Microbial Diseases of the Skin and Eyes
Chapter 15 Summary
Principal Portals of Entry
- Define the different pathways through which microbes gain entry into a host.Definitions
- ID50: Infectious dose for 50% of the population. A measure of virulence that indicates how many organisms are required to cause disease in half of the exposed hosts.
- LD50: Lethal dose for 50% of the population. A measure of the potency of a toxin that indicates how much toxin is required to kill half of the test subjects.Microbial Adherence to Host Cells
- Explanation of how microbes attach to host tissues to establish infection, often utilizing structures like fimbriae, pili, and specialized proteins.Pathogenicity Contributions of Capsules and Cell Wall Components
- Capsules offer protection from phagocytosis.
- Specific components of the cell wall can aid in adhesion, evasion of immune responses, and overall virulence.Comparison of Enzymatic Effects
- Coagulases: Enzymes that coagulate blood, aiding in combating host defense.
- Kinases: Break down fibrin, allowing bacteria to spread from localized infections.
- Hyaluronidase: Breaks down hyaluronic acid in connective tissue, facilitating the spread of pathogens.
- Collagenase: Dismantles collagen in connective tissue, aiding in tissue invasion.Antigenic Variation
- Definition: The ability of pathogens to alter their surface antigens to evade host immune responses.
- Example: Certain influenza viruses changing their surface proteins.Role of Host Cell Cytoskeleton in Pathogen Entry
- Explanation of mechanisms by which bacteria utilize host cell cytoskeletal components to enter cells.Avoiding Phagocytosis
- Identification of six mechanisms including:
1. Encapsulation
2. Production of surface proteins that inhibit phagocytosis
3. Inhibition of phagosome-lysosome fusion
4. Production of enzymes that destroy phagocytes
5. Mimicking host molecules to evade detection
6. Cell wall modifications that hinder adherence.Function of Siderophores
- Molecules produced by bacteria to scavenge iron from the host, an essential nutrient for microbial growth.Direct Damage vs. Toxin Production
- Direct damage: Pathogens disrupt normal cell function or cause cell death.
- Toxins: Produce specific effects on host cells, potentially leading to more significant damage even at low doses.Exotoxins vs. Endotoxins
- Exotoxins: Soluble proteins released by living bacteria; highly toxic and specific in action (e.g., botulinum toxin).
- Endotoxins: Lipopolysaccharides from the outer membrane of Gram-negative bacteria; less toxic than exotoxins and cause systemic effects (e.g., fever, septic shock).Mechanisms of Action of Toxins
- A-B toxins: Consist of an active (A) and binding (B) component; the A component inhibits protein synthesis within host cells.
- Membrane-disrupting toxins: Form pores in host cell membranes, causing lysis and cell death.
- Superantigens: Stimulate an excessive immune response and cytokine release.
- Genotoxins: Damage DNA, potentially leading to mutations and malignancies.Importance of the LAL Assay
- Limulus Amebocyte Lysate assay detects bacterial endotoxins in medical devices and pharmaceuticals.Roles of Plasmids and Lysogeny in Pathogenicity
- Plasmids: Carry genes for antibiotic resistance and virulence factors, enhancing bacterial survival.
- Lysogeny: Phage integration into bacterial genome can confer new pathogenic traits, including toxins.Cytopathic Effects of Viral Infections
- List of nine common effects including cell lysis, inclusion body formation, and apoptosis.Symptoms in Other Pathogen Induced Diseases
- Discussion of the causes of symptoms in fungal (e.g., mycoses), protozoan, helminthic, and algal diseases.Portals of Entry vs. Exit
- Distinction between how infectious agents enter and leave the host organism.
Chapter 21 - Microbial Diseases of the Skin and Eyes
Structure and Function of the Skin
Learning Objective: Describe the structure of the skin and mucous membranes and the ways pathogens can invade them.
Epidermis: Thin outer layer of skin, consisting of epithelial cells.
Keratin: A waterproofing protein that coats the outer layer of the epidermis, preventing water loss.
