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DR15.1-3 | Pyoderma — Practice Quiz

Practice 10 questions · Untimed · Unlimited attempts

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Q1 DR15.1 1 pt

A 6-year-old child presents with multiple clustered vesicles that rapidly rupture to leave golden-yellow crusted lesions around the mouth and nose. There is no fever. Which organism is most commonly responsible?

A Streptococcus pyogenes alone
B Staphylococcus aureus (most common) and/or Streptococcus pyogenes
C Pseudomonas aeruginosa
D Staphylococcus epidermidis

Correct. Non-bullous impetigo is caused by Staph aureus (predominant) and/or Strep pyogenes. The honey-coloured crust arises from serous exudate drying on a ruptured vesico-pustule.

Non-bullous impetigo is the most common pyoderma in children; Staph aureus is now the dominant pathogen, with Strep pyogenes less common but still implicated.

Incorrect. Non-bullous impetigo is predominantly caused by Staphylococcus aureus, often with Streptococcus pyogenes. Pseudomonas and S. epidermidis are not typical causes.

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Q2 DR15.1 1 pt

Bullous impetigo differs from non-bullous impetigo primarily because it is caused by a Staphylococcus aureus strain that produces which virulence factor?

A Protein A
B Exfoliative (epidermolytic) toxin
C Toxic shock syndrome toxin-1 (TSST-1)
D Leukocidin (Panton-Valentine)

Correct. ET-A/ET-B are serine proteases that target desmoglein-1 at the granular layer. Localised production causes bullous impetigo; haematogenous spread causes SSSS.

Exfoliative toxin (ET-A and ET-B) cleaves desmoglein-1 in the superficial epidermis, producing flaccid bullae in bullous impetigo and generalised skin separation in SSSS.

Incorrect. Exfoliative toxin is the key virulence factor for bullous impetigo. Protein A has an immunological role; TSST-1 causes toxic shock; PVL is linked to furunculosis and necrotising pneumonia.

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Q3 DR15.3 1 pt

A 25-year-old man has a tender erythematous nodule at a hair follicle on the nape of the neck with a central pus-point. Fluctuance is absent. What is the most appropriate first-line treatment?

A Incision and drainage alone
B Oral antistaphylococcal antibiotic (e.g., cloxacillin or cephalexin)
C Topical mupirocin only
D Immediate surgical debridement

Correct. A non-fluctuant furuncle responds to systemic antibiotics. Cloxacillin (beta-lactamase-stable penicillin) or cephalexin are first-line; consider doxycycline/co-trimoxazole if MRSA is suspected.

A furuncle without fluctuance (pre-suppurative) is treated with systemic antistaphylococcal antibiotics; I&D is reserved for a fluctuant furuncle.

Incorrect. I&D is appropriate only once fluctuance develops. Topical mupirocin does not penetrate deep follicular infections. Immediate surgical debridement is reserved for necrotising infections.

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Q4 DR15.1 1 pt

Erysipelas and cellulitis are both spreading skin infections, but they differ in an important clinical feature. Which statement correctly distinguishes erysipelas from cellulitis?

A Erysipelas has ill-defined borders; cellulitis has sharply demarcated borders
B Erysipelas is sharply demarcated and involves the upper dermis and lymphatics; cellulitis is poorly demarcated and involves deeper dermis and subcutis
C Erysipelas is caused exclusively by Staphylococcus aureus; cellulitis by Streptococcus pyogenes
D Erysipelas never causes systemic fever; cellulitis invariably does

Correct. The raised, clearly-demarcated, peau d'orange edge of erysipelas is its defining sign. The common site is the face and lower leg; Strep pyogenes is the usual pathogen. Cellulitis can be caused by both Staph aureus and Strep spp.

The sharply-demarcated raised border of erysipelas reflects superficial (upper-dermal) lymphatic involvement by Strep pyogenes; cellulitis' ill-defined border reflects deeper dermal/subcutaneous spread.

Incorrect. Erysipelas is sharply demarcated (upper dermis); cellulitis is poorly demarcated (deeper dermis/subcutis). Both can cause fever.

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Q5 DR15.1 1 pt

Staphylococcal scalded skin syndrome (SSSS) is seen predominantly in neonates and young children. The skin cleavage in SSSS occurs at which level?

A Dermal-epidermal junction
B Within the granular layer (stratum granulosum) of the epidermis
C Between the papillary and reticular dermis
D At the basement membrane zone

Correct. The granular-layer split accounts for Nikolsky's sign and the relatively good prognosis in children (shallow wound heals fast). In adults, SSSS carries a much higher mortality due to impaired renal excretion of toxin.

Exfoliative toxin cleaves desmoglein-1 selectively expressed in the stratum granulosum, producing intra-epidermal cleavage (Nikolsky sign positive) with a shallow split — hence rapid re-epithelialisation if treated promptly.

Incorrect. SSSS cleavage is intra-epidermal (granular layer), not at the dermal-epidermal junction or basement membrane zone. This distinguishes it from autoimmune blistering disorders like bullous pemphigoid.

