Chapter 22: Skin Structure, Microbiota, and Bacterial Skin Diseases

A Glimpse of History

This section introduces the historical context of bacterial skin diseases, focusing on the pioneering work of Howard Ricketts in the early 20th century.

• Howard Ricketts (University of Chicago, 1902) studied Rocky Mountain spotted fever (RMSF).

• Identified tiny rod-shaped bacteria in patient blood; could transmit disease to animals but could not culture on standard media.

• Demonstrated ticks as vectors; ticks remained healthy, but their eggs were often infected.

• Traveled to Mexico to study louse-borne typhus; both Ricketts and Stanislaus Prowazek (another researcher) died from the disease.

• Louse-borne typhus named Rickettsia prowazekii; RMSF agent named Rickettsia rickettsii.

Skin Surface: Remarkable Barrier to Invasion

The skin acts as a primary defense against microbial invasion, but its exposed nature makes it susceptible to injury and infection.

• Functions: Tough, flexible outer covering; regulates temperature; restricts fluid loss; senses environment.

• Vulnerabilities: Cuts, punctures, burns, chemical injury, insect/tick bites can breach the barrier.

• Examples: Staphylococcus aureus can enter surgical wounds; sandfly bites can introduce Leishmania species.

• Pathogens may reach the skin via the bloodstream from other infection sites.

22.1. Anatomy, Physiology, and Ecology of the Skin

The skin is a complex organ with multiple layers and functions, supporting a diverse microbial ecosystem.

• Epidermis: Surface layer of flat cells; outermost cells are dead, filled with water-resistant keratin, and constantly shed.

• Dermis: Contains nerves, glands, blood, and lymphatic vessels.

• Subcutaneous tissue: Composed of fat and other cells that support the skin.

Secretions and Microbiota

• Sweat glands: Deliver sweat via fine tubules; evaporation leaves salty residue that inhibits microbial growth.

• Sebaceous glands: Secrete oily sebum into hair follicles, keeping skin soft and water-repellent.

• Normal microbiota: Adapted to dry, salty, cool habitat; use sweat and sebum as nutrients; by-products (e.g., fatty acids) inhibit other microbes.

• Most pathogens cannot tolerate the skin's dryness, saltiness, acidity, and toxicity; those that do are shed with dead skin cells.

• Some normal microbiota are opportunistic pathogens; bacterial breakdown of sweat can cause body odor.

Microbial Inhabitants of the Skin

• Different skin regions have distinct microbial populations (e.g., drier back vs. moist groin/armpit).

• Main groups:

  • Diphtheroids: Found in oily regions; Propionibacterium (obligate anaerobes) grow in hair follicles.

  • Staphylococci: Salt-tolerant, produce antimicrobial substances active against other Gram-positive bacteria.

  • Malassezia: Tiny, lipid-dependent yeasts.

22.2. Bacterial Skin Diseases

Bacterial skin diseases arise when pathogens breach the skin barrier, often via hair follicles or injuries.

Acne Vulgaris

• Signs and Symptoms: Enlarged sebaceous glands, increased sebum secretion, thickened hair follicle epithelium, blackheads, and whiteheads.

• Causative Agent: Propionibacterium acnes, which multiplies in sebum.

• Pathogenesis: Metabolic products trigger inflammation; neutrophils release enzymes that damage follicle wall, leading to abscess formation.

• Epidemiology: Most people have P. acnes on their skin; increased acne during puberty due to hormonal changes.

• Treatment and Prevention: Usually mild; medications available; squeezing lesions can worsen infection.

Hair Follicle Infections

• Signs and Symptoms:

  • Folliculitis: Inflammation causing red bumps (pimples).

  • Furuncle: Infection extends to adjacent tissues, causing localized redness, swelling, pain, and pus drainage.

  • Carbuncle: Larger area of redness, swelling, pain, draining pus; fever may be present.

• Causative Agent: Staphylococcus aureus; produces coagulase and clumping factor (virulence factors).

