123. Pharmacology | Beta-lactam Antibiotics, Other Cell Wall Inhibitors, and Cell Membrane-Active Antibiotics, Part 2: Cephalosporins, Carbapenems, Monobactam, Vancomycin, and Daptomycin

A 68-year-old man with septic shock and acute kidney injury is started on broad-spectrum empiric antibiotics. Shortly after initiating one of the drugs, he develops new-onset seizures. Which antibiotic is the MOST likely cause of this effect?

A. Meropenem
B. Imipenem–cilastatin
C. Cefepime
D. Aztreonam
E. Ceftriaxone

B

Imipenem is well known (and emphasized in the transcript) for causing seizures, especially in renal insufficiency, because reduced clearance leads to accumulation. Cilastatin prevents renal degradation but does not prevent CNS toxicity.

• A. Meropenem – Lower seizure risk than imipenem.

• C. Cefepime – Can cause neurotoxicity in real-world practice, but this was not included in your lecture; thus not the correct answer.

• D. Aztreonam – No seizure risk.

• E. Ceftriaxone – Causes biliary sludging, neonatal issues, Ca-precipitation, NOT seizures.

A 3-day-old neonate is diagnosed with neonatal sepsis. The team wants to use a third-generation cephalosporin with excellent CSF penetration. Which drug is preferred specifically because it avoids risks associated with displacement of unconjugated bilirubin and calcium precipitation?

A. Cefepime
B. Ceftriaxone
C. Cefotaxime
D. Ceftazidime
E. Cefuroxime

C

Cefotaxime is preferred in neonates because ceftriaxone displaces bilirubin → ↑ risk of kernicterus, and forms fatal calcium–ceftriaxone precipitates.
Cefotaxime has excellent CSF penetration and avoids the neonatal dangers listed in the transcript.

Why the Other Choices Are Incorrect:

• A. Cefepime – Not preferred in neonates; not the drug mentioned in this context.

• B. Ceftriaxone – CONTRAINDICATED in neonates.

• D. Ceftazidime – CSF-penetrating, but no special neonatal safety benefit.

• E. Cefuroxime – Not a favored neonatal meningitis agent.

A 45-year-old man receiving therapy for MRSA bacteremia develops worsening muscle pain and rising creatine kinase levels. He is NOT taking any statins. Which mechanism explains the adverse effect of the drug causing his symptoms?

A. Inhibition of transpeptidase binding sites
B. Formation of pores in the membrane via calcium-dependent insertion
C. Binding to D-Ala-D-Ala termini
D. Chelation of iron for siderophore-mediated uptake
E. Inhibition of renal dehydropeptidase I

B

The patient is experiencing myopathy and elevated CK → classic adverse effect of daptomycin.
Mechanism: Calcium-dependent insertion of its lipid tail into the bacterial membrane, forming pores → depolarization.

• A. = β-lactam MOA (not associated with CK elevation).

• C. = vancomycin MOA; AE = Red Man, nephrotoxicity—not myopathy.

• D. = Cefiderocol mechanism (iron-siderophore uptake).

• E. = Cilastatin role, not related to CK elevation.

A 59-year-old woman with suspected ESBL-producing Enterobacterales bacteremia is started on empiric therapy. Which antibiotic is MOST appropriate as first-line treatment?

A. Cefuroxime
B. Cefazolin
C. Ceftriaxone
D. Meropenem
E. Ceftaroline

D

Carbapenems are the treatment of choice for ESBL-producing Enterobacterales.
Meropenem (and imipenem) remain the first-line agents until susceptibility results return.

• A/B/C – ESBLs inactivate all of these.

• E. Ceftaroline – Anti-MRSA, not an ESBL drug; limited Gram–.