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Q6 DR15.2 1 pt

A patient with widespread non-bullous impetigo covering more than three body sites is being started on treatment. Which topical antibiotic is considered first-line for localised impetigo, and what is its most clinically relevant adverse effect?

A Gentamicin cream; nephrotoxicity with prolonged use
B Mupirocin 2% ointment; transient local burning/stinging; high-level resistance emerging with overuse
C Fusidic acid; thrombocytopaenia
D Clindamycin gel; pseudomembranous colitis with topical use

Correct. Mupirocin 2% ointment TDS for 5–7 days is first-line for localised, superficial impetigo. However, widespread impetigo (>3 sites or bullous type) warrants systemic antibiotics.

Mupirocin inhibits bacterial isoleucyl-tRNA synthetase. It is first-line topical therapy for localised impetigo; local irritation is the main adverse effect, and resistance (especially high-level) is a growing concern with prolonged use.

Incorrect. Mupirocin 2% is the first-line topical agent. Gentamicin cream lacks evidence for impetigo; topical clindamycin carries negligible systemic absorption risk.

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Q7 DR15.3 1 pt

A 40-year-old man with poorly-controlled diabetes presents with a painful, indurated 4 cm mass on the back of the neck — multiple interconnected boils discharging through several pus-points. Systemic antibiotics are started. What additional intervention is indicated?

A Topical mupirocin application over the mass
B Surgical incision and drainage once fluctuance is confirmed
C Cryotherapy
D Intralesional corticosteroid injection

Correct. Carbuncles require I&D because the pus-filled cavity is inaccessible to antibiotics. Diabetes impairs neutrophil function, making surgical drainage essential. Post-drainage antibiotics treat surrounding cellulitis.

A carbuncle (multiple coalescing furuncles draining through several openings) in a diabetic requires surgical I&D in addition to systemic antibiotics. Antibiotics alone cannot drain pus.

Incorrect. Topical agents cannot penetrate a deep abscess. Cryotherapy and intralesional steroids are inappropriate for bacterial infection with pus.

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Q8 DR15.3 1 pt

Which of the following clinical features is the MOST important early warning sign of necrotising soft-tissue infection (NSTI) that should prompt urgent surgical referral?

A Erythema with well-defined margins
B Pain disproportionate to the visible skin signs
C Haemorrhagic bullae
D Crepitus on palpation

Correct. In NSTI, deep fascial necrosis far outpaces the visible skin changes. A patient who appears to have 'just cellulitis' but screams with light touch demands urgent surgical assessment.

Pain out of proportion to skin findings is the cardinal early sign of NSTI — act before the classic late signs (crepitus, haemorrhagic bullae, dusky discolouration) appear. Late-stage NSTI carries very high mortality.

Incorrect. Crepitus and haemorrhagic bullae are LATE signs of NSTI that indicate advanced disease. Pain disproportionate to visible signs is the critical early warning and must trigger immediate surgical referral.

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Q9 DR15.2 1 pt

For a patient with confirmed MRSA-positive cellulitis not responding to standard beta-lactam therapy, which systemic antibiotic is an appropriate oral option?

A Amoxicillin-clavulanate
B Cloxacillin
C Co-trimoxazole (trimethoprim-sulfamethoxazole) or doxycycline
D Penicillin G

Correct. Co-trimoxazole and doxycycline are standard oral options for CA-MRSA skin/soft-tissue infections. ADRs: co-trimoxazole — hypersensitivity, Stevens-Johnson, hyperkalemia, bone marrow suppression; doxycycline — photosensitivity, GI upset, avoid in pregnancy/children <8 years.

MRSA is resistant to all beta-lactams (penicillins and cephalosporins). Oral MRSA options include co-trimoxazole, doxycycline, and clindamycin (check susceptibility). IV vancomycin/linezolid is used for severe/hospitalised cases.

Incorrect. Amoxicillin-clavulanate, cloxacillin, and penicillin G are all beta-lactams and are ineffective against MRSA (which has altered PBP2a via mecA gene).

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Q10 DR15.1 1 pt

Ecthyma is best described as which of the following?

A A superficial blistering condition confined to the epidermis, caused by TSST-1
B An ulcerative pyoderma extending into the dermis, with a 'punched-out' ulcer covered by an adherent brown-black crust
C A deep-seated abscess of multiple adjacent follicles draining through several sinuses
D A non-suppurative spreading infection of the upper dermis and lymphatics

Correct. Ecthyma is commonly caused by Strep pyogenes (± Staph aureus), occurring on the legs of malnourished or immunocompromised patients. The thick adherent crust conceals a well-demarcated ulcer underneath.

Ecthyma is a deep form of impetigo extending into the dermis, producing a punched-out ulcer with an overlying adherent crust. It heals with scarring, unlike impetigo.

Incorrect. Ecthyma is a deep ulcerative variant of impetigo, not a blistering condition. The punched-out dermally-extending ulcer with brown-black crust is its hallmark.

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