Nelson Chapter 208 (Staphylococcus)

Question 1

1. Which single test differentiates S. aureus from all coagulase-negative staphylococci (CoNS)?
   A. Catalase test
   B. Hemolysis pattern on blood agar
   C. Coagulase test — S. aureus is coagulase POSITIVE
   D. Gram stain morphology

Answer 1

Answer: C
High-yield: Coagulase positive = S. aureus. CoNS = S. epidermidis, S. saprophyticus, S. haemolyticus, S. lugdunensis. This single test is the primary differentiator.

Question 2

3. Coagulase promotes S. aureus virulence by which mechanism?
   A. Directly destroys neutrophil membranes
   B. Reacts with fibrinogen causing plasma to clot — may wall off infection and interfere with phagocytosis promoting abscess formation
   C. Activates the exfoliative toxin cascade
   D. Inhibits complement C3b deposition on bacterial surface

Answer 2

Answer: B
High-yield: Coagulase + fibrinogen → fibrin clot → walls off abscess → protects bacteria from phagocytosis. Coagulase production = synonymous with invasive pathogenic potential of S. aureus.

Question 2

2. Protein A of S. aureus promotes virulence by which specific mechanism?
   A. Directly lyses neutrophil membranes via pore formation
   B. Absorbs serum immunoglobulins on the outer cell wall — preventing antibodies from acting as opsonins and inhibiting phagocytosis
   C. Activates complement via the alternative pathway
   D. Inhibits peptidoglycan synthesis in competing bacteria

Answer 2

Answer: B
High-yield: Protein A = binds Fc portion of IgG → blocks opsonization → prevents phagocytosis. Also used in diagnostic coagglutination tests. Key immune evasion mechanism.

Question 3

4. Panton-Valentine leukocidin (PVL) is clinically important because it is:
   A. The primary toxin causing toxic shock syndrome
   B. A superantigen stimulating massive T-cell activation
   C. A two-component toxin that combines with leukocyte cell membrane phospholipid → increased permeability → cell death; associated with severe skin infections, pneumonia, and osteomyelitis
   D. The cause of staphylococcal scalded skin syndrome in neonates

Answer 3

Answer: C
High-yield: PVL = leukocidin causing WBC destruction. Strongly associated with CA-MRSA (USA300). Causes necrotizing skin infections and necrotizing pneumonia in young healthy patients.

Question 3

5. The most significant risk factor for developing S. aureus infection is:
   A. Age under 5 years
   B. Disruption of intact skin — wounds, eczema, burns, surgical sites, indwelling catheters, ventriculoperitoneal shunts
   C. Exposure to crowded school environments
   D. Male sex

Answer 3

Answer: B
High-yield: Intact skin = primary barrier. Disruption = entry point. Additional risk factors = corticosteroids, malnutrition, azotemia, antibiotic-resistant organism colonization, viral respiratory infections.

Question 3

6. Which immune defects specifically predispose children to recurrent S. aureus infections?
   A. IgA deficiency and complement C3 deficiency
   B. Congenital defects in chemotaxis (Job syndrome, Chédiak-Higashi) and defective phagocytosis/killing (neutropenia, chronic granulomatous disease)
   C. DiGeorge syndrome (T-cell deficiency only)
   D. Selective IgM deficiency

Answer 3

Answer: B
High-yield: Recurrent staph infections = think neutrophil dysfunction. Job syndrome (hyper-IgE) = classic association with recurrent S. aureus skin abscesses. Children with recurrent S. aureus infections should be evaluated for immune defects.

Question 4

7. S. aureus pneumonia is characteristically associated with which radiological findings that suggest the diagnosis?
   A. Perihilar lymphadenopathy and miliary nodules
   B. Pleural effusion only without parenchymal involvement
   C. Pneumatoceles, pyopneumothorax, and lung abscesses — highly suggestive of S. aureus
   D. Diffuse bilateral ground-glass opacities

Answer 4

Answer: C
High-yield: Pneumatoceles = thin-walled air cavities = classic S. aureus pneumonia finding. Also: empyema, bronchopleural fistulas. Necrotizing pneumonia with cavity formation = S. aureus until proven otherwise.

