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3.16 Flashcards

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1
Q

Gram− bacilli

Some are common members of (2)

A

human and animal flora

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2
Q

Some are members of commensal groups that have become
pathogenic due to acquired virulence factors like toxins from
(3)

A

plasmids, bacteriophages or
“pathogenicity islands
”

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3
Q

Most can be motile with

A

peritrichous flagella (
H
-antigen
)

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4
Q

Some are non-motile (3)

A

Shigella, Klebsiella, Yersinia

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5
Q

Most have surface pili:

A

fimbriae for adherence and sex pili for

plasmid conjugation

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6
Q

Some species have capsules (2 antigen) (3 species)

A

(K or Vi antigen) (most Klebsiella

species, some Enterobacter and E.coli species)

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7
Q

All: (3)

A 
outer
-membrane LPS (heat
-stable endotoxin) with
enterobacterial common antigen and serotype
-specific
O
-
antigen
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8
Q

When bacteria have a toxin

like cholera toxin:

A

get watery diarrhea

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9
Q

When also have a toxin like

Shiga toxin:

A

get blood in diarrhea

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10
Q

When also have inflammation

and neutrophils:

A

get pus in diarrhea =

dysentery

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11
Q

Outer- and inner-core sugars are the

— common antigen

A

enterobacterial

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12
Q

LPS: Also known as the

A

“heat-stable

enterotoxin”

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13
Q

Type III secretion system is present in many bacteria like (4):

A 
Yersinia, Salmonella, Shigella,
enteropathogenic EPEC (E.coli); also present in other species like Pseudomonas and Chlamydia):
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14
Q

Type III secretion system

A

20-protein system that looks like a short, hollow flagellum (“needle”) to inject a variety of speciesspecific toxins into host cells

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15
Q

Escherichia coli

Transmission: (3)

A

• person-to-person
• contaminated food
• human and animal feces
(no hand washing; insect vectors)

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16
Q

E.coli Virulence Factors

Ø heat-labile enterotoxin “LT” (cholera-like AB-exotoxin): (4)

A

ADP-ribosylation of G protein ► cAMP ­ ►
loss of water + electrolytes ► watery diarrhea (e.g. foodborne enterotoxigenic ETEC E.coli)

Traveller’s diarrhea

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17
Q

In Shigella dysenteriae this set of symptoms “diarrhea with blood” is combined with

A

intestinal cell invasion, apoptosis and neutrophilia (► “pus”) to define “dysentery”.

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18
Q 
Name: EPEC, EnteroPathogenic
Virulence Factors: 
Clinical: 
Epidemiology: 
Treatment:
A

bundle-forming pili
adhesins with effacing
[see 16-3]

watery diarrhea
vomiting

infants (developing
world) hospital
nurseries, bottle-fed
infants

replenish fluids
unknown

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19
Q

Name: EHEC
EnteroHemorrhagic
(typically O157:H7)

Virulence Factors:
CLINICAL: (3)
Epidemiology:
TX: (2)

A

shiga toxin
adhesins with effacing

bloody diarrhea
hemorrhagic colitis
hemolytic uremic
syndrome

Foodborne &
waterborne
(developing world)

replenish fluids
(antibiotics are
contraindicated)

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20
Q

Name: ETEC
EnteroToxigenic

Virulence Factors:
Clinical:
Epidemiology:
Treatment:

A 
pili
heat-labile enterotoxin
(cholera-like toxin)
heat-stable enterotoxin
(LPS) [see Fig.16-2]

watery diarrhea

children (developing
world)
foodborne (picnic,
travel)

replenish fluids
prevention: PeptoBismol (bismuth)
ciprofloxacin (but
resistance!)

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21
Q

Name: EAggEC
EnteroAggressive

Virulence Factors:
Clinical:
Epidemiology:
Treatment:

A

pili
cytotoxins

diarrhea + mucus

children + HIV

replenish fluids
fluoroquinolones (if
AIDS)

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22
Q

Name: EIEC
EnteroInvasive

Virulence Factors:
Clinical:
Epidemiology:
Treatment:

A

invasion of colonic
epithelials (like
Shigella)

bloody diarrhea
hemorrhagic colitis

children (developing
world)

replenish fluids
antibiotics (gentamicin,
polymixin) to shorten

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23
Q 
Name: UroPathogenic
Virulence Factors: 
Clinical: 
Epidemiology: 
Treatment:
A

adhesins (bladder
epithelia)
hemolysin
pathogenicity islands

cystitis (bladder
infection)
pyelonephritis

nosocomial: catheter
women: intercourse,
diaphragm
men: enlarged prostate

prevent: drink enough
trimetaprimsulfamethoxazole
fluoroquinolones

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24
Q 
Name: Meningitis associated
Virulence Factors: 
Clinical: 
Epidemiology: 
Treatment:
A

