🧬 β-lactamases are bacterial enzymes that inactivate β-lactam antibiotics by breaking the β-lactam ring.
🧱 This prevents β-lactams (penicillins, cephalosporins, carbapenems) from binding PBPs → cell-wall synthesis continues → treatment failure.
⚠️ A major driver of resistance in Gram-negatives, but also important in Gram-positives (e.g. penicillinase in S. aureus).

High-yield types (exam + real-world)

🟦 Narrow-spectrum penicillinases (e.g. many S. aureus) → resistant to plain penicillins; often overcome by inhibitor combinations.
🧪 ESBLs (often E. coli, Klebsiella) → hydrolyse many 3rd-gen cephalosporins; often leave carbapenems active (stewardship matters).
🔁 AmpC (e.g. Enterobacter, Citrobacter, Serratia, Providencia, Morganella) → can “switch on” during therapy; inhibitor combos may not reliably work.
🚨 Carbapenemases (e.g. KPC, NDM, OXA-48-like) → threaten carbapenems; management often needs specialist microbiology input.

Common β-lactamase producers (clinical examples)

👃🫁 Haemophilus influenzae & Moraxella catarrhalis (URTI/LRTI): frequent β-lactamase production → plain amoxicillin may fail.
🫃🦠 Bacteroides fragilis group (intra-abdominal/aspiration/anaerobes): many strains produce β-lactamase → influences anaerobic cover choices.
🚽🩸 Enterobacterales (e.g. E. coli, Klebsiella): ESBL/AmpC patterns are key in UTIs, sepsis, biliary infection.
🧴🩹 Staphylococcus aureus: penicillinase common; note MRSA = altered PBP (PBP2a), not a β-lactamase mechanism.

Important correction

🧠 Enterococcus isn’t classically a routine “β-lactamase producer”; its resistance is usually due to low-affinity PBPs (and cephalosporins have poor intrinsic activity).

β-lactamase inhibitors

🛡️ These protect the partner β-lactam by inhibiting certain β-lactamases (they don’t fix resistance due to altered PBPs or porin loss).
🧩 Classic inhibitors:
- 🍋 Clavulanate (e.g. co-amoxiclav)
- 🧷 Sulbactam (with ampicillin in some settings)
- 🧯 Tazobactam (e.g. piperacillin–tazobactam)
🆕 Newer inhibitors (spectrum varies by agent):
- 🧠 Avibactam (ceftazidime–avibactam): many ESBL/AmpC + some carbapenemases (KPC, OXA-48-like), but not metallo-β-lactamases (e.g. NDM).
- 🔧 Relebactam (imipenem–relebactam): some KPC/AmpC patterns; not metallo-β-lactamases.
- 🧱 Vaborbactam (meropenem–vaborbactam): strong vs KPC; not metallo-β-lactamases.

Clinical significance (UK ward reality)

📈 β-lactamase producers can drive escalation to broader agents, but aim for targeted therapy once cultures/susceptibilities return.
🧼 ESBL & carbapenemase producers are IPC priorities (screen/isolate per local policy).
☎️ In severe sepsis or treatment failure, escalate early to micro/ID—choice depends on organism + site + MIC + patient factors.

Prevention and management

🎯 Stewardship: right drug, right dose, shortest effective duration; de-escalate when able.
🧰 Source control (drain pus, remove infected lines, relieve obstruction) is often as important as antibiotics.
🧽 Infection prevention: hand hygiene, isolation when indicated, surveillance in high-risk units.

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Beta-lactamases

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