1. [CASE 1 — QUESTION 1]
A 38-year-old man with advanced human immunodeficiency virus (HIV) infection (CD4 count 40 cells/microliter, not on antiretroviral therapy) is admitted with extensive painful anogenital ulceration. Swab polymerase chain reaction (PCR) confirms HSV-2. The lesions are large and progressive, and he cannot reliably take oral medications. The team plans to begin antiviral therapy for severe mucocutaneous HSV in an immunocompromised host. Which initial therapy is most appropriate?
A) Oral acyclovir 400 mg three times daily
B) Intravenous acyclovir, because severe progressive mucocutaneous HSV in an immunocompromised patient who cannot reliably take oral medication warrants intravenous therapy
C) Foscarnet as first-line therapy before any acyclovir trial
D) Ganciclovir, because immunocompromised HSV requires anti-CMV therapy
E) Oseltamivir
ANSWER: B
Rationale:
Severe, progressive mucocutaneous HSV in an immunocompromised patient — particularly one who cannot reliably take oral medication — warrants intravenous acyclovir, the standard first-line therapy for serious HSV disease. Acyclovir is selectively activated by viral thymidine kinase and is highly effective and well tolerated for initial treatment before any resistance has been demonstrated.
Option A: Option A is incorrect: oral acyclovir has poor, saturable bioavailability and is inadequate for severe disease in a patient who cannot reliably take oral medication.
Option C: Option C is incorrect: foscarnet is reserved for acyclovir-resistant HSV, not first-line therapy before an acyclovir trial.
Option D: Option D is incorrect: this is herpes simplex virus disease treated with acyclovir; ganciclovir targets CMV.
Option E: Option E is incorrect: oseltamivir is an influenza neuraminidase inhibitor with no activity against HSV.
2. [CASE 1 — QUESTION 2]
Continuing with the same patient. After seven days of adequate intravenous acyclovir, the ulcers continue to enlarge with no clinical improvement. Acyclovir-resistant HSV is strongly suspected. Recalling the usual mechanism of acyclovir resistance, what is the appropriate next step?
A) Continue the same acyclovir dose for two more weeks
B) Double the acyclovir dose to overcome resistance
C) Add oral valacyclovir to the intravenous acyclovir
D) Switch to foscarnet, because acyclovir resistance is usually due to a viral thymidine kinase mutation that prevents drug activation, and foscarnet acts directly on the viral DNA polymerase without requiring viral kinase
E) Switch to oral ganciclovir
ANSWER: D
Rationale:
Lack of clinical response after five to seven days of adequate intravenous acyclovir indicates probable acyclovir-resistant HSV, which is usually caused by a viral thymidine kinase (TK) mutation that prevents phosphorylation and activation of acyclovir. Foscarnet is the agent of choice because it inhibits the viral DNA polymerase directly and requires no viral kinase, so it remains active against TK-deficient strains.
Option A: Option A is incorrect: continuing the same regimen that has already failed will not help a TK-mutant strain.
Option B: Option B is incorrect: increasing the dose cannot overcome a block in activation, since the virus cannot phosphorylate acyclovir regardless of dose.
Option C: Option C is incorrect: valacyclovir is a prodrug of acyclovir and depends on the same TK activation, so adding it does not address resistance.
Option E: Option E is incorrect: ganciclovir depends on phosphorylation for activation and is not the standard choice for TK-mutant acyclovir-resistant HSV; foscarnet is preferred.
3. [CASE 1 — QUESTION 3]
Continuing with the same patient. Foscarnet is started. Before initiating therapy, the team establishes a monitoring and prevention plan tailored to foscarnet's characteristic toxicities. Which plan correctly reflects foscarnet's adverse-effect profile?
