Lecture 17- GI infections Flashcards
(90 cards)
1
Q
the gut is a tube- great way to get toxins into the body. name some potential toxins
A
- Chemical
- Bacterial
- Viruses
- Protozoa
- Nematodes (roundworms)
- Cestodes (tapeworms)
- Trematodes (flukes)
2
Q
Main defence against toxins:
A
commensal bacteria
- When we have an imbalance in commensal bacteria , ingesting other toxins are more likely to make us ill
3
Q
role of bacteria in the colon
A
produce short chain fatty acids (SCFA)
4
Q
name 3 SCFA
A
butyrate
acetate
propionate
5
Q
butyrate
A
energy source for colonocytes, helps regulate gut environment
6
Q
- Acetate-
A
involved in cholesterol metabolism
7
Q
- Propionate-
A
helps regulate satiety
8
Q
what icnreases composition of gut microbiotia
A
high fibre diet
9
Q
- …………..disrupt diversity of gut microbiota (bad)
A
Sweeteners
10
Q
- Gluten free diet people without gluten sensitivity or coelicac disease-
A
have a lower numbers of key species
11
Q
drug which causes increased GI infections
A
- proton pump inhibitors
- antibiotics (meat) linked to obesity
12
Q
- Probiotics
A
– live bacteria and yeasts put in foodà probs die in stomach
13
Q
- Prebiotics-
A
essentially food for the microbiota (accessible carbs and fibreà seen as more useful
14
Q
GI defences
A
- Sight , smell, memory
- Saliva (bacteriostatic secretions)
- Gastric acid (acidic environment)
- Small intestinalsecretions (bile)
- Colonic mucus
- Anaerobic environment (small bowel, colon)
15
Q
proximal gut microbiome
*
A
- Proximal gut is relatively sterile
- Stomach is microaerophilic environment e.g. H.pylori (not anaerobic yet)
16
Q
how much bacteria in the colon
A
- 10^11 bacteria in the colon (anaerobic environment)
17
Q
- More than ………of faecal matter is bacteria
A
20%
18
Q
- Benefits of gut microbiome
A
- Harmful bacterial cannot compete for nutrients
- Microbiome produces antimicrobial substances
- Helps to develop newborns immune system
- Produces certain nutrients (VitK)
19
Q
- Microbiome started when we
A
come out the birth canal
20
Q
obesity and fut microbiota
A
seems to be less diverse pop of bacteria
21
Q
- Inflammatory bowel disease-
A
less diversity
22
Q
- Microbiome composition affects response
A
to chemotherapy
23
Q
- Microbiome competition affects
A
insulin response to food
24
Q
Faecal microbiota transplant (FMT)
A
Stool is a biologically active complex mixture of living organisms with therapeutic potential
- Route of admin
- NG/duodenal tube (unappealing)
- Upper GI endoscopy
- Colonoscopy
- Transplant can be in caecum (allowed to move throughout colon)
- Distributed throughout length of the colon
25
which disease has FMT been used to treat
* E.g. pseudomembranous colitis has been treated by faecal enemas since 1985
* C.diff
* IBD
26
**Where do you get faeces from**
* 10-25 year olds
* Donors do not use (in past 3 months)
* Antibiotics
* Laxative
* Diet pills
* Do not have GI disease
* Completely screen for diseases e.g. HIV, hepatitis
* Transplant takes place within one hour
27
bacteria infections in the gut
* **Gram negative rods**
* Salmonella
* Campylobacter
* Shigella
* Enterotoxigenic E.coli
* **Gram positive**
* Clostridium difficile
28
**Salmonella-** gastroenteritis
* Symptoms
* Nausea
* Vomiting
* Diarrheal (mostly non-blood)
* Abdominal cramping
29
salmonella transmission
* -ingesting food and water contaminated by salmonella bacteria (symptoms develop 48 hours later)
30
MOA of salmonella
* Salmonella gain access to enterocyte via endocytosis
* Move to submucosa where encounters macrophages
* Macrophages transfer salmonella to RES where they multiply inside cells
* Lymphoid hyperplasia
* Re-enter gut from the liver
31
prognosis of salmonella
* Prognosis – self limiting (may need oral resus)
32
Campylobacter
* Bacteria is spiral shaped
* Microaerophilic (do not ferment carbs)
33
**Campylobacter-** gastroenteritis symptoms
* Fever
* Abdominal cramping
* Diarrhoea (can be bloody)
34
Campylobacter- gastroenteritis transmission
* Eating poultry
* Foaeco-oral route
35
**Campylobacter-** gastroenteritis MOA
* Needs to multiply within host before symptoms appear (food infection- not poisoning)
* Longer incubation period e.g. 1-7 days)
* Releases a cytotoxin (similar to cholera)
36
camplobacter prognosis
* Can last days to week- generally self limiting
* Fluid/electrolyte resus
* Consider Abx if bloody
37
**Shigella-** gastroenteritis causes
* **shigellosis- dysentery commonly affecting young children**
38
transmission of shigella
* Spread from infected stool
* Person to person (sometimes flies)
* Only need small dose to cause infection
39
MOA of shigella
* Invades **large intestine colonocyte**s, multiplies and invades neighbouring cells
* Kills **colonocytes** and forms abscesses in the mucosa
40
symptoms of shigella
* Blood diarrhoea with mucus and abdominal cramping
41
prognosis of shigella
42
Enterotoxigenic E.coli
* Commensal of the colon but can also be a pathogen
* Flagella helps transport
43
**Enterotoxigenic E.coli -gastroenteritis transmission**
* Faecal oral route by contaminated water
* Common cause of travellers diarrhoea
44
**Enterotoxigenic E.coli -gastroenteritis** MAO
* Adheres enterocytes in **small intestine**
* Produces enterotoxins
* These cause hypersecretion of chloride
* Water leaves cells in the gut lumen
45
different strains of e.coli cause different
symptoms and need different treatment
46
gram negative bacteria which cause bloody diarrhoea
shigell, campylobacter
(colon involvement)
47
Hemolytic-uremic syndrome (HUS) potential
shigell and campylobacter
- anaemia
- thrombocytopenia
- AKI
48
duration of gram engative infections shrotest to longest
ETEC, salmonella (days), shigella (week), campylobacter (weeks)
49
which is the main gram positive bacteria which causes gastroenteritis
clostridium difficile
50
clostridium difficile
* Gram positive
* anaerobic
* spore forming bacillus
* minor component of GI tract but can be transferred via faecal oral route
51
why is C.diff common in hospitals
spore very difficult to get rid of from environment e.g. hospital
up to 20% of hospitalised pts become colonised with C.difficile
52
MOA of C.diff
* **Following antibiotic therap**y C difficile can colonise gut (imbalance in microbiota and release toxins A and B
* A- enterotoxin results in excessive secretion and inflammation
* B- cytotoxin
53
cause of C.diff
Most antibiotics can precipitate C.difficile proliferation- esp broad spectrum.
