Helicobacter-Pseudomonas-Bordetella-Corynebacterium Flashcards

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1
Q

Helicobacter pylori

gram and shape

A

gram -

vibrio

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2
Q

Helicobacter pylori virulence factos

A
urease 
VacA
CagA
mucinase 
flagella
superoxide dimutase
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3
Q

Helicobacter pylori metabolize what?

A

AA not carbs

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4
Q

urease of Helicobacter pylori

A

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

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5
Q

VacA of Helicobacter pylori

A

acts on gastric mucosa epithelia and promotes urea flow into stomach

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6
Q

CagA of Helicobacter pylori

A

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

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7
Q

mucinase of Helicobacter pylori

A

degrades the mucus for invasion

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8
Q

flagella of Helicobacter pylori

A

used for colonization

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9
Q

superoxide dimutase of Helicobacter pylori

A

prevents phago/ intrcell killing

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10
Q

Gastric ulcer

A
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11
Q

inital infection response to heliobacter pylori

A
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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12
Q

prevention/ treatment of helio pylori infection

A

proton pump inhibitor and Ab

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13
Q

symptoms of heliobacter pylori infection

A

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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14
Q
Pseudomonas aeruginosa
gram 
shape
flagella 
O2 use  
nutrient req
temp range
A
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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15
Q

notable virulence factors of Pseudomonas aeruginosa

A
pili
flagellum
siderophores 
pyocyanin 
exotoxin A 
alginate 
LPS
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16
Q

pili of Pseudomonas aeruginosa

A

adherence function

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17
Q

flagellum of Pseudomonas aeruginosa

A

motility and adherence

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18
Q

siderophores of Pseudomonas aeruginosa

A

scavenge iron

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19
Q

pyocyanin of Pseudomonas aeruginosa

A

generates reactive O2 species

20
Q

exotoxin A of Pseudomonas aeruginosa

A

ADP ribosylation of EF-2

21
Q

alginate of Pseudomonas aeruginosa

A

adherence, protect from dehydration, immune evasion

22
Q

LPS of Pseudomonas aeruginosa

what the different protions do

A

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

23
Q

pathgenicity of Pseudomonas aeruginosa

where can it be and why?

A

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

  1. common in environment + Hot tubs are perfect culture conditions
  2. resistance to many chemical desinfectants
  3. R-plasmid based resistance to many antibiotics
24
Q

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

A

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

25
Q

Pseudomonas aeruginosa at burns

A

results in a greenish stain

Soluble blue-green dye pyocyanin and pyoverdin characterize P.aeriginosa

26
Q

Pseudomonas aeruginosa clinical features

A

respiratory (CF pts)

27
Q

Pseudomonas aeruginosa epidemiology

A

nocosomial infections

28
Q

Pseudomonas aeruginosa treatment

A

multi drug therapy due to resistances

29
Q
Bordetella pertussis
shape and gram
o2 use 
motility 
capsule
A

Gram− coccobacilli
strict aerobe
non-motile,
capsule

30
Q

Bordetella pertussis disease

invasive?

A

whooping cough in children

adhesion to ciliated respiratory tract cells
but NOT invasive

31
Q

Bordetella pertussis growth

A

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

32
Q

Bordetella pertussis virulence factors

A

ptx
secreted adenylate cyclase
tracheal cytotoxin

33
Q

B. pertusis pertusis toxin

A

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

34
Q

secreted adenylate cyclase of b pertusis

A

will also increase cAMP

35
Q

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

A

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.

36
Q

Bordetella pertussis vax

A

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

37
Q

Bordetella pertussis epidemiology

A

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

38
Q

Corynebacterium diphtheriae
gram and shape
O2

A

gram +
pleiomorphic
facultative anaerobe

39
Q

Corynebacterium diphtheriae pathogencity

A

opportunistic, often an oral pathogen with systemic effects

40
Q

Corynebacterium diphtheriae virulence factors

A
diptheria toxin (AB toxin)
throat adhesion
41
Q

diptheria toxin causes?

A

pseudomembrane in throat and heart/kidney damage

42
Q

how Diptheria toxin works

A

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

43
Q

pseudomembrane of diptheria made of?

can lead to?

A

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

44
Q

disease risks of diptheria toxin

local and systemic

A

local:
• paralysis; impaired swallowing, peripheral neuritis
• Suffocation (due to blockage)

systemic:
• cardiac arrythmia
• kidney failure

45
Q

treatment/ prevention of Corynebacterium diphteriae

A

neutralizing antitoxin/ penicillin and eryhtromyocin

toxoid vax

46
Q

Corynebacterium diphteriae epidemilogy (spreads thru)

A

saliva dropliets