Microbiology: Skin Structure, Microbiota, and Bacterial Skin Diseases (Chapter 22 Study Notes)

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.

Group	Characteristics
Diphtheroids	Gram-positive rods; non-pathogenic; metabolize sebum; e.g., Propionibacterium acnes
Staphylococci	Gram-positive cocci; salt-tolerant; produce antimicrobial peptides
Malassezia	Lipid-dependent yeast; can cause skin conditions in some cases

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.

Product	Effect
Capsule	Inhibits phagocytosis
Protein A	Binds IgG, inhibits opsonization
Coagulase	Clots plasma, walls off infection
Clumping factor	Attaches to fibrin, plastic devices
Exfoliatin	Separates layers of epidermis
Leukocidin	Kills white blood cells
Hyaluronidase	Breaks down connective tissue
Staphylokinase	Dissolves blood clots

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.