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Microbiology > 3.16 > Flashcards

3.16 Flashcards

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
E.coli --%; Klebsiella, Proteus --%; Staphylococcus saprophyticus --%
70-90 5-10 5-10
26
Shigella dysenteriae: induction of apoptosis (5)
``` 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. ```
27
Epidemiology:
Transmission via fecal-oral route; sometimes by fecally contaminated food or water, humans generally the only source
28
Virulence Factors
Dysentery: Shiga toxin: bloody watery diarrheal Cell invasion -neutrophils * pus
29
S.enterica (4)
* enteric fever * human reservoir * typhoid * high mortality
30
Many Salmonella species: (3)
* gastroenteritis * poultry reservoir * foodborne illness
31
``` Salmonella Virulence Factors (2) ``` in S.typhi serovars: (2)
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
32
Salmonella invasion of intestinal epithelia (4)
* 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
Gram- rods, aerobic / facultatively anaerobic species: Salmonella enterica (*serovar typhi) Virulence factors: Clinical features: Treatment: Epidemiology:
``` 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
Gram- rods, aerobic / facultatively anaerobic species: Shigella dysenteriae Virulence factors: Clinical features: Treatment: Epidemiology:
``` type III secretion intracellular spread induces apoptosis in macrophages R-plasmids ``` bacillary dysentery ampicillin trimetaprimsulfamethoxazole fluoroquinolones foodborne waterborne person-to-person
35
Gram- rods, aerobic / facultatively anaerobic species: Klebsiella pneumoniae Virulence factors: Clinical features: Treatment: Epidemiology:
capsule R-plasmids pneumonia urinary tract infections cephalosporins fluoroquinolones nosocomial infections alcoholism
36
Gram− vibrio (curved rods) (salt tolerant) found in (2)
estuaries and marine environments (e.g. in crabs)
37
Vibrio cholerae: | Virulence Factors: (4)
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
CTXφ (a bacteriophage) and Vibrio cholerae
``` 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
TCP =
Toxin coregulated pilus
40
(2) encode the | proteins that comprise cholera toxin
ctxA and ctxB
41
Cholera | formalinized whole-cell vaccine:
several doses; partial protection for 2-3 yrs
42
Common epidemic strain:
serovar O1
43
New strain:
serovar O139 with capsule as new virulence factor | India 1992) (O1 vaccine does not protect
44
``` Gram- vibrio (rods), aerobic / facultatively anaerobic Virulence factors (4) Clinical features (2) Treatment (1) Epidemiology (2) ```
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
Campylobacter jejune | shape
Gram− vibrio (short S- or | comma-shaped rods)
46
Campylobacter jejune | Virulence Factors: (3)
Ø Growth in intestinal tract: § invade intestinal epithelial cells or grow below epithelial layer. § inflammatory response
47
Campylobacter jejune | Zoonosis:
animal reservoir (intestinal)
48
Campylobacter jejune | Transmission:
``` contaminated food (poultry, milk) (e.g. in >89% of raw chicken) ```
49
Campylobacter jejune | Disease: (3)
Disease: gastroenteritis, diarrhea, dysentery
50
Campylobacter jejune Disease resolves without treatment in --- Creates ---
<1 week | protective immunity
51
Gram- vibrio (rods), aerobic / facultatively anaerobic | C.jenune
adhesion; invasion of mucosal epithelia gastroenteritis self-limited In severe cases: erythromycin, tetracycline or fluoroquinolones zoonotic infection (food, milk, water)
52
Helicobacter pylori classification
Gram− vibrio
53
Helicobacter pylori | Virulence Factors: (5)
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
Gastric ulcer
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
Symptoms of stomach and upper duodenum infection: | v in most people:
no symptoms (symptom-free carrier).
56
Pseudomonas aeruginosa | characteristics (5)
``` Gram− short rods polar flagella (one or more; high mobility) obligate aerobe simple nutrient requirements (acetate) broad temperature range: 20 to 43 ºC ```
57
alginate mechanism of action (3) contribution to virulence (1)
adherence, protection from dehydration, and immune evasion biofilm formation
58
lipopolysaccharide | mechanism of action
lipid A is endotoxic, core interacts CFTR (Cystic Fibrosis Transmembrane conductance Regulator); O antigen protects from complement mediated killing
59
opportunistic pathogen (in case of disease, cancer, weakened immunity): (3)
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
major problem in hospitals (nosocomial infections) (5)
``` 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
(2) characterize P.aeriginosa
Soluble blue-green dye pyocyanin and | pyoverdin
62
``` Pseudomonas aeruginosa Gram- rod, generally aerobic Clinical features (1) Treatment Epidemiology (1) ```
``` Pulmonary (CF patients) 1º skin infection urinary tract infection eye & ear infection bacteremia ``` ``` combination therapy: aminoglycoside + cephalosporins, piperacillin-tazobactam or carbapenem ``` nosocomial infection
63
Bordetella pertussis | characterization
Gram− coccobacilli strict aerobe non-motile, capsule
64
B.pertussis show dense surface growth in the
lower respiratory tract (bronchi, bronchioli) without cell invasion and with strong mucus secretion.
65
Virulence Factors of Bordetella pertussis (5)
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
Ø pertussis toxin ptx
(ADP-ribosylation of G-protein: cAMP­ increase | mucus­ and other secretions)
67
secreted invasive adenylate cyclase / hemolysin
(cAMP­ increase)
68
Ø tracheal cytotoxin (Nitric Oxide NO release) (2)
kills ciliated cells toxin is a component of peptidoglycan disaccharride-tetrapeptide
69
Ø tracheal cytotoxin (causes Nitric Oxide NO release) (2)
kills ciliated cells | toxin is a component of peptidoglycan disaccharride-tetrapeptide
70
Most gram negative bacteria keep --- within the cell wall by using a transporter protein to recycle it. is B. pertussis capable?
TCT | B. pertussis not capable of recycling TCT and it escapes to the surrounding environment.
71
``` Bordetella pertussis Gram- small coccobacilli, strict aerobic Virulence factors Clinical features Treatment Epidemiology ```
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
Corynebacterium diphtheriae characterization (3)
Gram+ pleiomorphic (club-shaped) rods opportunistic pathogen oral pathogen with systemic effects
73
Corynebacterium diphtheriae | 1 Virulence Factor: diphtheria toxin
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
``` diphtheria: Corynebacterium diphtheriae Virulence Factors (2) ```
throat adhesion | diphtheria toxin
75
diphtheria toxin
``` (ADP-ribosylation of EF-2 causing translation stop) cell death pseudomembrane Pseudomembrane = C.diphtheriae cells + damaged host cells + blood à Block air passage ```
76
Disease risks from toxin: local: (2) systemic: (2)
• paralysis impaired swallowing peripheral neuritis • Suffocation (due to blockage) * cardiac arrythmia * kidney failure
77
``` Corynebacterium diphteriae Gram+ rods, aerobic / facultatively anaerobic Virulence factors Clinical features TX (1) EPIDEMIOLOGY (1) ```
diphtheria toxin ``` diphtheria • respiratory • cutaneous (skin ulcers in vaccinated carriers) ``` neutralizing antitoxin penicillin or erythomycin prevent by toxoid vaccination Spread by saliva droplets
78
diseases DPT (3)
diptheria pertussis (whopping cough) tetanus

Microbiology (42 decks)

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