Microbial Diseases of the Skin and Wounds (Chapter 19) – Comprehensive Study Notes

Vocabulary & Key Terminology

• Acne – inflammatory disease of pilosebaceous units most frequently triggered by Propionibacterium (Cutibacterium) acnes.

• Carbuncle – deeply invasive cluster of interconnected furuncles; often accompanied by systemic signs (fever, malaise).

• Chicken pox – primary Varicella-Zoster Virus (VZV) infection producing diffuse vesicular rash.

• Cutaneous Anthrax – painless black eschar produced by Bacillus anthracis at site of entry.

• Dendritic cells – antigen-presenting cells (APCs) resident in epidermis (a.k.a. Langerhans cells).

• Dermis – vascular, innervated connective-tissue layer beneath epidermis; contains glands, follicles, macrophages.

• Epidermis – keratinized stratified squamous epithelium forming outermost barrier.

• Erysipelas – acute, well-demarcated erythematous infection of upper dermis caused by Streptococcus pyogenes.

• Eschar – dry, black scab or slough; classic in cutaneous anthrax or advanced burns.

• Exfoliative toxins – S. aureus serine proteases (ETA, ETB) that cleave desmoglein-1 ⇒ intra-epidermal blistering.

• Exoenzymes – secreted enzymes (e.g., hyaluronidase, collagenase) that degrade host tissues aiding spread.

• Exotoxin A – superantigen of S. pyogenes (and P. aeruginosa) triggering necrotizing fasciitis and toxic shock.

• Folliculitis – superficial infection of a single hair follicle (a “pimple”).

• Furuncle (boil) – painful dermal abscess arising from folliculitis; purulent core.

• Gas Gangrene – myonecrosis with crepitus caused by Clostridium perfringens α-toxin.

• Herpes Zoster – reactivation of latent VZV in dorsal-root ganglia; presents as unilateral dermatomal vesicles.

• Impetigo (Pyoderma) – contagious, honey-crusted epidermal infection; S. aureus (80%) or S. pyogenes.

• Ischemia – tissue hypoperfusion ⇒ \text{↓O_2}, predisposes to anaerobic infection.

• Keratin – water-resistant structural protein produced by keratinocytes.

• Koplik’s spots – pathognomonic enanthema on buccal mucosa in measles (Rubeola).

• Macules – flat, non-palpable lesions <1\;\text{cm}.

• Measles – febrile illness with maculopapular rash caused by Rubeola virus (Morbillivirus).

• Microbiota – resident skin flora (Staphylococcus epidermidis, Corynebacterium spp., etc.).

• Necrosis – uncontrolled cell death; hallmark of necrotizing infections.

• Necrotizing fasciitis – rapidly spreading infection of fascia; “flesh-eating disease.”

• Papillomas (warts) – benign hyperkeratotic lesions due to HPV-induced epithelial proliferation.

• Papules – raised, solid lesions <1\;\text{cm}.

• Pimple – colloquial folliculitis; may progress to pustule.

• Pox (general) – pustular diseases (smallpox, chicken pox, cowpox) producing scar-forming lesions.

• Protein A – S. aureus surface Fc-binding protein; blocks opsonization.

• Rubella – mild rash illness (“German measles”) caused by Rubivirus; teratogenic in pregnancy.

• Rubeola – synonym for measles.

• Staphylococcal Scalded Skin Syndrome (SSSS) – toxigenic exfoliation in neonates/children; skin desquamation.

• Shingles – common term for Herpes Zoster.

• Subacute sclerosing panencephalitis (SSPE) – fatal, late neurological sequela of measles ($\approx1/10{,}000$ cases).

• Sty – suppurative inflammation of eyelid glands (Zeis or Moll) by S. aureus.

• Varicella – chicken pox.

• Vesicles – fluid-filled lesions <1\;\text{cm} (blisters).

• Warts – see Papillomas; subtypes: seed (common), plantar, flat, genital.

