Pharmacology Quiz: Beta Lactams
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Beta LactamsQuestion 1 of 20

A patient in the intensive care unit on mechanical ventilation develops a new fever and purulent sputum. Empiric therapy with imipenem/cilastatin is initiated to cover a broad range of potential pathogens. Despite this, the patient's condition worsens. The causative organism is later identified from culture. Which of the following pathogens is most likely responsible for the treatment failure due to its intrinsic resistance to carbapenems?

Escherichia coli producing an extended-spectrum beta-lactamase (ESBL).
Pseudomonas aeruginosa with acquired porin loss and efflux pump upregulation.
Stenotrophomonas maltophilia.
Bacteroides fragilis.
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Pharmacology Quiz

Pharmacology Quiz: Beta Lactams

Practice Beta Lactams in Pharmacology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Beta Lactams, giving you a quick way to practice the rules, question types, and explanations that matter most for Pharmacology.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

All questions

Question 1

A patient in the intensive care unit on mechanical ventilation develops a new fever and purulent sputum. Empiric therapy with imipenem/cilastatin is initiated to cover a broad range of potential pathogens. Despite this, the patient's condition worsens. The causative organism is later identified from culture. Which of the following pathogens is most likely responsible for the treatment failure due to its intrinsic resistance to carbapenems?

  1. Escherichia coli producing an extended-spectrum beta-lactamase (ESBL).
  2. Pseudomonas aeruginosa with acquired porin loss and efflux pump upregulation.
  3. Stenotrophomonas maltophilia. (correct answer)
  4. Bacteroides fragilis.
Explanation: Stenotrophomonas maltophilia exhibits high levels of intrinsic resistance to carbapenems. This is primarily due to the production of two beta-lactamases: a zinc-dependent metallo-beta-lactamase (L1) and a cephalosporinase (L2). Imipenem is readily hydrolyzed by the L1 enzyme. (A) Carbapenems like imipenem are the drugs of choice for ESBL-producing organisms. (B) While P. aeruginosa can acquire resistance to carbapenems, it is not universally intrinsically resistant. (D) Carbapenems have excellent activity against most anaerobes, including B. fragilis.

Question 2

A patient is being discharged from the hospital after successful treatment of pyelonephritis with intravenous ceftriaxone. The physician wishes to transition the patient to an oral cephalosporin to complete a 14-day course of therapy. Which of the following would be an illogical choice for oral step-down therapy due to its pharmacokinetic properties?

  1. Cefixime
  2. Cefdinir
  3. Cefepime (correct answer)
  4. Cephalexin
Explanation: Cefepime is a fourth-generation cephalosporin that is only available in a parenteral (IV/IM) formulation. It has very poor oral bioavailability and is not manufactured as an oral medication. Therefore, it cannot be used for oral step-down therapy. (A), (B), and (D) are all examples of cephalosporins (third-, third-, and first-generation, respectively) that are available in oral formulations with adequate bioavailability for treating conditions like urinary tract infections.

Question 3

A patient in the intensive care unit on mechanical ventilation develops a new fever and purulent sputum. Empiric therapy with imipenem/cilastatin is initiated to cover a broad range of potential pathogens. Despite this, the patient's condition worsens. The causative organism is later identified from culture. Which of the following pathogens is most likely responsible for the treatment failure due to its intrinsic resistance to carbapenems?

  1. Escherichia coli producing an extended-spectrum beta-lactamase (ESBL).
  2. Pseudomonas aeruginosa with acquired porin loss and efflux pump upregulation.
  3. Stenotrophomonas maltophilia. (correct answer)
  4. Bacteroides fragilis.
Explanation: Stenotrophomonas maltophilia exhibits high levels of intrinsic resistance to carbapenems. This is primarily due to the production of two beta-lactamases: a zinc-dependent metallo-beta-lactamase (L1) and a cephalosporinase (L2). Imipenem is readily hydrolyzed by the L1 enzyme. (A) Carbapenems like imipenem are the drugs of choice for ESBL-producing organisms. (B) While P. aeruginosa can acquire resistance to carbapenems, it is not universally intrinsically resistant. (D) Carbapenems have excellent activity against most anaerobes, including B. fragilis.

