Host-Parasite Interaction 2 Flashcards
1
Q
the “opportunistic” pathogen
A
- Pseudomonas aureginosa
- biofilm formation in pathogens
2
Q
the commensal gone bad
A
- helicobacter pylori and hepaticas
- pathogenicity islands
3
Q
Pseudomonas aeruginosa
A
- only a pathogen in compromised hosts (burn victims and those with cystic fibrosis)
- accounts of 10% of hospital infections
- normally soil bacterium (very metabolically flexible)
- used as a bio-remediator.
4
Q
Characteristics of pseudomonas aeruginosa
A
- can grow on 75 other organic substrates and ammonium
- wide temperature range
- naturally resistant to antiseptic compounds and many antibiotics (LPS and EPS)
- forms biofilms
- possibly the most prevalent bacterium.
5
Q
Toxin
A
- Endotoxin (LPS)
- produces a large quantity of LPS used in biofilm formation.
6
Q
“mucoid” phenotype
A
- exopolysaccharide is made of alginate
- its expression is induced by environmental factors such as starvation and the alternative sigma factor.
- requires 25 alg genes to be produced, and is required for biofilm formation.
- typically the strains that cause human infection.
7
Q
biofilm
A
- physical barrier against chemical and immune responses.
8
Q
alginate composition
A
- composed of mannuronic acid and guluronic acid.
9
Q
Factors required for biofilm formation
A
- quorum sensing
- motility (both flagella and twitching)
- alginate production
10
Q
motility
A
- flagella bind to surface
- if they do not twitch and can’t move the biofilm is flat.
11
Q
quorum sensing
A
- use two homoserine lactones and a quinolone
- all are constitutively expressed
- only if intracellular concentration of any one reaches a critical level, biofilm formation is induced.
12
Q
steps in biofilm production
A
- alginate production is the first step in biofilm creation
- serves to secure the bacteria to the substrate and allow for the colony to grow vertically.
- channels in biofilm allow bacteria access to the nutrients in the medium.
13
Q
Pseudomonas and Cystic Fibrosis
A
- 80% of CF patients are infected with P. aeruginosa - will keep for life
- Infected patients have decreased pulmonary function and die sooner - lungs fill with mucus
- 80% of clinical isolates have acquired resistance
- Mucoid and biofilm production further makes eradication problematic
14
Q
Cystic Fibrosis Transmembrane conductive regulator
A
- have mutations in the protein CFTR
- CFTR is a membrane ABC transporter and chloride channel that controls concentration of chloride ion found near mucosal surfaces
15
Q
Result
A
- chloride imbalance in skin and mucosal surfaces affects viscosity of mucus covering the lung epithelia, making it harder to clear out bacteria.
- ciliary flow is disrupted in CF lungs which make it easier for biofilm formation.
- CF lungs are susceptible to many types of infection.
16
Q
Symptoms of CF after Pseudomonas infection
A
- increased frequency, duration, and intensity of cough
- increased or new onset of sputum production and appearance
- increased shortness of breath and decreased exercise tolerance
- decrease in overall well-being, increased fatigue, weakness, fever, poor appetite
17
Q
physical signs of CF after Pseudomonas infection
A
- increased work of breathing. intercostal retractions and use of accessory muscles
- increased respiratory rate
- increased air trapping
- fever
- weight loss
18
Q
Helicobacter pylori
A
- only lives in humans.
- about 50% of all people on earth are infected with it, but was probably higher in the past.
- first described in 1983 by Marshall and Warren
19
Q
Marshall and Warren
A
- noticed patients with gastric ulcers tended to have what looked to be bacteria in the stomach lining
- stomach was thought to be a sterile environment due to acidic pH and digestive enzymes.
- Marshall used Koch’s postulates on himself
20
Q
Epidemiology
A
- after infection most people will come down with chronic superficial gastritis - upset stomach
- a small percentage will develop gastric ulcers many years later
- if kept for decades, the person has a high risk for certain types of gastric cancer.
- researchers detected it in blood dating back 50 years
21
Q
Urease
A
- H. pylori doesn’t like an acidic pH and will burrow down into the stomach
- to combat stomach acid, it will produce large amounts of urease
22
Q
urease mechanism
A
- splits urea into CO2 and ammonia.
- ammonia will neutralize the acid but will also degrade the stomach lining causing the ulcer.
23
Q
detection
A
- will be given urea with radioactively labeled carbon
- patients breath is taken and analyzed for presence of labeled CO2
24
Q
Cag pathogenicity island
A
- Cag status is correlated with more severe pathologies, but is not required for colonization or persistence
- encodes a type four secretion system
- CagA is the delivered effector molecule
- CagA is phosphorylates by the host Src kinase, which causes actin rearrangement of epithelial cells
- induces IL-8 cytokines.
25
Helicobacter hepaticus
- certain strains of mice were developing liver cancer at an unusual frequency
- associated with enterocolitis and cancer
- lives in small intestine
26
Cag postive strains
- typically more pathogenic than those that do not have the island.
27
evidence of recent acquisition
- different G+C codon bias
| - strains are either completely + or -
28
How to recognize an Island?
- have a difference % G/C DNA content from the rest of the DNA
- have a different "codon bias" from the rest of the genes
- Are in the middle of a gene/operon where it doesn't belong
- Are present in some members of a species, absent in others.
- type III and IV secretion systems are sometimes found on islands.
29
Cag
- CagA is phosphorylated by the host Src kinase, which causes actin rearrangement of epithelial cells
- Cag is not required for colonization or persistence in the stomach.
30
codon bias
- bacteria tend to use the same triplet to encode an amino acids, even though the codon is redundant.
31
hummingbird phenotype
- actin polymerizes off the ends and looks like a hummingbird's beak
32
H. pylori and esophageal cancer
- if you have H. pylori, you will be less likely to get esophageal cancer.
33
The HHGI1 Pathogenicity Island
- found in helicobacter hepaticus
| - mice with pathogenicity island (+) strains are more likely to have liver infections.
34
Gram secretion systems
- analogous to type IV
- deliver a molecule directly across membrane into host.
- host cells with type IV mutants have dramatically different transcription profiles.
- transcribe a lot less
35
Type VI
- makes easier to bacteria and immune system to live together
