Bacterial Pathogenesis Flashcards
1
Q
Salmonella
A
1) M cell invasion
- SPI1 host cell ruffling and engulfment
- tight junctions disrupted
- macrophage apoptosis (gut limited) OR remain in macrophage - SPI2 (systemic infection)
2) epithelial cell invasion (apical side)
- SpI1 membrane ruffling and engulfment
- replicate in vacuoles
3) dendritic cells extend pseudopods to lumen to capture bacteria
2
Q
Cholera
A
- attach intestinal microvilli via TCP (pili)
- CTX binds host receptor and taken up
- increase cAMP
- increase CL-, Na+, HCO3- secretion into gut, H20 follows
3
Q
H pylori
A
- swim beneath mucus layer and attach gastric epithelial cells
- urease makes ammonia -> neutralizes stomach acid and is toxic to epithelial cells
- VacA and CagA inject into host -> VacA kills cells and disrupts tight jxn, CagA triggers inflammation
- choric inflammation + ammonia toxicity +VacA = stomach mucosa damage -> ulcers
4
Q
NTHi
A
- colonization: OMPs and pili bind nasopharynx, IgA protease degrades IgA
- invades LRT due to impaired defenses
- secreted LOS inhibits cilia mvmt, damages lung cells and induces pro-inflammatory response
- influx neutrophils to lung -> lung damage
5
Q
Hib
A
- bind epithelial cells via OMPs and pili
- invades sub epithelial tissue (paracellular route) and blood vessels
6
Q
Legionella pneumophilia
A
- host defenses impaired, Lp invades LRT and is phagocytksed by alveolar macrophages
- DOt/Icm injects effector molecules into cytosol (blocks fusion with lysosome, phagosome surrounded by RER forming replicative vacuole)
- replicates, ruptures -> bacteria escape
- inflammation, RBCs into lung -> lung damage
7
Q
Bodetella pertussis
A
- pili and hemagglutinin bind epithelial cell cilia
- pertussis toxin enter cell, increase cAMP and bacterial produced adenylate cyclase increase cAMP
- tracheal cytotoxin causes ciliostasis and kills ciliated cells (loss ciliary blanket)
8
Q
Mycoplasma pneumoniae
A
- attachment proteins bind ciliated epithelium (bronchi and bronchioles)
- secretes hydrogen peroxide -> ciliostasis
- CARDS toxin kills cells, slough off
- inflammation, WBCs infiltrate bronchial tissue
9
Q
Psuedomonas aeruginosa
A
- CFTR gene mutation: disrupted Cl- transport -> thick, sticky mucus (impaired ciliary clearance)
- hypoxic cond trigger alginate production/switch to mucoid -> chronic infection
10
Q
Clostridium tetani
A
- tetanospasm binds peripheral nerve receptors
- transported along axons to CNS
- block release of inhibitory NT -> uncontrolled activation motor neurons -> mm spasms
11
Q
Bacteroides fragilis
A
- intestinal spillage (phagocytes rapidly mobilized)
- B.fragilis capsule resist phagocytosis, O2 tolerant anaerobes survive at first (peritoneal cavity well oxygenated)
- strict anaerobes dominate when O2 gone
12
Q
Corynebacterium diphtheria
A
- C.dip binds URT epithelial cells
- DT blocks protein synthesis causing cell death, necrosis and inflammation -> pseudomembrane of small local plaque or extensive cover of tracheobronchial tree
- DT enter bloodstream, systemic effects on multiple cells primarily myocardial cells
13
Q
Listeria monocytogenes
A
- internalins promote binding and engulfment of bacteria by enterocytes
- LLO lyses vacuole
- bacterium replicates in host cell cytosol
- spreads to adj cells (ActA polymerizes host cell actin to propel bacteria to adj cell, membrane pinches off forming double membrane vacuole)
- LLO lyses vacuole
14
Q
Bacillus antrhacis
A
- spired deposited in alveoli spaces -> phagocytksed
- germinate in amcrophages
- vegetative cells released, multiply in lymph nodes (produce ER increasing cAMP -> edema and produce LF which causes secretion of TNFalpha and IL-1beta by macrophages)
- lymph nodes inflamed blocks pulmonary lymph drainage -> pulmonary edema
- bacteria enter blood, systemic spread -> sepsis
15
Q
Treponema pallidum
A
- 1˚
- enter mucous membrane
- enters sub epithelial tissue leading to extracellular replication, inflammation of blood vessels caution obstruction of blood flow -> necrosis and chancre
- spreads to lymph nodes systemically in hrs
- 2˚
- bacteria replicate in skin and goes latent (up to decades)
- 3˚
- host response to t.pallidum Ag
- develop gammas -> late benign syphilis
- neurosyphilis
cardiosyphilis
16
Q
Borrelia burgdorferi
A
- stage 1
- injected into skin during tick feeding
- replicates at site
- spreads in skin via BBA70
- enters bloodstream, disseminates systemically -> OspC helps evade phagocytosis
- stage 2
- host reponds to borrelia Ag
- mediated by IL-1beta and TNF alpha
- stage 3
- inflammation targets joints primarily
17
Q
Neisseria meningitidis
A
- binds nasopharynx via pili, replicate
- endocytose -> vacuoles traffic to basolateral side of cell
- bacteria released into submucosa
- Opc mediates invasion of vascular endothelium
- enter bloodstream, replicate, capsule resists phagocytosis and LOS resists complement deposition
- bacteria invade CNS, replicate -> Opc mediates invasion of brain endothelium
18
Q
Neisseria gonorrhea
A
- bind epithelial cells via pili and Opa proteins, replicate
- endocytosed -> vacuoles traffic to basolateral side of cell
- released into submucosa, replicate
- LOS, PTG etc trigger intense inflammation -> tissue damage
- pili and Opa proteins resist phagocytosis, LOS resist complement deposition
- catalase help survive oxidative bursts
19
Q
Chlamydia trachomatis
A
- elementary body binds genital epithelium
- Tarp injected into host cell, actin rearrangement, engulfment
- EB transforms to reticulate body
- RB forms inclusion (replicative vacuole) -> mem assoc IncA inhibits lysosomal fusion
- RB replicates, reorganizes and condense to for EBs
released by exocytosis - infected cells pro-inflammatory, influx WBCs leading to tissue damage, necrosis and scarring
20
Q
Rickettsia ricketsii
A
- injected from tick bite
- rOmpA binds vascular endothelial cells of local capillaries -> uptake into phagosome
- phospholipase lyses phagosome -> replicates, polymerizes actin and spread to adj cells
- lyses cells, damage blood vessels -> RBC and fluid leakage
- systemic spread via bloodstream
- massive endothelial injury: edema, hypotension, inadequate organ perfusion, dysfunction of affected organs
21
Q
Yersinia pestis
A
- injected into skin by flea bite
- invade lymphatic system and spread to lymph nodes
- replicates in lymph nodes -> inflammation and necrosis of LN, buboes
- enter bloodstream -> bacteremia -> sepsis
- F1 capsule, Yops help evade phagocytosis and killing