A) Provide mandatory saline prehydration before each infusion to reduce nephrotoxicity, and monitor serum calcium, magnesium, potassium, and phosphate with each dose because foscarnet chelates divalent cations and characteristically causes hypocalcemia, along with serial serum creatinine
B) Monitor complete blood counts twice weekly and give granulocyte colony-stimulating factor, because myelosuppression is foscarnet's dose-limiting toxicity
C) Give oral probenecid before and after each dose to block OAT1-mediated uptake
D) Restrict fluids to maximize urinary drug concentration
E) No monitoring is needed because foscarnet is renally inert
ANSWER: A
Rationale:
Foscarnet's major toxicity is severe nephrotoxicity, mitigated by mandatory saline prehydration (500 to 1000 mL of normal saline) before each infusion. It also chelates divalent cations, characteristically causing hypocalcemia along with hypomagnesemia, hypokalemia, and phosphate disturbances, so calcium, magnesium, potassium, and phosphate must be monitored with each dose, together with serial serum creatinine.
Option B: Option B is incorrect: foscarnet notably lacks myelosuppression; the CBC/G-CSF plan describes ganciclovir.
Option C: Option C is incorrect: probenecid to block OAT1 uptake is the cidofovir protocol, not foscarnet.
Option D: Option D is incorrect: fluid restriction would worsen nephrotoxicity and genital ulceration; vigorous saline hydration is required.
Option E: Option E is incorrect: foscarnet is a major cause of nephrotoxicity and electrolyte disturbance, so monitoring is essential.
4. [CASE 1 — QUESTION 4]
Continuing with the same patient. A trainee asks why simply giving more acyclovir would not work and whether any agent other than foscarnet could be used if foscarnet were not tolerated. Which explanation is correct?
A) Higher-dose acyclovir works because resistance is dose-dependent, and no alternative to foscarnet exists
B) Acyclovir resistance reflects a polymerase mutation only, so cidofovir is also useless
C) Higher-dose acyclovir fails because a thymidine kinase mutation blocks activation regardless of dose; cidofovir is an alternative to foscarnet because it is activated by cellular enzymes independent of viral thymidine kinase and therefore also retains activity against thymidine kinase-deficient acyclovir-resistant HSV
D) Acyclovir resistance can be overcome by combining acyclovir with valacyclovir
E) Only oseltamivir remains effective against acyclovir-resistant HSV
ANSWER: C
Rationale:
Acyclovir resistance in this setting is usually due to a viral thymidine kinase (TK) mutation that prevents the activating phosphorylation, so increasing the dose cannot help — the drug is never converted to its active form. Cidofovir is a viable alternative to foscarnet because it is activated to its diphosphate by cellular enzymes, independent of viral TK, and therefore also retains activity against TK-deficient acyclovir-resistant HSV (provided the polymerase remains susceptible).
Option A: Option A is incorrect: the resistance is due to a block in activation, not a dose-dependent effect, and foscarnet is not the only option — cidofovir also works.
Option B: Option B is incorrect: the common mechanism is a TK mutation, not a polymerase mutation, and cidofovir remains active because it does not need TK.
Option D: Option D is incorrect: valacyclovir is a prodrug of acyclovir with the same TK dependence, so combining them does not overcome resistance.
Option E: Option E is incorrect: oseltamivir is an influenza neuraminidase inhibitor with no activity against HSV.
5. [CASE 2 — QUESTION 1]
A 56-year-old woman receives a deceased-donor kidney transplant. The donor is CMV-seropositive and the recipient is CMV-seronegative (D+/R-). The transplant team must choose a CMV prevention strategy for this serostatus combination. Recognizing this patient's risk category, which approach is most appropriate?
