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Microbiology > Bacteria Ch16-17 Enteric Bacteria > Flashcards

Bacteria Ch16-17 Enteric Bacteria Flashcards

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Biology 101 flashcards
1
Q

describe enteric bacteria and where are they found

A

-gram negative bacilli
- human and animal flora
- commensal groups that have become pathogenic due to acquired virulence factors like toxins from plasmids, bacteriophages or pathogenicity islands

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2
Q

which enteric bacteria are motile and what flagella do they have

A

H-antigen with peritrichous flagella

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3
Q

which enteric bacteria are non motile

A

shigella, klebsiella, yersinia

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4
Q

what type of surface pili do enteric bacteria have

A

fimbriae for adherence and sex pili for plasmid conjugation

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5
Q

which enteric bacteria have capsules and what kind

A
  • klebsiella enterobacter and E coli
  • K or Vi antigen
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6
Q

the enteric bacteria have LPS with

A

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 bacteria have a toxin like shiga toxin

A

get blood in diarrhea

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9
Q

when inflammation and neutrophils what happens to diarrhea

A

pus in diarrhea = dysentery

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10
Q

how are enteric bacteria transferred

A
  • human to human
  • seven F’s: feces, food, fluids, fingers, flies, fomites and fornication
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11
Q

what are the enterobacterial common antigen in LPS

A

outer and inner core sugars

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12
Q

what is the LPS also known as

A

heat stable enterotoxin

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13
Q

what does Lipid A do

A

activates inflammatory responses of macrophages

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14
Q

LPS get shed from______ and is bound by _______.

A

bacteria; plasma protein

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15
Q

what is the primary basis for serotyping

A

O-antigen

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16
Q

what are the virulence factors of enterobacteriaceae

A
  • endotoxin
  • capsule
  • H antigen
  • antigenic and phase variation
  • sequestration
    -antibiotic resistance
  • type III secretion system
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17
Q

what enterobacteriaceae have endotoxin

A

aerobic and some anaerobic gram negative bacteria

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18
Q

what does endotoxin (LPS lipid A) do

A
  • complement activation
  • induces macrophages to secrete inflammatory cytokines which induces fever, clotting, vascular dilation, smooth muscle contraction, shock, death
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19
Q

what does capsule (K antigen or slime) do

A

antiphagocytic: ineffective humoral response

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20
Q

what is H antigen

A

flagella protein (flagellin)

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21
Q

what is pathogenicity island

A

chromosomal location with multiple virulence factors and toxin genes, readily transferable together by conjugation

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22
Q

what amount constitutes severe watery diarrhea

A

greater than 20L per day

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23
Q

what is the virulence factor for cholera

A

cholera like AB- exotoxin heat labile enterotoxin

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24
Q

what bacteria is type III secretion system present in

A

yersinia, salmonella, shigella

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25
Q

how is e coli transmitted

A

-person to person
- contaminated food
- human and animal feces

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26
Q

what are the E. coli virulence factors

A
  • heat labile enterotoxin LT
  • shiga toxin
27
Q

what is another name for heat labile enterotoxin LT and whats the mechanism

A
  • Traveller’s diarrhea
  • ADP ribosylation of G protein -> cAMP increase -> loss of water + electrolytes -> watery diarrhea
28
Q

what does the shiga toxin do

A

inactivation of 60S ribosome subunit by removal of a specific adenine base from a nucleotide of 28S rRNA -> stop translation -> cell death -> bloody diarrhea

29
Q

what are the symptoms of shigella dysenteriae

A

diarrhea with blood
- intestinal cell invasion
- apoptosis
- neutrophilia

30
Q

what is the general treatment for diarrhea

A
  • oral rehydration
  • to 1 liter of water add:
  • 1/2 teaspoon salt
  • 1/4 teaspoon bicarbonate
  • 1/4 teaspoon KCL
  • 4 tablespoon sugar
31
Q

what clinical symptoms does enterohemorrhagic E coli strain cause and whats the treatment

A
  • blood diarrhea, hemorrhagic colitis, hemolytic uremic syndrome
  • replenish fluids
  • antibiotics are contraindicated
32
Q

what is the clinical symptom of uropathogenic e coli strain

A

cystitis (bladder infection)

