroquinolones exhibited relatively low MIC values, indicating their sustained effectiveness against N. gonorrhoeae. DISCUSSION: Efflux pump systems are key to N. gonorrhoeae resistance and adaptability. Regional MIC variations indicate that local antibiotic use shapes resistance patterns. The high resistance to penicillin and spectinomycin highlights the need for alternative treatments, whereas zoliflodacin and fluoroquinolones remain effective but require monitoring. This study emphasizes global AMR surveillance, novel therapies, and targeted antimicrobial stewardship to address multidrug-resistant infections.

Neisseria gonorrhoeae↗
PubMed1978

In vitro activity of HR 756, a new cephalosporin compound.

The in vitro activity of HR 756, a new cephalosporin, has been determined against recent clinical isolates and compared with that of other beta-lactam antibiotics. The geometric means of the minimum inhibitory concentrations (MIC) for different isolates of Escherichia coli (100 isolates), Klebsiella pneumoniae (84), Pseudomonas aeruginosa (121), Proteus mirabilis (52), indole-positive Proteus species (9), Salmonella species (19), Staphylococcus aureus penicillin-sensitive (29) and penicillin-resistant (39) were: 0.095, 0.124, 11.1, 0.095, 0.0107, 0.078, 1 and 0.95 mcg/ml, respectively. Its activity was affected by rise in inoculum against S. aureus and P. aeruginosa but not against K. pneumoniae and E. coli. Bactericidal activity was determined by membrane filtration method. HR 756 was found to be bactericidal to E. coli, K. pneumoniae, P. aeruginosa and Proteus species. Although the MICs of the tested S. aureus strains were 1 mcg/ml, 5 mcg/ml of HR 756 failed to kill 99% of the inoculum within 24 hours.

Bacteria↗
PubMed1978

[The present situation of antibacterial resistance (author's transl)].

The various types of bacterial resistance (natural species resistance, chromosomal and plasmidic resistance) and their mechanisms are described. Thereafter, a survey on the resistance is given using investigations from different sources. The distribution of resistant strains dependent on the geographical location and the situation of the patients (ambulatory--hospitalized) is described, and the development of resistant strains in dependance of time is analyzed. Finally, the phenomena of resistance against aminoglycoside and beta-lactam antibiotics are explained in more detail.

Aminoglycosides↗
PubMed1978

Computer survey of antibiotic resistance--developments during 1973 to 1977.

Results of antibiotic resistance of strains belonging to 9 species of so-called Problem bacteria, recorded by 10 District Public Health Laboratories in Slovakia during 6 months of 1977 (altogether 32641 strains) have been compared with results, obtained with identical computer-assisted system in 1973. The position of "Reserve antibiotics" (gentamicin, colistin, cotrimoxazole, oxacillin, lincomycin, spiramycin) remained favourable during precedent 4 years and even improved (with exception of gentamicin in P. aeruginosa). In classical antibiotics a typical steady-state situation was establishedin that period. Beta-lactam antibiotics in general deteriorated in gramnegatives, with certain improvements in special cases. In "specific pathogens", i.e. enteropathogenic strains of E. coli and in strains of P. aeruginosa, resistance to antibiotics generally increased. On the other hand, in S. aureus strains a better susceptibility to almost all antibiotics could be recorded. Surgical services still seem to use the bacteriological services infrequently and this should improve on an all-nation basis.

Anti-Bacterial Agents↗
PubMed1978

Solubilization and characterization of the partially purified penicillin sensitive D-alanine carboxypeptidase of Neisseria gonorrhoeae.

Treatment of crude gonococcal cell envelopes with a solution of 2 M KCl + 1% Brij 36T resulted in the solubilization of a portion of the D-alanine carboxypeptidase activity of Neisseria gonorrhoeae envelopes. This soluble enzyme preparation was partially resolved by chromatography on a column of DEAE-cellulose. The partially purified enzyme eluted from the column with a gradient of NaCl (0-1 M), catalysed the release of D-alanine from a radioactively labelled UDP-N-acetylmuramyl-pentapeptide with a pH optimum of 8.6. The Km for the soluble enzyme acting on this substrate was 0.18 mM. The enzyme activity was sensitive to inhibition by low concentrations of the beta-lactam antibiotics, penicillin G, ampicillin, oxacillin and mecillinam.

Carboxypeptidases↗
PubMed2026

Occurrence of blaOXA-72 in a clinical isolate of carbapenem-resistant Acinetobacter pittii ST206 in Japan.