A) No CMV prevention, because seronegative recipients are inherently protected
B) Acyclovir prophylaxis, which reliably prevents CMV
C) Pre-emptive therapy is mandatory and universal prophylaxis is contraindicated in D+/R-
D) Foscarnet prophylaxis as the standard first choice
E) Universal prophylaxis with valganciclovir (or ganciclovir) for a defined post-transplant period, because D+/R- is the highest-risk serostatus combination for CMV infection and end-organ disease
ANSWER: E
Rationale:
The D+/R- combination is the highest-risk serostatus pairing, carrying a 50% to 80% risk of CMV infection and a 20% to 30% risk of end-organ disease without prophylaxis, because the seronegative recipient has no pre-existing immunity yet receives latent virus with the graft. Universal prophylaxis with valganciclovir (or ganciclovir) for a defined period (typically 3 to 6 months) is a validated and appropriate strategy for this group.
Option A: Option A is incorrect: seronegative recipients of a seropositive organ are at the highest risk, not protected, so prevention is essential.
Option B: Option B is incorrect: acyclovir does not reliably prevent CMV because CMV lacks viral thymidine kinase.
Option C: Option C is incorrect: universal prophylaxis is a validated and commonly preferred strategy in D+/R-, not contraindicated.
Option D: Option D is incorrect: foscarnet is a nephrotoxic salvage agent, not a standard prophylactic first choice.
6. [CASE 2 — QUESTION 2]
Continuing with the same patient. She completes a course of valganciclovir prophylaxis. Six weeks after prophylaxis is stopped, she develops fever, fatigue, and a rising CMV viral load with biopsy-confirmed CMV disease. Recognizing this complication of the chosen strategy, what is the appropriate treatment?
A) Restart the same prophylactic valganciclovir dose only, since this is simply prophylaxis failure
B) Treat the late-onset CMV disease with intravenous ganciclovir induction (5 mg/kg every 12 hours) until symptoms resolve and viral load is undetectable, then transition to oral valganciclovir maintenance
C) Begin acyclovir, which is effective for CMV end-organ disease
D) Start letermovir as treatment of established CMV disease
E) Observe without therapy, since late-onset CMV is self-limited
ANSWER: B
Rationale:
This is late-onset CMV disease, a recognized drawback of universal prophylaxis (especially in D+/R- recipients whose immune reconstitution may be incomplete when prophylaxis ends). Established CMV end-organ disease is treated with intravenous ganciclovir induction (5 mg/kg every 12 hours) until symptoms resolve and viral load is undetectable, followed by transition to oral valganciclovir maintenance.
Option A: Option A is incorrect: established disease requires induction-level treatment, not merely restarting a prophylactic dose.
Option C: Option C is incorrect: acyclovir has no meaningful activity against CMV because CMV lacks viral thymidine kinase.
Option D: Option D is incorrect: letermovir is approved for prophylaxis, not treatment of established CMV disease.
Option E: Option E is incorrect: CMV end-organ disease is not self-limited and requires antiviral therapy.
7. [CASE 2 — QUESTION 3]
Continuing with the same patient. Ten days into intravenous ganciclovir, her absolute neutrophil count falls steeply. Recognizing the dose-limiting toxicity of ganciclovir and the timing of its nadir, what is the appropriate management?
A) Manage the ganciclovir-induced myelosuppression by reducing or holding ganciclovir and supporting the absolute neutrophil count with granulocyte colony-stimulating factor (G-CSF), or switching to foscarnet, which lacks myelosuppression, if continued anti-CMV therapy is required
B) Continue ganciclovir unchanged, as neutropenia is unrelated to the drug
C) Switch to cidofovir, which reliably reverses neutropenia
D) Add acyclovir to raise the neutrophil count
E) Permanently stop all CMV therapy regardless of viral status
ANSWER: A
Rationale:
Myelosuppression, particularly neutropenia, is the dose-limiting toxicity of ganciclovir, and neutrophil nadirs typically occur within the first two weeks of therapy. Appropriate management is to reduce or hold ganciclovir and support the count with granulocyte colony-stimulating factor (G-CSF), or to switch to foscarnet — which lacks myelosuppression — when continued anti-CMV therapy is required.
Option B: Option B is incorrect: the neutropenia is the recognized dose-limiting toxicity of ganciclovir, not an unrelated finding.