Dermis: The thicker inner layer composed mainly of connective tissue.
Defense Mechanisms:
- Perspiration: Provides moisture and nutrients for growth, contains salt to inhibit microorganisms, and lysozyme to break down bacterial cell walls.
- Sebum: Secreted by oil glands; contains fatty acids that inhibit pathogens.
Mucous Membranes
Line body cavities open to the exterior, consisting of tightly packed epithelial cells attached to the extracellular matrix.
Cells secrete mucus which traps pathogens, and some have cilia that help move mucus out.
Often acidic, which can discourage pathogen survival, and the eyes are cleaned by tears containing lysozyme.
Normal Microbiota of the Skin
Learning Objective: Provide examples of normal skin microbiota and their ecological roles.
Characteristics:
- Resistant to drying and high salt concentration.
- Large numbers of gram-positive cocci: including Staphylococci and Micrococci.
- Microbiota density increases in moist areas; they metabolize sweat and produce body odor.
- Diphtheroids (e.g., Cutibacterium acnes): Inhabit hair follicles; anaerobic and produce acids that maintain low pH; Corynebacterium xerosis: Aerobic and occupy skin surface.
- Yeast (Malassezia furfur): Associated with dandruff.
Microbial Diseases of the Skin
Different types of skin lesions:
- Vesicles: Small fluid-filled lesions.
- Bullae: Vesicles larger than 1 cm in diameter.
- Macules: Flat, reddened lesions.
- Papules: Raised lesions.
- Pustules: Raised lesions with pus.
- Exanthem: Rash arising from a disease.
- Enanthem: Rash on mucous membranes arising from a disease.
Staphylococcal Skin Infections
Characteristics:
- Spherical gram-positive bacteria that form clusters.
- Coagulase-positive/negative: Differentiate via the enzyme coagulase, which clots blood and aids in identification.
- Staphylococcus epidermidis: Most common skin microbiota, healthcare-associated pathogen, forms biofilm on catheters.
- Staphylococcus aureus: Carried in nasal passages, responsible for various diseases, avoids host defenses, and can produce toxic proteins.Infections:
- Folliculitis: Infections of hair follicles.
- Impetigo: Crusting sores spread by autoinoculation.
- Scalded Skin Syndrome: Causes exfoliation via Toxin B.
- Toxic Shock Syndrome (TSS): Results from TSST-1, leading to severe systemic effects.
Streptococcal Skin Infections
Characteristics: Gram-positive cocci in chains; beta-hemolytic group A streptococci known as Streptococcus pyogenes.
Virulence factors include streptolysins and hyaluronidase.
Erysipelas: Infection of the dermal layer, can lead to sepsis.
Necrotizing fasciitis: Aggressive “flesh-eating” disease associated with streptococci toxins.
Infections by Pseudomonads
Pseudomonas aeruginosa: Gram-negative, causes opportunistic infections, resistant to many antibiotics, produces blue-green pus.
Conditions: Pseudomonas dermatitis from swimming pools and otitis externa.
Viral Diseases of the Skin
Warts: Small growths caused by papillomavirus.
Smallpox: Caused by orthopoxvirus, completely eradicated.
Chickenpox and Shingles: Virus remains latent and can reactivate.
Herpes Simplex: Spread via contact, latent infections trigger recurrent outbreaks.
Fungal Diseases of the Skin and Nails
Cutaneous Mycoses: Metabolize keratin in skin and nails, treated with topical drugs.
Subcutaneous Mycoses: More serious infections, usually soil-borne.
Candidiasis: Overgrowth of Candida, often occurs when normal microbiota are disrupted.
Microbial Diseases of the Eye
Conjunctivitis: Inflammation of conjunctiva; causes include Haemophilus influenzae.
Ophthalmia Neonatorum: Caused by Neisseria gonorrhoeae, can lead to blindness.
Trachoma: Leading cause of blindness caused by Chlamydia trachomatis.
Conclusion
Neglected Tropical Diseases: WHO goals for prevention and management strategies including enhanced sanitation and vector control.