• Pathogenesis: S. aureus attaches to hair follicle cells, multiplies, spreads to sebaceous glands, triggers inflammation, and can spread deeper to form carbuncles or enter the bloodstream.

• Epidemiology: S. aureus found in nostrils of nearly everyone; transmission usually by hands; survives well in the environment; fomites can transmit.

• Treatment and Prevention: Boils/carbuncles may require drainage and antibiotics; many strains are resistant (MRSA, VISA, VRSA); handwashing limits spread.

Staphylococcal Scalded Skin Syndrome (SSSS)

• Signs and Symptoms: Redness, malaise, irritability, fever; painful nose, mouth, genitalia; wrinkled skin and large fluid-filled blisters within 48 hours.

• Causative Agent: S. aureus strains producing exfoliatin toxin (only ~5% of strains).

• Pathogenesis: Exfoliatin carried by bloodstream, causes epidermis to split below keratinized layer, leading to peeling and fluid loss.

• Epidemiology: Most frequent in newborns; person-to-person transmission.

• Treatment and Prevention: Antibiotics and removal of dead skin; prompt therapy usually yields full recovery.

Streptococcal Impetigo

• Signs and Symptoms: Superficial skin infection with inflammation; thin-walled blisters break and are replaced by oozing yellowish crusts; little fever or pain; enlarged lymph nodes.

• Causative Agent: Streptococcus pyogenes (also S. aureus); both have group A carbohydrate.

• Pathogenesis: Minor injuries introduce bacteria into deeper epidermis; hyaluronic acid capsule and M protein interfere with phagocytosis; additional virulence factors include proteases, nucleases, hyaluronidase.

• Epidemiology: Most common among poor children in hot, humid areas; spread by contact, insects, fomites; patients may become throat/nasal carriers.

• Treatment and Prevention: S. pyogenes susceptible to penicillin, erythromycin; wound cleaning, antiseptics, avoiding contact; keep skin clean, avoid sharing personal items.

Rocky Mountain Spotted Fever (RMSF)

• Signs and Symptoms: Sudden onset of headache, muscle/joint pain, fever; rash from blood leakage on palms, wrists, ankles, soles; spreads to rest of body; bleeding may occur at other sites; damage to organs can cause shock and death without prompt treatment.

• Causative Agent: Rickettsia rickettsii (tiny Gram-negative, non-motile coccobacilli; obligate intracellular bacteria).

• Pathogenesis: Transmitted by tick bite (4–10 hours feeding); bacteria enter capillary endothelial cells, escape phagosome, multiply in cytoplasm/nucleus; use actin to move between cells, causing membrane damage and cell rupture; infection of blood vessel walls leads to clotting, necrosis, rash; release of lipopolysaccharide causes shock and disseminated intravascular coagulation.

• Epidemiology: Sporadic distribution in Americas; zoonosis maintained in ticks and mammals; humans are accidental hosts; wood tick and dog tick are major vectors (active April–September).

Key Terms and Concepts

• Keratin: Water-resistant protein in skin's outer layer.

• Abscess: Collection of pus (living/dead neutrophils, bacteria, tissue debris).

• Fomite: Inanimate object that can transmit pathogens.

• Virulence factors: Molecules produced by pathogens that enhance their ability to cause disease (e.g., coagulase, protein A, capsule).

• Obligate intracellular bacteria: Bacteria that must live within host cells to survive and replicate (e.g., Rickettsia rickettsii).

Example: MRSA (Methicillin-resistant Staphylococcus aureus)

• MRSA is a major cause of hospital- and community-acquired skin infections.

• Resistant to many antibiotics, including methicillin and sometimes vancomycin.

• Prevention includes handwashing and screening patients in healthcare settings.

Additional info:

• Tables have been recreated and summarized based on slide content and standard microbiology knowledge.

• Some details (e.g., full table entries, mechanisms) have been inferred for completeness.