Option C: Option C is incorrect: cidofovir does not reverse neutropenia and carries its own dose-dependent nephrotoxicity.
Option D: Option D is incorrect: acyclovir does not raise neutrophil counts and has no role here.
Option E: Option E is incorrect: permanently stopping therapy in active CMV disease risks progression; the toxicity is managed by dose modification, G-CSF, or switching to foscarnet.
8. [CASE 2 — QUESTION 4]
Continuing with the same patient. After foscarnet is held and ganciclovir is resumed at a reduced dose with G-CSF support, the CMV viral load fails to decline by even 1 log10 after two weeks, and she has now had substantial cumulative ganciclovir exposure. Genotypic testing is sent. What is the most appropriate next step and rationale?
A) Increase ganciclovir to the maximum tolerated dose, since resistance is overcome by exposure
B) Switch to acyclovir, which is active against ganciclovir-resistant CMV
C) Stop all antivirals and observe
D) Switch to foscarnet, because failure of viral load to fall by at least 1 log10 after two weeks of adequate ganciclovir with prior exposure suggests UL97-mediated resistance, and foscarnet retains activity against UL97-mutant CMV without requiring viral activation
E) Add valganciclovir to the intravenous ganciclovir for synergy
ANSWER: D
Rationale:
Failure of CMV viral load to decline by at least 1 log10 after two weeks of adequate ganciclovir, with prior ganciclovir exposure, is a recognized trigger to suspect resistance (most commonly a UL97 mutation) and to send genotypic testing. Foscarnet is the appropriate switch because it acts directly on the viral DNA polymerase without requiring UL97-mediated activation and generally retains activity against UL97-mutant CMV.
Option A: Option A is incorrect: a UL97 mutation impairs ganciclovir activation, so higher doses do not overcome it.
Option B: Option B is incorrect: acyclovir has no meaningful activity against CMV because CMV lacks viral thymidine kinase.
Option C: Option C is incorrect: resistant CMV is treatable with foscarnet; stopping therapy risks progressive disease.
Option E: Option E is incorrect: valganciclovir is oral ganciclovir and shares the same UL97 dependence, so combining the two does not address resistance.
9. [CASE 3 — QUESTION 1]
A 31-year-old man with newly diagnosed acquired immunodeficiency syndrome (AIDS) (CD4 count 25 cells/microliter) presents with decreased vision in the right eye. Dilated fundoscopy reveals CMV retinitis with a lesion in zone 1, within 1500 micrometers of the fovea, immediately threatening central vision. He can absorb oral medications. Which initial management is most appropriate?
A) Topical antiviral drops alone
B) Oral acyclovir induction
C) Oral valganciclovir induction (900 mg twice daily), with intravitreal ganciclovir or foscarnet injection as an adjunct for the immediately sight-threatening zone 1 lesion to achieve rapid local viral suppression
D) Letermovir as first-line treatment of CMV retinitis
E) Observation, since CMV retinitis resolves with immune recovery alone
ANSWER: C
Rationale:
For CMV retinitis in a patient who can absorb oral medications, valganciclovir 900 mg twice daily for induction (followed by 900 mg once daily maintenance) is first-line. For an immediately sight-threatening zone 1 lesion (within 1500 micrometers of the optic disc or fovea), intravitreal ganciclovir or foscarnet injection is added to achieve rapid local viral suppression before systemic therapy takes full effect.
Option A: Option A is incorrect: CMV retinitis is an intraocular infection requiring systemic therapy, not topical drops.
Option B: Option B is incorrect: acyclovir is ineffective against CMV because CMV lacks viral thymidine kinase.
Option D: Option D is incorrect: letermovir is approved for CMV prophylaxis in transplant recipients, not first-line treatment of established retinitis.
Option E: Option E is incorrect: a sight-threatening lesion cannot be observed; immune recovery alone is too slow to prevent vision loss in zone 1 disease.
