Microbial Diseases of the Skin and Wounds presented by Robert W. Bauman (2012)
Lecture prepared by Mindy Miller-Kittrell
Layers of Skin:
Epidermis: Outer layer, dead and impenetrable.
Dermis: Beneath the epidermis.
Prevents excessive water loss.
Regulates body temperature.
Involves sensory phenomena.
Acts as a barrier against microbial invaders.
Contains a salty surface.
Hosts normal flora, including halophiles resistant to sebum.
Generally harmless but cannot be completely removed through cleansing.
Composed of:
Yeasts: e.g., Malassezia, causing itchy pimples.
Bacteria: e.g., Staphylococcus, Micrococcus, diphtheroids.
Can cause disease if they breach the epidermis or if the immune system is compromised.
Trauma to body tissue, e.g., cuts, scrapes, surgery, burns, bites.
Allows microbes to infect deeper tissues.
Body defenses often eliminate infection, but severe or fatal diseases can result.
Infection of hair follicles often called a pimple.
If at eyelid base, referred to as a sty.
Spread can lead to:
Furuncles (boils)
Carbuncles (multiple furuncles growing together).
Images depict types of folliculitis, including carbuncles and furuncles.
Staphylococcus: Gram-positive, facultative anaerobes, cocci in clusters.
Salt-tolerant and can survive desiccation (>600°C for 30 min).
Two common species:
Staphylococcus epidermidis
Staphylococcus aureus (more pathogenic)
Beta-lactamase production and toxin production distinguish them.
Details on enzymes, toxins, and proteins affecting virulence:
Hyaluronidase, coagulase, and others.
Presence of polysaccharide slime layer and protein A that inhibits phagocytosis.
Isolation of gram-positive bacteria from pus.
Dicloxacillin: Preferred treatment.
Vancomycin: For resistant strains.
Hand antisepsis and proper hospital procedures to minimize MRSA infections.
Strains of Staphylococcus aureus producing exfoliative toxins cause SSSS.
No scarring occurs as the dermis remains unaffected.
Secondary infections may lead to death, but it's rare.
Primarily affects infants; spread via person-to-person contact.
How exfoliative toxins affect the skin.
Primary cause is S. aureus, occasionally by Streptococcus pyogenes.
Pathogenicity includes similar virulence factors (M protein, hyaluronic acid).
Bacteria invade compromised skin; can lead to complications like acute glomerulonephritis.
Common transmission through person-to-person contact or fomites.
Clinical pictures of impetigo.
Occurs primarily in elderly populations.
Usually caused by Streptococcus pyogenes (Group A).
Gram-positive cocci, tissue-invading enzymes, exotoxins damage tissue.
Enters through skin breaks, spreads person-to-person.
a### Diagnosis, Treatment, and Prevention
Hard-to-diagnose early due to nonspecific symptoms; treated with clindamycin and penicillin or broader antibiotics.
Pathogen enters and spreads rapidly; secretes enzymes to invade.
M protein helps survive phagocytosis; Streptolysin S and exotoxin A damage tissues.
Caused by Propionibacterium acnes; a common skin inhabitant.
Usually starts in adolescence but can appear later.
Diagnosed visually; treated with antimicrobial drugs and exfoliants; Accutane for severe cases.
Explanation of pore blockage and inflammation leading to various types of acne.
Causative agent: Pseudomonas aeruginosa; thrives in moist environments.
Infects burn victims, causes extensive tissue damage.
Difficult to diagnose; treated with specific antibiotics.
Image depicting Pseudomonas aeruginosa infections in the skin.
Caused by Bacillus anthracis through breaks in the skin, leads to a black eschar.
Treated with antimicrobial drugs; prevention demands animal disease control.
Caused by Clostridium species (e.g., C. perfringens).
Symptoms include tissue necrosis, blackening skin, and gas bubble presence.
Involves surgical removal of necrotic tissue and antibiotics; prevention focuses on wound cleaning.
Includes smallpox, orf, cowpox; smallpox was the first eradicated virus.
Requires immediate vaccination; previously widespread vaccination has been discontinued.
Illustration depicting the stages of lesions in poxvirus infections.
Caused by human herpesviruses 1 and 2; shows slow spreading lesions.
Symptoms stem from inflammation and cell death; can cause syncytia.
Diagnosis by lesions; control medications like acyclovir are available.
Shows herpes lesions and related anatomical structures.
Displays importance of ganglia in herpes virus latency and recurrence.
Chickenpox: lesions on back and trunk; Shingles: localized lesions along nerves.
Caused by varicella-zoster virus (VZV); often severe in adults.
Vaccines available for both conditions.
Diagrammatic representation of VZV becoming latent and reactivating.
Benign epithelial growths caused by various papillomaviruses.
Direct contact and fomites; some/onco- strains linked to cancer.
Diagnosed via observation; various removal techniques are available.
Occurs mostly in infants; can cause teratogenic birth defects.
Caused by rubella virus, preventable with vaccines focusing on pregnant women.
Graph depicting decrease in rubella cases since the introduction of a vaccine.
Identified by Koplik’s spots and highly contagious nature.
Caused by the measles virus; diagnosis based on symptoms; prevention through MMR vaccine.
Graph illustrating the decline of measles cases due to vaccination efforts.
Fungal diseases often opportunistic, classified by infection location:
Superficial, subcutaneous, systemic.
Ringworm and other conditions caused by dermatophytes.
Shared personal items spread fungi; treated by topical or oral medications.
Image depicting appearance of pityriasis versicolor.
Result from dermatophyte infections, leading to cutaneous lesions.
Confirmed through KOH preparations; treated with topical or oral agents.