Question 32
Card 1 — Correct prophylaxis choice
Label: Malaria prophylaxis — drug selection
The recommended medication for malaria prophylaxis for travel to East Africa is
Atovaquone–proguanil.
Card 2 — Why this is correct
Label: Malaria prophylaxis — mechanism
Atovaquone–proguanil acts as a
hepatic schizonticide, targeting Plasmodium in the liver stage.
Card 3 — Timing of therapy
Label: Malaria prophylaxis — dosing schedule
Atovaquone–proguanil should be taken:
Start: 1–2 days before travel
Continue: for 7 days after leaving the endemic area
Card 4 — Why not ciprofloxacin?
Label: Traveler’s medicine — common confusion
Ciprofloxacin is used for traveler’s diarrhea, not malaria.
Card 5 — Why not clarithromycin?
Label: Opportunistic infections
Clarithromycin is used for prophylaxis against
Mycobacterium avium complex in patients with advanced HIV.
Card 6 — Why not mebendazole?
Label: Parasite specificity
Mebendazole treats intestinal helminths, not malaria.
Card 7 — Why not nifurtimox?
Label: Tropical diseases
Nifurtimox is used to treat Chagas disease caused by
Trypanosoma cruzi.
Card 8 — Classes of malaria drugs
Label: Malaria pharmacology
Malaria drugs are classified as:
• Hepatic schizonticides (Atovaquone–proguanil)
• Blood schizonticides (chloroquine, doxycycline, mefloquine)
• Hypnozoiticides (primaquine)
Card 9 — Hypnozoite coverage
Label: Malaria species differentiation
Primaquine clears hypnozoites in
Plasmodium vivax and Plasmodium ovale
(requires G6PD screening).
Card 10 — Special populations
Label: Malaria prophylaxis — pregnancy
Pregnant patients should receive:
• Chloroquine in sensitive areas
• Mefloquine in resistant areas
Core diagnosis
Label: Transplant infections — CMV disease
Solid-organ transplant recipient with fever, leukopenia, transaminitis, diarrhea, and odynophagia most likely has cytomegalovirus (CMV) disease.
Card 2 — Why CMV fits
Label: CMV disease — classic presentation
CMV disease causes:
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Low-grade fever & malaise
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Leukopenia
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Hepatitis (↑ AST/ALT)
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GI involvement (diarrhea, esophagitis)
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Occurs after rejection treatment or increased immunosuppression
Card 3 — Timing clue
Label: Transplant timeline — CMV risk
Peak risk for CMV disease is 1–6 months post-transplant, especially:
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After stopping prophylaxis
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After pulse steroids
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After rejection therapy
Card 4 — Pathophysiology
Label: CMV in transplant — mechanism
CMV disease results from:
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Reactivation of latent virus
-
Or superinfection from donor strain
especially after immunosuppression escalation
Card 5 — Why not BK virus
Label: Transplant infections — BK vs CMV
BK virus presents with:
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Progressive renal dysfunction
-
Tubulointerstitial nephritis
NOT fever, diarrhea, or hepatitis.
Card 6 — Why not HSV
Label: Opportunistic infections — HSV vs CMV
HSV classically presents with:
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Painful oral/genital ulcers
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Localized disease
Does NOT cause leukopenia or systemic illness like CMV.
Card 7 — Why not tacrolimus toxicity
Label: Immunosuppressant toxicity
Tacrolimus toxicity causes:
-
Nephrotoxicity
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Neurotoxicity (tremor)
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Hyperkalemia, hypertension
Not fever, hepatitis, or diarrhea.
Card 8 — Why not Toxoplasma
Label: Post-transplant infections — Toxo
Toxoplasma gondii causes:
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Brain abscess
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Chorioretinitis
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Pneumonitis
Rare after kidney transplant and not GI-predominant.
Card 9 — Treatment
Label: CMV disease — management
Treatment includes:
-
IV ganciclovir or oral valganciclovir
Standard duration: 3 months (90–100 days)
-
Reduction in immunosuppression if possible
Card 10 — Exam pearl
Label: USMLE pearl — CMV
Any transplant patient with:
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Leukopenia
-
Transaminitis
-
Diarrhea or odynophagia
= Think CMV disease first.
Toxoplasma - Brain abscess, chorioretinitis, pneumonitis
Organisms that REQUIRE catheter removal:
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Staphylococcus aureus
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Pseudomonas aeruginosa
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Fungal species (eg, Candida)
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Mycobacteria
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Persistent bacteremia despite therapy
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Endocarditis, septic thrombophlebitis, or tunnel infection
Although coagulase-negative Staph forms biofilm, catheter salvage is allowed (with antibiotic lock) if the patient is stable and the organism is susceptible.
But Pseudomonas is aggressive and relapse-prone → salvage fails → remove.
Why this is norovirus:
This patient has the classic outbreak pattern and symptom profile of norovirus:
Key clues in the question
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Multiple residents affected → common-source outbreak
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Nursing home → classic risk environment
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Vomiting > diarrhea → hallmark of norovirus
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Negative stool culture → viral cause
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Fever, myalgias, headache → systemic viral illness
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Rapid onset, short duration → viral gastroenteritis
High-Yield Norovirus Profile
Transmission
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Fecal–oral
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Food and water
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Fomites
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Aerosolized vomitus (yes — airborne particles from vomiting)
Clinical Pattern
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Sudden-onset vomiting
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Watery diarrhea
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Fever
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Headache
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Myalgias
Settings that scream Norovirus
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Nursing homes
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Hospitals
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Cruise ships
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Schools
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Restaurants
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Daycares
Course
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Self-limited (48–72 hours)
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Supportive care only
Why this is correct
This patient has a cat bite to the hand with a deep puncture wound → this is a high-risk bite and requires empiric antibiotics.
Cat bites are dangerous because:
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They cause deep inoculation
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They frequently introduce Pasteurella multocida
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Hands have closed spaces → high risk for tenosynovitis, osteomyelitis, septic arthritis
First-line therapy for cat bites
✅ Amoxicillin–clavulanate
(covers Pasteurella + anaerobes + skin flora)
But…
She has a penicillin allergy → use an alternative
✅ Doxycycline + metronidazole
Provides coverage for:
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Pasteurella multocida (doxycycline)
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Anaerobes (metronidazole)
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Streptococci & skin flora
Why the other answers are wrong
❌ A. Azithromycin + clindamycin
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Macrolides (azithro) are unreliable against Pasteurella
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Inadequate empiric therapy
❌ C. Primary closure
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Never close animal bites on the hand
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↑ risk of abscess, tendon infection, osteomyelitis
❌ D. Tetanus immunoglobulin
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Booster within 5 years → already protected
❌ E. Culture + observe
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Cat bites need immediate prophylaxis, not watchful waiting
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Pasteurella grows poorly on culture
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