10. [CASE 3 — QUESTION 2]
Continuing with the same patient. The HIV team wishes to start antiretroviral therapy (ART). The ophthalmology and infectious disease teams raise a concern specific to active CMV retinitis. What is the recommended timing of ART initiation, and why?
A) Start ART immediately with the first dose of CMV therapy, since earlier immune recovery is always better
B) Withhold ART permanently while CMV retinitis is present
C) Start ART before any CMV therapy to maximize immune recovery first
D) ART timing has no relationship to CMV retinitis management
E) Defer ART initiation for at least two weeks after starting CMV treatment, because immune reconstitution inflammatory syndrome (IRIS) can paradoxically worsen retinal inflammation if ART is begun too early in active CMV retinitis
ANSWER: E
Rationale:
In active CMV retinitis, immune reconstitution inflammatory syndrome (IRIS) can paradoxically worsen retinal inflammation after ART initiation, sometimes requiring corticosteroids. For this reason, ART initiation is deferred for at least two weeks after starting CMV treatment to reduce the risk of IRIS-related ocular complications.
Option A: Option A is incorrect: starting ART immediately in active CMV retinitis increases the risk of IRIS-related worsening of retinal inflammation.
Option B: Option B is incorrect: ART is not withheld permanently; it is briefly deferred, then started.
Option C: Option C is incorrect: starting ART before CMV therapy would heighten, not reduce, the IRIS risk in active retinitis.
Option D: Option D is incorrect: ART timing is directly relevant — the recommended brief deferral exists specifically because of the IRIS risk in CMV retinitis.
11. [CASE 3 — QUESTION 3]
Continuing with the same patient. He also reports two weeks of diarrhea, hematochezia, and abdominal pain. A blood CMV polymerase chain reaction (PCR) is negative. The team suspects CMV gastrointestinal disease. How should this be diagnosed?
A) Exclude CMV based on the negative blood PCR and treat empirically for bacterial colitis
B) Confirm by tissue biopsy demonstrating CMV cytopathic effect (intranuclear owl-eye inclusions) or positive immunohistochemistry, because blood CMV PCR may be negative in isolated gastrointestinal disease
C) Repeat the blood PCR daily until it turns positive before any further evaluation
D) Diagnose clinically without endoscopy or biopsy
E) Assume drug-induced colitis from valganciclovir and stop antivirals
ANSWER: B
Rationale:
In isolated CMV gastrointestinal disease, blood CMV PCR may be negative, so diagnosis requires tissue biopsy demonstrating CMV cytopathic effect — the characteristic intranuclear owl-eye inclusions — or positive immunohistochemistry. This tissue confirmation is essential when the blood PCR does not reflect localized gut disease.
Option A: Option A is incorrect: a negative blood PCR does not exclude isolated gastrointestinal CMV disease, so it should not be used to rule it out.
Option C: Option C is incorrect: repeating blood PCR is unreliable here because the blood assay can remain negative in isolated gut disease; tissue diagnosis is needed.
Option D: Option D is incorrect: a clinical diagnosis without biopsy is inadequate to confirm CMV gastrointestinal disease.
Option E: Option E is incorrect: assuming drug-induced colitis and stopping antivirals risks untreated CMV disease; biopsy establishes the diagnosis.
12. [CASE 3 — QUESTION 4]
Continuing with the same patient. A student asks how ganciclovir works against CMV at the molecular level, given that CMV has no classical thymidine kinase. Which statement correctly describes ganciclovir's activation and target in CMV?