Question 4

A patient is diagnosed with native valve endocarditis due to Enterococcus faecalis that is susceptible to penicillin. A junior colleague suggests initiating therapy with intravenous nafcillin, arguing that it is a potent anti-Gram-positive agent. Why is nafcillin a clinically inappropriate choice for treating this infection?

  1. Nafcillin achieves poor concentrations in cardiac vegetations compared to other penicillins.
  2. Enterococcus faecalis rapidly develops resistance to nafcillin via beta-lactamase induction.
  3. Nafcillin has inherently poor binding affinity to the penicillin-binding proteins of Enterococcus species. (correct answer)
  4. Nafcillin is primarily hepatically metabolized, which is contraindicated in the inflammatory state of endocarditis.
Explanation: The anti-staphylococcal penicillins (nafcillin, oxacillin, dicloxacillin) have a bulky R-group side chain. This structure sterically hinders their hydrolysis by staphylococcal penicillinase, making them effective against MSSA. However, this same bulky structure also prevents them from binding effectively to the PBPs of other organisms, including enterococci, Listeria, and most anaerobes. Thus, despite the enterococcus being susceptible to penicillin, it is intrinsically resistant to nafcillin due to poor target affinity. (A) This is not the primary reason. (B) Enterococcal resistance is typically due to PBP modification, not beta-lactamase. (D) Hepatic metabolism is a feature, not a contraindication.

Question 5

A patient with a skin infection caused by Staphylococcus aureus is not responding to treatment. Subsequent culture and sensitivity testing identifies the isolate as methicillin-resistant (mecA-positive) and also resistant to ceftaroline. Which of the following provides the most likely molecular basis for the organism's acquired resistance to ceftaroline?

  1. Expression of a novel beta-lactamase enzyme that efficiently hydrolyzes the ceftaroline beta-lactam ring.
  2. A point mutation in the mecA gene leading to an altered PBP2a with significantly reduced binding affinity for ceftaroline. (correct answer)
  3. Downregulation of porin channels in the bacterial outer membrane, preventing ceftaroline from reaching its target site.
  4. Induction of high-level efflux pump expression that actively transports ceftaroline out of the bacterial cell.
Explanation: Ceftaroline's unique activity against MRSA stems from its high binding affinity for PBP2a, the protein encoded by the mecA gene. While initial MRSA isolates are typically susceptible, resistance to ceftaroline can develop. The most common mechanism for this is a mutation within the mecA gene that alters the allosteric or active binding site of PBP2a, thereby reducing ceftaroline's ability to bind and inhibit cell wall synthesis. (A) is less likely as ceftaroline is stable against standard staphylococcal beta-lactamases. (C) is incorrect because S. aureus is a Gram-positive bacterium and lacks an outer membrane with porin channels. (D) Efflux pumps are a mechanism of resistance for some antibiotics, but target alteration is the primary mechanism for ceftaroline resistance in MRSA.

Question 6

A patient is diagnosed with native valve endocarditis due to Enterococcus faecalis that is susceptible to penicillin. A junior colleague suggests initiating therapy with intravenous nafcillin, arguing that it is a potent anti-Gram-positive agent. Why is nafcillin a clinically inappropriate choice for treating this infection?

  1. Nafcillin achieves poor concentrations in cardiac vegetations compared to other penicillins.
  2. Enterococcus faecalis rapidly develops resistance to nafcillin via beta-lactamase induction.
  3. Nafcillin has inherently poor binding affinity to the penicillin-binding proteins of Enterococcus species. (correct answer)
  4. Nafcillin is primarily hepatically metabolized, which is contraindicated in the inflammatory state of endocarditis.
Explanation: The anti-staphylococcal penicillins (nafcillin, oxacillin, dicloxacillin) have a bulky R-group side chain. This structure sterically hinders their hydrolysis by staphylococcal penicillinase, making them effective against MSSA. However, this same bulky structure also prevents them from binding effectively to the PBPs of other organisms, including enterococci, Listeria, and most anaerobes. Thus, despite the enterococcus being susceptible to penicillin, it is intrinsically resistant to nafcillin due to poor target affinity. (A) This is not the primary reason. (B) Enterococcal resistance is typically due to PBP modification, not beta-lactamase. (D) Hepatic metabolism is a feature, not a contraindication.

