Mechanisms of Bacterial Pathogenesis Flashcards
Asymptomatic, inapparent, subclinical infection
-host defenses clear pathogen before any symptoms of disease are noted
Communicable infection
can be passed from host to host
Contagious infection
-high communicable
Noncommunicable infection
-comes from environment, not a previous host (botulism, Legionnaires Disease)
Latent infection
-disease subsides, but microorganisms remain in the body and restart disease later
Chronic carrier state
-host survives disease but continues to shed the pathogen indefinitely
Epidemic
-much more frequent infection than usual
Pandemic
worldwide distribution of infection
Parasitism
- pathogens are parasites in the sense that they harm the host by taking its resources to reproduce themselves
- all viruses and a few bacteria are obligate intracellular parasites, which must enter host cells to reproduce
- most bacteria are facultative intracellular parasites, meaning that they can reproduce outside host cells when they need to
- be careful of confusion with parasites, ie protozoa and helminthes
Nonpathogens
- very unlikely to cause disease
- most environmental bacteria and normal flora
- very low virulence: LD50 very high
- ID50 very high
Opportunistic pathogens
- are very unlikely to cause disease in a healthy person, but will take advantage of a host that is injured or immunosuppressed (pseudomonas, enterobacter, klebsiella)
- low virulence: LD50 is high
- ID 50 low- easy to colonize
Highly pathogenic organisms
- likely to cause disease on colonization of even a previously-healthy host
- STDs
- Mid-High Virulence Mid-Low LD50
- Mid low ID50
Pathogenicity
- enhanced by virulence factors, which are gene products needed for causing full-blown disease
- genes for several of these may be encoded together in pathogenicity islands
Functiions: survival in extreme environments, adhesion to host surfaces, take over host cells, and poison the host, immune evasion
Survive extreme environments
- pH tolerance
- siderophores- bind iron strongly
- resistance to drying
- resistance to detergents
Adhesion to host surfaces
- pili/fimbrae especially in movement
- slime layer
- adhesions
Immune Evasion
- capsules for resisting phagocytosis
- IgA proteases
- induces of macrophage apoptosis
- antigenic variation- different antigen for part of the infection, and then switch the antigen keeps the host taxed
- serum resistance factors for escaping complement
Host Cell Takeover
- Endosome Escape Routes- Legionella multiplies in phagosome and becomes motile and escapes, lyse the cell and spreads to another
- Actin Polymerization Pathways- cell to cell spread, Listeria
- type 3 and 4 secretion systems- type 3 inject proteins into cytooplasm were type 4 transport DNA and proteins
Poison the host
- exotoxins (secreted)
- endotoxins (cell wall components)- Gram(-)- LPS/LOS, Gram (+)- teichoic acids- symptoms are immunogenic so antibody is not protective and vaccination is not useful
- tissue degrading enzymes- section off itself a place where it isnt bothered by immune system or Oxygen
Stages of Pathogens
From previous human host:
1) Respiratory droplets
2) Fecal-oral
3) Direct contact
4) Sexual contact
5) Blood blood
6) Vertical- transplacental, vaginal delivery, breast milk
From animal reservoir: zoonosis (rabies)
Fomite (washcloth, countertop)
Vector (tick, mosquito)
Attachment of pathogen to host sufaces
- pili/fimbrae
- glycocalyx/ slime layer
- adhesins
- biofilm formation
- curli- recently-discovered, similar to pili
Invasion of host tissue
- collagenase/hyaluronidase: break down tissue so S pyogenes can penetrate
- coagulase: breaks down fibrinogen to form a fibrin clot around S. aureus
- IgA protease: cleaves IgA so N. meningitidis can adhere to mucus membranes
- leukocidins destroy macrophages
- capsule and M protein are protect against phagocytosis by macrophages
- S aureus protein A prevents complement acivation
Inflammatory response
- pyogenic: pus-forming, predominately neutrophils
- granulomatous: machrophages kill most of the bacteria but some survive inside macrophages within a granuloma
Survival inside host cells
- mycobacteria, legionella, brucella, listeria are facultative intracellular
- chlamydia and rickettsia are obligate intracellular
- invasins: virulence factors recognized by cell-surface integrins, docking leads to cell entry
- inhibit fusion of lysosome with phagosome/endosome, so bacteria continue to multiply rather than being degraded (legionella)
- allow lysosome fusion but inhibit endosome acidification (Legionella, Chlamydia)
- allows lysosome fusion and survive acidification (Q fever)
- escape from the endosome into the cytoplasm (Listeria)
- actin based motility
- inhibition of cytokine activation
Poisoning the host
- pseudomembrane formation: blocks airway in diphtheria, colon in pseudomembraneous colitis
- exotoxins
