Bacterial Adhesion Mechanisms and Virulence Factors

Bacterial Adhesion Mechanisms

• Bacteria use various mechanisms to adhere to host cells.
• Pili: Class IV pili are found at the poles of bacilli and exhibit 'twitching' motility. They enable bacteria to move along solid surfaces by retracting and extending, allowing for 'slingshot' motion.
• Adhesins: These are surface proteins or glycoproteins present on bacterial cell walls. Adhesins bind to specific receptor molecules on host cell surfaces, allowing the bacteria to adhere closely and resist physical removal.
• Capsules: Some bacteria produce capsules which aid in adhesion and immune evasion by preventing phagocytosis. Their composition prevents antibody adhesion and their size deters phagocytosis.

Virulence Factors

• Fimbriae: Some Streptococcus species have fimbriae containing M protein, which alters the bacterial surface inhibiting phagocytosis.
• Mycolic acid: This waxy substance is produced in the cell wall of Mycobacterium tuberculosis. It serves as a protective coat that deters killing mechanisms when the bacterium is phagocytosed.
• Exoenzymes: Secreted by bacteria to invade deeper tissues and support their growth by breaking down host structures.
• Toxins: Biological poisons produced by certain pathogens that damage tissues.
  • Endotoxins: Derived from gram-negative bacteria and trigger systemic inflammatory responses. They are heat-stable and require high temperatures for inactivation. High concentrations can lead to severe consequences like blood pressure drops, multi-organ failure, and death.
  • Exotoxins: Potent protein molecules produced primarily by gram-positive bacteria. They exhibit specific action and target specific cells, damaging them through various molecular mechanisms. They are heat-sensitive and even low concentrations can be lethal.

Terminology

• Bacteraemia: Presence of bacteria in the bloodstream.
• Pyaemia: Presence of pus-forming bacteria in the bloodstream.
• Toxaemia: Presence of toxins in the bloodstream.
• Septicaemia: Multiplying bacteria in the bloodstream.

Virulence Factors Promoting Infection

• Coagulase: Produced by Staphylococcus aureus, this exoenzyme triggers fibrinogen-to-fibrin conversion, enabling the bacteria to be coated by fibrin clots and prevent phagocytosis.
• Kinases: These enzymes digest fibrin clots, allowing the pathogen to escape and spread from the clot.
• Antigenic Variation: Surface proteins are altered to evade recognition by the host's immune response, a mechanism employed by pathogens like influenza and COVID-19.
• Leukocidins: Destroy phagocytic cells, hindering the immune system's defense.
• Intracellular Position: Some pathogens reside inside host cells, making them inaccessible to immune defenses.
• Escape Methods: Intracellular pathogens employ strategies to avoid killing mechanisms within phagocytes.

Viral Virulence

• Adhesins: Found on viral capsids or membrane envelopes, these proteins mediate viral attachment to host cells by interacting with specific cell receptors (tropism). Examples include the spike protein hemagglutinin on influenza virus and glycoprotein g20 found on HIV.
• Antigenic Variation: Found in some enveloped viruses, it involves changes in surface proteins.
  • Antigenic Drift: Point mutations cause minor changes in spike proteins, leading to gradual immune evasion.
  • Antigenic Shift: Gene reassortment results in major changes in spike proteins, leading to significant immune evasion.

Virulence Factors in Oral Health

• Porphyromonas Gingivalis: This bacterium produces fimbriae that modify and stimulate immune responses, influencing cytokine production and inhibition in the periodontium. It also produces gingipains (proteases) that break down periodontal structural proteins like collagen, elastin, and fibronectin.
• Streptococcus Mutans: Key factors contributing to tooth decay include adhesion, acidogenicity, and acid tolerance. These factors work together to alter the dental plaque ecology, increasing acidity and enamel susceptibility to demineralization.
• Herpes Simplex Virus: This virus hides in neurons and non-neuronal cells, persisting for years. It becomes pathogenic when immune resistance is low, manifesting as herpes labialis.
• Candida Albicans: The main cause of opportunistic human fungal infections, it employs several virulence factors:
  • Exoenzymes: Secretes aspartyl proteases known as 'Sap proteins.'
  • Adhesins: Promotes adherence.
  • Pleomorphism: Adapts to changing environmental conditions and biological niches.

Adhesins in Candida albicans

• Candida albicans utilizes several adhesins, including ALS proteins, to attach to host cells.

Conclusion

• Pathogens continuously evolve to increase their virulence and evade immune responses.
• The dynamic interaction between pathogens and host cells involves the production of new virulence factors by pathogens and the host’s immune response.
• The emergence of new pathogens is driven by their ability to exploit the host without causing immediate death.

Explore the various mechanisms bacteria use to adhere to host cells and the virulence factors that enable their survival. This quiz covers pili, adhesins, capsules, fimbriae, and mycolic acid, highlighting their roles in bacterial pathogenesis. Test your knowledge on these critical aspects of microbiology!