The development of carbapenem resistance in Acinetobacter spp., which are recognized as significant opportunistic pathogens, is of critical importance as it poses challenges to therapy and the control of healthcare-associated infections in clinical settings. This study investigated the genetic characteristics of a carbapenem-resistant A. pittii clinical isolate from a university hospital using whole-genome sequencing. The A. pittii strain SU8507, which was detected in the abdominal drainage fluid of a patient, exhibited resistance to imipenem (MIC: 128&#x202f;&#x3bc;g/mL) and meropenem (MIC: 64&#x202f;&#x3bc;g/mL) and produced positive results by the CIMTris method. A. pittii SU8507, belonging to ST206, harbored the blaOXA-72 and new variants of intrinsic blaOXA-213-like gene blaOXA-1222, which lacks an upstream insertion sequence element, and blaADC-1-like gene blaADC-343. The blaOXA-72 gene, flanked by XerC/XerD-like recombination sites, was located on a plasmid pSU8507, sized at 10,913 bp, carrying 13 predicted protein-coding genes. Complete pSU8507 containing mobA, repB, and the yoeB-yefM toxin-antitoxin genes, showed 98.9% nucleotide sequence identity and 75% coverage with plasmid pA2702 of the A. baylyi strain A2702, but a low BLAST MAX score. SU8507 harbored virulence genes involved in biofilm formation, types II and VI secretion systems, type IV pilus system, and serum resistance. This study describes the first isolation of an OXA-72-producing, carbapenem-resistant A. pittii clinical isolate in Japan. Given that the isolation rate of carbapenem-resistant Acinetobacter spp. Remains low in Japan, it is crucial to expand the scope of rapid, accurate carbapenemase detection to include not only A. baumannii, but also non-baumannii Acinetobacter spp.

Humans↗
PubMed2026

Dual &#x3b2;-lactam therapy against high-risk Pseudomonas aeruginosa isolates: a dynamic in-vitro infection model study integrating population genomics with quantitative systems pharmacology modelling and simulations.

BACKGROUND: Pseudomonas aeruginosa has an extraordinary capacity for resistance emergence during treatment, even with newer antipseudomonals. There is a gap in understanding how resistance mechanisms affect the time-course of bacterial response to these newer agents. Traditional approaches for predicting pathogen response to an antibiotic do not apply to combination therapy. We aimed to develop a modelling framework to predict treatment response based on resistome information, using isolates of the worldwide-disseminated high-risk clone sequence type (ST) 235 and &#x3b2;-lactam antibiotics as the example. METHODS: In this hollow-fibre in-vitro infection study, we used three extensively drug-resistant ST235 clinical isolates from the national collection of the Clinical Microbiology Department of the Hospital Son Espases (Palma de Mallorca, Spain) that were hospital-acquired, were isolated following routine microbiological procedures from different patients between 2017 and 2022, were susceptible to ceftolozane-tazobactam, and had different levels of meropenem resistance. The selected isolates (ST235-05, ST235-09, and ST235-10) showed classical &#x3b2;-lactam resistance mechanisms pre-treatment. The isolates were investigated in 240-h dynamic hollow-fibre in-vitro infection models (HFIMs). The studies exposed the isolates to pharmacokinetic profiles of ceftolozane-tazobactam (simulating 1 g of ceftolozane and 0&#xb7;5 g of tazobactam as a 3-h infusion every 8 h) and meropenem (simulating 6 g per day continuous infusion) as observed in hospitalised patients, as monotherapy and in combination. Treatment response was assessed through the quantification of the time-courses of viable total and resistant bacteria. Whole-genome sequencing identified the mechanisms of emerging resistance. A quantitative systems pharmacology (QSP) approach was used to model total and resistant bacterial counts and corresponding pharmacokinetic data from the HFIM. Monte Carlo simulations were used to predict treatment responses in 1000 virtual infected patients treated with ceftolozane-tazobactam and meropenem as monotherapies or in combination over 10 days. FINDINGS: In the HFIMs, each antibiotic alone amplified resistance by approximately 48 h for all isolates; that is, monotherapies resulted in a higher concentration of resistant bacteria compared with the control treatment at the respective time, except ceftolozane-tazobactam against ST235-10. Combination of ceftolozane-tazobactam and meropenem was synergistic (bacterial counts &#x2265;2 log10 colony forming units [CFU] per mL lower than the best performing monotherapy and initial inoculum) against all isolates and suppressed resistance. Against ST235-10, ceftolozane-tazobactam monotherapy reduced counts to less than 1 log10 CFU per mL from 192 h onwards, whereas the combination reached less than 1 log10 CFU per mL by 24 h. Across strains, population genomics confirmed monotherapy failures were associated with emerging resistance mechanisms (ceftolozane-tazobactam: ampC &#x3a9;-loop mutations; meropenem: ftsl mutation). The developed QSP model incorporated baseline resistance mechanisms and those emerging in resistant mutant subpopulations. The model explained and predicted the monotherapy failures involving amplification of these subpopulations, and synergistic killing and resistance suppression by the combination. Simulations using the model predicted bacterial regrowth above the initial inoculum for more than 90% of patients after 0 to approximately 3 days for meropenem monotherapy across all strains and for ceftolozane-tazobactam monotherapy against ST235-05 and ST235-09. For ceftolozane-tazobactam monotherapy against ST235-10, regrowth was predicted for approximately 30% of patients. In contrast, the simulations predicted sustained bacterial killing of at least 2 log10 CFU per mL compared with the initial inoculum by the combination for more than 89% of patients across all strains. INTERPRETATION: To our knowledge, this model is the first to characterise and predict the time-course of responses of clinical isolates to antibiotics only by the resistance mechanisms present and their complex interplay, representing a step towards pathogen-specific, personalised medicine. FUNDING: Australian National Health and Medical Research Council.

