Gastroenteritis

Question 1

what are the risk factors of gastroenterititis

Answer 1

Malnutrition (micronutrient) deficiency
Closed/ semi-closed communities
Exposure to contaminated food/water /travel
Winter congregating/ summer floods
Age <5 , not breastfeeding
Older age

Question 2

pathogenesis of gastroenteritis

Answer 2

Osmotic/Malabsorptive (various mechanisms)
Secretory (toxin mediated)
Intestinal tight junction dysruption (leak-flux)
Inflammatory (mucosal invasion)
Intestinal motility (through the enteric nervous system)

Question 3

how does diarrhoea happen

Answer 3

Adherence/attachment to the gastrointestinal mucosa
Cellular invasion
Production of exotoxins
Changes in epithelial cell physiology
Loss of brush border digestive enzymes, and/or cell death
Increased intestinal motility, net fluid secretion, influx of inflammatory cells, and/or intestinal hemorrhage

Question 4

≥3 unformed stolls/day more than 250g/day
no other cause (exclude laxatives)
hold shape of container
departure from normal bowel habit
use bristol stool chart

Answer 4

diarrhoea

Question 5

inflammation of the intestine particularly the colon causing diarrhoea associated with blood and mucus
generally associatated with fever, abdominal pain, and rectal tenesmus

Answer 5

dysentry

Question 6

volume of diarrhoea in large bowel and small?

Answer 6

Large volume tends to be small bowel, large bowel small volume

Yersinia enterocolitica may mimic appendicitis as it may invade mesenteric nodes

Question 7

what should you ask in a history for gastroenteritis

Answer 7

associated symptoms
exposure history and predisposing factors
travel history
stool appearance

Question 8

1 to 6 hours
gram positive
from starchy food (reheated Rice)
profuse vomiting

Answer 8

bacillus cereus

Question 9

1-6 hrs
gram positive coccus
preformed toxin in food, rapid absorption, acts on vomiting centres on brain
food left at room temp
milk, meat, fish

Answer 9

staphylococcus aureus

Question 10

investigations for gastroenteritis

Answer 10

stool sample

Blood culture

Question 11

gram negative rod, nonmotile, anaerobic, enterobacteriaceae

four species

Answer 11

shigella

Question 12

what are the 4 species of shigella

Answer 12

s. dysenterae (serogroup A), S. flexneri (serogroup B), shigella boydii (C), s sonnei (D)

Question 13

what species of shigella can cause the hemolytic-uremic syndrome (HUS) and what is it mediated by ?

Answer 13

s. dysenterae 1

and shiga toxin (Stx)

Question 14

what are the symptoms of a shigella infection

Answer 14

fever
abdominal pain
mucoid diarrhoea
watery/bloody diarrhoea
vomiting

Question 15

what does shiga toxin do

Answer 15

binds to receptors found on renal cells, RBC and others
inhibit protein synthesis
cause cell death

Question 16

ecoli classes

Answer 16

enteroToxigenic(ETEC)
enteroPathogenic (EPEC)
enteroInvasive (EIEC)
enteroAggregative (EAIC)

Question 17

how does Ecoli produced toxin

Answer 17

Adhere to the intestinal epithelial cells, and elaborate Shiga toxin

Toxins bind to absorptive enterocytes on the luminal surface of the small and large intestines, enter the cell, and irreversibly inhibit protein synthesis, resulting in death of enterocytes.