K1 capsule
S fimbriae
cellular invasion

acute meningitis

neonates (birthassociated infection)

broad-spectrum
cephalosporins

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25
Q

E.coli –%;
Klebsiella, Proteus –%;
Staphylococcus saprophyticus –%

A

70-90
5-10
5-10

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26
Q

Shigella dysenteriae: induction of apoptosis (5)

A 
1) Shigellas are taken up by M cells
and transported beneath the
epithelium. Macrophages take up
shigellas, die and release the
bacteria.
(2) The bacteria enter the inferior and
lateral aspects of the epithelial cells
by inducing endocytosis. The
endosomes are quickly lysed,
leaving the shigellas free in the
cytoplasm.
(3) Actin filaments quickly form a tail,
pushing the shigellas into the next cell
(4) Shigellas multiply in the cytoplasn
and the infection extends to the
next cell.
5) Infected cells die and slough off.
Intense response of acute
inflammatory cells (neutrophils),
bleeding and abscess formation.
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27
Q

Epidemiology:

A

Transmission via fecal-oral route; sometimes by
fecally contaminated food or water, humans
generally the only source

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28
Q

Virulence Factors

A

Dysentery:
Shiga toxin: bloody watery diarrheal
Cell invasion -neutrophils * pus

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29
Q

S.enterica (4)

A
  • enteric fever
  • human reservoir
  • typhoid
  • high mortality
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30
Q

Many Salmonella species: (3)

A
  • gastroenteritis
  • poultry reservoir
  • foodborne illness
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31
Q 
Salmonella
Virulence Factors (2)

in S.typhi serovars: (2)

A

Ø Type III secretion induces enteric epithelial uptake via M cells
Ø intracellular endosome growth in macrophages: secretes protein that
prevents phagosome-lysosome fusion

in S.typhi serovars:
Ø through macrophages: invasive into different tissues and organs
Ø destruction of Peyer’s Patches ► intestinal rupture

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32
Q

Salmonella invasion of intestinal epithelia (4)

A
  • M cell uptake through ruffles: transport through epithelial layer.
  • Electrolyte release to lumen (diarrhea/gastroenteritis).
  • Release of inflammatory exudate.
  • Transport to lymph nodes / transient bacteremia
33
Q

Gram- rods, aerobic / facultatively anaerobic
species: Salmonella
enterica
(*serovar typhi)

Virulence factors:
Clinical features:
Treatment:
Epidemiology:

A 
type III secretion
epithelial cell
invasion
intracellular growth
(in macrophages)
R-plasmids

diarrhea
enteric fever*
(serovar typhi)

(antibiotic treatment
may prolong carrier
state)
*fluoroquinolones
attenuated oral
vaccine
gal bladder resection

contaminated food
bacteremia if
immunecompromised

34
Q

Gram- rods, aerobic / facultatively anaerobic
species: Shigella
dysenteriae

Virulence factors:
Clinical features:
Treatment:
Epidemiology:

A 
type III secretion
intracellular spread
induces apoptosis in
macrophages
R-plasmids

bacillary dysentery
ampicillin
trimetaprimsulfamethoxazole
fluoroquinolones

foodborne
waterborne
person-to-person

35
Q

Gram- rods, aerobic / facultatively anaerobic
species: Klebsiella
pneumoniae

Virulence factors:
Clinical features:
Treatment:
Epidemiology:

A

capsule
R-plasmids

pneumonia
urinary tract
infections

cephalosporins
fluoroquinolones

nosocomial
infections
alcoholism

36
Q

Gram− vibrio (curved rods) (salt tolerant) found in (2)

A

estuaries and marine environments (e.g. in crabs)

37
Q

Vibrio cholerae:

Virulence Factors: (4)

A

Ø toxin co-regulated pilus (tcp): adhesion to small intestinal epithelia
Ø cholera toxin (heat-labile exotoxin “LT”): protein A causes cAMP rise + watery diarrhea
Ø an additional toxin “ST” can raise cGMP levels with a similar effect
Ø Neuraminidase-increase cholera toxin binding

