Term
| How does Dysentery differ from Diarrhea? |
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Definition
Dysentery involves frequent, low volume stools with blood and pus (usually involving inflammation in the COLON)
Diarrhea is frequent, profuse, water discharge common in bacterial gastroenteritis (toxins in the SMALL INTESTINE). |
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Term
| What are the major determinants of outcome in the context of exposure to ingested gastric pathogens? |
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Definition
1) Virulence
- Shigella >>>Cholerae
2) Dose of pathogen and type
- Bacteria is more severe than virus, but virus can be virulent
3) Host flora |
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Term
| What are the normal defenses in the human GI tract that protect against gastroenteritis? |
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Definition
1) Normal flora-compete out organisms
2) Gastric acid
3) Motility
4) Mucus
5) Bile
6) Shedding of epithelium
7) IgA
8) Local lymphoid tissue (cellular immunity) |
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Term
| How is infectious diarrhea produced in gastroenteritis |
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Definition
1) Enterotoxins produce increased secretion, altering levels of cyclic nucleotides (cholera, ETEC)
2) Decreased absorption from intestinal damage (viral or enterotoxin)
3) Inflammation from invasion (Salmonella, shigella) or enterotoxin
** LOOK FOR FECAL LEUKOCYTES **
4) Changed motility
- viruses can impede motility or cause vomiting. |
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Term
| How do Cholera toxin and E. coli Heat-labile enterotoxin produce infectious diarrhea? |
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Definition
Increased Secretion
1) Bind ganglioside receptor Gm1 on apical membrane of enterocyte, leading to vesicle-mediated endocytosis.
2) A1 chain is released and ADP-ribosylates Adenylate cyclase in basolateral membrane, leading to uncontrolled cAMP production (prevents inactivation)
3) PKA phosphorylates Apical CFTR (more Cl secretion and less sodium/water reabsorption)
**No inflammation
3) Cholera toxin is an ADP-ribosyltransferease |
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Term
How might norovirus produce infectious diarrhea?
What about C. perfringens? |
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Definition
| Both decrease intestinal absorption, increasing luminal osmotic pressure by damaging epithelium |
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Term
| How do Salmonella/Shigella induce infectious diarrhea? |
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Definition
Inflammation due to invasion (remember, Cholera causes no inflammation!)
1) Salmonella undergoes epithelial transcytosis and then binds TLR5 on the on basolateral membrane, which increases Ca2+, activating NF-kb.
- NF-kb activates IL8, which is released from the basolateral membrane and attracts PMNs.
2) PMNs cause 5' AMP production, which binds A2B receptor and leads to Gs activation.
- cAMP production leads to PKA phosphorylation and Cl secretion. |
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Term
| How does Rotavirus produce gastroenteritis? How do you diagnose and treat it? |
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Definition
Endemic infection (occurs in usual living conditions of patient and family) VACCINE NOW GIVEN.
Reovirus with segmented dsRNA genome that exhibits fecal-oral transmission in young children and infants.
1) Kills intestinal cells, resulting in malabsorption (enterotoxin also?)
2) Diagnose with antigen detection in stool and EM, and treat with rehydration. |
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Term
| How does Vibrio cholerae cause gastroenteritis and what kind of infection is it? How do you diagnose/treat? |
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Definition
Epidemic (more than family unit) presenting with severe dehydration and perhaps cardiac and kidney sequelae
Gram-negative bacterial rod (oxidase positive) usually transmitted in fecally-contaminated water.
1) Enterotoxin-mediated increase in cAMP that increases chloride secretion causing watery diarrhea without inflammation (does not damage mucosa)
2) Culture and treat with fluid/electrolyte replacement and antibiotics. |
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Term
| How does Norovirus cause gastroenteritis and what kind of infection is it? How do you diagnose/treat? |
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Definition
"Adult with sudden-onset vomiting and diarrhea"
Caliciviruses (ssRNA) with fecal-oral transmission in contaminated food/water causing epidemic infection.
