Helicobacter-Pseudomonas-Bordetella-Corynebacterium Flashcards
Helicobacter pylori
gram and shape
gram -
vibrio
Helicobacter pylori virulence factos
urease VacA CagA mucinase flagella superoxide dimutase
Helicobacter pylori metabolize what?
AA not carbs
urease of Helicobacter pylori
converts urea to ammonia and raises the pH to neturalize stomach acid
VacA of Helicobacter pylori
acts on gastric mucosa epithelia and promotes urea flow into stomach
CagA of Helicobacter pylori
protien injected into host cells, cells change, prelude to cancer
mucinase of Helicobacter pylori
degrades the mucus for invasion
flagella of Helicobacter pylori
used for colonization
superoxide dimutase of Helicobacter pylori
prevents phago/ intrcell killing
Gastric ulcer
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.
prevention/ treatment of helio pylori infection
proton pump inhibitor and Ab
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.
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
notable virulence factors of Pseudomonas aeruginosa
pili flagellum siderophores pyocyanin exotoxin A alginate LPS
pili of Pseudomonas aeruginosa
adherence function
flagellum of Pseudomonas aeruginosa
motility and adherence
siderophores of Pseudomonas aeruginosa
scavenge iron
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
