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Bacteria > GI > Flashcards

GI Flashcards

1
Q

What happens when there’s a shift in the bidrectional flux in the small bowel?

A

Can result in overload of colonic absorptive capacity, leading to diarrhea

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2
Q

How do infections change the normal physio of the intestines?

A

Penetration through intact mucosa
Inflammatory or cytotoxic destruction of ileal/colonic mucosa
Shift in bidrectional water and electrolyte flow in upper small intestine

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3
Q

Ex of penetration through intact mucosa–organisms

A

Listeria

Salmonella typhi

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4
Q

Ex of inflammation or cytotoxic destruction of ileal or colonic mucosa

A 
Shigella
Non typhoidal salmonella types
enterohermoorhagic e coli
campylobacter
helicobacter
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5
Q

ex of shift in bidirectional water and electrolyte flow–name organism

A

vibrio cholerae

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6
Q

listeria metabolism, spore/no spore, stain and shape

A

aerobic
no spores
gram positive
rod

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7
Q

What is unique about Listeria?

A

grows at 1-45 C and high salt (think stored foods!)

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8
Q

motility/non-motility of listeria?

A

motile at room temp

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9
Q

What helps to ID listeria microscopically?

A

Tumbling

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10
Q

Who does Listeria cause disease in?

A

neonates, elderly, pregnant, immunocompromised

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11
Q

Pathogenesis of Listeria

A

consume contaminated food
L. monocytogenes survives in acid and bile salts
adheres to host cell
enters enterocytes or M cells
pH in phagosome induces listeriolysin O and 2 phospholipase C enzymes
Listeria replicates freely in cytoplasm
ActA on Listeria polymerizes host actin and enables it to move intracellularly to membrane
Actin polymerization

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12
Q

What kind of symptoms do you see for Listeria in the healthy?

A

mild flu like
acute
self limited gastroenteritis

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13
Q

What kind of symptoms do you see for Listeria in the immunocrompromised adult?

A

meningitis, high mortality

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14
Q

symptoms of listeria in neonate?

A

early onset-abortion, stillbirth, premature birth
granuloma formation in many organs
late onset-meningitis

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15
Q

Stain and shape of Salmonella

A

gram negative

rod

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16
Q

Where are salmonella found

A

soil, water, normal intestinal flora

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17
Q

Does Salmonella ferment or not ferment lactose?

A

does not

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18
Q

Pathogenesis of Salmonella

A

withstands stomach acid
attaches to small intestine and invades M cells and enterocytes
Replicates in endocytic vacuoles
endocytic vacules are stabilized by injection of Salmonella proteins with two type III secretion systems

Type III secretion systems (pathogenicity island 1=injected into host cell to tell cell to take up Salmonella) (pathogenicity island 2=injected into cytoplasm of host cell to resist phago-lysosome fusion)

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19
Q

Salmonella can cause

A

Gastroenteritis (serotypes other than Typhi and paratyphi)
enteric or typhoid fever (for typhi, bacteria not only invade enterocytes but replicates in macrophages–spreads through reiculoentheolial system to liver, spleen, blood)

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20
Q

Salmonella causes gastroenteritis commonly in?

A

children and elderly, more frequent in summer

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21
Q

Where is Salmonella found?

A

food (poultry, eggs, ground beef)

pet turtle feces

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22
Q

Differences between salmonella typhi and salmonella causing gastroenteritis?

A

inoculum is low for typhi

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23
Q

How does one get Salmonella typhi?

A

person to person, fecal contamination

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24
Q

Which has a vaccine? Listeria or Salmonella

A

Salmonella (use for travel)

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25
Q

diseases of Salmonella

A 
gastroenteritis (fever, abd cramps, headache, nonbloody diarrhea)
salmonella septicemia (can be caused by all species)
enteric fever-(colonizes gall bladder and reinfects intestines)
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26
Q

Salmonella is lactose positive or negative?

A

lactose negative

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27
Q

Salmonella is motile or non motile?

A

motile

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28
Q

What chemical does Salmonella make?

A

H2S

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29
Q

stain, motility, metabolism of shigella

A

gram negative
non motile
does not ferment lactose

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30
Q

Does shigella have or not have a capsule?

A

no capsule

31
Q

How is Shigella spread?

A

fecal oral

32
Q

Pathogenesis of shigella

A

replicate intracellulary in COLON
invade M cells initially in small intestine
inject type III proteins into host cells to be engulfed (proteins are IpaA, IpaB, IpaC, IpaD)
inside cells, shigella lyses the vacuole and replicates freely in cytoplasm
polymerizes host actin to move to other cells
induce apoptosis of phagocytic cells
make Shiga toxin

33
Q

How does Shiga toxin work?

A

enzymatic A component cleaves 28S ribosomal RNA–causes colon’s epithelium to die

34
Q

Who does Shigella cause disease in?

A

mostly children

35
Q

symptoms of shigella

A 
abdominal cramps
tenesmus (strain to defecate)
diarrhea
pus and blood in stool
neutrophils and mucous in stool
dysentery (frequent stool w blood and mucous-cells sloughed off)
36
Q

What do Shigella appear like in culture?

A

lactose negative on selective medium (colorless colony on MacConkey agar)

37
Q

Differences btwn Shigella and Salmonella? Similarities?

A

both are lactose negative
shigella is non motile, salmonella has flagella
shigella doesn’t make H2S

38
Q

How do you treat Shigella?

