Helicobacter-Pseudomonas-Bordetella-Corynebacterium Flashcards by Caleb Houghton

Helicobacter pylori

gram and shape

gram -

vibrio

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Helicobacter pylori virulence factos

urease 
VacA
CagA
mucinase 
flagella
superoxide dimutase

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Helicobacter pylori metabolize what?

AA not carbs

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urease of Helicobacter pylori

converts urea to ammonia and raises the pH to neturalize stomach acid

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VacA of Helicobacter pylori

acts on gastric mucosa epithelia and promotes urea flow into stomach

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CagA of Helicobacter pylori

protien injected into host cells, cells change, prelude to cancer

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mucinase of Helicobacter pylori

degrades the mucus for invasion

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flagella of Helicobacter pylori

used for colonization

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superoxide dimutase of Helicobacter pylori

prevents phago/ intrcell killing

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Gastric ulcer

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inital infection response to heliobacter pylori

Initial infection induces a low grade
immune response with IgM, followed
by IgA and IgG production.
This suppresses bacterial growth
and leads to the typical low-level
persistent infection which remains
symptom-free for 80-90% of carriers.

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prevention/ treatment of helio pylori infection

proton pump inhibitor and Ab

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symptoms of heliobacter pylori infection

Symptoms of stomach and upper duodenum infection:
in most people: no symptoms (symptom-free carrier).

in some: gastritis, peptic and duodenal ulcers, Potential for gastric adenocarcinoma

If ulcers/cancer: stomach pain, tenderness and bleeding.

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Pseudomonas aeruginosa
gram 
shape
flagella 
O2 use  
nutrient req
temp range

Gram− 
short rods
polar flagella (one or more; high mobility)
obligate aerobe
simple nutrient requirements (acetate)
broad temperature range: 20 to 43 ºC

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notable virulence factors of Pseudomonas aeruginosa

pili
flagellum
siderophores 
pyocyanin 
exotoxin A 
alginate 
LPS

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pili of Pseudomonas aeruginosa

adherence function

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flagellum of Pseudomonas aeruginosa

motility and adherence

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siderophores of Pseudomonas aeruginosa

scavenge iron

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pyocyanin of Pseudomonas aeruginosa

generates reactive O2 species

exotoxin A of Pseudomonas aeruginosa

ADP ribosylation of EF-2

alginate of Pseudomonas aeruginosa

adherence, protect from dehydration, immune evasion

LPS of Pseudomonas aeruginosa

what the different protions do

lipid A is endotoxic
core interacts with CTFR
O Ag protects from complement killing

pathgenicity of Pseudomonas aeruginosa

where can it be and why?

opportunistic pathogen (in case of disease, cancer, weakened immunity)

common in environment + Hot tubs are perfect culture conditions
resistance to many chemical desinfectants
R-plasmid based resistance to many antibiotics

Pseudomonas aeruginosa major problem where?
affected tissues?
all infections could lead to?

major problem in hospitals (nosocomial infections)

lungs: artificial ventilators, cystic fibrosis (mucoid strains)
skin: burn victims, folliculitis
bladder infections
ear infections (swimmers ear: otitis externa)
eye infections(from contact lenses)

All infections could lead to septicemia and shock

Pseudomonas aeruginosa at burns

results in a greenish stain | Soluble blue-green dye pyocyanin and pyoverdin characterize P.aeriginosa

Pseudomonas aeruginosa clinical features

respiratory (CF pts)

Pseudomonas aeruginosa epidemiology

nocosomial infections

Pseudomonas aeruginosa treatment

multi drug therapy due to resistances

``` Bordetella pertussis shape and gram o2 use motility capsule ```

Gram− coccobacilli strict aerobe non-motile, capsule

Bordetella pertussis disease | invasive?

whooping cough in children adhesion to ciliated respiratory tract cells but NOT invasive

Bordetella pertussis growth

B.pertussis show dense surface growth in the lower respiratory tract (bronchi, bronchioli) without cell invasion and with strong mucus secretion

Bordetella pertussis virulence factors

ptx secreted adenylate cyclase tracheal cytotoxin

B. pertusis pertusis toxin

ADP ribo of G pro to increase cAMP which increases mucus secretion and others

secreted adenylate cyclase of b pertusis

will also increase cAMP

tracheal cytotoxin of B pertusis component of? how does B pertusis differ from other bacteria with this?

NO relase to kill ciliated cells toxin is a component of peptidoglycan disaccharride-tetrapeptide Most gram negative bacteria keep TCT within the cell wall by using a transporter protein to recycle it. B. pertussis not capable of recycling TCT and it escapes to the surrounding environment.

Bordetella pertussis vax

used to use killed whole cell vax now we use DTaP (diphtheria, tetanus, acellular pertusis)

Bordetella pertussis epidemiology

aerosol transmission childrens disease (mild symptoms in adults who are the reservoir

Corynebacterium diphtheriae gram and shape O2

gram + pleiomorphic facultative anaerobe

Corynebacterium diphtheriae pathogencity

opportunistic, often an oral pathogen with systemic effects

Corynebacterium diphtheriae virulence factors

``` diptheria toxin (AB toxin) throat adhesion ```

diptheria toxin causes?

pseudomembrane in throat and heart/kidney damage

how Diptheria toxin works

inactivates elongation factor in host cells and kills them (ADP-ribosylation), can also be carried in blood to various organs

pseudomembrane of diptheria made of? | can lead to?

Pseudomembrane = C.diphtheriae cells + damaged host cells + blood Block air passage

disease risks of diptheria toxin | local and systemic

local: • paralysis; impaired swallowing, peripheral neuritis • Suffocation (due to blockage) systemic: • cardiac arrythmia • kidney failure

treatment/ prevention of Corynebacterium diphteriae

neutralizing antitoxin/ penicillin and eryhtromyocin | toxoid vax

Corynebacterium diphteriae epidemilogy (spreads thru)

saliva dropliets