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microbiology > enteric bacteria > Flashcards

enteric bacteria Flashcards

1
Q

enteric bacteria
gram?
shape?
common in what flora?

A

Gram−
bacilli
Some are common members of human and animal flora

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2
Q

pathogenic enteric bacteria

A

Some are members of commensal groups that have become pathogenic due to acquired virulence factors like toxins from plasmids, bacteriophages or“pathogenicity islands”

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3
Q

motility of enteric bacteria

A

Most can be motile with peritrichous flagella (H-antigen)

Some are non-motile (Shigella, Klebsiella, Yersinia)

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4
Q

pili of enteric bacteria

A

Most have surface pili: fimbriae for adherence and sex pili for
plasmid conjugation

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5
Q

capsules of enteric bacteria
named antigen?
which species

A

Some species have capsules (K or Vi antigen)

most Klebsiella species, some Enterobacter and E.coli species

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6
Q

enteric bacteria LPS

A

all strains with outer-membrane LPS (heat-stable endotoxin) with enterobacterial common antigen and serotype-specific O- antigen

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7
Q

When bacteria have a toxin like cholera toxin:

A

get watery diarrhea

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8
Q

When also have a toxin like

Shiga toxin:

A

get blood in diarrhea

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9
Q

When also have inflammation

and neutrophils:

A

get pus in diarrhea =dysentery

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10
Q

Characterization of various
pathogenic E. coli strains is
based on

A

toxins produced and pattern of cell invasion and destruction

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11
Q

transmission modes of enteric bacteria

A

Transmission: • person-to-person • “seven F’s” = feces, food,
fluids, fingers, flies, fomites, and fornication

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12
Q

other virulence factors of gram- enteric bac could cause?

A

bacteremia

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13
Q

LPS of enteric bac common antigen? variable portion?

A

Outer- and inner-core sugars are the enterobacterial common antigen
O antigen is the variable portion

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14
Q

LPS also known as

A

heat stable enterotoxin

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15
Q

LPS shedding

A

LPS gets shed from bacteria and is bound by plasma protein LBP (LPS-binding protein).
This facilitates binding to macrophages and enhances inflammatory response

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16
Q

lipid A of LPS activates?

A

inflammatory response of macrophages

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17
Q

“pathogenicity island”

A

= chromosomal location with multiple virulence factors and toxin genes, readily transferable together by conjugation.
Example: uro-pathogenic E.coli

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18
Q

cholera-like AB-exotoxin mechanism

A

B component binds the membrane of the host cell and A component penetrates
A component will act as an ADP ribotrasferylase and activate a G pro
G pro causes adenylate cyclase to increase cAMP leading to increased electrolyte and water secretion= severe watery diarhea

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19
Q

cholera-like AB-exotoxin known as

A

heat liable enterotoxin

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20
Q

Type III secretion system
found in what strains?
mechanism?

A

present in: Yersinia, Salmonella, Shigella, enteropathogenic EPEC (E.coli), Pseudomonas and Chlamydia (all gram-)

20-protein system that looks like a short, hollow flagellum (“needle”) to inject a variety of species specific toxins into host cells; often affects actin filaments/ rearranges them to allow bacteria to adhere (EPEC)

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21
Q

intimin/ TIR
strains seen in?
how is TIR delivered?

A

seen in both EPEC and EHEC

TIR delivered to host cell mem via type III secretion, allows both e coli strain to bind

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22
Q

Escherichia coli transmission

A
  • person-to-person
  • contaminated food
  • human and animal feces (no hand washing; insect vectors)
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23
Q

additonal pathogenic e coli strains

A

Uro-Pathogenic E.coli

• Meningitis-associated E.coli

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24
Q

e coli gram?

A

negative

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25
Q

e coli virulence factors

A 
heat-labile enterotoxin “LT" (cholera-like AB-exotoxin)
shiga toxin (AB-exotoxin cytotoxin)
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26
Q

Ø heat-labile enterotoxin “LT” of E coli

A

(cholera-like AB-exotoxin): ADP-ribosylation of G protein ► cAMP ­ ►
loss of water + electrolytes ► watery diarrhea (e.g. foodborne enterotoxigenic ETEC E.coli)
cause of travellers diarhea

27
Q

Shiga toxin of E coli
mechanism?
strain?
additonal complication?

A

(AB-exotoxin cytotoxin): inactivation of 60S ribosome subunit by removal of a specific adenine base from a nucleotide of 28S rRNA ► stop translation ► cell death ►bloody diarrhea

(e.g. foodborne enterohemorrhagic EHEC E.coli O157:H7)

In addition: ► hemolytic uremic syndrome ► kidney damage

28
Q

Shigella dysenteriae

A

In Shigella dysenteriae this set of symptoms “diarrhea with blood” is combined with
intestinal cell invasion, apoptosis and neutrophilia (► “pus”) to define “dysentery

29
Q

treatment of mild forms of diarhea

A

oral rehydration

mixture of water with salts and sugars

30
Q

seasonal occurance of GI diseases

A

more common when warm= spoiled food

31
Q

EHEC EnteroHemorrhagic (typically O157:H7) clinical presentation

A

bloody diarrhea
hemorrhagic colitis
hemolytic uremic syndrome

32
Q

EHEC EnteroHemorrhagic (typically O157:H7) treatment

A

replenish fluids
(antibiotics are
contraindicated)

33
Q

UroPathogenic presentation

casuative strains %?