• Whitlow – painful HSV lesion on finger (thumb-sucking children, healthcare workers).

• Zoster – same as shingles.

Study Objectives (Global Expectations)

For each pathogen below be prepared to detail:
• Disease(s) produced
• Morphology & physiology of the microbe
• Route of transmission & epidemiology
• Virulence factors/mechanisms
• Hallmark clinical signs & possible sequelae
• Prevention, control, chemotherapeutic agents, and available vaccines

Objective 1 – Staphylococcus aureus Skin Infections

• Physical traits

  • Gram-positive cocci in irregular clusters; catalase +, coagulase +; golden β-hemolytic colonies.

  • Tolerant of high $\text{NaCl}$ and desiccation → survives on fomites.

• Reservoir & Transmission

  • Normal nasal/skin microbiota (30–40 % carriage) ⇒ direct contact, autoinoculation, or contaminated surfaces.

• Major Diseases

  • Folliculitis → Furuncles → Carbuncles

  • Impetigo (bullous form)

  • SSSS (toxin-mediated, no organisms in blisters)

  • Wound infection / cellulitis

  • Sties, paronychia

• Virulence factors

  • Protein A, capsule, coagulase, hyaluronidase, lipases, DNase

  • Exfoliative toxins (ETA, ETB) – scalded skin

  • Hemolysins, leukocidins, Toxic Shock Syndrome Toxin-1 (TSST-1)

• Clinical picture & sequelae

  • Localized pustules/abscesses; severe toxins → desquamation, septic shock.

  • Possible bacteremia → osteomyelitis, endocarditis.

• Treatment & Prevention

  • Incision & drainage of abscesses + antibiotics.

  • Methicillin-resistant S. aureus (MRSA) requires $\text{Vancomycin}$, $\text{Linezolid}$, $\text{Daptomycin}$.

  • Hand hygiene, mupirocin nasal decolonization, proper wound care; no vaccine currently.

Objective 2 – Streptococcus pyogenes (Group A Strep) Wound/ Skin Infections

• Microbiology

  • Gram-positive cocci in chains; β-hemolytic; bacitracin-sensitive; catalase −.

• Transmission

  • Respiratory droplets, skin-skin; colonizes oropharynx and damaged skin.

• Clinical Entities

  • Non-bullous Impetigo (pyoderma)

  • Erysipelas – fiery, raised borders, high fever

  • Cellulitis – ill-defined margins

  • Necrotizing fasciitis (“Type II”): rapid tissue death within hours.

• Virulence arsenal

  • M protein (anti-phagocytic), hyaluronic-acid capsule

  • Streptolysins O & S, DNases, streptokinase

  • Exotoxin A (superantigen) → streptococcal toxic shock

• Sequelae

  • Post-streptococcal glomerulonephritis possible after impetigo.

• Management

  • $\text{Penicillin V/G}$ first-line; clindamycin added for toxin suppression in NF.

  • Early surgical debridement for necrotizing fasciitis.

  • No licensed vaccine yet; M-protein multivalent candidates in trials.

Objective 3 – Propionibacterium (Cutibacterium) acnes & Acne

• Characteristics: Anaerobic, Gram-positive pleomorphic rods; resides deep in sebaceous follicles.

• Pathogenesis

  • Pubertal androgen surge ⇒ $\text{↑ sebum}$; P. acnes lipases → free fatty acids → inflammation.

• Lesion progression: Microcomedone → Closed comedone (whitehead) → Papule/pustule → Nodule/cyst.

• Treatment

  • Topicals (benzoyl peroxide, clindamycin, retinoids), systemic doxycycline or isotretinoin.

Objective 4 – Clostridium perfringens Wound Infections (Gas Gangrene)

• Biology: Gram-positive, spore-forming anaerobic rod; double zone of hemolysis.

• Epidemiology: Spores in soil, GI tract; introduced via trauma, surgery, war/bite injuries.

