micro 2
Acne: overview
Acne is a superficial skin infection/inflammatory condition centered around hair follicles and sebaceous glands.
Key lesion types:
Whitehead: pore closed, pus accumulation.
Blackhead: pore open, thick sebum/oxidized material at the surface.
Cystic acne: deeper infection with surrounding inflammation; squeezing causes rupture into surrounding tissue and potential scarring.
Primary organism in typical acne: Propionibacterium acnes (P. acnes).
Management (general): regular gentle cleansing; exfoliating/antibacterial cleansers with benzoyl peroxide to reduce organism load; avoid squeezing to prevent spread and cystic progression.
When to consider antibiotics: if widespread P. acnes proliferation with inflammation persists, topical antibiotics may be used to reduce organism load; avoid self-extraction.
Anatomy and progression
Most acne is superficial and centered at or just below the keratinized layer of the epidermis; superficial infections start in the epidermis or dermal-epidermal junction.
Boil/furuncle vs carbuncle involves more tissue: typically follicles for a furuncle; follicles for a carbuncle.
Boils (furuncle/carbuncle)
Causative organism: Staphylococcus aureus (often yellow/“golden” pus with a brassy tint; AU = gold).
Boil characteristics: large, purulent lesions that are painful, often well into the dermis/subcutaneous tissue; purulent drainage is key.
Diagnosis: clinical appearance; sterile drainage sample for Gram stain and culture (to confirm cocci in clusters for Staph aureus).
MRSA note: MRSA = Staphylococcus aureus with antibiotic resistance; not all Staph aureus are MRSA. If methicillin kills the organism, beta-lactams can be used; if MRSA resistant, alternatives are needed (sometimes IV antibiotics such as vancomycin in severe cases).
Treatment strategy:
Drainage of the boil (sterile technique).
Antibiotics (topical for minor cases; oral or IV for more severe cases; MRSA may require non-beta-lactam options).
Education: monitor for fever, spreading redness, deep pain, or non-resolution; hospital admission only if systemic involvement.
MRSA in the bloodstream is especially dangerous; invasive MRSA has higher mortality risk; prevalence has increased in the past decades.
Impetigo
Very superficial infection; honey-colored crusts around the mouth/face, can extend to neck/body.
Common causes: Staphylococcus aureus or Streptococcus pyogenes (group A Streptococcus).
Diagnosis: Gram stain from lesion swab (cocci in clusters for Staph; cocci in chains for Strep).
Treatment: topical antibiotics; emphasize hygiene to prevent spread (schools/daycares, etc.).
Staphylococcal Scalded Skin Syndrome (SSSS)
Also called Ritter disease; mostly affects newborns/infants.
Etiology: Staphylococcus aureus producing exfoliative toxins Eta and EtB; causes massive epidermal detachment within the keratinized layer (desquamation) but generally no deep tissue infection.
Distinct from SJS/TEN: SSSS splits within the epidermis (keratinized layer); SJS/TEN involves the dermis-epidermis junction and can be life-threatening.
Management: antibiotics to eradicate toxin-producing Staph; strict hand hygiene; supportive care; usually heals without scarring.
Cellulitis
Definition: infection of the dermis and subcutaneous tissue; may spread from a skin break or puncture wound.
Hallmarks: painful, red, warm, swollen skin with rapid progression; often shows lymphangitis (tracking lines) and regional lymph node swelling.
Common causative organisms:
Staphylococcus aureus
Streptococcus pyogenes (group A strep)
Other scenarios: animal bites can introduce Pasteurella multocida or Bartonella henselae (gram-negative rods); these are important to consider with animal exposure.
Diagnosis: Gram stain/culture from drained tissue; look for gram-positive cocci in clusters (Staph) or chains (Strep); in animal bite cases, expect gram-negative rods.
Treatment: systemic antibiotics (oral or IV); topical antibiotics are not sufficient due to depth of infection; imaging or cultures may be needed if severe or spreading.
Fungal cellulitis is rare; usually treated differently (antifungal therapy).
Implications and quick comparisons
Acne vs boils vs impetigo vs SSSS vs cellulitis: depth of infection and causative organism drive management and prognosis.
Key diagnostic cues:
Acne: superficial, comedones with possible inflammation.
Boil: localized, purulent, larger and deeper infection; golden pus; may require drainage.
Impetigo: honey-colored crusts on face, superficial; Gram stain to differentiate Staph vs Strep.
SSSS: widespread desquamation in infants; toxin-mediated, epidermal split within keratinized layer.
Cellulitis: dermal/subcutaneous infection with rapid spread and lymphangitis; often Staph/Strep; consider animal-bite organisms.
Quick reference rules for exam recall
Furuncle vs carbuncle sizes: follicles vs follicles.
MRSA concept: all MRSA are Staphylococcus aureus, but not all Staph aureus are MRSA; resistance guides antibiotic choice.
P. acnes is the typical skin commensal involved in acne; reducing its numbers helps with acne management.
Honey-colored crusts strongly suggest impetigo; Gram stain helps distinguish Staph vs Strep in impetigo.
SSSS toxins (Eta/EtB) cause epidermal split within the keratinized layer; not necessarily MRSA; treat with antibiotics and supportive care.
Cellulitis requires systemic antibiotics; depth (dermis/subcutaneous) differentiates it from epidermal infections.
Key numbers to remember
Boil follicle involvement: follicles; carbuncle: follicles.
Invasive MRSA mortality impact:
Invasive MRSA incidence: about cases per year in the US (approx. 100,000).
Treatment durations: some antibiotics are given for short courses; severe cases may require hospital-based IV therapy for several days, e.g., days or more depending on severity.
Notes on lab tests and timing
Gram stain results: typically within minutes to hour.
Culture results: usually around hours.
Culture helps confirm organism and guide antibiotic choice, especially for boils and cellulitis.