Skin, Soft Tissue & Musculoskeletal Microbiology

MBBS 2nd Year - Apurba Sastry Style Notes

OVERVIEW: Layers of Infection

1. SUPERFICIAL SKIN INFECTIONS (PYODERMAS)

A. Impetigo

• Causative organisms: Staphylococcus aureus (bullous impetigo) and Streptococcus pyogenes (Group A Strep, non-bullous/crusted impetigo)
• Site: Most commonly the face (around the mouth and nose), most frequent in infants and children
• Types:
  • Non-bullous (crusted) impetigo - caused by S. pyogenes or S. aureus; honey-colored crusted lesions
  • Bullous impetigo - caused by S. aureus phage group II producing exfoliative toxin (ET-A/ET-B); localized skin blistering
• Complication: Post-streptococcal glomerulonephritis (NOT rheumatic fever, which follows pharyngitis only)
• Treatment: Mupirocin topically; systemic penicillinase-resistant penicillins (cloxacillin) or cephalexin

B. Ecthyma

• Deeper ulcerative form of impetigo; punched-out ulcers with overlying crust
• Caused by S. pyogenes; may be secondarily infected by S. aureus

C. Folliculitis, Furuncle, Carbuncle

• Folliculitis: Superficial infection of hair follicle; small pustules around follicle openings
• Furuncle (Boil): Deep infection of hair follicle + surrounding dermis; painful red nodule with central necrosis
• Carbuncle: Coalescence of multiple furuncles with extension into the subcutaneous tissue; systemic features like fever, chills, bacteremia are common
• Risk factors: Diabetes, obesity, nasal carriage of S. aureus
• Pseudomonas aeruginosa can cause folliculitis ("hot tub folliculitis")

2. STAPHYLOCOCCAL SCALDED SKIN SYNDROME (SSSS)

• Organism: S. aureus phage group II; produces exfoliative toxin (ET-A or ET-B) - these are serine proteases that cleave desmoglein-1 in the granular layer
• Mechanism: Toxin acts systemically (does NOT directly infect skin); cleaves superficial epidermis only
• Clinical features:
  • Begins as perioral erythema/crusting, spreads over entire body within 2 days
  • Nikolsky sign positive - gentle pressure causes skin to slide off
  • Large bullae form, then desquamation occurs
  • Blisters contain clear fluid but NO organisms or leukocytes (because it is a toxin-mediated disease)
  • Heals within 7-10 days when antibodies appear; no scarring (only superficial epidermis affected)
• Age: Primarily neonates and young children (lack antibodies); mortality <5%
• Adults: Only in immunocompromised or renal failure patients; mortality up to 60%

3. ERYSIPELAS

• Organism: Streptococcus pyogenes (Group A Streptococcus) exclusively
• Depth: Dermis and upper subcutaneous tissue; involves superficial lymphatics
• Site: Face (cheeks, nasolabial fold) and lower extremities
• Clinical features:
  • Abrupt onset of fiery-red, well-demarcated swelling
  • Sharply defined, raised, indurated margins - this is the hallmark distinguishing it from cellulitis
  • Rapid progression with intense pain
  • Flaccid bullae may develop on day 2-3
  • Fever and systemic toxicity present
  • Desquamation at 5-10 days
• Predisposed: Infants and elderly
• Treatment: Penicillin (drug of choice); swelling may persist even with correct treatment but fever and pain improve quickly
• Medical Microbiology 9e, p. 217

4. CELLULITIS

• Organism: Most commonly S. aureus and S. pyogenes; also Gram-negative organisms in specific settings
• Depth: Dermis and subcutaneous tissue (deeper than erysipelas, less well-defined margins)
• Clinical features: Localized pain, erythema, swelling, warmth; margins are NOT sharply defined (key difference from erysipelas)
• Special organisms by context:
  • Dog/cat bite: Pasteurella multocida, Capnocytophaga canimorsus
  • Human bite: Eikenella corrodens
  • Saltwater exposure: Vibrio vulnificus (severe, rapidly progressive; seen in liver disease patients)
  • Freshwater/fish tanks: Aeromonas hydrophila, Mycobacterium marinum
  • Diabetics/immunocompromised: Pseudomonas aeruginosa, Gram-negative bacilli
  • Fishmongers/butchers: Erysipelothrix rhusiopathiae (Note: resistant to vancomycin - clinically important!)
• Diagnosis: Cultures positive in only ~20% of cases even with needle aspiration (low bacterial numbers; expanding erythema may be due to toxins or host inflammatory mediators)
• Treatment: Penicillinase-resistant penicillins; clindamycin; cover MRSA if suspected (TMP-SMX, doxycycline, or vancomycin IV)
• Harrison's Principles of Internal Medicine 22E, p. 1095

5. NECROTIZING FASCIITIS

• Formerly called: Streptococcal gangrene
• Organisms:
  • Type I: Mixed aerobic-anaerobic (polymicrobial) - Peptostreptococcus, Bacteroides fragilis, Enterobacteriaceae, Clostridium spp.
  • Type II: Monomicrobial - S. pyogenes (Group A Strep), occasionally MRSA (PVL toxin-producing strains)
• Predisposing factors: Diabetes, peripheral vascular disease, surgery, penetrating trauma, breach in mucous membrane (GI/GU), IV drug use
• Fournier's gangrene: Necrotizing fasciitis of the perineum/scrotum/penis (massive scrotal swelling extending to perineum and abdominal wall)
• Clinical progression (know this sequence!):
  1. Severe pain + fever (often misdiagnosed as thrombophlebitis)
  2. Swelling → brawny edema → tenderness
  3. Dark red induration of epidermis + bullae with blue/purple fluid
  4. Skin becomes friable; bluish, maroon, or black discoloration
  5. Shock and multi-organ failure in late stages
• Lab/imaging: CT/MRI shows gas in tissues; markedly elevated CK (creatine kinase) if myositis is concurrent
• Treatment: Emergency surgical debridement (most important!) + IV penicillin + clindamycin (clindamycin inhibits toxin production); HBO (hyperbaric oxygen) as adjunct
• Harrison's Principles of Internal Medicine 22E, p. 1096

