Mechanisms of microbial attachment, invasion, persistence, and toxin-mediated damage
Microbial Mechanisms of Attachment
Microorganisms employ distinct surface molecules and structures to adhere to host cells, initiating infection.| Organism | Attachment method | Clinical relevance |
|---|---|---|
| Influenza virus | Haemagglutinin binds to sialic acid on respiratory epithelium | Initiates viral entry into airway epithelial cells, leading to influenza |
| Giardia lamblia | Sucking disc attaches to intestinal mucosa | Enables colonisation of the duodenum and malabsorption syndromes |
| Plasmodium falciparum | Induces expression of PfEMP1 on infected RBCs | PfEMP1 binds endothelial receptors, causing sequestration and cerebral malaria |
| HIV | gp120 binds strongly to CD4 antigen on T-helper cells | Allows viral entry and destruction of CD4+ lymphocytes, impairing immunity |
| Neisseria gonorrhoeae | Fimbriae/pili bind to mucosal surfaces | Promotes colonisation of the genital tract and immune evasion |
Mechanisms of invasion and immune evasion
To persist in the host, pathogens must evade innate and adaptive defences using highly evolved molecular tools.
| Organism | Invasion or evasion strategy | Clinical relevance |
|---|---|---|
| Neisseria meningitidis | Secretes IgA protease | Disrupts mucosal immunity, facilitating entry across nasopharyngeal epithelium |
| Staphylococcus aureus | Expresses protein A that binds Fc region of IgG | Inhibits opsonisation and complement activation |
| Streptococcus pneumoniae | Possesses polysaccharide capsule | Prevents phagocytosis by neutrophils, enhancing survival in the bloodstream |
| Vibrio cholerae | Flagellated and highly motile | Penetrates intestinal mucus barrier, aiding colonisation and toxin delivery |
| Mycobacterium tuberculosis | Inhibits phagosome–lysosome fusion in macrophages | Enables long-term intracellular persistence |
Mechanisms of host damage via toxins
Some pathogens produce potent exotoxins that disrupt host cell function, leading to major clinical syndromes:
| Organism | Toxin | Mechanism of damage | Clinical effect |
|---|---|---|---|
| Vibrio cholerae | Cholera toxin | Activates adenylate cyclase in enterocytes → ↑cAMP → ion & water loss | Profuse watery diarrhoea |
| Clostridium tetani | Tetanospasmin | Blocks inhibitory neurotransmitter release (GABA, glycine) | Muscle rigidity, spasms (tetanus) |
| Corynebacterium diphtheriae | Diphtheria toxin | Inhibits EF-2 → halts protein synthesis | Cell death, pseudomembrane formation in pharynx |
| Escherichia coli (ETEC) | Heat-labile and heat-stable enterotoxins | Stimulate secretion via cAMP/cGMP pathways | Traveller’s diarrhoea |
| Bacillus anthracis | Lethal factor | Cleaves MAPK pathway kinases | Cell death, systemic inflammation (anthrax) |