A

mild infections are self limiting

antibiotics only given for serious cases

39
Q

Why is giving an antidiarrheal drug not good for Shigella

A

can make toxin stay longer in host instead of allowing it to be flushed out–causes more cell death

40
Q

What are the Enterobacteriaceae in gram stain?

A

negative

41
Q

How is enterohemorrhagic E. coli spread?

A

fecal oral

42
Q

Is Enterohemorrhagic E coli an opportunistic pathogen or true pathogen?

A

true pathogen

43
Q

What do EHEC produce that is cytotoxic?

A

Shiga toxin

44
Q

EHEC pathogenesis

A

makes a type III secretion system to enable it to be ingested by host cell
Also injects Tir, which binds to EHEC’s OM protein intimin
EHEC grows in place and produces Shiga toxin

45
Q

How are Shiga toxin genes in EHEC?

A

Bacteriophage

46
Q

How does one get EHEC?

A

consume undercooked beef, meat, anything contaminated with cattle feces

47
Q

Disease symptoms of EHEC?

A

ranges from mild diarrhea to hemorrhagic colitis

48
Q

What is hemorrhagic colitis?

A

intense abdominal pain and bloody diarrhea happening 3-4 days after eating food contaminated with EHEC

49
Q

In children, what can EHEC cause?

A

hemolytic uremic syndrome (acute renal failure, hemolytic anemia)

50
Q

How to differentiate EHEC in culture?

A

unable to ferment sorbitol–differential sorbitol containing MacConkey agar on which E coli are pink but EHEC is colorless

51
Q

Treatment for EHEC?

A

not given antibiotics –(in experiments antibiotics increased Shiga toxin release)
monitor in case develop microangiopathic complications (HUS)

52
Q

Stain, shape, metabolism, motility of Campylobacter

A

gram negative
curved rod (spiral or comma)
non-fermentative (microaerophilic)
motile with single flagella at one or two poles

53
Q

What temp can Campylobacter grow?

A

42

54
Q

Pathogenesis of Campylobacter

A

inflammation of small intestine and colon, diarrhea
Ulcers
infections linked with autoimmune disorders (guillain barre, reactive arthritis)—so due to LPS and cross reactivity
Makes toxin that stops cell division

55
Q

How do you get campylobacter?

A

consume contaminated food (especially chicken)

56
Q

When are Campylobacter infections most abundant?

A

summer and early fall

57
Q

Symptoms of Campylobacter infection

A

diarrhea (MORE THAN 10 bowel mvmts/day)
bloody stool
fever
abd pain, inflammation, ulcer

58
Q

Microscopy of Campylobacter

A

darting motility
S shaped in stool
RBCs and WBCs in stool

59
Q

Culture of Campylobacter

A

difficult–slowly grows, microaerophile, higher temps

60
Q

Treatment of Campylobacter

A 
fluid replacement (for diarrhea)
Serious cases-give antibiotics
61
Q

Stain, shape, motility, metabolism of Helicobacter

A

gram negative
curved rod
multiple flagella
microaerophilic

62
Q

What enzyme in helicobacter converts urea to NH3 and CO2?

A

urease

63
Q

Culture of Helicobacter

A

difficult. also difficult to isolate

64
Q

How does urease help Helicobacter?

A

helps it survive in acidic conditions of stomach

65
Q

Survivial mechanisms of Helicobacter in stomach

A

urease for acid
swim through mucus with flagella
stick to gastric epithelium (lewis blood group Ags and laminin)
pH at epithelial surface = 7

66
Q

Pathogenesis of Helicobacter

A

2 LOCI:
Toxin VacA–makes an anion specific channel, forms large vacuoles in cells, changes tight jxns, causes gastric epithelial erosion
SECOND locus: multiple genes (type IV secretion system that injects CagA inducing IL-8 release, enhance IL-8 transcription, Type IV effectos that cause pedestal formation)

67
Q

Symptoms of Helicobacter infection

A

gastritis
gastric ulcer formation
but asymptomatic in 70-80% of infected

68
Q

Transmission of Helicobacter

A

fecal oral

69
Q

Diagnosis of Helicobacter

A

urea breath test (labeled urea)
histology of gastric biopsy
biochemical detect. urease in gastric biopsy
h pylori antigens from stool samples

70
Q

Stain, shape of vibrio, motility

A

gram negative
curved rod
single polar flagella

71
Q

Pathogenesis of Vibrio

A

Cholera toxin.
Cholera toxin is encoded by bacteriophage
Toxin binds to ganglioside receptor on intestinal epithelial cells
A subunit ADP ribsylates Gs–increased cAMP—stimulates CFTR causing Cl- secretion, inhibts NaCL absoprtion, results in net water loss
OSMOTIC DIARRHEA

Also encoded from phage:
TCP-toxin coregulated pilus for attachment
chemotaxis proteins to get vibrio to host epithelial cells

72
Q

How does vibrio still produce diarrhea without cholera toxin?

A

zonnula occludens toxin–disrupts tight jxns

accessory cholera enterotoxin–increases fluid secretion

73
Q

Where are Vibrio found?

A

marine environments

74
Q

How is cholera spread to humans?

A

contaminated water and food (asymptomatic individuals can shed organism)
NO human to human transmission b/c high infectious dose needed

Bacteria (6 decks)

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