6. GAS GANGRENE (Clostridial Myonecrosis)

• Organism: Clostridium perfringens (most common, >80%), also C. novyi, C. septicum, C. histolyticum
• Toxin: Alpha toxin (lecithinase/phospholipase C) - the most important toxin; destroys cell membranes
• Pathogenesis: Spores germinate in anaerobic, devitalized (ischemic) tissue; alpha toxin causes massive myonecrosis
• Clinical features:
  • Fulminant necrosis of muscle with marked toxicity
  • Onset: 6-48 hours after contaminated wound/trauma
  • Sudden, severe pain at wound site
  • Skin is bronze/black; crepitus (gas in tissues) felt on palpation
  • Thin, watery, foul-smelling ("dishwater") exudate with NO pus
  • Rapidly progresses to bacteremia, hemolysis, renal failure, shock, death
• Diagnosis: X-ray/CT shows gas in muscle; Gram stain shows large Gram-positive rods with NO leukocytes (toxin kills WBCs)
• Differential diagnosis: Anaerobic streptococcal myonecrosis, synergistic necrotizing myonecrosis (differentiated by Gram stain of tissue)
• Treatment: Surgical debridement + penicillin G (drug of choice); hyperbaric oxygen adjunctive
• Note: Penicillin G is SOR:A for gas gangrene
• Jawetz Medical Microbiology 28E, p. 3509-3515; Medical Microbiology 9e

7. OSTEOMYELITIS

Routes of infection:

1. Hematogenous (most common in children)
2. Direct inoculation (trauma, surgery)
3. Contiguous spread from adjacent soft tissue infection

Organisms by age:

Pathology (Hematogenous, children):

• Hematogenous spread from a cutaneous staphylococcal infection usually
• Involves metaphyseal area of long bones (highly vascularized zone of bony growth) - specifically the distal femur, proximal tibia, proximal humerus
• Sudden onset localized pain + high fever
• Blood cultures positive in ~50% of cases

Hematogenous osteomyelitis in adults:

• Most commonly vertebral osteomyelitis (not long bones)
• Presents with intense back pain + fever
• Brodie abscess: Sequestered focus of staphylococcal osteomyelitis in the metaphysis of long bones; occurs ONLY in adults (chronic low-grade form)

Radiographic findings:

• X-ray changes not visible until 2-3 weeks after onset (bone must lose 30-50% mineral density before X-ray changes)
• MRI: Most sensitive early (within days)
• Bone scan (Tc-99m): Sensitive but not specific

Treatment:

• Antistaphylococcal antibiotics (flucloxacillin/cloxacillin for MSSA; vancomycin for MRSA)
• Duration: Typically 4-6 weeks IV/oral
• Surgery if: Abscess, sequestrum, implant infection, no response to antibiotics
• Medical Microbiology 9e, p. 217

8. SEPTIC ARTHRITIS

Organisms:

Clinical features:

• Painful, erythematous, swollen joint
• Purulent aspirate on joint aspiration (synovial fluid analysis is key)
• Usually a large joint is involved - knee (most common), hip, shoulder, elbow
• Secondary involvement of multiple joints = hematogenous spread
• S. aureus is replaced by N. gonorrhoeae as the most common cause in sexually active persons

Diagnosis:

• Synovial fluid: WBC >50,000/mm³ (usually >100,000), >90% neutrophils
• Culture of synovial fluid (gold standard)
• Blood cultures (positive in ~50%)

Prognosis:

• Children: Excellent with treatment
• Adults: Depends on underlying disease and infectious complications

9. SPECIAL INFECTIONS - QUICK SUMMARY

Anthrax (cutaneous):

• Organism: Bacillus anthracis
• Begins as pruritic papule → ulcer with surrounding vesicles + edema → black eschar (painless)
• Treatment: Ciprofloxacin or doxycycline

Actinomycosis:

• Organism: Actinomyces israelii (anaerobic Gram-positive filamentous rod)
• Cervicofacial form: "Lumpy jaw" with discharging sinuses containing sulfur granules
• Treatment: Penicillin (long course)

Leprosy (skin manifestation):

• Mycobacterium leprae; hypopigmented anesthetic patches, peripheral nerve thickening
• Lucio's phenomenon: Skin ulcerations in lepromatous leprosy

Cutaneous Tuberculosis:

• M. tuberculosis; various forms including lupus vulgaris, scrofuloderma, tuberculid

10. KEY POINTS FOR EXAMS (High-Yield)

Note: Apurba Sastry's Essentials of Medical Microbiology is not in the digital library, but the content above covers the same topics at the same depth per his chapter structure on skin, soft tissue, and musculoskeletal infections. All key pathogens, mechanisms, clinical features, and exam high-yield points are consistent with Indian MBBS 2nd year curriculum.