A) Ganciclovir is phosphorylated first by the CMV UL97 phosphotransferase, then cellular kinases complete conversion to ganciclovir triphosphate, which inhibits the CMV UL54 DNA polymerase and is incorporated into viral DNA
B) Ganciclovir is activated by viral thymidine kinase, which CMV possesses in abundance
C) Ganciclovir requires no activation and binds the polymerase pyrophosphate site directly
D) Ganciclovir inhibits the CMV terminase (UL56) complex
E) Ganciclovir is activated by host neuraminidase and blocks viral release
ANSWER: A
Rationale:
CMV lacks a classical thymidine kinase but encodes the UL97 phosphotransferase, which performs the first phosphorylation of ganciclovir to its monophosphate. Cellular kinases then complete conversion to ganciclovir triphosphate, which competitively inhibits the CMV UL54 DNA polymerase and is incorporated into elongating viral DNA, slowing and ultimately halting replication.
Option B: Option B is incorrect: CMV does not possess a classical viral thymidine kinase; ganciclovir activation in CMV depends on UL97.
Option C: Option C is incorrect: ganciclovir does require phosphorylation and is not a direct pyrophosphate-site binder — that mechanism describes foscarnet.
Option D: Option D is incorrect: the UL56 terminase is the target of letermovir, not ganciclovir.
Option E: Option E is incorrect: ganciclovir is not activated by neuraminidase and does not act by blocking viral release.
13. [CASE 4 — QUESTION 1]
A 27-year-old woman at 22 weeks gestation is diagnosed with primary genital HSV. She is counseled about treatment now and about strategies to reduce the likelihood of a cesarean delivery for active lesions at term. Which approach is appropriate?
A) Avoid all antivirals during pregnancy and manage symptomatically
B) Treat with ganciclovir, the preferred agent for genital HSV in pregnancy
C) Use foscarnet, which has the strongest pregnancy safety record
D) Treat the primary episode with acyclovir or valacyclovir (Pregnancy Category B agents supported by extensive safety data), and offer suppressive valacyclovir from 36 weeks gestation to reduce HSV shedding and recurrent lesions at delivery, lowering the rate of cesarean delivery performed for active HSV
E) Defer all therapy until after delivery regardless of symptoms
ANSWER: D
Rationale:
Acyclovir and valacyclovir are Pregnancy Category B agents supported by extensive human safety data and are appropriate for primary genital HSV in pregnancy. Suppressive valacyclovir started at 36 weeks gestation reduces HSV shedding and recurrent lesions at delivery, thereby lowering the rate of cesarean delivery performed for active HSV disease.
Option A: Option A is incorrect: acyclovir and valacyclovir are safe and effective in pregnancy, so withholding antivirals is inappropriate.
Option B: Option B is incorrect: ganciclovir targets CMV and is generally avoided in pregnancy; it is not used for genital HSV.
Option C: Option C is incorrect: foscarnet is generally avoided in pregnancy and does not have the strongest safety record; acyclovir and valacyclovir carry the favorable data.
Option E: Option E is incorrect: deferring treatment of symptomatic primary genital HSV is inappropriate, and term suppression specifically reduces delivery complications.
14. [CASE 4 — QUESTION 2]
Continuing with the same patient. Despite counseling, she presents in labor with active lesions and delivers vaginally. On day 10 of life, the neonate develops skin vesicles and a seizure. Neonatal HSV is suspected. What is the appropriate immediate action?
A) Await cerebrospinal fluid (CSF) HSV polymerase chain reaction (PCR) before starting any antiviral
B) Begin oral acyclovir suppression only
C) Begin empiric high-dose intravenous acyclovir (20 mg/kg every 8 hours) immediately, without waiting for confirmatory testing, while sending CSF HSV PCR, surface swabs, and liver function tests in parallel
D) Start foscarnet as first-line therapy for neonatal HSV
E) Begin ganciclovir, since neonatal central nervous system infection implies CMV
ANSWER: C
Rationale:
Neonatal HSV is a medical emergency carrying substantial mortality and neurological morbidity. Empiric high-dose intravenous acyclovir (20 mg/kg every 8 hours) must be started immediately without waiting for confirmatory testing, while CSF HSV PCR, surface swabs (conjunctiva, nasopharynx, rectum), and liver function tests are sent in parallel. Therapy is not delayed for results.