Shiga toxins can then enter the bloodstream via damaged intestinal epithelium and cause the death of vascular endothelial cells by the same mechanism

Endothelial cell lysis is accompanied by platelet activation and aggregation, cytokine secretion, vascular constriction contributing to fibrin deposition, and clot formation within the capillary lumen

Microangiopathy propagates distally as the toxins are carried to the kidneys, causing the clinical syndrome of hematuria and renal failure (HUS). The development of HUS is associated primarily with serotypes that produce Shiga toxin 2

Question 18

bloody diarrhoea
very low infectious dose
food - beef (raw milk, water)
person to person direct/indirect
children and elderly at risk of complications
outbreak potential

Answer 18

E Coli 0157

Question 19

effect of verotoxin (VTEC)

Answer 19

mild to severe (Death)
bloody diarrhoea
haemorrhagic collitis

Question 20

Haemolytic Ureamic Syndrome (HUS) presentation

Answer 20

abdomen pain
fever
pallor
petechiae
oliguria
blood diarrhoea
under 16 years old

Question 21

Haemolytic Ureamic Syndrome (HUS) signs

Answer 21

High white cells
Low platelets
Low HB
Red cell fragments
LDH>1.5 x normal
May develop after diarrhoea stopped

Question 22

Haemolytic Ureamic Syndrome (HUS) investigations and what treatments should be avoided

Answer 22

Send stool culture samples: all patients with bloody faeces

Send U&E, FBC, film, LFT, clotting, urine, (dipstick/micro), lactate dehydrogenase

Close monitoring
Admission usually needed
Look for: acute renal failure, thrombocytopaenia, haemolytic anaemia

NO antibiotics: may precipitate HUS
NO anti-motility agents
NO NSAIDS

Question 23

produces heat liable and heat stable toxin
Heat stable toxin similar to cholera and Yersinia toxins
Travel related

Answer 23

enteroTOXIgenic (ETEC)

Question 24

Attaching and effacing lesions. No toxin, not invasive
Synthesises, secretes and inserts its own receptor into cell membranes
Non breastfed children
Can be asymptomatic

Answer 24

enteroPATHOgenic (EPEC)

Question 25

Watery diarrhoea, rare dysentery Demonstrates invasion Sereny test

Answer 25

enteroINVASIVE (EIEC)

Question 26

Travellers diarrhoea New kid on the block Cytogenic, secretogenic, proinflammatory

Answer 26

enteroAGGREGATIVE (EAIC)

Question 27

``` Gram negative, Enterobacteriales family 16- 48 hrs incubation Sporadic – rarely outbreaks Low inoculum Invasive Pain, blood (30%), fever May be admitted food hygiene (raw poultry especially) Sel limiting macrolide (maybe if co-morbid factors: but increasing resistance) less likely to spread person to person Most common ```

Answer 27

Campylobacter

Question 28

corkscrew appearance

Answer 28

campylobacter

Question 29

campylobacter post infectious consequences

Answer 29

``` Guillain Barré (1-2 weeks after infection) Reactive arthritis ( associated with HLA B-27) Miller-Fischer variant ```

Question 30

Motile gram negative bacilli. Enterobacteriales family 8-72 hours hrs incubation Fecal oral route Food: poultry, meat, raw egg animal gut, multiplies in food Toxin and invasion D&V, blood, fever (severity depends on inoculum) Achloridia, IBD and sickle cell disease associated with more severe

Answer 30

salmonella

Question 31

Non spore forming Gram positive rod. It has 1 to 5 flagella Infection acquired from contaminated food -unpasteurised milk products, deli counter It can grow at low temperature ``` Extract of cell membrane causes monocytosis ……. in rabbits Rarely causes monocytosis in humans !!! Despite the name 67% csf has neutrophils Effect of iron overload Food borne transmission, mother to child ```