Question 5

12. The treatment of staphylococcal TSS requires which combination approach?
    A. Vancomycin alone for all cases
    B. Antistaphylococcal beta-lactam (nafcillin/oxacillin/cefazolin) PLUS clindamycin — clindamycin added specifically to inhibit toxin production
    C. Ampicillin-sulbactam plus gentamicin
    D. Penicillin G plus rifampin

Answer 5

Answer: B
High-yield: Clindamycin = inhibits protein synthesis → reduces toxin production. Beta-lactam kills organism. Dual approach = treat infection + suppress toxin. If MRSA suspected = vancomycin replaces beta-lactam.

Question 6

8. S. aureus staphylococcal food poisoning differs from other forms of food poisoning in which key clinical way?
   A. Long incubation period of 24–72 hours with prominent fever
   B. Short incubation period of 2–7 hours, sudden severe vomiting, watery diarrhea, NO fever or low-grade fever — symptoms rarely persist beyond 12–24 hours
   C. Bloody diarrhea with high fever and abdominal cramps lasting 5–7 days
   D. Gradual onset over 2–3 days with persistent nausea and jaundice

Answer 6

Answer: B
High-yield: Preformed enterotoxin = rapid onset. No fever = key distinguishing feature from infectious gastroenteritis. Resolves rapidly. Source often = colonized food handler. Enterotoxins A and B most common.

Question 6

10. The diagnosis of staphylococcal TSS requires which combination of major criteria?
    A. Positive blood cultures for S. aureus plus fever and rash
    B. Acute fever, hypotension, AND erythematous rash with convalescent desquamation — ALL three major criteria required
    C. Fever plus any two of the minor criteria
    D. Strawberry tongue plus vomiting and diarrhea

Answer 6

Answer: B
High-yield: TSS major criteria = ALL THREE required: fever >38.8°C + hypotension + erythroderma with desquamation. Minor criteria = any 3 or more from mucosal inflammation, vomiting/diarrhea, liver/renal/muscle/CNS abnormalities, thrombocytopenia.

Question 6

14. Why are penicillin G and ampicillin NOT appropriate for empirical S. aureus treatment?
    A. They do not penetrate biofilms formed by S. aureus
    B. Nearly all S. aureus isolates, regardless of source, produce beta-lactamase and are resistant to these agents
    C. They cause more adverse effects than nafcillin
    D. They are active only against Gram-negative organisms

Answer 6

Answer: B
High-yield: >90% of S. aureus produce penicillinase/beta-lactamase. Requires either penicillinase-resistant beta-lactam (nafcillin, oxacillin) or combination with beta-lactamase inhibitor. Penicillin only if rare susceptible strain confirmed.

Question 6

13. Which of the following statements about clindamycin use in S. aureus infections is TRUE?
    A. Clindamycin is the drug of choice for S. aureus endocarditis
    B. Clindamycin is bacteriostatic and should NOT be used for endocarditis, persistent bacteremia, or CNS infections; inducible resistance must always be ruled out by D-test
    C. Clindamycin is effective against all MRSA strains without resistance testing
    D. Clindamycin has no role in toxin-mediated S. aureus disease

Answer 6

Answer: B
High-yield: Clindamycin limitations = bacteriostatic (not bactericidal) = cannot use for endocarditis/persistent bacteremia/CNS infection. D-test = must be done before using clindamycin for erythromycin-resistant strains. Good for toxin inhibition in TSS.

Question 6

15. The mechanism of methicillin/nafcillin resistance in MRSA is:
    A. Beta-lactamase production encoded on a plasmid
    B. Altered penicillin-binding protein PBP2a encoded by the mecA gene — low affinity for all beta-lactams including cephalosporins (except ceftaroline)
    C. Efflux pump overexpression
    D. Reduced outer membrane permeability to beta-lactams

Answer 6

Answer: B
High-yield: mecA gene → PBP2a → low affinity for ALL beta-lactams → resistance to all penicillins, cephalosporins, and carbapenems EXCEPT ceftaroline (novel cephalosporin with MRSA activity).

Question 7

11. TSS is differentiated from Kawasaki disease by which clinical features?
    A. Rash with desquamation — seen only in TSS
    B. TSS features diffuse myalgia, vomiting, diarrhea, azotemia, hypotension, ARDS, and shock — rare in Kawasaki. Kawasaki typically occurs in children under 5 years and is not as rapidly progressive
    C. Fever — present only in TSS
    D. Conjunctival hyperemia — seen only in Kawasaki disease

Answer 7

Answer: B
High-yield: Both = fever + mucous membrane hyperemia + rash + desquamation. Key differentiators: TSS = shock, myalgia, GI symptoms, azotemia, ARDS. Kawasaki = children <5 years, coronary aneurysms, no shock.

