Free USMLE Step 2 CK Infectious Disease practice questions

This hospitalized woman developed diarrhea after a cephalosporin and a fluoroquinolone while taking a PPI, and stool testing confirms C. difficile infection. A leukocyte count of 15,000/mm3 or more or a creatinine above 1.5 mg/dL defines severe disease; she has both. She is not fulminant, which requires hypotension or shock, ileus, or megacolon. For an initial episode, whether nonsevere or severe, the 2021 IDSA and SHEA focused update recommends fidaxomicin (preferred, because it lowers recurrence) or oral vancomycin 125 mg four times daily for 10 days; among the options listed, oral vancomycin is correct. The ciprofloxacin should be stopped if possible (her pyelonephritis course is nearly complete), and the PPI should be reconsidered. She also needs contact precautions, and staff and visitors should wash their hands with soap and water, because alcohol-based gels do not kill spores.

B. Intravenous vancomycin is not secreted into the colonic lumen and has no effect on C. difficile colitis. C. Oral metronidazole is no longer recommended as first-line therapy for adults because it is less effective; it is an alternative only for nonsevere disease when vancomycin and fidaxomicin are unavailable. D. Fecal microbiota transplantation is reserved for patients with multiple recurrences after appropriate antibiotic therapy. E. Intravenous metronidazole is added to high-dose oral or rectal vancomycin for fulminant disease, particularly with ileus; it is never used alone.

This is blastomycosis. Blastomyces dermatitidis lives in moist soil and decaying wood near rivers and lakes of the Great Lakes region and the Ohio and Mississippi River basins, so hunters, canoeists and their dogs are infected from the same exposure; illness in a hunting dog is a classic clue. The pulmonary form is often a chronic, mass-like consolidation that mimics lung cancer. Blastomycosis disseminates even in healthy hosts, and the skin is the most common extrapulmonary site: verrucous, crusted plaques with heaped-up borders that look like squamous cell carcinoma. The pathology seals the diagnosis: large (8 to 15 micrometer) yeasts with a thick, double-contoured wall and a single broad-based bud. Culture confirms it, and treatment of mild to moderate disease is itraconazole for 6 to 12 months; most experts treat every case.

A. Squamous cell carcinoma of the lung could produce an upper-lobe mass in a former smoker, but it does not explain broad-based budding yeasts in a skin lesion, and the skin plaque is infectious, not metastatic. C. Histoplasmosis shows tiny (2 to 4 micrometer) yeasts inside macrophages and typically causes hilar adenopathy or calcified granulomas rather than verrucous skin plaques. D. Cryptococcosis shows yeasts with narrow-based budding and a polysaccharide capsule, and it favors the lungs and meninges. E. Coccidioidomycosis occurs in the desert Southwest and appears in tissue as large spherules filled with endospores, not budding yeasts.

Back pain with fever in a person who injects drugs is spinal epidural abscess or vertebral osteomyelitis until proven otherwise. This woman has focal spinous process tenderness, fever, markedly elevated ESR and CRP, and new radicular pain wrapping around the chest wall, which marks the second stage of the classic progression (back pain, then radicular pain, then weakness and sphincter dysfunction, then paralysis). She is still neurologically intact, which is exactly the window in which rapid diagnosis prevents permanent deficits.

The test of choice is urgent MRI with gadolinium, which shows the epidural collection, disk and vertebral body involvement and any cord compression. The entire spine should be imaged because noncontiguous (skip) lesions are common in hematogenous S. aureus infection and can change surgical planning. Because she is febrile and possibly bacteremic, empiric therapy with vancomycin plus ceftriaxone (or cefepime when Pseudomonas is a concern) should follow the blood cultures rather than wait for imaging. Neurologic decline or cord compression on MRI would prompt emergent surgical decompression.

B. Plain radiographs are insensitive early; bony destruction takes weeks to appear and they cannot show an epidural collection. C. Lumbar puncture is not indicated: CSF is often nonspecific, and passing a needle near an abscess risks seeding the subarachnoid space. D. Noncontrast CT shows bone but poorly visualizes epidural soft tissue and the cord; CT myelography is only a fallback when MRI is impossible. E. A bone scan is nonspecific, slow and does not show the abscess or cord compression.

Any fever in a person without a functioning spleen must be treated as overwhelming post-splenectomy infection (OPSI) until proven otherwise. Without splenic filtering and splenic IgM memory B cells, encapsulated bacteria, above all Streptococcus pneumoniae, followed by Haemophilus influenzae and Neisseria meningitidis, can progress from a flulike prodrome to septic shock, DIC, and purpura within hours, with mortality as high as 50%. The risk is lifelong, and vaccination reduces but does not eliminate it, especially when boosters are missed. This patient is tachycardic and borderline hypotensive. Management is to draw blood cultures and give empiric IV ceftriaxone plus vancomycin (for penicillin-resistant pneumococcus) without delay, along with IV fluids and close monitoring for shock. Once he recovers, his vaccines should be updated (pneumococcal conjugate vaccine, MenACWY with boosters every 5 years, MenB, annual influenza), and he should carry standby antibiotics.

A. Standby amoxicillin-clavulanate is self-treatment to begin at the first fever while seeking care; it is not adequate for a patient with signs of sepsis. B. Abdominal imaging is not indicated without localizing abdominal findings and must never delay antibiotics. D. He has no headache, meningismus, or altered mentation, and even when meningitis is suspected, antibiotics should not wait for a lumbar puncture. E. Withholding antibiotics until cultures result is dangerous in OPSI, where hours determine survival.