Answer 31

Listeria monocytogenes

Question 32

what can invasive listeria monocytogenes causes

Answer 32

meningitis/bacteriaemia | brain abscess, rhomboencephalitis

Question 33

what are examples of viruses causing viral gastroenteritis

Answer 33

Rotavirus | Norovirus

Question 34

``` Commonest cause in kids <3 yrs ~ all kids get it before 5 person-person Faecal oral Direct & indirect Usually in the winter Subclinical or mild in adults Immunocompromised? can be severe Range of clinical effects Mild watery to profuse and shock May have moderate fever first, vomiting then diarrhoea Not bloody Self limiting Lasts a week Children may have post infection malabsorption which leads to more diarrhoea Repeat infections: milder each time Can cause outbreaks PCR diagnosis on faeces Hydration is the key to management Oral where possible in mild to moderate ```

Answer 34

rotavirus

Question 35

describe the rotavirus vaccine

Answer 35

Oral Live attenuated Excreted in faeces From sept 2013 1200 babies/yr need hospital treatment 2 doses 2 and 3 months 120 cases per 100,000 children < 1 yo per year 2 in 100,000 with vaccine Risk of intususseption increases as babies get older So 1st dose is not given to babies over 15 weeks No dose given to babies over 24 weeks Capable of coughing spitting & sneezing oral vaccine: careful technique!

Question 36

‘Winter Vomiting Disease’- lately all year round! Affect all ages: HIGHLY infectious 5 billion viruses per gram of faeces Faecal-oral/droplet routes of spread Person to person (or on contaminated food/water) Environmental survival on fomites for days- weeks Low infectious dose Community circulation is the reservoir Asymptomatic shedding (48 hrs post cessation of symptoms) Abrupt & unpredictable onset D&V explosive & sudden! Vomiting can lead to widespread environmental contamination & onward transmission All lead to potential for numerous and large outbreaks especially in hospitals, schools etc

Answer 36

norovirus

Question 37

norovirus symptoms

Answer 37

Also some general systemic symptoms Short incubation (<24 hours): lasts 2-4 days Diagnosis: PCR on stool PCR on vomit using red Copan viral swabs Usually self limiting : very unpleasant Hydration is the key Can contribute to death in frail elderly patients Early ward closure/isolation/cohorting required

Question 38

inflammation of lining of stomach, small and large intestine

Answer 38

gastroenteritis

Question 39

what is the pathophysiology of gastroenteritits

Answer 39

enteric pathogens cause diarrhoea via several mechanisms: stimulation of net fluid and electrolyte secretion increased propulsive muscle contractions mucosal destruction and increased permeability nutrient malabsorption

Question 40

what investigations would you do for gastroenterititis

Answer 40

``` stool microscopy (HX of giardia, amoeba) stool culture (eg salmonella, campyl, shigella) stool toxin for C diff (enter- and cyto-toxin) blood cultures (Salmonella) PCR (norovirus) FBC (assess WCC) U&Es (renal function) AXR ```

Question 41

what is the treatment for gastroenteritis

Answer 41

``` usually supporting (oral rehydration + IV fluids) specific C.diff managments ```

Question 42

what are the two short incubation (1-6hrs) pathogens

Answer 42

``` staph aureus (gram positive coccus, very fast preformed toxin, acts on vomiting centre on brain, milk/meat/fish) bacillus cereus (gram positive bacillus rod, profuse vomiting, REHEATED RICE) ```

Question 43

What are the two medium incubation pathogens

Answer 43

salmonella (12-48hrs) [outbreaks can also cause bacteriaemia pultry/meat/rawegg blood diarrhoea, vomiting, fever] listeria monocytogenes (9-48hrs) [fever, muscle aches, diarrhoea, pregnant women may have mild sympoms, unpasteurised milk products, deli counter, gram positive rod]

Question 44

what are the two longer incubation pathgogens

Answer 44

campylobacter (16-48hrs) [most common, usually self limiting, associated with food hygiene, guillan barre syndrome complication] e.coli 0157 (1-14 days) [rare but mobidity and outbreaks, produces verotoxin and shiga-like toxins, verotoxins, blood diarrhoea, notify health protection unit, avoid ABs -> can progress to haemolytic uraemic syndrome)

Question 45

management of c.diff

Answer 45

non severe = metrondiazole PO 400 m tds (10 days) | severe = vancomycin 125mg qds PO/NG +/- metrondiazole (10 days) isolate patient

Question 46

4Cs causing C diff

Answer 46

cephalosporins clindamycin ciprofloxacin co-amoxiclav