Bacterial Pathogenesis and Immunology II Flashcards
1
Q
Multiplication
A
- Binary fission
- Location:
- -Extracellular
- -Intracellular - cytoplasm
- -Intracellular - within a vesicle
2
Q
Parasitophorous vacuole
A
Coxiella burnetti (causative agent of Q-fever in humans)
- Target cells: monocytes and macrophages (obligate intracellular)
- Lives and replicates in acidic environment of phagolysosomes
- Disseminates throughout the body via monocytes and macrophages
- Excreted in milk, urine, and feces, and found in placental and fetal tissues
- Acquired through inhalation, ingestion, or arthropod bites
3
Q
Cell to cell movement
A
Listeria monocytogenes
- Invades phagocytic and non-phagocytic cells
- Surface proteins (internalins) facilitate adherence to host cell membranes and subsequent uptake - Survives and replicates intracellularly
- Cytolytic toxin (listeroiolysin) destroys the membranes of phagocytic vacuoles, allowing escape into the cytoplasm - Transfers from cell-to-cell without exposure to humoral defense mechanisms
- Hijacks actin filaments of the host cell to induce formation of pseudopod-like projections - High level of multiplication leads to destruction of host cell and release of bacteria
- Spread via lymph and blood free of (extracellular) or within phagocytic cells (intracellular)
4
Q
Type III secretion systems
A
- Complex protein secretion system employed by many gram-negative pathogenic bacteria
- Transports bacterial effector proteins into eukaryotic host cytoplasm
- Effector proteins modulate (interfere with) the host cellular processes
5
Q
T3SS effectors
A
Pseudomonas aeruginosa
- One of the leading causes of hospital-acquired pneumonia in human hospitals
- Pneumonia can lead to bacteremia:
- -P. aeruginosa uses T3SS to inject the effector ExoS into pulmonary epithelial cells –> disruption of the pulmonary vascular barrier –> dissemination to the bloodstream
- High correlation between T3SS expression and patient death
- T3SS mutants display attenuated virulence
6
Q
Exotoxin
A
Pseudomonas aeruginosa
- Exotoxin A –> cytotoxic
- Works by suppressing protein expression in host cell
- -Invasion of tissues
- -Local tissue damage
- -Immune evasion (via killing macrophages)
7
Q
Flagella
A
- Confer motility
- Found on pathogens (not all flagella are pathogenic)
- Found on probiotic bacteria
Proteus mirabilis - swarming motility
- Observed in culture
- May aid in spread in vivo
- -Bladder infection –> kidney infection
8
Q
Damage
A
- Direct damage
- Immune-mediated damage
9
Q
Damage - direct
A
Toxins:
- Endotoxins: remains inside or on the surface of the bacteria; part of the bacterial structure
- -Example: LPS of gram-negative bacteria
- Exotoxins: secreted by the bacteria (into the space around it)
- -Example: Leukotoxin
10
Q
Damage - toxins
A
- E. coli heat-stable and heat-labile enterotoxins –> act upon intestinal enterocytes by disrupting the electrolyte homeostasis –> fluid loss –> secretory diarrhea
- Phospholipases - a group of ubiquitous and diverse enzymes that hydrolyze phospholipids
- Clostridium perfringens - phospholipase C
- -Acts on cell membranes and vesicle membranes
- -Hemolytic activity
- -Phospholipase C is also the way Pseudomonas aeruginosa breaches the cornea
- Clostridium botulinum - botulinum toxins A-G
11
Q
Botulinum neurotoxins
A
- Enter cell by endocytosis
- Cleave specific sites on SNARE proteins
- Block acetylcholine release
- Results in flaccid paralysis
12
Q
Exotoxin - Leukotoxin
A
- Manheimia haemolytica leukotoxin: an exotoxin that attacks host leukocytes (see lots of tissue damage)
- Ovine pneumonic pasteurellosis
- -Leukotoxin is a major contributor to the pathogenesis of lung injury
13
Q
Damage - immune-mediated, Purpura hemorrhagica
A
=Aseptic necrotizing vasculitis characterized primarily by edema and petechial or ecchymotic hemorrhage
