Lecture 14 - Eye Infections

Lecture 14 - Eye infections The Skin as a Barrier to Infection ●​ Hostile environment for microbes: Skin is dry, high in salt (due to sweat), and contains antimicrobial substances like lysozyme. ●​ Normal flora: Mostly Gram-positive bacteria. ●​ Microbial presence: Washing reduces numbers but does not eliminate normal flora since they re-establish from hair follicles and glands. ●​ Moisture-rich areas: Support higher microbial populations. Normal Flora of the Skin ●​ Aerobic and anaerobic bacteria: ○​ Staphylococcus epidermidis (dominant) ○​ Other Micrococci sp. ○​ Corynebacterium sp. (aerobes) ○​ Propionibacterium sp. (anaerobes) ○​ Yeasts (Malassezia furfur) Mucous Membranes (“Internal Skin”) ●​ Line body cavities, acting as a protective barrier ●​ Shets of epithelial cells attach to the basement membrane ●​ Goblet cells secrete mucus for additional protection. ●​ Cilia on some cells help trap and move pathogens. ●​ Acidic pH limits microbial growth (e.g., alpha streptococci in the respiratory tract, Lactobacillus in the vaginal canal). Normal Flora of the Eye - Conjunctival surface: ●​ Micrococcus sp. (S. epidermidis), alpha-hemolytic streptococci, and Diphtheriods (Corynebacterium sp.) in small amounts. ●​ The interior of the eye is sterile. Eye Infections Protective Mechanisms ●​ Eyelids: Mechanical barrier. ●​ Tears: Contain lysozyme and IgA (chemical defense). ●​ Conjunctiva: Thin, moist epithelial layer susceptible to infections. Types of Eye Infections: 1.​ Viral Conjunctivitis - A thin layer of mucus lining the eyelids and covering the surface of the eye ○​ Red, watery eyes, highly contagious, less pus then bacteria conjunctivitis 2.​ Bacterial Conjunctivitis ○​ Thick, purulent discharge, more pus then viral conjunctivitis 3.​ Keratitis (Corneal Inflammation) ○​ Bacterial keratitis: Pus present. ○​ Viral keratitis: Less pus, often from HSV-1. 4.​ Blepharitis & Styes ○​ Caused by Staphylococcus aureus. ○​ Blepharitis = eyelid and lid margin inflammation and infection ○​ Stye = infected eyelid follicles and glands. 5.​ Acanthamoeba Keratitis → Parasitic - cytes live ib dirty in the air and sometime get into eye or contact lens ○​ Associated with contact lens use. 6.​ Trachoma (Chlamydia trachomatis A-C) (A-C are eye infections) - caused by flies in the eye ○​ Chronic conjunctivitis leading to blindness. ○​ Causes eye lashes to turn inside out ○​ Gentical types - D-K, LGV 7.​ Inclusion Conjunctivitis ○​ C. trachomatis D-K infection in the eye from genital infections. 8.​ Ophthalmia Neonatorum ○​ Caused by Neisseria gonorrhoeae. ○​ Prevented with antibiotic eye drops in newborns. Skin Infections Common Pathogens 1.​ Staphylococcus species (Gram-positive cocci in clusters) - Non-motile, non-spore forming, and capsules ○​ S. aureus (pathogenic, coagulase-positive, yellow colonies on BAP) ○​ S. epidermidis (opportunistic) ○​ S. saprophyticus (urinary tract infections in young women) 2.​ Virulence Factors of S. aureus - converts fibrinogen (sol) to fibrin (insol): “coagulase positive staphylococci” ○​ Produces Coagulase (converts fibrinogen to fibrin) ○​ BAP- yellowish colonies - staphylococci ○​ Adhesion molecules ○​ Toxins: Exotoxins, superantigens (e.g., TSST-1), DNase, leucocidins (membran damaging toxin) ○​ Protein A (binds Fc region of antibodies) MSSA (methicillin susceptible S. aureus) MRSA (methicillin-resistant S. aureus) Skin Diseases ●​ Impetigo: Epidermal infection (caused by Staphylococcus & Streptococcus) ○​ Treatment: removal of crusts, washing of lesions and application of topical antibiotics - oral antibiotics only if infection spreads ●​ Toxic Shock Syndrome (TSST-1): Multi-system effects due to superantigens ○​ Caused by S. aureus, but can also be caused by GAS (group A streptococcus = S. pyogenes) ○​ Treatment: IV antibiotic (usually semisynthetic penicillin like oxacillin) ●​ Scalded Skin Syndrome: