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Gi Infecions Flashcards

1
Q

What are toxins that can affect the gi trac Chloride secretion • Creates gradient for the movement of Na into lumen
• Water moves by osmosis • Diarrhoea
•SGLT1 disruption
• Reduced movement of Na/glucose into enterocyte
• Higher osmotic load in gut
• Water moves by osmosis
•Brush border dysfunction • General malabsorption

A

• Chemical •Bacteria •Viruses •Protozoa •Nematodes (Roundworms) •Cestodes (Tapeworms) •Trematodes (Flukes)

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2
Q

What are gi defences

A
  • Sight, smell, memory
  • Saliva (bacteriostatic secretions)
  • Gastric acid (acidic environment)
  • Small intestinal secretions (Bile)
  • Colonic mucus - Mucus esp in colon keeps mucus and bacteria seperate
  • Anaerobic environment (small bowel, colon) - does nto suit aerobes
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3
Q

Describe the gut microbiome

A

Proximal gut is relatively sterile environment
• Stomach (microaerophilic environment)
•1011 bacteria in colon (anaerobic environment)
•More than 20% of faecal mass is bacteria
• Benefits of microbiome
• Harmful bacteria cannot compete for nutrients
• Microbiome produces antimicrobial substances
• Helps to develop newborn’s immune system
• Produce certain nutrients (Vit K)
When normal flora is interrupted - start to get problems . Infections can follow antibiotics for another infection bc normal flora is disrupted
C section - do not go through the birth canal - underdeveloped microbiome in the gut. Very vital.

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4
Q

What do bacteria in the gut produce

A

Bacteria in colon produce SCFAs (acetate, propionate, butyrate)
• Butyrate- energy source for colonocytes, helps regulate gut environment
•Acetate- involved in cholesterol metabolism
•Propionate- helps regulate satiety

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5
Q

What aer he likes between microbiome and health

A
  • Gut microbiota and health
  • Obesity- seems to be less diverse population of bacteria
  • Inflammatory bowel disease- less diversity
  • Microbiome composition affects response to chemotherapy
  • Microbiome composition affects insulin response to food
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6
Q

Describe microbiota and dietmedications

A

High fibre diets influence the composition of gut microbiota (increase in health)
• Sweeteners disrupt diversity of gut microbiota (bad)
•Gluten free diet in people without gluten sensitivity or coeliac disease- lower numbers of key species (bad)
•Proton pump inhibitors- increased GI infections
•Antibiotics (in meat) possible link to obesity (possibly mediated through disruption of microbiota)
•Probiotics- Live bacteria (and yeasts) put in food
•Prebiotics –essentially food for the microbiota (accessible carbs and fibre)

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7
Q

What is fmt

A

Stool is a biologically active complex mixture of living organisms with therapeutic potential Faecal transfer from healthy donors to the sick in order to treat disease has been described in the ancient medical literature. In the 4th century in China, Ge Hong described the use of human faecal suspension by mouth for patients with food poisoning or severe diarrhoea
• Pseudomembranous colitis has been treated by faecal enemas since 1985
•Route of administration includes
• NG/duodenal tubes (unappealing for most patients)
• Can be done under anaesthetic
• Upper GI endoscopy
• Colonoscopy
• Transplant can be put in Caecum (allowed to move throughout colon)
• Distributed throughout length of colon

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8
Q

What are successful uses of fmt

A

Successful uses of FMT
• Up to 90% resolution of diarrhoea following C difficile infection (No adverse side effects)
- Compared with vancomycin treatment (30% resolution)

Case reports (some questionable)
• Up to 70% resolution of IBD symptoms and reduction/cessation of IBD medications within 6 weeks
• Crohn’s disease
• Clinical remission in 50% of patients

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9
Q

Where is faeces from my obtined rom

A

10-25 year olds • Donors do not use (in past 3 months)
• Antibiotics • Laxatives • Diet pills
•Do not have GI disease •Completely screened (inflammatory markers, Hepatitis, HIV) •Fresh stool to transplantation or storage (1 hour!)
• Stool is centrifuged, filtered and diluted

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10
Q

What are some organisms that can cause infections of the gut

A 
• Gram negative rods
• Salmonella
• Campylobacter
• Shigella
• Enterotoxigenic E-coli
Gram positive •Clostridium difficile (gram positive)
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11
Q

Describe salmonella

A

Nausea, vomiting and diarrhoea (mostly non-bloody), fever, abdominal cramping
• Spread by ingesting food and water contaminated by salmonella bacteria (symptoms develop 48 hours later)
•In healthy individuals this is self limiting (2-3 days)

