Yu- GI Bacteria X4- Melissa** Flashcards
How many species of bacteria colonize the human GI tract?
How was this determined?
1000 different species in human gut (determined by 16s rRNA sequencing)
How many species of bacteria colonize the human BODY?
100 trillion (10^13) bacteria in human body (more bacteria than human cells)
How does the micro biome shift between healthy patients and patients with bowel disease? (2)
- # pathogenic ‘proteobateria’ like e. coli ^ in patients with IBD + Necrotizing enterocolitis
- patients with DM2 have more bacteriodetes
What is the function of the microbiota in the GI tract?
What is one factor that can dramatically change GI microiota?
Describe the layers of the GI tract from the lumen outward.
- Microbiota identified by immune system as non-foreign early in life; Provides barrier to colonization by foreign bacteria
- Microbiota dramatically changed by ABX use
- Microbiota–> Mucus layer–> Epi–> Mucosa
Three important bacteria in the stomach microbiome
- Lactobacillus
- Streptococcus
- H. pylori (associated with PUD)
Two important bacteria in the duodenum and jejunum microbiome, also found in standard probiotics?
- Streptococcus
- Lactobacillus
How does the micro biome change at the point of the ileum through the colon?
- *Overall increase in # of species
* *Overall increase in anaerobic species (Clostridium, Bacteroides, etc)
In the colon, what is a vital function of the microbiome outside the realm of immunologic defense?
**Many anaerobes that ferment polysaccharides and oligosaccharides (used by epi cells)
Segmented Filamentous Bacteria (SEM): What are these bacteria and what purpose do they serve?
- Spore forming anaerobic bacteria (like clostridium)
- Live in mucus layer on top of lymphoid tissue
- Enter M cells; Stimulate B and T cells to induce maturation of T17 cells; modulate gut immunity in animal models
4 mechanisms of bacterial gastroenteritis:
Also: what is the point of methylene blue staining of poop?
1) Toxin mediated (endo/exo)
2) Superficial invasion local inflammation
3) Deep invasion of blood or lymph
4) Mechanical trauma +/- abscess
Methylene blue: detects leukos in poop; + in INVASIVE diarrhea
(Shigella, salmonella, campy)
H. Pylori:
Gram/ motility/ O2 ?
Oxidase and Catalase present or absent?
Optimal pH?
Gram (-) curved rod Motile (unipolar flagella) Microaerophillic Oxidase, catalase, and ALK phos + Lives at pH 7--> 8; dies at pH 4.
H. pylori: 6 important virulence factors
- Sheathed flagellae
- Urease (+) –> ^ NH3, neutralize stomach acid
- VacA (vacuolating toxin)
- CagA (pathogenicity gene islands, passed bw strains)
- Phospholipase
- Protease
How common is H. pylori infection?
How does H. pylori induce infection?
What are 4 possible sequelae of H. pylori infection?
1 stomach infection
Normal microbiota overgrowth in mucin layer–>
Adhesion + cytotoxin–> Gastric atrophy–>
Class I carcinogen
1) Chronic gastritis
2) Peptic Ulcer Disease
3) MALT Lymphoma
*will shrink with irradication of the pathogen
4) Stomach Adenocardinoma
E.Coli/ EHEC (O157H7):
Gram/ MacConkeys/ Fermentation? Disease?
ETEC:
Fermentation and disease?
Gram (-) rod Pink = MacConkey’s EHEC: (Lactose +, Sorbatol -) Bloody diarrhea and HUS ETEC: Lactase and sorbitol fermenting; watery diarrhea
E.Coli/ EHEC (O157H7): most importnat virulent factor?
-Shiga Like Toxin (SLT) on phage stops protein synthesis
E.Coli/ EHEC (O157H7): Mechanism of infection and sequelae of disease (3)
Ingest LOW infectious load in undercooked meet–> Attachment-Effacement in Large intestine = ruffling of membranes–>
Bacteria make SLT–>
SLT penetrates cells–>
Pediatric Hemorrhagic colitis +/- HUS +/- Renal failure
***EHEC DOES NOT enter the cell; other e. coli might…
Shigella:
Gram, McConkeys, fermentation, motility?
Gram (-) rod
White = MacConkey’s
(Lactose -; produces no gasses)
Nonmotile
NO GAS. NO FERMENTATION. NO MOBILITY.
Two important shigella virulence factors:
- Shiga Toxin (Binds GB3-R,cleaves 28s rRNA in 60s subunit)
- Type III secretion system
Pathogenesis of shigella gastroenteritis + sequelae of disease? Which population is infected?
INVASIVE.
#1 effective GI pathogen (similar to invasive e. coli)
Type III secretion system–>
Membrane ruffling–>invades M cells in Colon–>
Cell to cell spread via actin tail–>
Mucosal abscess/cell–>
Host cell apoptosis–> Pediatric Dysentery
Dx/ Tx/ Px for shigella infection?
Dx: Methylene Blue stain of feces
Tx/Px: FLUIDS +/- FQN (Cipro) for close contact px
Salmonella Typhi/Paratyphi: gram?
Gram (-) rod