Question 7

A patient is being treated for a serious infection caused by an Enterobacter species that is known to produce an inducible AmpC beta-lactamase. The use of a third-generation cephalosporin like ceftriaxone carries a risk of treatment failure due to the selection of derepressed, resistant mutants. Why is cefepime, a fourth-generation cephalosporin, often a more reliable choice in this specific scenario?

  1. Cefepime is a much weaker inducer of AmpC beta-lactamase expression and is more stable to hydrolysis by the enzyme. (correct answer)
  2. Cefepime's zwitterionic structure allows it to completely bypass the porin channels used by ceftriaxone.
  3. Cefepime has the additional ability to inhibit the synthesis of the AmpC enzyme at the ribosomal level.
  4. Cefepime has a significantly longer half-life than ceftriaxone, which helps to overcome inducible resistance.
Explanation: The advantage of cefepime in treating infections caused by AmpC-producing organisms (like Enterobacter, Serratia, Citrobacter) lies in its relationship with the enzyme. Third-generation cephalosporins are potent inducers of AmpC gene expression and are also readily hydrolyzed by the resulting enzyme. In contrast, cefepime is a poor inducer of AmpC and is significantly more stable against hydrolysis by it. This combination of properties makes it less likely to select for resistant mutants during therapy. (B) It uses porin channels but may do so more efficiently. (C) It has no effect on enzyme synthesis. (D) Ceftriaxone actually has a much longer half-life than cefepime.

Question 8

An elderly patient with a creatinine clearance of 20 mL/min and a history of a seizure disorder is being treated with imipenem/cilastatin for a severe, polymicrobial infection. This patient requires particularly close monitoring because this specific clinical scenario significantly elevates the risk of which adverse drug event?

  1. Drug-induced immune hemolytic anemia.
  2. Severe nephrotoxicity leading to acute tubular necrosis.
  3. Neurotoxicity, manifesting as confusion or seizures. (correct answer)
  4. Biliary sludging and pseudocholelithiasis.
Explanation: Imipenem carries the highest risk of CNS toxicity, including seizures, among the carbapenems. This risk is substantially increased in patients with pre-existing CNS conditions (like a seizure disorder) and in those with renal impairment, as reduced clearance leads to drug accumulation. The dose of imipenem must be adjusted for renal function to mitigate this risk. (A) Hemolytic anemia is a rare reaction. (B) Imipenem's nephrotoxic potential is low, particularly when combined with cilastatin. (D) Biliary sludging is characteristic of ceftriaxone.

Question 9

A patient has a documented history of an IgE-mediated anaphylactic reaction to amoxicillin. The patient now requires treatment for a serious infection where a beta-lactam is strongly preferred. Based on current understanding of cross-reactivity, which of the following agents would carry the highest risk of eliciting a similar allergic response?

  1. Cefpodoxime
  2. Cefadroxil (correct answer)
  3. Aztreonam
  4. Meropenem
Explanation: The risk of cross-reactivity between penicillins and cephalosporins is largely determined by the similarity of the R1 side chain, not the beta-lactam ring itself. Amoxicillin and cefadroxil (a first-generation cephalosporin) share a nearly identical R1 side chain (a p-hydroxy-phenylglycyl group). This structural similarity significantly increases the risk of an IgE-mediated cross-reaction. (A) Cefpodoxime has a dissimilar R1 side chain. (C) Aztreonam, a monobactam, has virtually no cross-reactivity with penicillins. (D) Meropenem, a carbapenem, has a very low rate of cross-reactivity (<1%) with penicillins.

Question 10

A hospital-acquired pneumonia is being treated with piperacillin-tazobactam. The causative organism is identified as an Enterobacter cloacae isolate that is found to be resistant to the combination. The isolate remains susceptible to meropenem. What is the most probable resistance mechanism explaining this susceptibility pattern?

  1. Production of a KPC-type carbapenemase.
  2. Alteration of penicillin-binding protein targets.
  3. High-level, stable expression of an AmpC beta-lactamase. (correct answer)
  4. Production of an extended-spectrum beta-lactamase (ESBL).
Explanation: Enterobacter species are known for producing inducible AmpC beta-lactamases. While tazobactam is effective against many Class A beta-lactamases (including many ESBLs), it is a weak inhibitor of Class C (AmpC) enzymes. High-level expression of AmpC will hydrolyze piperacillin, rendering the combination ineffective. Meropenem is stable to hydrolysis by AmpC, explaining its retained activity. (A) A KPC carbapenemase would also confer resistance to meropenem. (B) PBP alteration is a less common mechanism for this pattern in Enterobacter. (D) Tazobactam is generally effective against ESBLs, making this mechanism less likely than AmpC to be the sole cause of resistance.

