M- Bacterial Infections of the Gut Flashcards Preview

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

Flashcards in M- Bacterial Infections of the Gut Deck (72)
Loading flashcards...

What is the most communicable of the bacterial diarrheas?



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

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

It has the greatest incidence in children under 5


What is dysentery?

GI disease characterized by :
1. frequent small bowel movements
2. cramps, tenesmus (straining)
3. blood, mucus, inflammatory cells in the feces


What media is used to culture vibrio cholerae?

TCBS- thiosulfate buffered sucrose agar


What are the 2 common features of all enteric bacteria?

1. gram negative
2. found in the GI tract of humans and animals


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

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)


What are the 3 tests used to identify enteric bacterial?

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)


What 3 structures are used in serotyping enteric bacteria?

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


What are the 3 components of LPS?
Where do the toxic properties of the endotoxin lie?

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


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

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


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 -

1. G-
2. lactose fermenting
3. either
4. not H2S producing
5. methyl red positive (indicating low pH


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

150 O
90 K
50 H


What are the 6 diseases caused by E. coli?

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


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

What is ETEC the leading cause of?

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.


How is the diagnosis of ETEC made?
What is the treatment?

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


What is the pathogenesis of EPEC?

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

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


How is EPEC diagnosed and treated?

Diagnosis- O antigen is identified by serotyping

Treatment: fluid and electrolyte replacement therapy


What is the pathogenesis of EIEC?
Who is most affected by this strain?

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


What is the diagnosis and treatment for EIEC?

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

Treatment: fluid and electrolyte replacement


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

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:
2. community-acquired diarrhea in infants
3. traveler's diarrhea (2nd to ETEC)

Diagnosis: Hep2 attachment assay, PCR, DNA probes

Treatment: ciprofloxacin


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

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

It affects children

Diagnosis: Hep2 attachment assay, DNA probe

Treatment = ?


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

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

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


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

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


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

O157 does NOT ferment sorbitol.
non-O157 do ferment sorbitol


What is the treatment of EHEC/STEC infections?

Antimicrobials should NOT be used because they:

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


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

1. UTI
2. bacteremia/respiratory tract infections
3. K1 antigen--> neonatal meningitis


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?

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


What are the 2 major subgroups of salmonella?

1. S. cholerasuis ----> S. enterica
2. S. bongori


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

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

S. typhi has a polysaccharide capsule Vi antigen


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

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.