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GI, Liver, GallBladder, Pancreas > M- Bacterial Infections of the Gut > Flashcards

M- Bacterial Infections of the Gut Flashcards

1
Q

What is the most communicable of the bacterial diarrheas?

A

Shigellosis

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2
Q

What 3 diseases can salmonella cause? What age great group has the greatest incidence of Salmonella disease?

A
  1. septicemia
  2. typhoid fever
  3. food-borne disease

It has the greatest incidence in children under 5

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3
Q

What is dysentery?

A

GI disease characterized by :

  1. frequent small bowel movements
  2. cramps, tenesmus (straining)
  3. blood, mucus, inflammatory cells in the feces
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4
Q

What media is used to culture vibrio cholerae?

A

TCBS- thiosulfate buffered sucrose agar

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5
Q

What are the 2 common features of all enteric bacteria?

A
  1. gram negative

2. found in the GI tract of humans and animals

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6
Q

How is media for the isolation of enteric bacteria both selective and differential?

A
  1. It has bile salts (sodium deoxycholate) to inhibit non-enteric bacteria (selective)
  2. It has one or 2 sugars and a pH indicator to determine sugar fermentation (differential)
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7
Q

What are the 3 tests used to identify enteric bacterial?

A
  1. Lactose fermentation ability [pink on MacConkey’s = ferments lactose]
  2. biochemical tests based on metabolic activity on different media
  3. Serological typing (especially important for salmonella)
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8
Q

What 3 structures are used in serotyping enteric bacteria?

A
  1. O antigen - LPS of outer membrane (endotoxin)
  2. H antigen - flagella
  3. K antigen - capsule (usually polysaccharide, but sometines protein)
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9
Q

What are the 3 components of LPS?

Where do the toxic properties of the endotoxin lie?

A

There is:
Lipid A - where the toxic properties lie
Core polysaccharide
O antigen (polysaccharide side chain)

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10
Q

What are the two major types of bacteria that can be considered enteric pathogens?

A
  1. Primary pathogens- salmonella, shigella that ALWAYS cause disease when they enter the digestive tract
  2. Opportunistic pathogens - normal gut flora like E. coli that only cause disease when the gain access to another region of the body besides the GI tract
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11
Q

Describe the microbiology of E. coli.

  1. G- or G+
  2. lactose fermenting or non-lactose fermenting
  3. motile or non-motile
  4. H2S production?
  5. methyl red? + or -
  6. Voges-PRoskaur? + or -
A
  1. G-
  2. lactose fermenting
  3. either
  4. not H2S producing
  5. methyl red positive (indicating low pH
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12
Q

E. coli has approximately ________O, ________K and ___________H antigenic types.

A

150 O
90 K
50 H

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13
Q

What are the 6 diseases caused by E. coli?

A
  1. ETEC - enterotoxigenic
  2. EPEC - enteropathogenic
  3. EIEC- enteroinvasive
  4. EAEC- enteroaggregative
  5. EHEC- enterohemorrhagic/STEC (shiga toxin)
  6. DAEC- diffusely adhering
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14
Q

What is the pathogenesis of ETEC?
What 2 toxins are involved?
What is the mechanism of action?

What is ETEC the leading cause of?

A

ETEC has a heat labile (LT) and heat stabile (ST) toxin.
LT is an ab toxin like cholera. B binds to GM1 ganglioside receptor and glycoprotein receptor in the brush border of the intestine. A activates adenyl cyclase –> cAMP–> intestinal secretion

ST binds transmembrane guanylate cyclase–>cGMP–> intestinal secretion

Increased secretions lead to TRAVELER’S DIARRHEA.

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15
Q

How is the diagnosis of ETEC made?

What is the treatment?

A

Diagnosis is made with DNA probes and immunological tests.

Treatment: fluid and electrolyte replacement

*usually it does not need antimicrobial treatment, but if it does use TMP-SMX or ciprofloxacin

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16
Q

What is the pathogenesis of EPEC?

Who is most likely to get disease from an EPEC strain of E. coli?