Question 11

A urine culture from a patient with a recurrent urinary tract infection grows Escherichia coli. The susceptibility report shows the isolate is resistant to ceftriaxone but susceptible to piperacillin-tazobactam and meropenem. Which mechanism of resistance is most consistent with this antibiogram?

  1. Production of a simple, plasmid-mediated penicillinase.
  2. Expression of a KPC-type carbapenemase.
  3. Target site modification via alteration of PBP2a.
  4. Production of an extended-spectrum beta-lactamase (ESBL). (correct answer)
Explanation: This susceptibility pattern is classic for an ESBL-producing organism. ESBLs are enzymes that hydrolyze most penicillins and cephalosporins (including third-generation agents like ceftriaxone), conferring resistance. However, they are inhibited by beta-lactamase inhibitors like tazobactam, restoring the activity of piperacillin. Carbapenems like meropenem are stable to hydrolysis by ESBLs. (A) A simple penicillinase would not inactivate ceftriaxone. (B) A carbapenemase would confer resistance to meropenem. (C) PBP2a alteration is the mechanism of methicillin resistance in S. aureus, not E. coli.

Question 12

A patient develops a widespread, non-pruritic, maculopapular rash on day 9 of a 10-day course of amoxicillin for a sinus infection. The patient has no fever, urticaria, angioedema, or difficulty breathing. Which immunological mechanism is most likely responsible for this reaction?

  1. A Type I, IgE-mediated immediate hypersensitivity reaction.
  2. A Type II, antibody-dependent cytotoxic hypersensitivity reaction.
  3. A Type III, immune complex deposition-mediated reaction.
  4. A Type IV, delayed-type, T-cell mediated hypersensitivity reaction. (correct answer)
Explanation: This clinical presentation is classic for a benign, delayed-type hypersensitivity reaction to a beta-lactam. These reactions are mediated by drug-specific T-lymphocytes, classifying them as Type IV hypersensitivity. They typically occur 5-14 days after drug initiation and manifest as a morbilliform or maculopapular exanthem. (A) Type I reactions are immediate (minutes to hours) and present with urticaria/angioedema. (B) Type II reactions cause cytopenias (e.g., hemolytic anemia). (C) Type III reactions can cause serum sickness or vasculitis, which present differently.

Question 13

A patient with cystic fibrosis has a pulmonary exacerbation caused by Pseudomonas aeruginosa. The patient's allergy history is significant for a severe anaphylactic reaction to ceftazidime. Which of the following beta-lactam antibiotics should be avoided due to a structurally predictable and high risk of allergic cross-reactivity?

  1. Piperacillin-tazobactam
  2. Meropenem
  3. Cefepime
  4. Aztreonam (correct answer)
Explanation: This question tests a critical exception in beta-lactam allergy. While aztreonam (a monobactam) generally has no cross-reactivity with other beta-lactams in penicillin-allergic patients, it shares an identical R1 side chain with ceftazidime (a third-generation cephalosporin). Because IgE-mediated allergies are often directed at the side chain, there is a significant risk of cross-reactivity between these two specific drugs. Therefore, aztreonam should be avoided in a patient with a known severe allergy to ceftazidime. The other options have dissimilar side chains and low predicted cross-reactivity risk.

Question 14

Aztreonam's spectrum of activity is uniquely limited to aerobic Gram-negative bacteria, making it useful in certain clinical situations. This selectivity is a direct consequence of its molecular structure and its interaction with bacterial targets. Which statement best explains this narrow spectrum?