Ghana is a high-transmission area for chloroquine-resistant Plasmodium falciparum, so prophylaxis must be active against resistant falciparum. The first-line choices there are atovaquone-proguanil, doxycycline, mefloquine, or tafenoquine, and the choice is driven by the patient's contraindications.

Atovaquone-proguanil is the best option for this patient. It is well tolerated, taken once daily from 1 to 2 days before entering the area until 7 days after leaving, which suits a short trip. It is avoided in pregnancy (insufficient safety data) and with creatinine clearance below 30 mL/min; neither applies, since her pregnancy test is negative and she has reliable contraception and normal renal function. It has no relevant interaction with levetiracetam. Bite prevention with DEET or picaridin repellent, permethrin-treated clothing, and bed nets should accompany any regimen, and she should be told that fever during or after travel is malaria until proven otherwise.

A. Chloroquine is used only where P. falciparum remains chloroquine sensitive, which excludes West Africa, and it can lower the seizure threshold.

B. Doxycycline is effective and inexpensive, but her history of doxycycline-induced esophageal ulceration argues against reexposure, and it must be continued for 4 weeks after return.

D. Mefloquine is contraindicated with a history of seizures or psychiatric illness because of neuropsychiatric adverse effects, including seizures.

E. Primaquine for primary prophylaxis is reserved mainly for areas where P. vivax predominates, and it requires documented normal G6PD activity before use because it causes hemolysis in G6PD deficiency.

This patient has foodborne botulism: home-canned low-acid vegetables, an afebrile and alert patient, and symmetric descending flaccid paralysis beginning with the cranial nerves (diplopia, ptosis, dysarthria, dysphagia), with dilated sluggish pupils and normal sensation. A second person with symptoms after the same meal is a strong epidemiologic clue. Laboratory confirmation is by detection of botulinum toxin in serum, stool, gastric contents or the implicated food (the mouse bioassay remains the reference method, and public health laboratories also use mass spectrometry or PCR for the organism). Specimens should be collected before antitoxin is given, because antitoxin neutralizes circulating toxin and can make serum testing negative. Results take days, which is why antitoxin is released and given on clinical suspicion rather than after confirmation, as was done here. Serial vital capacity monitoring and early intubation remain essential while results are pending.

A and E are wrong because they test for myasthenia gravis, which causes fatigable weakness and ptosis but spares the pupils and lacks autonomic features; the edrophonium test is also obsolete and can be falsely positive in botulism. B is wrong because CSF studies are used to support Guillain-Barre syndrome (albuminocytologic dissociation); in botulism the CSF is normal, so a normal result would not confirm the diagnosis. C is wrong because anti-GQ1b antibodies support the Miller Fisher variant of Guillain-Barre syndrome, which causes ophthalmoplegia, ataxia and areflexia rather than a food-linked descending paralysis with dilated pupils in two people.

The tuberculin skin test cutoff depends on the person's risk. An induration of 5 mm or more is positive in people with HIV, organ transplant or other immunosuppression, fibrotic changes on chest x-ray and recent close contacts of a person with infectious TB. Her 6-mm reaction is therefore a positive test. A positive PPD or IGRA cannot distinguish latent from active TB, so the next step is a symptom review (done, negative) and a chest x-ray. A normal film in an asymptomatic person means latent TB infection, which should be treated (for example, with 4 months of rifampin or 12 weekly doses of isoniazid plus rifapentine) because recent infection carries the highest risk of progression. An abnormal film would prompt sputum studies for active disease.

A. Calling the test negative applies the 15-mm cutoff for people with no risk factors (or the 10-mm cutoff for moderate-risk groups); a household contact of a smear-positive patient is a 5-mm group. B. Confirming a positive skin test with an IGRA is not required in a high-risk contact, would delay evaluation and could falsely reassure if discordant; a prior BCG vaccine, the usual reason to prefer an IGRA, is absent. C. Repeat skin testing 8 to 10 weeks after the last exposure is for a contact whose initial test is negative, to catch conversion. E. Sputum examination is needed when symptoms or chest x-ray findings suggest active disease; it comes after the chest x-ray, not before.

This patient has septic shock that remains vasopressor-dependent despite adequate fluid resuscitation, norepinephrine at a moderate to high dose for more than 4 hours, and added vasopressin. The Surviving Sepsis Campaign suggests adding intravenous hydrocortisone, typically 200 mg/day (given as 50 mg every 6 hours or as a continuous infusion), for adults with septic shock and an ongoing vasopressor requirement, commonly defined as norepinephrine of at least 0.25 µg/kg/min for at least 4 hours. Hydrocortisone shortens the duration of shock and vasopressor support; mortality benefit is less consistent, but the effect on shock reversal is reproducible. A cosyntropin stimulation test or random cortisol level is not needed before starting it. Hyperglycemia is the main adverse effect, and insulin is started if glucose exceeds about 180 mg/dL.

The usual vasopressor ladder is norepinephrine first, vasopressin second and epinephrine third, all titrated to a mean arterial pressure of at least 65 mm Hg.

A. Dopamine causes more tachyarrhythmias than norepinephrine and is not recommended in septic shock except in highly selected patients with bradycardia. B. Dobutamine is added for persistent hypoperfusion with cardiac dysfunction; her left ventricle is hyperdynamic, and dobutamine's vasodilating effect would worsen her hypotension. D. High-dose pulse methylprednisolone increased harm (secondary infection) without benefit in older sepsis trials and is not used. E. Fludrocortisone has been studied only as an adjunct to hydrocortisone, not alone, and oral absorption is unreliable in shock; it does not replace hydrocortisone.