A

EPEC strains attach to intestinal epithelial cells, and use a type II secretion system. They inject their own receptor into the host cell and sent signals to rearrange the cytoskeleton.

This results in effacement/loss of microvilli –>decreased surface area–>malabsorption–> diarrhea

Affects young children and infants

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17
Q

How is EPEC diagnosed and treated?

A

Diagnosis- O antigen is identified by serotyping

Treatment: fluid and electrolyte replacement therapy

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18
Q

What is the pathogenesis of EIEC?

Who is most affected by this strain?

A

EIEC are closely related to shigella. They invade the mucosa through M cells in Peyer’s patches (sampling cells that lack a brush border) and cause watery/bloody diarrhea.

It causes diarrhea and dysentery in children in developing countries

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19
Q

What is the diagnosis and treatment for EIEC?

A

Diagnosis:

  1. serotyping the O antigen using slide agglutination
  2. direct PCR

Treatment: fluid and electrolyte replacement

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20
Q

What is the pathogenesis of EAEC?
Who is most commonly affected?
What is diagnosis and treatment?

A

EAEC does not secrete toxins. It binds to Hep2 human cell line in vitro in stacked bridges. It is thought to cause diarrhea via cell-signaling.

Most commonly affected:

  1. AIDS
  2. community-acquired diarrhea in infants
  3. traveler’s diarrhea (2nd to ETEC)

Diagnosis: Hep2 attachment assay, PCR, DNA probes

Treatment: ciprofloxacin

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21
Q

What is the pathogenesis of DAEC?
Who is most commonly affected?
What is diagnosis/treatment?

A

It adheres to Hep2 human cell line in vitro in a diffuse pattern.

It affects children

Diagnosis: Hep2 attachment assay, DNA probe

Treatment = ?

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22
Q

What is the pathogenesis of EHEC/STEC?
What toxin is involved?

What symptoms are associated with disease caused by EHEC/STEC?

A

There are 2 modes of pathogenesis for EHEC/STEC.

  1. type III secretion producing “attach and efface” lesions like in EPEC
  2. Phage-encoded Shiga toxin binds to G3 glycolipid receptor on epithelial cells and cause secretion.
    It is also renal toxic by attaching to renal epithelial cells

This causes:

  1. diarrhea, bloody or not
  2. HUS in children
  3. TTP in adults
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23
Q

How is the EHEC/STEC virus spread?
What is the reservoir?
What is the “classic strain”?
Who is at the highest risk of infection?

A

It has a very low infectious dose and CAN be transmitted person-to-person, but is normally acquired from ingestion of contaminated food (like hamburger meat)

The reservior is : cattle, sheep, goats, deer

The classic strain is O157:H7, although non O157 diarrhea cases is slightly more than O157.

Highest risk of infection in children and the elderly

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24
Q

What will the difference between O157 and non-O157 be on a sorbitol-MacConkey agar be?

A

O157 does NOT ferment sorbitol.

non-O157 do ferment sorbitol

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25
Q

What is the treatment of EHEC/STEC infections?

A

Antimicrobials should NOT be used because they:

  1. increase expression of the shiga toxin
  2. worsen kidney problems
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26
Q

What extra- GI diseases are caused by E. coli?

A
  1. UTI
  2. bacteremia/respiratory tract infections
  3. K1 antigen–> neonatal meningitis
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27
Q

What 5 organisms found in the normal flora are known to cause disease when the host immune system is circumvented (catheter) or inhibited (chemo, steroids)?
What disease/problem is each organism associated with?

A
  1. Klebsiella - pneumonia in alcoholics
  2. Enterobacter- contaminated IV lines
  3. Serratia- pink/red colonies on agar. Catheters, neonatal disease [s. marcescens]
  4. e. coli - resp. tract infections, neonatal meningitis, UTI
  5. proteus - UTI, struvite kidney stones
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28
Q

What are the 2 major subgroups of salmonella?

A
  1. S. cholerasuis —-> S. enterica

2. S. bongori

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29
Q

Describe the microbiology of salmonella.