  1. Its monocyclic structure prevents it from being recognized and hydrolyzed by beta-lactamases from Gram-positive bacteria.
  2. It has a high binding affinity for penicillin-binding protein 3 (PBP3) of aerobic Gram-negatives but very low affinity for the PBPs of Gram-positives and anaerobes. (correct answer)
  3. It cannot effectively penetrate the thick peptidoglycan layer of Gram-positive bacteria to reach its PBP targets.
  4. It is actively transported out of Gram-positive bacteria and anaerobes by specific efflux pumps not present in aerobic Gram-negatives.
Explanation: The basis for aztreonam's selective spectrum is its differential affinity for penicillin-binding proteins. Its monobactam structure binds with high avidity to PBP3, an essential enzyme for cell septum formation in aerobic Gram-negative rods. In contrast, it has negligible affinity for the PBPs found in Gram-positive organisms and anaerobes, rendering it inactive against them. (A) While it has some stability, it can be hydrolyzed by certain Gram-negative beta-lactamases (like ESBLs). (C) Beta-lactams can generally penetrate the peptidoglycan layer. (D) Efflux is not the primary reason for its lack of activity against these entire classes of bacteria.

Question 15

A patient with cystic fibrosis has a pulmonary exacerbation caused by Pseudomonas aeruginosa. The patient's allergy history is significant for a severe anaphylactic reaction to ceftazidime. Which of the following beta-lactam antibiotics should be avoided due to a structurally predictable and high risk of allergic cross-reactivity?

  1. Piperacillin-tazobactam
  2. Meropenem
  3. Cefepime
  4. Aztreonam (correct answer)
Explanation: This question tests a critical exception in beta-lactam allergy. While aztreonam (a monobactam) generally has no cross-reactivity with other beta-lactams in penicillin-allergic patients, it shares an identical R1 side chain with ceftazidime (a third-generation cephalosporin). Because IgE-mediated allergies are often directed at the side chain, there is a significant risk of cross-reactivity between these two specific drugs. Therefore, aztreonam should be avoided in a patient with a known severe allergy to ceftazidime. The other options have dissimilar side chains and low predicted cross-reactivity risk.

Question 16

A patient presents with a severe intra-abdominal infection, and cultures grow a Klebsiella pneumoniae isolate that produces both an extended-spectrum beta-lactamase (ESBL) and a KPC-type carbapenemase. Which of the following beta-lactam/beta-lactamase inhibitor combinations is specifically designed to overcome this dual resistance mechanism?

  1. Meropenem-vaborbactam (correct answer)
  2. Ceftolozane-tazobactam
  3. Piperacillin-tazobactam
  4. Ampicillin-sulbactam
Explanation: When you encounter questions about multidrug-resistant organisms with multiple resistance mechanisms, focus on matching the specific inhibitor to the resistance enzymes present. This Klebsiella isolate produces both ESBL (which breaks down penicillins, cephalosporins, and aztreonam) and KPC carbapenemase (which destroys carbapenems), creating a formidable double threat. Meropenem-vaborbactam (A) is specifically engineered for this scenario. Vaborbactam is a next-generation beta-lactamase inhibitor that effectively inhibits both Class A enzymes (including ESBLs and KPC carbapenemases) and some Class C enzymes. When combined with meropenem, it restores the carbapenem's activity against KPC-producing organisms while also handling the ESBL. Ceftolozane-tazobactam (B) targets Pseudomonas and some ESBL-producers, but tazobactam cannot reliably inhibit KPC carbapenemases, making this ineffective against the dual resistance. Piperacillin-tazobactam (C) faces the same limitation—tazobactam is a first-generation beta-lactamase inhibitor that doesn't cover carbapenemases effectively. Ampicillin-sulbactam (D) is primarily used for Acinetobacter and some gram-positive infections; sulbactam has minimal activity against either ESBLs or carbapenemases. Study tip: Remember the carbapenemase coverage hierarchy: vaborbactam and relebactam (newer inhibitors) can handle KPC carbapenemases, while tazobactam and sulbactam (older inhibitors) generally cannot. When you see "carbapenemase-producing" organisms, look for these newer combination agents.

Question 17

A patient with a vague history of a non-urticarial rash to penicillin as a child undergoes penicillin allergy skin testing (PST), which is negative. The medical team plans to treat the patient's serious infection with a penicillin. What is the most accurate interpretation of the negative PST result in this context?