• Mechanisms

  • α-toxin (lecithinase) causes myonecrosis & hemolysis.

  • Fermentation gases (H2, CO2) expand tissues (crepitus).

• Clinical hallmarks: Sudden pain, bronze discoloration → black, bullae, foul odor.

• Therapy: Immediate surgical debridement/amputation, high-dose IV penicillin + clindamycin, hyperbaric \text{O_2}.

• Prevention: Proper wound cleansing, prophylactic antibiotics in high-risk trauma.

Objective 5 – Pseudomonas aeruginosa Wound/Burn Infections

• Traits: Gram-negative, oxidase +, motile rod; produces blue-green pigment (pyocyanin) & grape-like odor.

• Ecology: Water, soil; minimal growth requirements; biofilm former (alginate slime).

• Risk groups: Burn patients, cystic fibrosis lungs, immunosuppressed.

• Virulence

  • Exotoxin A (ADP-ribosylates EF-2), elastases, phospholipase C, Type III secreted effectors.

• Clinical features: Greenish purulence, ecthyma gangrenosum; may progress to sepsis.

• Treatment: Antipseudomonal β-lactams (piperacillin-tazobactam) + aminoglycoside; resistance common.

Objective 6 – Bacillus anthracis (Cutaneous Anthrax)

• Morphology: Gram-positive spore-forming rod with poly-D-glutamate capsule.

• Exposure: Contact with infected animals/hides; spores enter via cuts.

• Disease stages: Papule → Vesicle → Black eschar with edema (“malignant pustule”).

• Virulence factors: Protective antigen (PA), Edema factor (EF, cAMP increase), Lethal factor (LF, MAPKK cleavage).

• Outcome: Untreated mortality $\approx20\%$; systemic spread → septic shock.

• Therapy & Prevention: Oral doxycycline or ciprofloxacin; vaccine for high-risk personnel (PA subunit).

Objective 7 – Human Papillomavirus (HPV) Skin Infections

• Virology: Non-enveloped, dsDNA, >200 genotypes.

• Transmission: Direct contact, fomites, autoinoculation; incubation weeks–months.

• Cutaneous Wart Types

  • Common/seed (HPV-2, 4)

  • Plantar (HPV-1)

  • Flat (HPV-3, 10)

  • Filiform

• Pathogenesis: Viral early genes E6/E7 modulate keratinocyte cell cycle ⇒ hyperkeratosis.

• Treatment: Cryotherapy, salicylic acid, imiquimod; recurrences common.

• Vaccine: Quadrivalent (types 6,11,16,18) & 9-valent protect mainly genital strains, limited skin benefit.

Objective 8 – Human Herpesvirus 1 & 2 (HSV-1, HSV-2)

• Structure: Enveloped dsDNA with icosahedral capsid, tegument.

• Latency: HSV-1 trigeminal ganglia; HSV-2 sacral ganglia.

• Skin manifestations

  • Herpes labialis (cold sores), herpetic whitlow, gladiatorum (wrestlers), eczema herpeticum.

• Lesion evolution: Painful grouped vesicles on erythematous base → crust.

• Reactivation triggers: Stress, UV, fever.

• Antiviral therapy: Acyclovir, valacyclovir; topical for mild, IV for severe.

• Prevention: Gloves for HCWs, safe sex; no vaccine licensed (in development).

Objective 9 – Varicella-Zoster Virus (VZV)

• Primary disease (Varicella/Chicken pox)

  • Transmission: Inhalation of respiratory droplets & lesion fluid; extremely contagious (secondary attack rate >90\%).

  • Prodrome: Fever, malaise → pruritic vesicles in “dew-drop on rose petal” crops (macule → papule → vesicle → crust) at different stages.

  • Complications: Bacterial superinfection, pneumonia, encephalitis.

• Latency & Reactivation (Herpes Zoster/Shingles)

  • Viral DNA persists in dorsal-root ganglia.