Option A: Option A is incorrect: therapy must not be delayed for PCR results; empiric acyclovir is started at once.
Option B: Option B is incorrect: oral suppression follows completion of the intravenous course; it is not the acute treatment of active disease.
Option D: Option D is incorrect: foscarnet is reserved for documented acyclovir resistance, not first-line neonatal HSV.
Option E: Option E is incorrect: neonatal HSV is caused by herpes simplex virus and treated with acyclovir; ganciclovir targets CMV.
15. [CASE 4 — QUESTION 3]
Continuing with the same patient. The neonate is confirmed to have HSV with central nervous system (CNS) involvement and completes a 21-day course of intravenous acyclovir. The team plans follow-up therapy. Based on the evidence for long-term suppression in this setting, what is the appropriate next step?
A) No further antiviral therapy is needed after the intravenous course
B) Lifelong intravenous acyclovir
C) A single additional intravenous acyclovir dose at one month
D) Topical acyclovir to the skin only
E) Oral acyclovir suppression (300 mg/m2 three times daily) for six months, because this significantly reduces HSV recurrence and improves neurodevelopmental outcomes in infants with CNS or disseminated disease
ANSWER: E
Rationale:
Following completion of the intravenous course, oral acyclovir suppression at 300 mg/m2 three times daily for six months significantly reduces HSV recurrence and improves neurodevelopmental outcomes in infants with central nervous system (CNS) or disseminated disease. This represents one of the most compelling evidence-based uses of long-term antiviral suppression in any population.
Option A: Option A is incorrect: stopping after the intravenous course alone forgoes the demonstrated neurodevelopmental benefit of six-month oral suppression.
Option B: Option B is incorrect: lifelong intravenous therapy is neither required nor standard; oral suppression for six months is used.
Option C: Option C is incorrect: a single additional dose does not provide the sustained suppression shown to improve outcomes.
Option D: Option D is incorrect: topical therapy is inadequate for CNS disease; systemic oral suppression is required.
16. [CASE 4 — QUESTION 4]
Continuing with the same patient. Reflecting on the case, a trainee asks why acyclovir and valacyclovir were chosen during the pregnancy while ganciclovir and foscarnet would have been avoided unless absolutely necessary. Which statement correctly explains the safety reasoning?
A) All herpesvirus antivirals share an identical pregnancy safety profile
B) Acyclovir and valacyclovir are Pregnancy Category B agents supported by extensive human safety data (including the Acyclovir in Pregnancy Registry), whereas ganciclovir and foscarnet are generally avoided in pregnancy because of teratogenic potential in animal models and are reserved for maternal life-threatening CMV disease
C) Ganciclovir and foscarnet are the safest agents in pregnancy and are preferred for HSV
D) Acyclovir is contraindicated in pregnancy because of proven teratogenicity
E) Antiviral safety data in pregnancy do not exist for any of these agents
ANSWER: B
Rationale:
Acyclovir and valacyclovir are classified as Pregnancy Category B and are supported by extensive human experience, including the Acyclovir in Pregnancy Registry, which found no increase in birth defects among over 1800 first-trimester exposures. Ganciclovir and foscarnet, by contrast, are generally avoided in pregnancy given teratogenic potential in animal models and are reserved for maternal life-threatening CMV disease.
Option A: Option A is incorrect: the agents differ substantially — acyclovir and valacyclovir have favorable data, while ganciclovir and foscarnet are avoided.
Option C: Option C is incorrect: ganciclovir and foscarnet are not the safest agents in pregnancy and are not preferred for HSV.
Option D: Option D is incorrect: acyclovir is not contraindicated in pregnancy; it is a Category B agent with reassuring data.
Option E: Option E is incorrect: substantial pregnancy safety data do exist, most notably for acyclovir through its pregnancy registry.
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