Neonatal (2nd degree toxic shock) exfoliative toxin production. ○​ Caused by S. aureus ○​ Begins as skin lesions, causes loss of epidermal cells ○​ Treatment: IV antibiotics ●​ Erysipelas ○​ Infection of the dermal layer of skin ○​ Can progress to septicemia and fatal outcome ○​ Can begin as a pharyngitis ○​ Treatment: Antibiotics ●​ Necrotizing Fasciitis (Flesh-eating disease): Rapidly progressing tissue destruction by S. pyogenes or GAS ○​ Gram-positive cocci in chains, and growth of beta-hemolytic streptococci ○​ Exotoxin: SpeA toxin detected in bacterial isolate. (superAg) ○​ Diagnosis: Disproportionate pain to injury - distroys fascia, 40% MORALITY Streptococcus sp. ●​ Facultative Gram positive cocci in chains ●​ Divided into three groups based on their hemolytic reactions on blood agar: ○​ Alpha hemolytic - a partial or "green" hemolysis characterized by a greenish discoloration around bacterial colonies ○​ Beta hemolytic - Involves complete lysis of RBCs, resulting in a clear zone around the colonies. ○​ gamma hemolytic - No hemolysis occurs, and there is no change in the appearance of the agar around the colonies Group A Streptococcus (S. pyogenes) -GAS ●​ Beta-hemolytic, highly pathogenic ●​ Transmiossion: Direct contact ●​ Virulence factors: ○​ M protein: Immune evasion. ○​ Streptokinase: Dissolves blood clots. ○​ Hyaluronidase: Breaks down connective tissue. ○​ Erythrogenic toxin: Causes Scarlet Fever rash. ●​ Diseases: ○​ Erysipelas: Infection of the dermis. ○​ Cellulitis & Impetigo: Deeper infections. ○​ Necrotizing Fasciitis: Tissue liquefaction, 40%+ mortality rate. Post-infectious disease (S. pyogenes) - acute glomerulonephritis, rheumatic fever​ Group B Streptococcus agalactiae Alpha, gamma and variable hemolysis: Group C: Several strains, clinical significance? Group D: (enterococci also known as S. faecalis) Group G: several strains, clinical significance? Streptococcal toxins and enzymes ●​ ●​ ●​ ●​ ●​ ●​ Streptokinase (dissolves blood clots - fibrin) Hyaluronidase (breaks down connective tissue) Deoxyribonucleases (degrade DNA) Proteases (e.g. IgA protease) Erythrogenic toxin (rash of Scarlet Fever) (superantigen) Spe toxins (superantigens sometimes present in NF strains are exotoxins that cause massive tissue damage and inflammation, like Flesh Eating Disease) Viral Skin Diseases 1.​ Warts (Human Papillomavirus - HPV) ○​ Benign skin growths. 2.​ Herpes Simplex Virus (HSV) ○​ HSV-1: Cold sores, latent in trigeminal nerve. i.​ Very common, > 90% infected, most in childhood ii.​ transmitted by oral route or direct contact iii.​ causes “cold sores” iv.​ Remains latent in nerve endings (trigeminal nerve ganglia) and flare up with stress ○​ HSV-2: Genital herpes. ○​ Herpes Gladiatorum: Common in wrestlers. ○​ Herpes Whitlow: Infects fingers of healthcare workers. Measles (Rubeola)- enveloped paramyxovirus (RNA) ●​ Highly contagious (airborne transmission). ●​ Symptoms: ○​ Fever, malaise, conjunctivitis, photophobia, Koplik’s spots (diagnostic). ○​ Maculopapular rash starting at ears → spreads. ●​ Complications: ○​ Secondary bacterial infections caused by Staphylococcus aureus (pneumonia, ear infections). ○​ Subacute Sclerosing Panencephalitis (SSPE): A Fatal neurological complication years later. ●​ Immunosuppression Effects: ○​ Dendritic cells and monocytes are infected, and antigen presenting activity is compromised ○​ Decreased T cells. ○​ Skewed immune response towards Th2 (antibody-mediated immunity) ○​ Reduced macrophage activity ●​ Prevention: Vaccination cha ○​ Live attenuated MMRV vaccine (Measles, Mumps, Rubella, Varicella). ○​ 95% efficacy after one dose; booster at 4-6 years. Key Review Questions 1.​ Which enzyme dissolves blood clots? ○​ Answer: Streptokinase. 2.​ How is Necrotizing Fasciitis transmitted? ○​ Answer: Direct contact. 3.​ What is the diagnostic sign of measles before rash onset? ○​ Answer: Koplik’s spots.