Learning Objective
By the end of this section, students should be able to describe the major mechanisms by which pathogens establish infection, evade host defenses, acquire nutrients, and cause damage, including both extracellular and intracellular strategies.
Pathogenicity: Major Mechanisms
Colonization
- Colonization is necessary for infection unless the organism is directly implanted via trauma.
- Adherence to host cells:
| Mechanism | Organisms / Notes |
|---|---|
| Pili / Fimbriae | Most Gram-negative bacteria; primary adherence factor. |
| Teichoic acids | Most Gram-positive bacteria. |
| Adhesins | Colonizing factors like pertussis toxin, hemagglutinins |
Partial adherence/biofilms: Staphylococcus epidermidis, Streptococcus mutans, Pseudomonas aeruginosa
Mnemonic – “Some Killers Have Pretty Nice Capsules”
- S. pneumoniae
- K. pneumoniae
- H. influenzae
- P. aeruginosa
- N. meningitidis
- C. neoformans
Avoiding Immediate Destruction by Host Defense
- Anti-phagocytic surface components: prevent uptake by phagocytes: Capsules/slime layers:
- S. pyogenes: M protein
- N. gonorrhoeae: pili
- S. aureus: Protein A
- IgA proteases: degrade mucosal IgA
- Neisseria, Haemophilus, S. pneumoniae
Acquiring Nutrients
- Siderophores: molecules that chelate iron and import it into the bacteria
Antigenic Variation
- Changing surface antigens to escape immune detection: Examples:
- N. gonorrhoeae: pili & outer membrane proteins
- Trypanosoma brucei: phase variation
- Enterobacteriaceae: capsular and flagellar antigens
- HIV, Influenza: antigenic drift
Intracellular Pathogens
| Strategy | Examples / Notes |
|---|---|
| Evade phagocytic killing | M. tuberculosis: inhibits phagosome-lysosome fusion |
| Escape phagosome | Listeria: moves into the cytoplasm before fusion |
| Invasins | Yersinia pseudotuberculosis: binds & invades non-phagocytic cells |
| Damage via replication | Viruses: kill, transform, or remain latent in host cells |
Type III Secretion System
- Acts as a tunnel delivering bacterial toxins directly into host cells
- Found in: E. coli, Salmonella, Yersinia, Pseudomonas, Chlamydia
Inflammation / Immune-Mediated Damage
- Mechanisms:
- Cross-reactive antibodies → e.g., Rheumatic fever
- Delayed hypersensitivity & granulomatous response → e.g., TB, leprosy, Chlamydia PID
- Immune complexes → e.g., post-streptococcal glomerulonephritis
- Structural toxins: peptidoglycan-teichoic acid fragments (chemotactic for neutrophils)
Physical Damage
- Swelling in fixed spaces → e.g., meningitis, cysticercosis
- Large organism size → e.g., Ascaris lumbricoides blocking the bile duct
Teaching Tools / Memory Aids
- Mnemonic for Capsules & Biofilm Pathogens:
“Some Killers Have Pretty Nice Capsules” → S. pneumoniae, K. pneumoniae, H. influenzae, P. aeruginosa, N. meningitidis, C. neoformans - Mnemonic for Anti-Phagocytic Proteins:
- M protein → S. pyogenes
- Protein A → S. aureus
- Pili → N. gonorrhoeae
- Flow for Intracellular Pathogens:
- Entry → Evade phagosome → Replicate → Cause damage / latent infection
