Gi #8: Bacteriology And The Gastrointestinal Tract

Front 1

What area of the GI tract has the highest concentration of bacteria? What type of bacteria do you find most frequently?

Back 1

Colon- 10^10 to 10^12 bacteria. Typically anaerobes and bacteroides.

Front 2

What type of organisms are typically found in the Upper GI? At what point in the GI tract do you find barely any bacteria?

Where is the turning point at which you see the most amount of bacteria?

Back 2

Mouth has a lot of bacteria that get swallowed and killed in HCl of stomach.

After the ileo-cecal valve, you get increase in # of organisms (in the colon).

Front 3

What factors contribute to the type of fecal flora an individual has?

What is the difference between a baby that is breast fed vs. formula fed?

Back 3

- genetics
- Mother's microbiota
- vaginal vs. cesarean birth
- birth environment (developed vs. undeveloped country)

Breast fed = higher conc. of bifidobacteria (good bacteria) vs. formula fed= more clostridia and E.coli, more likely to get infection

Front 4

Increase in fat cause an abundance of what bacteria?
What about a high carb diet?

What bacterial changes would occur if a person with Crohn's was put on an elemental diet?

Back 4

Bacteriodes- increase with fat intake
Bifidobacteria- increase with CHO (carb) intake
Elemental diet- DECREASE enterococci & lactobacili

Front 5

What is the effect on gut bacteria when someone eats a lot of red meat?

In general, what are the benefits of having host microbia in the gut?

Back 5

It causes an increase in glucuronidase, nitro & azoreductase. Can lead to colon cancer.

Host microbes can inhibit potential pathogens, help synthesize and use vitamins and nutrients, metabolize medications, and promote metabolism.

Front 6

What important nutrients are produced by bacteria?

What is the role of bacteria in the coloring of stool?

Back 6

Bacteria produce folate, B vitamins (biotin) , vit K, and SCFA (short chain fatty acids) used for energy.

Bacteria important in biotransformation of bile acids. Made bilirubin --> urobilinogen (which oxidizes and is called stercobilin in stool- brown).

Front 7

What is the role of the firmicutes bacteria?

How do bacteria contribute to the formation of gall stones?

Back 7

It helps extract calories and regulate fat storage (implicated as an infectious cause of obesity).

Bacteria deconjugate primary bile acids to secondary bile acids- deoxycholic and lithocolic acid (important in stone formation).

Front 8

What are the various Intraluminal and Extraluminal defense roles of host bacteria?

Back 8

Intraluminal Defense= decrease oxygen tension (limits aerobic bacteria survival), depletes nutrients needed for other bacteria to grow, form biofilm that produces bacteriocins

Extraluminal= stimulates antibody production, phagocytosis, and augmentation of interferon production

Front 9

Describe how bacteria population in the gut changes from birth to when baby starts to eat food?

Back 9

At birth you are sterile, with exposure to air colonization begins. Baby has a lot of lactobacilli and E.coli (Aerobes) early on. With introduction of solid food, you see transition to Bacteroides (anaerobes).

*note: babie's gut flora resemble that of parents (mainly mom)

Front 10

Host microbes play an important role in drug metabolism. Describe their importance in drugs used to treat UC.

If a patient's heart failure medication is not helping to increase contractility, what bacteria do you have to be concerned about in the gut?

Back 10

Sulfasalazine = sulfapyridine + 5-aminosalicylic acid joined with diazo bond. Bacteria break the diazo bond releasing active 5-ASA.

Eubacteria lentum --> inactivates digoxin

*note: cyclamate is a sugar that bacteria can convert to cyclohexylamine (leading to bladder tumors)- thus it was taken off the market

Front 11

How does a neonate, who does not produce IgA for the first 3-4 months of life, get mucosal protection?

What changes would you see in intestinal structure in a germ free patient vs. normal person?

Back 11

Initially, breast feeding allows transfer of maternal IgA to baby. Commensal organisms also stimulate secretory IgA production (helping protect neonate).

DECREASED lamina propria cellularity, ↓ T-cell/ cell enzyme activity, small lymphoid follicles, thin muscle wall (↓ protection)

Front 12

What is the main component of formed stool?

What is the difference between soluble and insoluble fibers?

Back 12

Bacteria (25% of stool is solid, 75% water)

Soluble = hemicelluloses, increase stool bulk, and colonic emptying. Insoluble = cellulose, increase flatus. **Note- SCFA are produced from bacterial fermentation of fibers. Important source for nutrition and growth of colonocytes.

Front 13

What is the main gas produced from bacterial degradation of cellulose?

What contributes to the odorous smell of stool?

Back 13

Main = nitrogen (other odorless = H2, CO2, CH4 methane, O2)

Odorous = H2S (from the decarboxylation of sulfur amino acids), Skatoles, and Mercaptans

Front 14

What are some symptoms of SIBO?

Back 14

Small Intestinal Bacterial Overgrowth- excess bacteria in proximal small intestine.

Sxs= non-specific, bloating, flatulence, diarrhea, distension, pain, symptoms related to nutrient and vitamin malabsorption.

Front 15

What is the pathogenesis of SIBO?

Back 15

1. Congenital or Structural abnormality (diverticuli, surgical blind limb, etc. into which bacteria and stool settle)
2. ↓ gastric acid (PPI use)
3. ↓ peristalsis (scleroderma, diabetes)
4. mucosal damage/atrophy (CD, celiacs, elderly)

Front 16

What is the gold standard for diagnosis of SIBO?

What is the most common method used today?

Back 16

Gold standard = jejunal aspirate with bacteria >105

Most common is the breath test- pt fasts overnight. Baseline H2 is collected. Then pt ingests lactulose or glucose, serial breath samples are collected and bacteria release H2 gas when they ferment. Positive >20ppm

Front 17

What does the "double peak" seen with lactulose ingestion mean?

How do you treat SIBO?

Back 17

1st peak = small bowel microflora activity
2nd peak = enteric cecum activity

Treat SIBO with antibiotics (amox, clavulanate, norfloxicin, etc.). Patients may need surgical correction of a blind loop.

Front 18

How do probiotics work?

What are some commonly prescribed probiotics?

Back 18

Alter flora, provide antimicrobial activity, provide barrier protection that interferes with bacterial translocation, and immunomodulation.

Lactobacilli, bifidobacteria, saccharomyces boulardii

Front 19

Name the probiotic that works well for the following situations-

1. Recurrent C. dif infections
2. Irritable bowel syndrome- diarrhea predominant variant
3. Pouchitis

Back 19

C.diff/infections = Saccharomyces boulardii (increase sIgA, decrease NFkB)

IBS-Diarrhea= Bifidobacter infantis

Pouchitis (inflammation of surgical pouch)= VSL#3 (a combination of 7 probiotics)

Front 20

What is a prebiotic?
What is a synbiotic?

Back 20

Prebiotic=Short chain carb that is poorly absorbed but used to stimulate pre-existing GI microbiota (ex: bran, lactulose, etc.)

Synbiotic= prebiotic + probiotic

Front 21

What is the downside of using probiotics (especially in elderly or very sick)?

What is an unusual treatment method for recurrent C.Dif infections (besides probiotic therapy)?

Back 21

It can lead to bacteremia and sepsis (remember, they are live organisms!)

Fecal transplants (help restore natural flora of the colon)