Microbial Mechanisms of Pathogenicity: Study Notes

Microbial Mechanisms of Pathogenicity

Introduction to Pathogenicity

Pathogenicity refers to the ability of a microorganism to cause disease in a host organism. Understanding the mechanisms by which microbes cause disease is fundamental in microbiology.

• Pathogenicity: The capacity of a microbe to cause disease.

• Opportunistic Pathogen: Microorganisms that cause disease only when the host's defenses are compromised.

• Virulence: The degree of pathogenicity; often measured by the severity of disease produced.

• ID50: The infectious dose required to infect 50% of a test population.

• LD50: The lethal dose required to kill 50% of a test population.

Example: Streptococcus pneumoniae is more virulent than Streptococcus mitis due to its capsule and ability to evade host defenses.

Portals of Entry

Microorganisms must enter the host through specific portals to initiate infection. The portal of entry can influence the outcome of infection.

• Common Portals of Entry:

  • Skin

  • Mucous membranes (respiratory, gastrointestinal, genitourinary tracts)

  • Parenteral route (injections, cuts, bites)

• Preferred Portal of Entry: Some pathogens are more effective when entering through a specific portal (e.g., Salmonella via ingestion).

• Special Cases: Skin is a strong barrier, but some pathogens can enter through hair follicles or sweat glands.

Mechanisms of Pathogenesis

Pathogenesis involves a series of steps that allow microbes to establish infection and cause disease.

• Adherence: The process by which microbes attach to host tissues, often via adhesins on their surface.

• Establishing Infection: Microbes must overcome host defenses to colonize and multiply.

Adherence Mechanisms

Adherence is the first step in infection, allowing pathogens to attach to host cells.

• Adhesins: Surface molecules on pathogens that bind to specific receptors on host cells.

• Biofilms: Communities of microorganisms attached to a surface, encased in a protective matrix. Biofilms increase resistance to antibiotics and host defenses.

• Importance of Biofilms: Biofilms are significant in chronic infections and medical device contamination.

Penetration of Host Defenses

Pathogens employ various strategies to evade or penetrate host immune defenses.

• Capsules: Polysaccharide layers that inhibit phagocytosis by host immune cells.

• Enzymes: Pathogens produce enzymes that aid in invasion and evasion.

Enzyme	Activity	Role in Pathogenicity
Coagulase	Clots fibrin in blood	Protects bacteria from phagocytosis
Kinase	Digests fibrin clots	Allows spread of bacteria
Hyaluronidase	Hydrolyzes hyaluronic acid	Facilitates tissue penetration
Collagenase	Breaks down collagen	Enables deeper invasion into tissues

• Antigenic Variation: Pathogens alter their surface antigens to evade immune detection.

How Bacterial Pathogens Damage Host Cells

Bacterial pathogens can damage host cells through direct mechanisms or by producing toxins.

• Siderophores: Molecules that bind and sequester iron from the host, essential for bacterial growth.

• Toxins: Poisonous substances produced by microbes that contribute to disease.

Toxin Type	Characteristics	Examples
Exotoxins	Proteins secreted by bacteria; highly toxic; specific effects	Diphtheria toxin, botulinum toxin
Endotoxins	Lipopolysaccharide (LPS) component of Gram-negative bacteria; released upon cell death	Salmonella endotoxin

• Exotoxins:

  • Deadly due to specific action on host cells

  • Measured by LD50

  • Types: cytotoxins, neurotoxins, enterotoxins

  • Superantigens: Cause excessive immune response

• Endotoxins:

  • Cause fever, inflammation, and shock

  • Less specific than exotoxins

Antitoxins: Antibodies that neutralize toxins. Used in treatment of toxin-mediated diseases.

Comparison of Exotoxins and Endotoxins:

Feature	Exotoxin	Endotoxin
Chemical Nature	Protein	Lipid A of LPS
Source	Gram-positive and Gram-negative bacteria	Gram-negative bacteria only
Effect on Host	Specific (e.g., neurotoxicity)	General (fever, shock)
Heat Stability	Unstable	Stable

Viruses: Entry and Immune Evasion

Viruses must enter host cells and evade immune responses to replicate and cause disease.

• Entry: Viruses attach to specific receptors and enter cells via endocytosis or membrane fusion.

• Immune Evasion: Viruses can inhibit antigen presentation, mutate surface proteins, or produce proteins that interfere with immune signaling.

• Cytopathic Effects (CPE): Observable changes in host cells due to viral infection, such as cell lysis, syncytia formation, or inclusion bodies.

• Examples of CPE: Herpesvirus causes inclusion bodies; HIV causes syncytia formation.

Portals of Exit

Microorganisms leave the host through specific portals, facilitating transmission to new hosts.

• Common Portals of Exit:

  • Respiratory tract (coughing, sneezing)

  • Gastrointestinal tract (feces, saliva)

  • Genitourinary tract (urine, vaginal secretions)

  • Skin and wounds

  • Blood (insect bites, needles)

• Examples: Influenza virus exits via respiratory droplets; hepatitis B virus via blood.

Additional info: Academic context and examples have been added to expand upon the brief outline provided in the original notes.