Pseudomonas aeruginosa↗
PubMed2026

Complicated urinary tract infections: evolving definitions, clinical burden, and treatment landscape amid antimicrobial resistance.

INTRODUCTION: Complicated urinary tract infection (cUTI) is a common and heterogeneous infection associated with substantial morbidity, high healthcare utilization, and increasing antimicrobial resistance. Evolving definitions, increasing device use, and changing patient populations have altered its epidemiology and management. Marked variability in diagnostic criteria, clinical trial endpoints within and outside registrational settings, and treatment strategies complicates clinical decision-making and interpretation of therapeutic advances. AREAS COVERED: This review examines contemporary cUTI epidemiology, classification frameworks, and drivers of disease burden. It evaluates resistance trends and their therapeutic implications, alongside stewardship-based management strategies, including empiric antibiotic selection, intravenous-to-oral transition, treatment duration, and source control. Challenges in catheter-associated infection, recurrence, and regulatory endpoint design are discussed, together with the emerging role of novel agents targeting resistant Gram-negative pathogens. EXPERT OPINION: Rising multidrug resistance and limited oral options are reshaping cUTI management, necessitating individualized, stewardship-aligned therapy guided by illness severity and local epidemiology. Current regulatory endpoints inadequately reflect patient-centered outcomes, particularly in the context of asymptomatic bacteriuria. Expanding availability of effective oral agents may enable earlier discharge and outpatient care. Integration of rapid diagnostics and risk stratification will be essential to optimize therapy, limit resistance, and improve outcomes.

Humans↗
PubMed2025

Characterization of blaOXA-542-mediated carbapenem resistance in Acinetobacter baumannii.

BACKGROUND: Carbapenem-resistant Acinetobacter baumannii (CRAB) causes multiple anatomical site infections, representing a significant public health threat. AIM: This study reports the isolation and characterization of a carbapenem-resistant A. baumannii harbouring blaOXA-542, followed by a comprehensive investigation of its antimicrobial resistance mechanisms and genomic characteristics. METHODS: Firstly, antimicrobial susceptibility testing was performed using the broth microdilution method. Subsequently, whole-genome sequencing was employed to identify and characterize the resistance and virulence determinants. The functional validation of resistance mechanisms was performed by gene knockdown and construction of expression vectors. The fitness cost of &#x3b2;-lactamase expression was identified by a bacterial growth kinetic test. Molecular docking was utilized to predict potential binding sites of &#x3b2;-lactamase and carbapenems. Finally, the genetic characteristics of the isolates were analysed through comparative genomics analyses and phylogenetic tree construction. RESULTS AND CONCLUSIONS: The results demonstrated that blaOXA-542 confers resistance to carbapenem and penicillin in A. baumannii and Escherichia coli while exhibiting no significant impact on cephalosporins. The ability of blaOXA-542 to hydrolyze meropenem was further confirmed by modified carbapenem inactivation assay (mCIM). Expression of blaOXA-542 in E. coli BL21 showed no significant growth rate alteration. Comparative analysis of the blaOXA-542 genetic environment revealed a close association with Acinetobacter pitti. This study reports the emergence of blaOXA-542-mediated carbapenem and penicillin resistance in a novel A. baumannii lineage (ST2795Pas/ST3464Oxf), highlighting the urgent need for rational antibiotic use against specific pathogens.

Acinetobacter baumannii↗
PubMed2025

Chromosomal resistance mutations facilitate acquisition of multidrug-resistant plasmids in Escherichia coli.

