LESSON-7-HOST-DEFENSE-AND-PHATOGENICITY
Pathogenesis II: Host Defense and Pathogenicity of the Microbes in Microbiology
Overview
Study of host defense mechanisms against infectious diseases.
Examination of microbial pathogenicity.
Outline of Host Defense Against Infectious Disease
Define Normal Flora
Distribution of Normal Flora
Protective function and clinical significance of Normal Flora
Stages of Bacterial Pathogenesis
Mode of Transmission
Routes of Transmission
Mechanisms of Host Defense
Innate Immunity
Physical Barriers
Skin: Keratin layer, fatty acids from sebaceous glands, low pH, support from normal flora.
Mucous Membranes: Lines respiratory and gastrointestinal tracts.
Phagocytic Cells: Including macrophages and polymorphonuclear leukocytes (PMN).
Soluble Molecules
Complement: Set of proteins aiding in immune response.
Lysozyme: Enzyme that breaks down bacterial cell walls.
Antibodies: Produced by B cells.
T Lymphocytes: Key players in adaptive immunity.
Physical Barriers
Skin: Important for preventing pathogen entry.
Respiratory Tract: Mucus lining, IgA presence, ciliary action, and alveolar macrophages to trap pathogens.
Gastrointestinal Tract: Acidic stomach pH and digestive enzymes protect against ingested pathogens.
Vagina: Maintains low pH through Lactobacilli bacteria.
Factors Contributing to Bacterial Infection
Impact of Barrier Damage
Intravenous Catheter: May lead to skin infections like Staphylococcus epidermidis and S. aureus.
Diabetes: Higher risk for skin infections by S. aureus.
Burns: Vulnerability to infections from Pseudomonas aeruginosa.
Dental Extraction: Can lead to infections from Streptococcus viridans due to disruptions in mucosal integrity.
Host Defense Mechanisms
Inflammation
Phagocytosis as a response to infection.
Inflammatory Response Types
Pyogenic Response: Leads to pus formation; involves acute, extracellular pathogens and activated by complements and antibodies.
Granulomatous Response: Formation of granulomas; involves chronic responses with macrophages and helper T cells against intracellular pathogens.
Complement Activation Pathways
Classical, Alternative, and Lectin Pathways: Various mechanisms for complement activation that enhances immune response.
Involvement of C3 and C5 convertases in amplification and facilitation of pathogen opsonization and lysis.
Inflammatory Response Against Bacterial Infection
Responses differ for pyogenic versus intracellular bacteria.
Activation leads to mediator release (e.g., histamine) that increases vascular permeability, causing edema and erythema.
Phagocytosis Process
Steps in Phagocytosis
Migration: Mediated by IL-8 and C5a; adhesion mechanisms via selectins and integrins.
Ingestion: Phagosome formation, aided by opsonization (IgG, C3b).
Killing: Mechanisms deployed to destroy ingested pathogens.
Normal Flora and its Role in Host Defense
Definition
Normal Flora: Permanent residents of body sites (e.g., skin, colon).
Commensals
Organisms that benefit from the host without causing harm.
Significance of Normal Flora
Disease potential when immune system compromised or when organisms move to unusual sites.
Important for colonization resistance; limits pathogenic bacteria by occupying binding sites.
Metabolic Functions: Synthesis of vitamins like B12 and K.
Normal Flora Distribution by Body Sites
Skin: Includes species like Staphylococcus epidermidis, Propionibacterium acnes.
Respiratory Tract: Different flora in nose and throat (e.g., Staphylococcus aureus, Viridans streptococci).
Intestinal Tract: Presence of E. coli and various lactobacilli; yeasts like Candida albicans.
Genitourinary Tract: Includes Group B Streptococci and Candida albicans.
Stages of Bacterial Pathogenesis
Transmission: Entry through the portal.
Evasion: Overcoming host defenses.
Adherence: Attachment to host tissues.
Colonization: Establishing presence.
Disease: Resulting from toxin production or invasion.
Host Responses: Reactions from the immune system.
Progression or Resolution: Outcome of the infection.
Summary of Key Points
Host defense involves innate and acquired immunity mechanisms; macrophages and T-cells control intracellular pathogens.
Complement, antibodies, and inflammatory responses play pivotal roles in combating extracellular pathogens.
Disease types vary; some involve toxin production, while others are related to invasive mechanisms.
Normal flora function as both protective agents and potential pathogens under specific conditions.
References
Levinson, W. (2010). Review of Medical Microbiology and Immunology, 11th ed.
Brooks, G. F., Carroll, K. C., Butel, J. S., Morse, S. A., Mietzner, T. A. (2010). Medical Microbiology, 25th ed.