  1. G+ or G-
  2. lactose fermenting or non-lactose fermenting
  3. motile or non-motile
  4. capsule or no capsule
A

Salmonella are G- rods.
They do NOT ferment lactose.
They are motile and have flagella

S. typhi has a polysaccharide capsule Vi antigen

30
Q

How is S. typhi spread?
What is the incubation period?
Describe the pathogenesis of S. typhi.

A

It is spread via contaminated water and food.
The incubation is 4 days- 3wks

S. typhi can:

  1. travel down to the ileum where it penetrates through Peyer’s patches into the bloodstream.
  2. make intestinal epithelial cells ingest them via type III secretion where they induce cytoskeleton rearrangement and enter via membrane ruffle.

They can be facultative intracellular parasites in phagocytes, enter the RES, and reinfect intestinal tissue.

31
Q

How do people with S. typhi present?

A
  1. asymptomatic carrier due to chronic carriage in the gall bladder
  2. rash on the trunk “rose spots” with or without diarrhea.
32
Q

Who is most likely to be infected by S. typhi?

A

Children under the age of 1 in developing countries.

S. typhi is only found in humans (no animal reservoir)

33
Q

How is S. typhi diagnosed?
What is treatment?
What can be done as prevention?

A

It is diagnosed by isolating the species from:

  1. blood
  2. recent stool
  3. bone marrow
  4. punch biopsies from the “rose spots”

The species are plated on MacConkey agar (should grow and be grey) and Hektoen (blue due to peptone metabolism)

Treatment is TMP-SMX, ampicillin or cephalosporin

Prevention -

  1. live vaccine of attenuated Ty21a mutant
  2. purified Vi capsular antigen delivered by injection
34
Q

What strain of salmonella can cause gastroenteritis?

What is their reservoir?

A

nontyphoidal strains of salmonella like:

  1. s. enteritidis
  2. s. typhimurium

The reservoir is in the GI tract of animals

35
Q

What are the symptoms of infection for nontyphoidal salmonella?
How long does the infection last?
What is the pathogenesis?

A

fever, nausea, vomiting, diarrhea.

The infection can last up to 7 days but is self-limiting.

Salmonella invades the intestinal epithelial cells and causes inflammatory events.

36
Q

What is the most important cause of food borne bacterial disease in the US?
Where else is this infection found?
What is the most susceptible populations?

A

nontyphoidal salmonella like:
S. typhimurium, S. enteriditis, S. newport

Salmonella can also be contracted from :

  1. pet turtles (turtles are carriers)
  2. egg yolks (0.01% of shell eggs have it)

The most susceptible populations are the elderly, neonates and immunocompromised

37
Q

What is the diagnosis, treatment and prevention for salmonella?

A

Diagnosis: isolate culture from fresh stool

Treatment: antibiotics are ONLY used for

  1. infections in healthy people that have spread out of the GI tract
  2. immunocompromised, infants, over 50

Prevention: virtually impossible

38
Q

What are the 4 strains of shigella?
Do they ferment lactose?
Are they motile or non-motile?
Which strain makes a phage endcoded Shiga toxin?

A
  1. S, sonnei - ferments lactose slowly
  2. S. dysenteriae- type 1 produces phage encoded Shiga toxin necessary for HUS
  3. s. flexneri
  4. s. boydii

Aside from sonnei, the other shigella are NOT lactose fermenters.
They all lack flagella (H) and are non-motile

39
Q

What is the most infectious organism to cause GI problems? What is the inoculum?
What are the signs/symptoms?
What are the fatal complications?

A

Shigella is the most infectious with an inoculum of 10 organisms.
The symptoms will be watery diarrhea, bloody diarrhea or dystentery (blood, pus, mucus in the stool). Cramping is common and ulcerative lesions are in the colon.

Fatal complications are bacteremia and HUS ( from the Shiga toxin production)

40
Q

Describe the pathogenesis of shigella.