38
Q

CTXφ (a bacteriophage) and Vibrio cholerae

A 
TCP production is
induced within the
intestine, while
production in other
environments appears to
be minimal

(toxin is phage CTXφ-encoded and regulated by pilin-regulating chromosomal gene)

39
Q

TCP =

A

Toxin
coregulated
pilus

40
Q

(2) encode the

proteins that comprise cholera toxin

A

ctxA and ctxB

41
Q

Cholera

formalinized whole-cell vaccine:

A

several doses; partial protection for 2-3 yrs

42
Q

Common epidemic strain:

A

serovar O1

43
Q

New strain:

A

serovar O139 with capsule as new virulence factor

India 1992) (O1 vaccine does not protect

44
Q 
Gram- vibrio (rods), aerobic / facultatively anaerobic
Virulence factors (4)
Clinical features (2)
Treatment (1)
Epidemiology (2)
A

cholera toxin
toxin-coregulated pili
toxins
neuraminidase

severe watery diarrhea
Disease is self-limiting as
intestinal cells with surface
bacteria are shed.

Rehydration + electrolytes
to shorten course:
doxycycline, trimethoprimsulfamethoxazole or
furazolidone

fecal transmission in
developing countries
under-cooked coastal
crabs

45
Q

Campylobacter jejune

shape

A

Gram− vibrio (short S- or

comma-shaped rods)

46
Q

Campylobacter jejune

Virulence Factors: (3)

A

Ø Growth in intestinal tract:
§ invade intestinal epithelial cells or
grow below epithelial layer.
§ inflammatory response

47
Q

Campylobacter jejune

Zoonosis:

A

animal reservoir (intestinal)

48
Q

Campylobacter jejune

Transmission:

A 
contaminated food (poultry, milk)
(e.g. in >89% of raw chicken)
49
Q

Campylobacter jejune

Disease: (3)

A

Disease: gastroenteritis, diarrhea, dysentery

50
Q

Campylobacter jejune
Disease resolves without treatment in —
Creates —

A

<1 week

protective immunity

51
Q

Gram- vibrio (rods), aerobic / facultatively anaerobic

C.jenune

A

adhesion; invasion
of mucosal
epithelia

gastroenteritis

self-limited
In severe cases: erythromycin,
tetracycline or fluoroquinolones

zoonotic infection
(food, milk, water)

52
Q

Helicobacter pylori classification

A

Gram− vibrio

53
Q

Helicobacter pylori

Virulence Factors: (5)

A

Ø urease (urea ® ammonia pH increase, neutralization of stomach acid)
Ø VacA protein acts on gastric mucosal epithelia and promotes flow of urea into stomach
Ø CagA protein: injected into host epithelia cells change (prelude to cancer)
Ø mucinase
Ø flagella

54
Q

Gastric ulcer

A

Organisms survive the acidity of stomach juices
by producing a powerful urease. Upon reaching the
layer of mucus, they penetrate to the epithelial
surface, where bacterial products incite an
inflammatory response. Thinning of the mucus
layer occurs, and 10 to 20% of infected individuals
develop ulcerations. Only a small percentage
develop cancer, but more than 90% of individuals
with stomach cancers are infected with H. pylori

No proven preventive. Most infections are cured
using two antibiotics together, plus a medication to
suppress stomach acid (see next slide)

55
Q

Symptoms of stomach and upper duodenum infection:

v in most people:

A

no symptoms (symptom-free carrier).

56
Q

Pseudomonas aeruginosa

characteristics (5)

A 
Gram− short rods
polar flagella (one or more; high mobility)
obligate aerobe
simple nutrient requirements (acetate)
broad temperature range: 20 to 43 ºC
57
Q

alginate
mechanism of action (3)
contribution to virulence (1)

A

adherence, protection from dehydration, and immune evasion

biofilm formation

58
Q

lipopolysaccharide

mechanism of action

A

lipid A is endotoxic, core interacts CFTR (Cystic Fibrosis Transmembrane conductance Regulator); O antigen protects from complement mediated killing

59
Q

opportunistic pathogen (in case of disease, cancer, weakened immunity): (3)

A
  1. common in environment (water, soil) +
    Hot tubs are perfect culture conditions (due to heat tolerance)
  2. resistance to many chemical desinfectants (like iodine) +
  3. R-plasmid based resistance to many antibiotics
60
Q

major problem in hospitals (nosocomial infections) (5)

A 
ü lungs: artificial ventilators, cystic fibrosis (mucoid strains)
ü skin: burn victims, folliculitis
ü bladder infections
ü ear infections
(swimmers ear:
otitis externa)
ü eye infections
(from contact lenses)
61
Q