Bacteria can gain multiple resistance mechanisms in a single step by the acquisition of multidrug-resistant (MDR) plasmids, but it is unclear how antibiotic selection during the acquisition of MDR plasmids affects the evolution of additional resistance mechanisms. Through conjugating separate extended-spectrum &#x3b2;-lactamase (ESBL)- and carbapenemase-producing MDR plasmids into plasmid-naive Escherichia coli hosts, we examine the effects of acquisition of a single plasmid or co-acquisition of multiple plasmids upon fitness costs, resistance and subsequent genomic adaptation. We show that acquisition of pOXA-48, encoding OXA-48 carbapenemase, is associated with highly variable fitness costs and levels of resistance to ertapenem in transconjugants independent of the presence of pLL35. This phenomenon was not observed during the acquisition of ESBL CTX-M-15-encoding pLL35 alone. Within a single growth cycle, transconjugants receiving pOXA-48 rapidly gained parallel mutations affecting the membrane porin OmpF, or its regulators OmpR or EnvZ. These chromosomal mutations were not compensatory for the fitness costs imposed by the plasmid, nor did they provide significant increases in resistance to carbapenems in the absence of the pOXA-48. Rather, they acted synergistically with the plasmid-encoded carbapenemase, which alone only provided marginal resistance, together providing high-level resistance to ertapenem. Such rapid evolutionary processes may play an important role in plasmid dynamics within environments with strong antibiotic selection for plasmid-encoded antimicrobial resistance genes (ARGs), particularly when these ARGs provide only marginal resistance.

Escherichia coli↗
PubMed2026

Variations in carbapenem resistance associated with the VIM-1 metallo-&#x3b2;-lactamase across the Enterobacterales.

The VIM-1 metallo-&#x3b2;-lactamase enzyme, encoded within class 1 integrons, is found in Gram-negative clinical isolates worldwide and has been linked to outbreaks of bacterial pathogens in nosocomial settings. Six vim-1+ clinical isolates, from the genera Escherichia, Klebsiella and Enterobacter, were obtained from Kingston, Ontario, Canada. Whole-genome sequencing revealed that vim-1 was plasmid-borne in all strains and situated as the first gene in In916 or In110 integrons. Analysis of related plasmids suggested that these vim-1-containing plasmids are globally disseminated and have spread via horizontal gene transfer and autochthonous vertical spread within Ontario. Interestingly, the MICs of ertapenem and meropenem, two clinically relevant carbapenem antibiotics, against these six isolates varied more than tenfold, suggesting that the effects of VIM-1 are dependent on the genomic content of the host microbe. Introducing vim-1 into three common Enterobacterales laboratory strains was not sufficient to confer resistance to ertapenem and meropenem. Instead, adaptive laboratory evolution of the vim-1 + laboratory strains revealed that vim-1-mediated carbapenem resistance in these strains was dependent on epistatic interactions with ompC mutations, likely due to decreased outer membrane permeability to these antibiotics. Together, these results provide additional support for the role of gene epistasis in modulating the antimicrobial resistance phenotypes of acquired resistance genes, as well as previous results suggesting that the presence of a &#x3b2;-lactamase gene is insufficient to confer strong resistance to carbapenems without being paired with reduced outer membrane permeability.

beta-Lactamases↗
PubMed1978

Inhibition of beta-lactamase in Neisseria gonorrhoeae by sodium clavulanate.

Sodium clavulanate at subinhibitory concentrations affected the activity of penicillin G, ampicillin, or amoxicillin on beta-lactamase-positive strains of Neisseria gonorrhoeae as demonstrated by marked reduction in the minimal inhibitory concentrations of the drugs for the organisms. The compound did not affect the activity of these penicillins on beta-lactamase-negative strains of N. gonorrhoeae. It also had no effect on the activity of cefoxitin against either beta-lactamase-negative or -positive strains. The reduction in minimal inhibitory concentrations of the penicillins for the beta-lactamase-positive organisms brought about by sodium clavulanate is probably due to inhibition of the beta-lactamase by the compound.

Anti-Bacterial Agents↗
PubMed1978

Clavulanic acid inhibition of beta-lactamase I from Bacillus cereus 569/H.

Inactivation of beta-lactamase I by clavulanic acid was investigated. Clavulanic acid induced inhibition of the enzyme was found to be progressive with time. Benzylpenicillin provided protection against the adverse effects of the inhibitor initially, however, the enzyme was irreversibly inhibited in a progressive manner even in the presence of substrate. Reaction of beta-lactamase I with clavulanic acid, in the presence of ampicillin, led to a very rapid inactivation of the enzyme.

Ampicillin↗