oxacillin
Regulatory sources consulted
Approved indications
- Infections caused by penicillinase-producing staphylococci susceptible to oxacillin.
Contraindications
Absolute
- Hypersensitivity to oxacillin or a history of hypersensitivity to a penicillin.
Clinical warnings
- Major warning · It may cause severe hypersensitivity or anaphylaxis. Review any history of immediate beta-lactam reactions before use and discontinue if an allergic reaction occurs. — FDA, set_id 152758c0-d225-4761-abeb-3f1cb0190806
- Major warning · It may cause Clostridioides difficile-associated diarrhea during or after treatment; assess significant diarrhea and avoid antiperistaltic drugs if colitis is suspected. — FDA, set_id 152758c0-d225-4761-abeb-3f1cb0190806
Drug interactions
- ModerateProbenecid
Mechanism: It reduces renal tubular secretion and may increase and prolong antibiotic exposure.
Recommendation: Avoid the combination unless deliberately indicated and monitor toxicity.
FDA, set_id 152758c0-d225-4761-abeb-3f1cb0190806
- ModerateTetracyclines
Mechanism: They may antagonize oxacillin bactericidal activity.
Recommendation: Avoid the combination.
FDA, set_id 152758c0-d225-4761-abeb-3f1cb0190806
Adverse events
Common (≥1%)
Nausea, diarrhea, and rash
Rare but serious
Anaphylaxis, C. difficile colitis, and severe cytopenias
Pregnancy and lactation
Use during pregnancy only when clearly indicated. Small amounts pass into milk; monitor the infant for diarrhea, candidiasis, or sensitization and assess continuation according to the product.
Recent literature (PubMed)
This article provides an overview of the mechanisms behind carbapenem resistance and the antibiotic management for severe infections caused by key carbapenem-resistant gram-negative bacteria, specifically Enterobacterales, Acinetobacter baumannii, and Pseudomonas aeruginosa. For Enterobacterales, it highlights the relative advantages of meropenem-vaborbactam and imipenem-relebactam in treating Klebsiella pneumoniae carbapenemase (KPC)-producing strains with resistance to ceftazidime-avibactam, the preference for ceftazidime-avibactam in addressing oxacillin-hydrolyzing carpapenemase (OXA)-48-like -producing organisms, and the combination of ceftazidime-avibactam with aztreonam for metallo-β-lactamase (MBL)-producing Enterobacterales. Regarding A baumannii, sulbactam-durlobactam is identified as the preferred treatment, while ceftolozane-tazobactam, ceftazidime-avibactam, and imipenem-relebactam are viable options for P aeruginosa. Additionally, cefiderocol is presented as an alternative for MBL-producing carbapenem-resistant gram-negative bacteria.
The Clinical and Laboratory Standards Institute (CLSI) Subcommittee on Antimicrobial Susceptibility Testing (AST) develops and publishes standards and guidelines for AST methods and results interpretation in an annual update to the Performance Standards for Antimicrobial Susceptibility Testing (M100). This minireview will discuss changes to M100 for the 31st edition, including new and revised breakpoints and testing recommendations. New MIC and disk diffusion breakpoints are described for azithromycin (Shigella spp.), imipenem-relebactam (Enterobacterales, Pseudomonas aeruginosa, and anaerobes), and lefamulin (Staphylococcus aureus, Haemophilus influenzae, and Streptococcus pneumoniae), and disk breakpoints are described for azithromycin and Neisseria gonorrhoeae. The rationale behind revised oxacillin MIC breakpoints for select staphylococci is discussed. Updates to test methods include a method for disk diffusion using positive blood culture broth and use of linezolid to predict tedizolid susceptibility. There is clarification on which drugs to suppress on bacteria isolated from the cerebrospinal fluid and clarification on the use of a caret symbol attached to the intermediate category ("I^") to indicate those antimicrobials that concentrate in the urine.
The pathogenic bacterium Staphylococcus aureus is the most common pathogen isolated in skin-and-soft-tissue infections (SSTIs) in the United States. Most S. aureus SSTIs are caused by the epidemic clone USA300 in the USA. These infections can be serious; in 2019, SSTIs with S. aureus were associated with an all-cause, age-standardized mortality rate of 0.5 globally. Clinical presentations of S. aureus SSTIs vary from superficial infections with local symptoms to monomicrobial necrotizing fasciitis, which can cause systemic manifestations and may lead to serious complications or death. In order to cause skin infections, S. aureus employs a host of virulence factors including cytolytic proteins, superantigenic factors, cell wall-anchored proteins, and molecules used for immune evasion. The immune response to S. aureus SSTIs involves initial responders such as keratinocytes and neutrophils, which are supported by dendritic cells and T-lymphocytes later during infection. Treatment for S. aureus SSTIs is usually oral therapy, with parenteral therapy reserved for severe presentations; it ranges from cephalosporins and penicillin agents such as oxacillin, which is generally used for methicillin-sensitive S. aureus (MSSA), to vancomycin for methicillin-resistant S. aureus (MRSA). Treatment challenges include adverse effects, risk for Clostridioides difficile infection, and potential for antibiotic resistance.
There is debate on whether cefazolin or antistaphylococcal penicillins should be the first-line treatment for methicillin-susceptible Staphylococcus aureus (MSSA) bacteraemia. Ongoing trials are investigating whether cefazolin is non-inferior to (flu)cloxacillin, but it remains uncertain whether these findings apply to other antistaphylococcal penicillins. We conducted a systematic review and meta-analysis comparing cefazolin with each of the individual antistaphylococcal penicillins for MSSA bacteraemia. Data sources: We updated a 2019 systematic review but specifically focused on evaluating outcomes by individual antistaphylococcal penicillins. Study eligibility criteria include comparative observational studies. Participants include patients with MSSA bacteraemia. Interventions include cefazolin vs. the antistaphylococcal penicillins. Assessment of risk of bias involved the risk of bias in non-randomized studies of interventions tool. The primary outcome was 30-day all-cause mortality and we assessed for non-inferiority of cefazolin using a pre-specified non-inferiority margin of a pooled OR <1.2 using raw unadjusted data. Secondary outcomes were 90-day mortality, treatment-related adverse events (TRAEs), discontinuation due to toxicity, and nephrotoxicity. No randomized data have been published. A total of 30 observational studies at moderate or high risk of bias were included, which comprised 3869 patients who received cefazolin and 11 644 patients who received antistaphylococcal penicillins (flucloxacillin = 6721, unspecified = 2440, nafcillin = 1305, cloxacillin = 1258, and oxacillin = 120). Cefazolin was associated with a reduced odds of 30-day all-cause mortality (OR = 0.73, 95% CI: 0.62-0.85) compared with antistaphylococcal penicillins, meeting pre-specified non-inferiority. This effect was consistent vs. flucloxacillin (OR = 0.92, 95% CI: 0.73-1.16), nafcillin (OR = 0.58, 95% CI: 0.28-1.17), cloxacillin (OR = 0.42, 95% CI: 0.11-1.58), and oxacillin (OR =