  • Inside gut:
  • Salmonella gain access to enterocytes (endocytosis)
  • Move to submucosa where encounter macrophages
  • Macrophages transfer salmonella to reticuloendothelial system where they multiply inside cells
  • Causing lymphoid hyperplasia
  • Re-enter gut from the liver
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12
Q

Describe campylobacter

A

Spiral or ‘s’ shaped organism
• Mainly microaerophilic (do not ferment carbs)
•Spread to humans via faeco-oral route
•Needs to multiply within host before symptoms appear (food infection- not food poisoning)
• Longer incubation period (1-7 days) •Fever, abdominal cramping, diarrhoea (can be bloody)
•Releases a cytotoxin (similar to cholera)
•Can lasts days to weeks (generally self limiting)
•Treatment
• Fluid/electrolyte replacement
• Consider antibiotics if bloody diarrhoea

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13
Q

Describe shigella

A

Causes shigellosis which is a dysentery commonly affecting young children
• Spread from infected stools, person to person (sometimes flies)
•Only needs a small dose to cause infection (spreads between family members)
•Invades large intestine colonocytes, multiplies in cells and invades neighbouring cells
•This kills colonocytes and forms abscesses in the mucosa
•Bloody diarrhoea with mucus and abdominal cramping
•Usually resolves in a week

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14
Q

Describe enterotoxigenic E. coli

A

Commensal of the colon but can also be a pathogen
• Spread by faecal oral route by contaminated water
•Common cause of travellers diarrhoea
•Invade enterocytes (produces enterotoxins)
•These cause the hypersecretion of chloride ions
•Water leaves cells into the gut lumen
Hypersecretion fo chloride iris - sodium ions will follow- after will follow . Movement of water across epithelia of small intestine. Unpleasant watery diarrhoea

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15
Q

Give a summary of gram negative rods

A
  • Gram negative rods (all) •Spread (oral route from different sources- faecal, food, water)
  • Diarrhoea (all)
  • Potentially bloody (Shigella, campylobacter)
  • Watery (ETEC, salmonella)
  • Toxin production (all)
  • Potential HUS (Shigella, campylobacter)
  • Antibiotics are carefully prescribed for serious cases (resistance becoming a problem)
  • Duration –shortest to longest
  • ETEC, salmonella (days), Shigella (week), campylobacter (weeks)
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16
Q

Descrbe c dficile

A

Gram positive , anaerobic, spore forming bacillus
• Minor component of the GI tract but can be transferred via faecal-oral route
•Spores are very difficult to get rid of from an environment (like a hospital)
• In US 20% of hospitalised patients become colonised with C difficile

  • Following antibiotic therapy C-difficile can colonise gut and release toxins
  • Toxins A & B
  • A- enterotoxin that results in excessive secretion (+ inflammation)
  • B- Cytotoxin
17
Q

What are teh symptoms of c dif

A

Most antibiotics can precipitate C- difficile proliferation (especially broad spectrum)
Resulting in:
• Asymptomatic (most people)
• Varying degrees of diarrhoea (mild to terrible, rarely bloody)
• Abdominal cramping In a few cases (<5%)
• Pseudomembranous colitis
• Toxic megacolon (worst case scenario)
• Surgery

18
Q

Wha this pseudomembranoud colitis

A

Inflammatory condition
• Elevated yellow plaques join to form a pseudomembrane

Treatment of C. difficile infection •Remove offending antibiotic
•Fluid resuscitation
•Metronidazole/Vancomycin
•Probiotics

19
Q

Describe rotavirus

A

Very common cause of gastroenteritis in the under 5s
• Double stranded RNA virus
•Spread faecal-oral route (only very small dose required)
•Adults rarely affected (immunity lasts into adulthood)
•Vomiting with a fever are first symptoms
•Diarrhoea follows (lasting up to a week)
- Chloride secretion
- SGLT1 disruption
- Reduced brush border enzyme function •Treatment involves managing dehydration

20
Q

How can rotavirus cause diarrhoea

A

Chloride secretion
• Creates gradient for the movement of Na into lumen
• Water moves by osmosis
• Diarrhoea

SGLT1 disruption
• Reduced movement of Na/glucose into enterocyte
• Higher osmotic load in gut
• Water moves by osmosis

Brush border dysfunction
• General malabsorption

21
Q

What is norovirus

A

Previously known as the Norwalk virus (RNA virus) • Most common cause of non bacterial gastroenteritis in the world •Can affect any age as there are huge number of strains (don’t develop immunity) •Only requires small dose so highly contagious •Virus resistant to cleansing •Incubation is 1-2 days and symptoms last 1-3 days •Infects the small intestine and damages microvilli (brush border enzymes disruption) •Symptoms include vomiting, watery diarrhoea, fever
• Anion secretion, so movement of water into gut lumen • Vomiting is due to delayed gastric emptying
•Treatment is oral rehydration therapy