33
Q

what percentage is e coli of enteric bacteria

A

70-90%

34
Q

what is the mechanism of uptake for shigella dysenteriae

A

-shigellas are taken up by M cell and transported beneath the epithelium. macrophages take up shigellas, die and release the bacteria
- 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
- actin filaments quickly form a tail pushing the sigella into the next cell
- shigellas mutliply in the cytoplasm and the infection extends to the next cell
- infected cells die and slough off. intense response of acute inflammatory cells, bleeding and abscess formation
- apoptosis

35
Q

what is the epidemiology of shigella dysenteriae

A

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

36
Q

what are the shigella dysenteriae virulence factors and what do they cause

A

-shiga toxin: bloody watery diarrhea
- cell invasion -> neutrophils -> pus

37
Q

describe S. enterica

A
  • enteric fever
  • human resevoir
  • typhoid
  • high mortality
38
Q

what do many salmonella species cause

A

-gastroenteritis
- foodborne illness
-poultry resevoir

39
Q

what are the virulence factors for salmonella

A
  • type III secretion induced enteric epithelial uptake via M cells
  • intracellular endosome growth in macrophagaes
  • through macrophages: invasive into different tissues and organs
  • destruction of peyers patches -> intestinal rupture
40
Q

describe the mechanism of salmonella invasion of intestinal epithelia

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

41
Q

what is the mechanism of typhoid fever

A
  • ingestion of S.typhi -> small intestine -> inflammation and ulceration of peyer patches -> diarrhea, hemorrhage and perforation
  • AND goes to mesenteric lymph nodes -> thoracic duct -> transient bacteremia -> multiplication in macrophages in liver, spleen, and bone marrow -> bile-> gallbladder -> bile -> small intestine
  • galbladder -> cholecystitis, carrier state
  • multiplication of macrophages -> speticemia -> fever, kidney and other organs infected
42
Q

describe vibrio cholerae and where is it found

A
  • gram negative vibrio
  • estuaries and marine environments
43
Q

what are the virulence factors of vibrio cholerae

A
  • toxin co-regulated pilus: adhesion to small intestinal epithelia
  • cholera toxin: protein A causes cAMP rise and watery diarrhea
  • an additional toxin “ST” can raise cGMP levels with a similar effect
  • neuraminidase-increase cholera toxin binding
44
Q

what is CTX phi

A

a bacteriophage

45
Q

where is TCP production induced

A

within the intestine while production in other environments appears to be minimal

46
Q

what does TCP stand for

A

toxin coregulated pilus

47
Q

what encodes the proteins that comprise cholera toxin

A

ctxA and ctxB

48
Q

what is the treatment for cholera

A

-formalinized whole cell vaccine
- several sodes; partial protection for 2-3 years

49
Q

what is the common epidemic strain for cholera

A

serovar O1

50
Q

what is the new strain of cholera and the new virulence factor

A
  • serovar O139 with capsule
51
Q

what are the virulence factors for vibrio cholerae

A
  • cholera toxin
  • toxin coregulated pili
  • toxins
  • neuraminidase
52
Q

what are the clinical features for vibrio cholerae

A
  • severe watery diarrhea
  • disease is self limiting as intestinal cells with surface bacteria are shed
53
Q

what is the treatment for vibrio cholerae

A

rehydration and electrolytes

54
Q

what is the epidemiology for vibrio cholerae

A

-fecal transmission in developing countries
- under cooked coastal crabs

55
Q

what type of microbe is vibrio cholerae

A
  • aerobic/ facultatively anaerobic
56
Q

what type of microbe is enterobacteriaeae

A

aerobic/facultatively anaerobic

57
Q

describe campylobacter jejune

A

-gram negative vibrio
- short S or comma shaped rods
-oxidase positive

58
Q

how is campylobacter jejune transmitted and what disease does it cause

A
  • zoonosis: animal reservoir (intestinal)
  • transmission: contaminated food (poultry, milk)
  • disease: gastroenteritis, diarrhea, dysentery
59
Q

how long does it take for campylobacter jejune to resolve without treatment and what type of immunity does it create

A

-less than a week
- creates protective immunity

60
Q

what are the virulence factors for campylobacter jejune

A
  • LPS
  • capsule
  • cytolethal distending toxin
  • growth in intestinal tract: invade intestinal epithelial cells or grow below epithelial layer and inflammatory response
61
Q

does campylobacter jejune cause bacteremia

A

rarely

62
Q

what type of microbe is campylobacter

A

aerobic/facultatively anaerobic

63
Q

what are the virulence factors for C jejune

A

-adhesion
- invasion of mucosal epithelia

64
Q

what clinical symptom does C jejune cause

A

gastroenteritis

Microbiology (39 decks)

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