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American Society of Microbiology ABMM Sample Questions:

1. A microbiology laboratory receives a CSF sample from a patient with suspected fungal meningitis. India ink staining reveals encapsulated yeast cells. Culture on Sabouraud dextrose agar grows creamy white colonies.
The MOST likely organism is:

A) Aspergillus flavus
B) Cryptococcus neoformans
C) Candida albicans
D) Mucor species

2. A microbiology laboratory is investigating an outbreak of bloodstream infections in a neonatal intensive care unit. Isolates of Staphylococcus epidermidis from multiple infants show indistinguishable banding patterns by pulsed-field gel electrophoresis (PFGE). This finding MOST strongly suggests:

A) Spontaneous mutations leading to increased pathogenicity.
B) A common source of infection and clonal spread of the organism.
C) Recent horizontal gene transfer of virulence factors.
D) Widespread antibiotic resistance within the S. epidermidis population.

3. A patient presents with a pruritic rash consisting of raised, serpiginous tracks on their skin. The patient recently returned from a Caribbean vacation and reported walking barefoot on the beach. The MOST likely causative organism is:

A) Sarcoptes scabiei
B) Larvae of Ancylostoma braziliense
C) Pediculus humanus
D) Larvae of Strongyloides stercoralis

4. Microscopic examination of a potassium hydroxide (KOH) preparation of skin scrapings from a patient with tinea versicolor typically reveals:

A) Septate hyphae and arthroconidia
B) Cigar-shaped yeast cells
C) Broad, aseptate hyphae with sporangiophores
D) Short, unbranched hyphae and globose yeast cells in clusters ("spaghetti and meatballs")

5. A clinical microbiology laboratory is monitoring the emergence of resistance to colistin in Gram-negative bacteria. Resistance to colistin is often mediated by modifications of the bacterial lipopolysaccharide (LPS).
The genetic basis for acquired colistin resistance most commonly involves:

A) Acquisition of genes encoding efflux pumps that specifically target colistin.
B) Mutations in genes encoding enzymes that modify the lipid A component of LPS.
C) Alterations in the outer membrane porin proteins, reducing colistin uptake.
D) Production of enzymes that directly inactivate the colistin molecule.

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