54
symptoms of c.diff
* Asymptomatic – most people
* Varying degrees of diarrhoea (mild to terrible, rarely bloody)
* Abdominal cramping
55
rare complications of C,diff
* Pseudomembranous colitis
* Toxic megacolon (worst case scenario)- surgery
56
* Pseudomembranous colitis
* Inflammatory condition
* Elevated yellow plaques which join to form a pseudomembrane
57
megacolon
needs surgery
58
treatment of C.diff
**Treatment**
* Remove offending antibiotic
* Fluid resus
* Metronidazole/vancomycin
* Probiotics
59
viruses which can cause gastroenteritis
rotavirus
noravirus
60
Parasites which cause gastroenteritis
* Cryptosporidium
* Giardia
* Entamoeba
61
**Viral gastroenteritis- Rotavirus characteristics**
* Common in under 5s
* The virus
* dsRNA
62
* transmission of rotavirus
* faecal oral route (only small dose required)
* adults rarely affected (immunity lasts into adulthood)
63
symptoms of rotavirus
* fever and vomiting first
* diarrhoea follows
64
diarrhea in rotavirus
* **chloride secretion**
* creates gradient for movement of Na into lumen
* water moves by osmosis
* diarrhoea
* **SGLT 1 disruption**
* Reduced movement of Na/glucose into enterocyte
* Higher osmotic load in gut
* Water moves by osmosis
* **Reduce brush border enzyme function- malabsorption**
65
* Treatment of rotavirus
Managing dehydration
66
**Viral gastroenteritis- Norovirus can affect**
* Can affect any age – huge number of strains- don’t develop immunity
67
68
norovrius
* RNA virus
* Only requires small dose-highly contagious
69
* norovirus Transmission
* Person to person
* Resistant to cleaning
70
* MOA norovirus
* Incubation 1-2 days
* Symptoms last 1-3 days
* Affecting **small intestine** and damages microvilli (brish border enzyme disruption)
71
* Symptoms norovirus
* Vomiting
* Delayed gastric emptying
* Watery diarrhoea
* Anion secretion- movement of water into gut
* Fever
72
* Treatment of norovirus
* Oral rehydration therapy
73
* **Protozoal infects the intestinal tract**
* **Cryptosporidium- sporozoan**
* Non motile
* **Giardia lamblia- flagellate**
* Motile - flagella
* **Entamoeba- amoeba**
* Motile- move by extending cytoplasmic projections
74
**Cryptosporidium is a**
**sporozoan- protozoa**
75
transmission of cryptosporidium
* Faecal oral route but can also survive and spread via bodies of water
76
who does Cryptosporidium effect
77
MOA of cryptosporidium
MOA
* Disease is caused by ingestion of oocysts (cyst containing parasitic)
* Reproduces inside the epithelial cells of the distal small intestine
* Oocysts are excreted in faces and continue cycle
78
Symptoms of cryptosporidium
*
* Watery diarrhoea (S.intestine)
* Malabsorption (brush border enzymes affected)
* Chloride secretion
79
**Treatment of cryptosporidium**
* Fluids
* Occasionally need an anti-parasitic treatment if pt immunocompromised e.g. HIV
80
giardia is a
flagellate
81
symptoms of giardia
* Most infections asymptomatic (symptoms in children)
* If symptomatic (appear after 10+ days incubation period)
* Diarrhoea
* Abdominal cramping
* Can last 6 weeks
* Common cause of persistent diarrhoea
82
transmission of giardia
* Faecal oral route with water supplies often affected
83
* **MOA of giardia**
**Life cycle in 2 stages**
84
* **Treatment of giardia**
Antibiotics and fluid rehydration therapy (lactase deficiency common after infection- lactose intolerance)
85
entamoeba has a higher prevalence in
developing coutnries
86
entamoeba symptom
* Most cases are asymptomatic (80%)
* Diarrhoea
* Liver abscesses (rare)
87
transmission of entamoeba
* Transmission
* Faecal oral route
88
MOA of entemoeba
* **MOA**
* Infection following ingestion of cysts
* Excystation occurs in colon where trophozoites invade mucosa
* Bloody diarrhoea and inflammatory changes occur (similar to IBD)
* Infection can spread to liver- abscesses
* Cysts then pass out with faeces- infect others
89
treatment of entamoeba
* **Treatment**
* Anti-protozoal= metronidazole
* Severe colitis/toxic megacolon= surgery
90
travellers diarhhoea