Question 8

9. TSST-1 causes toxic shock syndrome through which immunological mechanism?
   A. Direct cytotoxicity to vascular endothelial cells
   B. Endotoxin-like activation of TLR4 on macrophages
   C. Superantigen — stimulates massive non-specific T-cell activation → IL-1 and TNF release → hypotension, fever, and multisystem involvement
   D. Molecular mimicry leading to autoantibody formation

Answer 8

Answer: C
High-yield: TSST-1 = prototypical superantigen = bridges MHC class II on APC with T-cell Vβ receptor non-specifically → massive cytokine storm → TSS. Most S. aureus TSS strains are MSSA (not MRSA/USA300).

Question 9

16. For empirical treatment of a critically ill child with suspected S. aureus infection of unknown susceptibility, which combination is recommended?
    A. Penicillin G plus gentamicin
    B. Vancomycin PLUS nafcillin/oxacillin — covers both MRSA and MSSA until culture results available
    C. Ceftriaxone alone
    D. Clindamycin monotherapy

Answer 9

Answer: B
High-yield: Critically ill + unknown susceptibility = vancomycin + nafcillin empirically. Covers MRSA (vancomycin) AND MSSA (nafcillin more effective than vancomycin for MSSA). Narrow once susceptibility confirmed.

Question 10

17. Daptomycin is an important anti-MRSA agent with one critical limitation in clinical practice. What is it?
    A. Cannot be used in patients with renal failure
    B. Inactivated by pulmonary surfactant — CANNOT be used to treat pneumonia
    C. Does not achieve adequate CNS penetration for meningitis
    D. Ineffective against endocarditis due to poor valve penetration.

Answer 10

Answer: B
High-yield: Daptomycin = inactivated by surfactant → CANNOT treat pneumonia. FDA warning also links it to eosinophilic pneumonitis. Excellent for bacteremia and endocarditis. Key limitation to memorize

Question 11

18. CoNS (coagulase-negative staphylococci) cause disease primarily through which mechanism, distinguishing them from S. aureus?
    A. Production of powerful exotoxins similar to TSST-1
    B. Biofilm formation on indwelling medical devices — resists phagocytosis and antibiotic penetration; low intrinsic virulence requires presence of foreign body
    C. Direct tissue invasion via coagulase activity
    D. Polysaccharide capsule that prevents complement activation

Answer 11

Answer: B
High-yield: CoNS virulence = biofilm on devices + impaired host immunity. Without a foreign body, CoNS rarely causes disease. Biofilm = resistant to antibiotics + phagocytosis = explains why device removal often required.

Question 12

19. When should CoNS growing in a blood culture be considered TRUE bacteremia rather than contamination?
    A. Any positive CoNS blood culture in a hospitalized patient
    B. Rapid growth within 24 hours + multiple positive cultures with same strain + cultures from both line and peripheral sites positive + clinical signs compatible with sepsis that resolve with treatment
    C. CoNS growing in a single blood culture bottle with gram stain showing cocci in clusters
    D. Positive blood culture in any neonate regardless of clinical status

Answer 12

Answer: B
High-yield: CoNS = common blood culture contaminant (skin flora). True bacteremia criteria = rapid growth + multiple positives + same strain + line AND peripheral positives + clinical improvement with treatment. Never dismiss CoNS in neonates or CVC patients without careful assessment.

Question 13

20. The most effective strategy for preventing spread of S. aureus including MRSA in both hospital and community settings is:
    A. Routine prophylactic antibiotics for all high-risk contacts
    B. Universal screening of all patients for MRSA nasal colonization
    C. Strict hand hygiene — use of chlorhexidine or alcohol-based hand wash; contact isolation for MRSA patients; decolonization protocols for recurrent infections
    D. Routine environmental fumigation of hospital rooms

Answer 13

Answer: C
High-yield: Hand hygiene = single most effective infection control measure. MRSA control = hand hygiene + contact precautions + surveillance cultures + decolonization (mupirocin nasal + chlorhexidine baths) for recurrent infections. Influenza vaccination indirectly prevents S. aureus co-infection.