  • Dermatomal vesicular rash, severe neuralgia.

  • Post-herpetic neuralgia: pain >90\text{ days} (older adults).

• Prevention & Control

  • Two-dose live attenuated Varivax for children; Zoster vaccine (Shingrix, recombinant gE + AS01B adjuvant) for adults $\ge50$ y.

  • Acyclovir/Valacyclovir for treatment; corticosteroids sometimes for PHN.

Objective 10 – Rubella Virus (Rubivirus)

• Togaviridae, enveloped +ssRNA.

• Disease features

  • Mild maculopapular rash, low-grade fever, posterior auricular lymphadenopathy.

  • Arthralgias common in adults.

• Congenital Rubella Syndrome (CRS)

  • Maternal infection in 1st trimester ⇒ cataracts, PDA, sensorineural deafness, “blueberry muffin” rash.

• Prevention

  • Live attenuated MMR/MMRV vaccine (two doses); contraindicated in pregnancy.

Objective 11 – Rubeola Virus (Morbillivirus)

• Paramyxoviridae, enveloped −ssRNA; uses hemagglutinin (H) & fusion (F) glycoproteins.

• Clinical course

  1. Incubation $10–12\;\text{days}$.

  2. Prodrome: 3 C’s – Cough, Coryza, Conjunctivitis + photophobia & fever.

  3. Koplik’s spots (buccal) precede rash.

  4. Maculopapular rash spreads cephalocaudal, confluent.

• Complications

  • Otitis media (most common), pneumonia, acute encephalitis, SSPE (years later).

• Immunology: Transient but profound $\text{↓ cell-mediated immunity}$ ⇒ secondary infections.

• Prevention

  • Two-dose MMR/MMRV vaccine; herd immunity threshold >95\%.

  • Vitamin A reduces morbidity in children.

Lesion Morphology Recap & Diagnostic Clues

• Macule (flat) → Papule (raised) → Vesicle (fluid) → Pustule (purulent) → Crust/Scar.
• Umbilicated vesicles: Poxviruses.
• Honey-crust: Impetigo.
• Black eschar: Anthrax.
• Dermatomal pain: Shingles.

Comparative Table (selected parameters)

Ethical & Practical Considerations

• Vaccine hesitancy threatens herd immunity (measles resurgence).

• MRSA & multidrug-resistant P. aeruginosa demand antimicrobial stewardship.

• Occupational risk: HSV whitlows in dentists, anthrax in tannery workers.

• Bioterrorism: Anthrax spores weaponizable ⇒ surveillance & stockpiled antibiotics/vaccine.

Integration With Previous Concepts

• Innate barriers: Keratinized epidermis, sebum acidity, microbiota competitively exclude pathogens.

• Adaptive immunity: Memory responses exploited in live attenuated vaccines (MMR, VZV).

• Superantigens (TSST-1, Exotoxin A) link to cytokine storm concept from immunology lectures.

High-Yield Numbers & Equations (for recall)

• Measles basic reproduction number $R_0 = 12–18$ (most contagious viral disease).

• VZV secondary attack rate >90\% among susceptible household contacts.

• Clostridial myonecrosis doubling time $\approx8\text{ min}$ (one of the fastest).

• Case-fatality untreated cutaneous anthrax $20\%$ ; treated <1\%.

• Post-herpetic neuralgia risk increases $\approx3\%$ per decade over age 50.

Study Tips

• Associate lesion description with likely pathogen (e.g., honey-crust → GAS/G+ cocci).
• Remember exotoxin nomenclature: A for Attack (S. pyogenes and P. aeruginosa share Exotoxin A).
• Visualize dermatomal map for shingles questions.
• Use “4 P’s” for HPV warts: Pain-less, Proliferative, Papillomatous, Persistence.
• Link vaccine schedule (2-dose) to measles, mumps, rubella, varicella.

End of Notes