22
Q

Which parasites can cause parasitic astronteritis

A
  • Cryptosporidium
  • Sporozoan- •Giardia lamblia
  • Flagellate •Entamoeba
  • Amoeba
23
Q

Whar is cryptosporidium

A

Cryptosporidium is a protozoa
• Transmitted by the faecal-oral route but can also be survive and spread via bodies of water (infected by animal faeces) •Affects: (list from Wikipedia)
• People who swim regularly in pools with insufficient sanitation (certain strains of Cryptosporidium are chlorine-resistant) • Child-care workers • Parents of infected children • People caring for other people with cryptosporidiosis • Backpackers, hikers, and campers who drink unfiltered, untreated water • Petting Farms and open farms with public access • People, including swimmers, who swallow water from contaminated sources • People handling infected cattle • People exposed to human faeces

24
Q

How can cryptosporidium cause infecto

A
  • Disease is caused by the ingestion of an oocyst (a cyst containing the parasite)
  • This reproduces inside the epithelial cells of the distal small intestine
  • Oocysts are excreted in faeces to continue cycle •Produces watery diarrhoea that is normally self limiting
  • Malabsorption (brush border enzymes affected)
  • Chloride secretion •Treatment is supportive (fluids) •Occasionally anti-parasitic treatment in at risk groups
  • AIDS- can produce severe symptoms
25
Q

What is giardiasis

A

• Most infections are asymptomatic but symptoms are more common in children •Spread via faecal-oral route with water supplies often affected (in developing countries)
• Swallowing Giardia picked up from surfaces (such as bathroom handles, changing tables, diaper pails, or toys) that contain infected faeces • Drinking water or using ice made from water sources where Giardia may live (for example, untreated or improperly treated water from lakes, streams, or wells) • Swallowing water while swimming or playing in water where Giardia may live, especially in lakes, rivers, springs, ponds, and streams • Eating uncooked food that contains Giardia organisms • Having contact with someone who is ill with giardiasis • Traveling to countries where giardiasis is common
• If symptomatic (appear after 10+ days incubation period)
• Diarrhoea
• Abdominal cramping
• Can last up to 6 weeks
Common cause of persistent diarrhoea

26
Q

Describe the life cycle of giardia

A

Life cycle is in two stages 1. Cyst is ingested
• Stomach acid/ pancreatic enzymes release parasite from cyst
• which then multiplies in small intestine- incubation 1-2 weeks • Damages proximal small intestine causing symptoms (diarrhoea) • Villous atrophy occurs
2. Parasite then goes back into cyst stage in colon
• Excreted to repeat the cycle Treatment •Antibiotics and fluid rehydration therapy Note
• Post Giardia infection, lactase deficiency is common
• Lactose intolerance

27
Q

What is entamoeba histilytica

A

Higher prevalence in developing countries • Most cases are asymptomatic (80%)
• If symptomatic
• Diarrhoea
• Liver abscesses (rare)
•Transmitted by faecal-oral route (from contaminated food or water)
Affects:
• People who have travelled to tropical places that have poor sanitary conditions • People who live in institutions that have poor sanitary conditions • Men who have sex with men

28
Q

What happens following the ingestion of cults

A
  • Infection follows the ingestion of cysts •Excystation occurs in colon where trophozoites invade mucosa
  • Bloody diarrhoea and inflammatory changes occur (similar to IBD) •Infection can also spread to liver (abscesses form) •Cysts then pass out with faeces- infect others •Treatment
  • Anti-protozoals/metronidazole
  • Severe colitis/toxic megacolon may require surgery
29
Q

What is travellers diarrhoea

A

Diarrhoea is the most common symptom of travel related illnesses • Enterotoxic Escherichia coli (ETEC) is the most common cause of acute travellers’ diarrhoea globally •Defined as passing 3 or more loose/watery stools
• +/- fever, abdominal pain •Greater than 14 days of symptoms makes it less likely to be bacterial in cause •Antibiotics are only recommended for vulnerable patients (immunosuppressed)
• Halves duration of symptoms (to 1.5 days on average) Risk of getting diarrhoea •Place you are visiting (south and east asia, central America, west and north Africa) •Dietary exposure (backpacking) •Less than 6 years, PPIs, Blood group O (shigellosis, cholera)

30
Q

Describe teh prevention and treatment of travelers diarrhoea

A
  • Prevention
  • Good hand hygiene
  • Food and water precautions •Treatment •Mild/moderate (less than 6 stools/24 hrs)
  • Hydration (oral rehydration solutions/ safe water)
  • Antidiarrhoeal agents
  • Severe (more than 6 stools/24 hrs)
  • IV fluids (potentially)
  • Antibiotics (if appropriate)

Gi (15 decks)

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