Disease Transmission and Zoonosis Quiz

Mechanisms of Bacterial Virulence

• Bacterial pathogens cause disease
• Pathogenicity is the ability to initiate disease
• Virulence is the severity of disease. Measures virulence using LD₅₀
• Transmissibility is the ability to spread from one host to another
• Survival is the ability to withstand host immunity and reproduce
• Infectivity is the ability to breach host defenses
• Virulence factors are essential proteins or molecules for pathogenicity

Virulence Factors

• Cytosolic factors involve metabolic, physiological, and morphological changes
• Membrane-associated factors aid adhesion to host tissues/cells and evade host immunity
• Secretory factors invade tissues and evade innate and adaptive immunity

Steps to Infection

• Transmission: Exposure to pathogens
• Adherence: Binding to skin/mucosa
• Invasion: Breaking through barriers
• Survival: Growth at original and distal sites, production of virulence factors
• Tissue Damage: Toxicity and disease

Transmission: Reservoirs

• Human: Person-to-person transmission, asymptomatic carriage (e.g., COVID, HIV)
• Animal: Animal-to-animal, with humans as incidental hosts (e.g., Brucellosis, Anthrax, Plague)
• Environmental: Plants, soil, and water (e.g., Cholera, Legionnaires disease)

Transmission: Mechanisms

• Direct Contact: Physical transfer between infected individuals (e.g., skin-to-skin, sexual)
• Indirect Contact: Contact with a contaminated object (fomites) (e.g., Cholera, Salmonellosis)
• Droplets: Transmission via airborne droplets produced by coughing, sneezing (e.g., Influenza, Pneumonia)
• Zoonoses: Transmission from animals to humans (e.g., Animal bites, food products, animal hide products, invertebrate vector-borne)

Portals of Entry and Exit

• Portals of entry include mucous membranes, skin damage, placenta/birth transmission, specialised entry, and vector transmission.
• Portals of exit include respiratory tract, gastrointestinal tract, genitourinary tract, skin, and blood.

Factors Affecting Pathogen Transmission

• Environmental conditions: temperature, pH, oxygen levels, salt levels, host immune responses, nutrient availability

How Pathogens Achieve Infection

• Cell Surface Components: Adhesion, entry and structural defence against immunity
• Active Combat: Invasive enzymes, nutrient acquisition, toxins
• General Strategies: Dealing with phagocytosis, communication, subverting apoptosis

Adhesion

• The process of organisms attaching to tissues or cells
• Necessary for successful colonization
• Adhesion factors:
  • Attachment proteins (pili, fimbriae, flagella)
  • Specialized surface structures (EPS, CPS)

Adhesion Structures

• Initial attachment often mediated by protein appendages:
  • Fimbriae/pili: Short fibers for sticking to host cells
  • Flagella: For movement

Surface Structure (EPS)

• Exopolysaccharides (EPS): Consist of monosaccharide polymers secreted by bacteria into their environments
• Function: Hydrophobic, displace water, promoting closer contact, protective shield (capsule), prevent phagocytosis

Biofilms

• Formed by bacteria after initial attachment to enhance survival
• Locations: Inside host tissues, on abiotic surfaces (dental plaque, intestines)
• Structure: Contain biological polymers (exocellular polysaccharides, DNA, proteins)
• Function: Barrier against harmful factors, antibiotics and immune factors cannot penetrate.

Active Combat: Invasive Enzymes

• Coagulase: Coagulates fibrinogen, facilitates bacterial entry
• Kinases: Digest fibrin clots, breakdown host clots
• Hyaluronidase: Digests intercellular hyaluronic acid, spreading bacteria through tissues
• Collagenase: Hydrolyses collagen tissue, allowing bacteria greater freedom
• IgA protease: Destroy IgA antibodies, combating the host's immune system.

Active Combat: Toxins

• Toxin: Substance contributing to pathogenicity
• Toxigenicity: Ability to produce toxin
• Toxemia: Presence of toxin in the host's blood
• Toxoid: Inactivated toxin used in a vaccine
• Antitoxin: Antibodies against a specific toxin
  • Examples are botulinum, shiga toxins, staphylococcal.
• Toxins vary in effect and potency and can be quite specific

Active Combat: LPS

• Gram-negative bacteria outer membrane component
• Triggers TLR4, causing inflammatory responses and fever
• Little innate toxicity itself

Active Combat: Exotoxins

• Specifically synthesized and released in response to host signals
• Types:
  • Single polypeptide toxins
  • Multiple polypeptide toxin complexes
  • Small "drug-like" molecules
  • Toxins directly "injected" by specialist secretion systems

Active Combat: Single Chain Toxins

• Example: S. aureus α-toxin creates pores in host cell membranes
• Many toxins disrupt phospholipid bilayers

Active Combat: Superantigens

• Directly target immune system
• Trigger non-specific T-cell activation, cytokine storm
• Bridge between class II MHC and TCR

Active Combat: Multiple Subunit Protein Toxins

• Multi-protein injection machines delivering toxic payloads across host cell membranes

Active Combat: Non-protein Small Drug-like Toxins

• Other toxins are evolved specifically to damage or manipulate the host
• Some examples include toxins, immune inhibitors, antibiotics, siderophores

Multi-enzyme "Factories"

• Secondary metabolite genes like NRPS act as factories to produce molecules
• Molecules include toxins, immune inhibitors, antibiotics, siderophores

Active Combat: Specialized Toxin Delivery Systems

• Secretion systems for toxin release into host cells
• Types:
  • Type I, Type II, Type III, Type IV, Type V, Type VI, Type VII
• Occur in both Gram-positive and Gram-negative bacteria