- Pathogenesis: thought to be vasculitis caused by deposition of immune complexes in blood vessel walls
- Possible association with S. equi ssp. equi (strangles) infection
14
Q
Damage - immune-mediated, Sepsis
A
=Severe, whole body inflammatory response to bacteria
- Response to bacterial components such as the endotoxin lipopolysaccharide (LPS)
- Causes vascular damage, hypotension, multiple organ damage
15
Q
Damage - immune-mediated, Superantigens
A
- Non-specific activation of T-cells
- Most powerful T-cell mitogens ever discovered
- Massive, non-specific inflammation:
- -Shock
- -Multiple organ failure
- -Death
- S. aureus
- S. equi ssp. zooepidemicus
- Y. pseudotuberculosis
16
Q
Transmission - exiting the host
A
- Respiratory droplets
- Feces
- Urine
- Milk
- Reproductive fluid/tissues
- Decomposing host tissues
-Back to the environmental reservoir OR directly to another host
17
Q
Transmission - extremes
A
- Minimal effect on host - keep host healthy to encourage transmission
- -Sexually transmitted diseases
- -Vector borne diseases
- Major effect on host - make host sick to encourage transmission
- -Increase respiratory spread (coughing and sneezing)
- -Increase fecal spread (diarrhea)
- -Kill the host then sit and wait
18
Q
Minimal effect on host
A
- Campylobacter fetus ssp. venerealis
- Bovine venereal campylobacteriosis
- Bulls - bacterium lives in preputial crypts
- Sexually transmitted from asymptomatic bulls to cows
- Cows - infertility, abortion
19
Q
Major effect on host
A
- Bordetella bronchiseptica - kennel cough
- Spread by respiratory droplets
- ETEC (Enterotoxigenic E. coli) - calf scours
- Spread by fecal-oral route
- Bacillus anthracis
- -Increase host exploitation
- -Forms spores in decomposing carcasses while awaiting another host (sit and wait)
20
Q
Spores
A
- Bacterial spores are highly resistant, dormant structures (no metabolic activity) formed in response to adverse environmental conditions (limited nutrients)
- Bacterial spores are highly resistant to:
- -Heat
- -Dehydration
- -Radiation
- -Chemicals
- Bacillus anthracis (central spores)
- Clostridium tetani (terminal spores, looks like drumstick)
21
Q
Fungal spores v. Bacterial spores
A
- Fungal spores are about reproduction
- Bacterial spores are about survival
22
Q
Dead end hosts
A
- Not helpful for the pathogen
- End of transmission
23
Q
Lyme disease
A
- Borrelia burgdorferi
- Enzootic life-cycle = endemic in animals = constantly present in an animal population
- Dogs and humans are dead end hosts (they cannot transmit it to a new host)
24
Q
Zoonotic bacteria
A
- Can be transmitted from animals to people
- Do NOT confuse with common source infections
- -This is when both animals and people can be infected with the same organism, but they catch it from the same source, not from each other.
- -The pathogen is not transmitted from animals to people in common source infections
25
Q
Fungi
A
- Molds = multi-celled hyphae; fuzz on solid media
- -Form in the environment
- Yeasts = single-celled; colonies on solid media
- -Form in host tissues
- Dimorphic = can convert to the other form
26
Q
Immunity to fungal infections
A
- Innate:
- -Fungal PAMPs bind PRRs on innate cells (macrophages, dendritic cells)
- -Phagocytosis
- Adaptive:
- -Th1 and Th17 pathways provide the best protection against fungal infections –> killing by effector cells (neutrophils, macrophages)
- -Th17 - acute inflammation
- -Th1 - chronic inflammation
27
Q
Immunity to fungal infections
A
How fungi survive the immune response:
- Escape from phagolysosome
- Too large to be phagocytosed
- -Neutrophils cannot totally ingest some fungal structures due to their large size:
- –Neutrophils release enzymes and oxidants –> damage fungal hyphae –> small fungal fragments –> ingestion by macrophages or NK cells