  1. The test definitively proves the patient was never truly allergic to penicillin.
  2. The patient is not at risk for any delayed, T-cell mediated reactions like Stevens-Johnson syndrome to penicillin.
  3. The patient has a very high likelihood (>97%) of tolerating penicillin without an immediate, IgE-mediated hypersensitivity reaction. (correct answer)
  4. The test result indicates safety for penicillin use, but the patient remains at high risk for cross-reactivity with all cephalosporins.
Explanation: A negative penicillin skin test has a very high negative predictive value (NPV), typically reported as 97-99%. This means that it effectively rules out the presence of penicillin-specific IgE antibodies, and the patient has a very low risk of experiencing an immediate (Type I) hypersensitivity reaction upon receiving a penicillin. (A) It doesn't prove a prior allergy didn't exist; many people lose their IgE-mediated sensitivity over time. (B) PST does not predict the risk of delayed, Type IV reactions. (D) A negative PST suggests a very low risk of IgE-mediated reaction to penicillins and, by extension, a low risk of cross-reactivity to cephalosporins.

Question 18

Aztreonam's spectrum of activity is uniquely limited to aerobic Gram-negative bacteria, making it useful in certain clinical situations. This selectivity is a direct consequence of its molecular structure and its interaction with bacterial targets. Which statement best explains this narrow spectrum?

  1. Its monocyclic structure prevents it from being recognized and hydrolyzed by beta-lactamases from Gram-positive bacteria.
  2. It has a high binding affinity for penicillin-binding protein 3 (PBP3) of aerobic Gram-negatives but very low affinity for the PBPs of Gram-positives and anaerobes. (correct answer)
  3. It cannot effectively penetrate the thick peptidoglycan layer of Gram-positive bacteria to reach its PBP targets.
  4. It is actively transported out of Gram-positive bacteria and anaerobes by specific efflux pumps not present in aerobic Gram-negatives.
Explanation: The basis for aztreonam's selective spectrum is its differential affinity for penicillin-binding proteins. Its monobactam structure binds with high avidity to PBP3, an essential enzyme for cell septum formation in aerobic Gram-negative rods. In contrast, it has negligible affinity for the PBPs found in Gram-positive organisms and anaerobes, rendering it inactive against them. (A) While it has some stability, it can be hydrolyzed by certain Gram-negative beta-lactamases (like ESBLs). (C) Beta-lactams can generally penetrate the peptidoglycan layer. (D) Efflux is not the primary reason for its lack of activity against these entire classes of bacteria.

Question 19

A patient has a documented history of an IgE-mediated anaphylactic reaction to amoxicillin. The patient now requires treatment for a serious infection where a beta-lactam is strongly preferred. Based on current understanding of cross-reactivity, which of the following agents would carry the highest risk of eliciting a similar allergic response?

  1. Cefpodoxime
  2. Cefadroxil (correct answer)
  3. Aztreonam
  4. Meropenem
Explanation: The risk of cross-reactivity between penicillins and cephalosporins is largely determined by the similarity of the R1 side chain, not the beta-lactam ring itself. Amoxicillin and cefadroxil (a first-generation cephalosporin) share a nearly identical R1 side chain (a p-hydroxy-phenylglycyl group). This structural similarity significantly increases the risk of an IgE-mediated cross-reaction. (A) Cefpodoxime has a dissimilar R1 side chain. (C) Aztreonam, a monobactam, has virtually no cross-reactivity with penicillins. (D) Meropenem, a carbapenem, has a very low rate of cross-reactivity (<1%) with penicillins.

Question 20

An elderly patient with a creatinine clearance of 20 mL/min and a history of a seizure disorder is being treated with imipenem/cilastatin for a severe, polymicrobial infection. This patient requires particularly close monitoring because this specific clinical scenario significantly elevates the risk of which adverse drug event?

  1. Drug-induced immune hemolytic anemia.
  2. Severe nephrotoxicity leading to acute tubular necrosis.
  3. Neurotoxicity, manifesting as confusion or seizures. (correct answer)
  4. Biliary sludging and pseudocholelithiasis.
Explanation: Imipenem carries the highest risk of CNS toxicity, including seizures, among the carbapenems. This risk is substantially increased in patients with pre-existing CNS conditions (like a seizure disorder) and in those with renal impairment, as reduced clearance leads to drug accumulation. The dose of imipenem must be adjusted for renal function to mitigate this risk. (A) Hemolytic anemia is a rare reaction. (B) Imipenem's nephrotoxic potential is low, particularly when combined with cilastatin. (D) Biliary sludging is characteristic of ceftriaxone.