A

cystitis/ bladder infections

70-90% caused by E coli, 5-10 by klebsiella/proteus amd 5-10 by s. saprophyticus

34
Q

Shigella dysenteriae cell entry/infection

35
Q

Shigella dysenteriae epidemiology

A

oral-fecal route, contaminated food/ water, humans the only source

36
Q

Shigella dysenteriae virulence factors

lead to?

A

Shiga toxin: bloody and watery diarrhea
cell invasion: neutrophils/ pus
both lead to dysentery

37
Q 
Salmonella 
strain 
causes what fevers? 
reservoir?
mortality?
A

S.enterica
• enteric fever, typhoid fever
• human reservoir
• high mortality

38
Q

Many Salmonella species cause?

from what source outside humans?

A
  • gastroenteritis

* poultry reservoir= foodborne illness

39
Q

Virulence Factors of salmonella

A

type III secretion

growth within macrophages

40
Q

type III secretion in salmonella induces?

A

Type III secretion induces enteric epithelial uptake via M cells

41
Q

endosomal growth in macrophages by salmonella
allows for?
how can it not be destroyed in macrophages?
destruction of what gut structure?

A

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 (bacteremia)
Ø destruction of Peyer’s Patches ► intestinal rupture

42
Q 
Salmonella invasion of intestinal epithelia
which cells?
causes? 
release of? 
transport to?
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, can lead to further disease
43
Q

Typhoid Fever diagram
how can it lead to speticemia?
carrier state?

44
Q

Enterobacteriaceae
gram
shape
respiration

A

Gram-
rods,
aerobic / facultatively anaerobic

45
Q

Vibrio cholerae
gram
shape
found where?

A

Gram−
vibrio (curved rods)
(salt tolerant) found in estuaries and marine environments

46
Q

Virulence Factors of vibro cholarae

A 
toxin co-regulated pilus
cholera toxin
additional toxin “ST”
Neuraminidase
other toxins
47
Q

virulence factors of Vibro cholera delivered how (to the bac)?

A

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

48
Q

Ø toxin co-regulated pilus (tcp) of Vibro cholera allows for?

A

adhesion to small intestinal epithelia

49
Q

cholera toxin/ ST toxin of Vibro Cholera

A 
cholera toxin (heat-labile exotoxin “LT”): protein A causes cAMP rise + watery diarrhea
an additional toxin “ST” can raise cGMP levels with a similar effect
50
Q

Neuraminidase of vibro cholera

A

-increase cholera toxin binding

51
Q

CTXφ (a bacteriophage) and Vibrio cholerae

A

TCP = Toxin coregulated pilus, TCP production is induced within the intestine, while production in other environments appears to be minimal, allows the phage to deliver genes to the bacteria for replication, expression and secretion (contains the genes for various virulence factors)

52
Q

which genes of CTXφ (a bacteriophage) encode the cholera toxin for Vibrio cholerae

A

ctxA and ctxB encode the
proteins that comprise
cholera toxin

53
Q

cholera vax

A

formalinized whole-cell vaccine (inactivated cell) : several doses; partial protection for 2-3 yrs

54
Q

epidemic strains of cholera

common one/ new one?

A

Common epidemic strain: serovar O1

New strain: serovar O139 with capsule as new virulence factor (O1 vaccine does not protect)

55
Q

clincal features vibro cholera

limited?

A

severe watery diarrhea

self-limiting: intestinal surface cells with bacteria are shed

56
Q

treatment vibro cholera

A

rehydration

57
Q

epidemiolgy of vibro cholera

A

fecal transmission

under cooked coastal crabs

58
Q

Campylobacter jejune

gram and shape

A

Gram−

vibrio (short S- or comma-shaped rods)

59
Q

Campylobacter jejune virulence factors

A

Ø LPS
Ø capsule
Ø cytolethal distending toxin
Ø Growth in intestinal tract:

60
Q

Campylobacter jejune growth in intestinal tract
where?
can lead to?

A

§ invade intestinal epithelial cells or grow below epithelial layer.
§ inflammatory response

61
Q

Campylobacter jejune disease resolution

A

resolves without treatment in 1 week, creates protective immunity

62
Q

Campylobacter jejune
often from?
transmission?
diseases caused?

A

Zoonosis: animal reservoir (intestinal)
Transmission: contaminated food
Disease: gastroenteritis, diarrhea, dysentery

63
Q

bacteremia of Campylobacter jejune:

A

rarely causes bacteremia

microbiology (42 decks)

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