1) Damages intestinal mucosa, resulting in malabsorption
2) Diagnose with Em/serology of feces/PCR and treat with fluid/electrolyte replacement |
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Term
| What are the major food-borne causes of gastroenteritis from intoxications? |
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Definition
1) Botulism- may or may not cause gastroenteritis, but you will see flacid paralysis (treat with anti-toxin)
2) Staph or Bacillus cereus (onset <6h) |
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Term
What are the major food-borne causes of gastroenteritis from in-vivo toxin production??
How do you treat? |
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Definition
Viable pathogen must be ingested
1) C. perfringens
2) B. cereus
3) EHEC
Symptomatic treatment without antibiotics |
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Term
| How can you most easily tell between intoxications and infections from food poisoning? |
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Definition
Onset time.
1) Intoxication (Staph, B. cereus, Botulism) is FAST onset (<6h)
2) Infection (C. perfringens, B. cereus) is slowing (8-16h) |
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Term
| What 2 illnesses are caused by EHEC? |
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Definition
Gram-negative rod (O157:H7) ingested through food.
1) Hemorhhagic colitis (4 days after ingestion)
- shiga toxin affects colon, inhibiting protein synthesis and causing bloody diarrhea, but without invasion (no leukocytes in stool or substantial fever)
2) Hemolytic uremic syndrome (mostly in children- life-threatening)
- Shiga toxin is absorbed in gut in high amounts and enter circulation, leading to kidney damage and acute renal failure |
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Term
| How do you diagnose/treat EHEC infection? |
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Definition
Gram-negative rod (O157:H7) ingested through food.
1) Diagnose with culture and DNA hybridization test for shiga toxin, or serology
2) Treatment depends on disease
- DONT USE ANTIMICROBIALS
- For HUS, may need dialysis
- For H coloitis, fluid replacement is sufficient. |
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Term
Patient presents with bloody diarrhea, 4 days after eating a large hamburger. They have no fever or leukocytes in their stool.
Culture reveals gram-negative rod.
How do you treat? |
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Definition
This is hemorrhagic colitis due to EHEC ingestion.
Treat with fluid replacement and AVOID Ab!
** IF this was HUS, you would get circulation of protein-synthesis-inhibiting shiga toxin, leading to renal failure, and you might also need dialysis** |
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Term
Severely dehydrated patient presents with watery diarrhea.
Culture reveals gram-negative bacterial rod (oxidase positive)
How do you treat? |
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Definition
Vibrio cholerae infection causing diarrhea by enterotoxin-mediated increase in cAMP and CFTR activation.
Treat with fluid/electrolyte replacement and antibiotics. |
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Term
| What signs/labs would indicate gastroenteritis from food ingestion of an invasive bacterial species? |
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Definition
1) Fever (inflammation)
2) Fecal leukocytes (maybe)
3) Relatively slow disease onset (>1-2 days usually).
Shigella, Salmonella are examples |
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Term
Patient presents with fever and diarrhea with fecal leukocytes. He tells you that he ate some strange food a couple weeks ago, but nothing since then.
Culture reveals gram-negative bacterial rode.
What is the likely diagnosis/treatment? |
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Definition
Salmoenella typhi infection causing typhoid fever.
S. typhi invades M cells in PPs and is taken up and carried by macrophages to reticuloendothelial tissue, inducing inflammation.
**nontyphoid Salmonella produces a gastroenteritis and remains localized in the intestines following entry through M cells**
Treat with Antimicrobials (may be used for gastroenteritis also, but not necessarily), with fluid and electrolyte replacement. |
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Term
| How do typhoid fever and salmonella gastroenteritis differ in terms of pathogenesis? |
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Definition
Both gram-negative rods that invade through M cells
1) nontyphoid Salmonella produces a gastroenteritis and remains localized in the intestines
- 1-2 days after ingestion of food
2) S. typhi enters macrophages and is transported to reticuloendothelial organs, producing systemic inflammation (fever).