A
  1. penetrate into M cells
  2. taken up by macrophages in lamina propria
  3. macrophages secrete cytokines and undergo apoptosis
  4. intestinal epithelial cells produce attractants for neutrophils
  5. neutrophils migrate between the epithelial cells breaking down tight junctions
  6. bacteria are released from dead macrophages and invade epithelial cells from the basolateral side
41
Q

Where do the majority of shigella lesions form?

A

The rectosigmoid region

42
Q

In the US in what population is shigellosis most frequently seen? What strains?

A

Seen in children under 5 (often in day care centers)

  1. s. sonnei
  2. s. flexneri

Persons in custodial institutions are also at risk

43
Q

What is diagnosis and treatment for Shigella?

How do you prevent it?

A

Diagnosis:

  1. fresh stool sample - examined for leukocytes (from the ulcerative lesions the invasive shigella caused)
  2. rectal swabs
  3. PCR test and DNA probes

Treatment:

  1. fluid and electrolytes
  2. antibiotics for really severe (normal drugs will be resistant)
  3. medicines (loperamide) that reduce diarrhea should NOT be used

Prevention:
hygiene practices- handwashing, preventing contamination of food and water

44
Q

Despite the fact that vibrio cholerae has 190LPS serotypes, only 2 cause epidemic cholera in humans. What are they?

A

1 O1

2. O139

45
Q

Are vibrio cholera oxidase + or -?

motile or non-motile?

A

Oxidase + and motile using a single polar flagellum

46
Q

How is vibrio cholerae transmitted? What is incubation period?
What occurs in mild disease?
What occurs in cholera gravis?

A

It is transmitted in food and water. The incubation is 1-3 days.
Mild disease will be asymptomatic or watery diarrhea.

Cholera gravis is severe diarrhea, vomiting that leads to dehydration. If there is no treatment, shock ensues. Fluid loss is 1L/hr and is “rice water stool”

47
Q

Describe the pathogenesis of vibrio cholera.

A
  1. enters the GI tract, passes the acid barrier of the stomach
  2. the organisms that survive attach to brush border of the small intestine using pili/fimbrae
  3. Secrete cholera toxin (A-B with one A and five B)
  4. the five B form a pentamer and bind to GM1 ganglioside
  5. the A subunit cleaves to A1 and A2
  6. A1 catalyzes ADP ribosylation of GTP binding protein in the intestinal epithelium–> constant activation of adenyl cyclase–>cAMP
  7. increased Cl secretion and fluid loss
48
Q

What is the reservoir for V. cholera?

How does it survive for extended periods of time?

A

It lives in brackish water and estuarine waters and attaches to plankton, algae and shellfish.

It lives for long time by converting itself from growing and metabolically active cell into a dormant one

49
Q

What is diagnosis and treatment for V. cholera?

A

Diagnosis- cultured from stool and appears as yellow colonies on TCBS, vibrios on gram stain, motile vibrios on dark field.

Treatment:

  1. fluid and electrolyte replacement
  2. maybe doxycycline or tetracycline
50
Q

What is prevention of cholera infections?

A

It is transmitted fecal-oral in water and food supplies so make sure that water supply is chlorinated and food are pasteurized and cooked completely.

51
Q

What disease is caused by vibrio cholera that is not O1 or O139 ( dont make cholera toxin)?
How is this infection obtained?

A

gastroenteritis caused by ingestion of undercooked shellfish

52
Q

How is V. parahemolyticus transmitted?

What does it cause?

A

It is transmitted by ingesting raw or undercooked shellfish. It can also infect open wounds.

It causes gastroenteritis

53
Q

Where is V. vulnificus found?

What does it cause?

A

It is found in warm sea water and can spread by ingestion (oysters).
It can cause vomiting and diarrhea.

It can also directly infect open wounds and abrasions leading to skin breakdown and ulceration

54
Q

Which is more virulent, V. vulnificus or v. parahemolyticus?

A

V. vulnificus can cause septicemia and serious wound infection in alcoholics, chronic liver disease and immunocompromised.

55
Q

Describe the lab features of campylobacter.