(2) characterize P.aeriginosa

A

Soluble blue-green dye pyocyanin and

pyoverdin

62
Q 
Pseudomonas aeruginosa
Gram- rod, generally aerobic
Clinical features (1)
Treatment 
Epidemiology (1)
A 
Pulmonary (CF patients)
1º skin infection
urinary tract infection
eye & ear infection
bacteremia
combination therapy:
aminoglycoside +
cephalosporins,
piperacillin-tazobactam
or carbapenem

nosocomial infection

63
Q

Bordetella pertussis

characterization

A

Gram− coccobacilli
strict aerobe
non-motile, capsule

64
Q

B.pertussis show dense surface growth in the

A

lower
respiratory tract (bronchi, bronchioli) without cell
invasion and with strong mucus secretion.

65
Q

Virulence Factors of Bordetella pertussis (5)

A

Whooping cough (pertussis)
adhesion to ciliated respiratory tract cells
but NOT invasive

toxins:
Ø pertussis toxin ptx
Ø secreted invasive adenylate cyclase / hemolysin
Ø tracheal cytotoxin (Nitric Oxide NO release)
Ø tracheal cytotoxin (causes Nitric Oxide NO release)

66
Q

Ø pertussis toxin ptx

A

(ADP-ribosylation of G-protein: cAMP­ increase

mucus­ and other secretions)

67
Q

secreted invasive adenylate cyclase / hemolysin

A

(cAMP­ increase)

68
Q

Ø tracheal cytotoxin (Nitric Oxide NO release) (2)

A

kills ciliated cells
toxin is a component of peptidoglycan
disaccharride-tetrapeptide

69
Q

Ø tracheal cytotoxin (causes Nitric Oxide NO release) (2)

A

kills ciliated cells

toxin is a component of peptidoglycan disaccharride-tetrapeptide

70
Q

Most gram negative bacteria keep — within the cell wall by using a transporter protein to recycle it.
is B. pertussis capable?

A

TCT

B. pertussis not capable of recycling TCT and it escapes to the surrounding environment.

71
Q 
Bordetella pertussis
Gram- small coccobacilli, strict aerobic
Virulence factors 
Clinical features 
Treatment 
Epidemiology
A

pertussis toxin
adenylate cyclase toxin
tracheal toxin
adhesins

pertussis (whooping
cough)

DTaP vaccine (Diphtheria,
Tetanus, acellular Pertussis)
supportive treatment
erythromycin (partially
effective if given early;
prophylaxis)

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

72
Q

Corynebacterium diphtheriae characterization (3)

A

Gram+ pleiomorphic (club-shaped) rods
opportunistic pathogen
oral pathogen with systemic effects

73
Q

Corynebacterium diphtheriae

1 Virulence Factor: diphtheria toxin

A

diptheria; diptheria toxin (phage β coded)
(expressed only as prophage)
(toxin gene is induced if iron is LOW)

pseuodomembrane in the throat; heart, kidnet damage Inhibits protein synthesis by inactivating an elongation
factor of eukaryotic cells. Kills local cells (in the throat)
but can also be carried in the bloodstream to
various organs.
NAD + EF2 = ADP + ribose-EF2 + nicotinamide

74
Q 
diphtheria: Corynebacterium diphtheriae
Virulence Factors (2)
A

throat adhesion

diphtheria toxin

75
Q

diphtheria toxin

A 
(ADP-ribosylation of EF-2
causing translation stop)
 cell death  pseudomembrane
Pseudomembrane = C.diphtheriae
cells + damaged host cells + blood
à Block air passage
76
Q

Disease risks from toxin:

local: (2)
systemic: (2)

A

• paralysis
impaired swallowing
peripheral neuritis
• Suffocation (due to blockage)

  • cardiac arrythmia
  • kidney failure
77
Q 
Corynebacterium diphteriae
Gram+ rods, aerobic / facultatively anaerobic
Virulence factors 
Clinical features 
TX (1) 
EPIDEMIOLOGY (1)
A

diphtheria toxin

diphtheria 
• respiratory
• cutaneous
(skin ulcers in
vaccinated carriers)

neutralizing antitoxin
penicillin or erythomycin
prevent by toxoid vaccination

Spread by saliva droplets

78
Q

diseases DPT (3)

A

diptheria
pertussis (whopping cough)
tetanus

Microbiology (42 decks)

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