- takes a while to occur after food ingestion |
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Term
| Why do some patients in hospitals end up contracting a gastroenteritis? What is the most likely pathogen and what do you do? |
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Definition
Antibiotic-mediated alterations to normal flora (C. dificile)
1) C. dificile (gram-positive, anaerobic, spore-forming rod) with person-to-person transmission
**New strains are emerging that are very toxin, ranging from mild diarrhea to pseudomembranous colitis)*
2) Fluid/electrolyte replacement and metronidazole or vancomycin |
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Term
Patient presents with high fever and severe dehydration from diarrhea after being in the hospital for 1 week.
What test should you run to confirm your diagnosis and what is the pathogenesis? |
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Definition
Pseudomembranous colitis due to C. dificile (SERIOUS).
1) Run fecal toin test for toxin A/B
2) Toxins damage colonic mucosa by glucosylating Rho proteins, causing severe inflammation
**Treat with fluid/electrolyte replacement of metro or vanco** Maybe fidoxomycin or fecal transplant? |
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Term
An AIDS patient presents with severe, chronic diarrhea.
A modified acid-fast stain of concentrated stool reveals cysts.
How do you treat this condition? |
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Definition
Sounds like parasitic Cryptosporidium parvum infection in immunocompromised individual
Anti-retroviral therapy, but not antimicrobial
**IF immunocompetent, try Nitazoxanide** |
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Term
A patient with a recent travel history presents with watery diarrhea, but no fever.
DNA tests reveal the presence of specific toxins.
What is the pathogenesis of the most likely organism and how do you treat? |
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Definition
Enterotoxigenic E. coli (ETEC) causing traveler's diarrhea
1) Enterotoxin
- heat-labile increases intestinal cAMP and CFTR activation
- heat-stable increase intestinal cGMP and K+ channel activity.
2) Fluid/electrolyte replacement and symptomatic treatment |
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Term
| What are your initial steps in working up a patient with fever and bloody diarrhea? |
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Definition
Remember, if this wasn't present, just treat symptomatically.
1) Do microscopic exam for fecal WBCs (may also detect parasites).
2) Culture for routine pathogens; if patient is immunocompromised may need to consider exotic pathogens if there is no response (but don’t attempt culture initially).
3) If on antibiotics, run C. dif toxin test |
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Term
| What is the basic management strategy for an immunocompetent patient with gastroenteritis? |
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Definition
1) Address fluid/electrolyte loss (particularly in children).
- For mild diarrhea, can use pedialyte or mineral water plus saltine crackers.
- For moderate diarrhea (particularly in developing countries) may use ORS.
-For severe diarrhea, may need to use i.v. fluids.
2) If noninflammatory diarrhea, treat SYMPTOMATICALLY
- Absorbants
- Anti-intestinal motility agents (loperamide)
- Anti-secretory agent (Bismuth salt like Pepto bismol)
3) If inflammatory
- DO NOT use anti-motility agents like loperamide
- Give antimicrobials (watch out for EHEC!) |
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Term
| Why might you give Oral Rehydration Solution to a patient with gastroenteritis? |
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Definition
ORS is good for fluid/electrolyte replacement in cases of moderate diarrhea (IV for severe).
Salt and glucose enter intestinal mucosal cells and pull water in! |
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Term
True or False:
Loperamide should not be given for non-inflammatory diarrhea related to gastroenteritis? |
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Definition
False.
Should should give anti-motility drugs in this case, but NOT in the case of invasive pathogens, where it will increase their infectious time of occupancy. |
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Term
| How do you manage gastroenteritis in AIDS patients? |
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Definition
1) If routine cultures grow a typical GI pathogen (e.g., Shigella or Salmonella), treat this first with an appropriate antimicrobial.
2) If routine cultures are negative, treat symptomatically (e.g., with loperamide). If no response, then order more extensive cultures. |
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