A

They are zoonotic bacteria that are :

  1. obligate microaerophilic
  2. grow at 43-43 degrees celcius
56
Q

What is the pathogenesis of C. jejuni?

A

It invades the small intestine and colon mucosa and causes fever, cramping and diarrhea (that may or may not be bloody).
Leukocytes are often in stool (like shigella)

57
Q

What are the sequelae of C. jejuni infections?

A
  1. Guillen-Barre

2. hypersensitivity phenomena (reactive arthritis)

58
Q

What is the incidence of campylobacter?

A

bimodal with children less than 1 year and a second around 15-24 years of age.

59
Q

How is Campylobacter diagnosed and treated? How can spread be prevented?

A

Diagnosed:
isolation from fecal samples

Treatment:
electrolyte and fluid replacement

Prevention
Ther is no vaccine and it is zoonotic so it is hard to keep it out of the food supply. Cook your chicken all the way.

60
Q

Describe the pathogenesis of vibrio cholera.

A
  1. enters the GI tract, passes the acid barrier of the stomach
  2. the organisms that survive attach to brush border of the small intestine using pili/fimbrae
  3. Secrete cholera toxin (A-B with one A and five B)
  4. the five B form a pentamer and bind to GM1 ganglioside
  5. the A subunit cleaves to A1 and A2
  6. A1 catalyzes ADP ribosylation of GTP binding protein in the intestinal epithelium–> constant activation of adenyl cyclase–>cAMP
  7. increased Cl secretion and fluid loss
61
Q

What is the reservoir for V. cholera?

How does it survive for extended periods of time?

A

It lives in brackish water and estuarine waters and attaches to plankton, algae and shellfish.

It lives for long time by converting itself from growing and metabolically active cell into a dormant one

62
Q

What is diagnosis and treatment for V. cholera?

A

Diagnosis- cultured from stool and appears as yellow colonies on TCBS, vibrios on gram stain, motile vibrios on dark field.

Treatment:

  1. fluid and electrolyte replacement
  2. maybe doxycycline or tetracycline
63
Q

What is prevention of cholera infections?

A

It is transmitted fecal-oral in water and food supplies so make sure that water supply is chlorinated and food are pasteurized and cooked completely.

64
Q

What disease is caused by vibrio cholera that is not O1 or O139 ( dont make cholera toxin)?
How is this infection obtained?

A

gastroenteritis caused by ingestion of undercooked shellfish

65
Q

How is V. parahemolyticus transmitted?

What does it cause?

A

It is transmitted by ingesting raw or undercooked shellfish. It can also infect open wounds.

It causes gastroenteritis

66
Q

Where is V. vulnificus found?

What does it cause?

A

It is found in warm sea water and can spread by ingestion (oysters).
It can cause vomiting and diarrhea.

It can also directly infect open wounds and abrasions leading to skin breakdown and ulceration

67
Q

Which is more virulent, V. vulnificus or v. parahemolyticus?

A

V. vulnificus can cause septicemia and serious wound infection in alcoholics, chronic liver disease and immunocompromised.

68
Q

Describe the lab features of campylobacter.

A

They are zoonotic bacteria that are :

  1. obligate microaerophilic
  2. grow at 43-43 degrees celcius
69
Q

What is the pathogenesis of C. jejuni?

A

It invades the small intestine and colon mucosa and causes fever, cramping and diarrhea (that may or may not be bloody).
Leukocytes are often in stool (like shigella)

70
Q

What are the sequelae of C. jejuni infections?

A
  1. Guillen-Barre

2. hypersensitivity phenomena (reactive arthritis)

71
Q

What is the incidence of campylobacter?

A

bimodal with children less than 1 year and a second around 15-24 years of age.

72
Q

How is Campylobacter diagnosed and treated? How can spread be prevented?

A

Diagnosed:
isolation from fecal samples

Treatment:
electrolyte and fluid replacement

Prevention
Ther is no vaccine and it is zoonotic so it is hard to keep it out of the food supply. Cook your chicken all the way.

GI, Liver, GallBladder, Pancreas (24 decks)

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