Gastroenteritis Flashcards
what are the risk factors of gastroenterititis
Malnutrition (micronutrient) deficiency Closed/ semi-closed communities Exposure to contaminated food/water /travel Winter congregating/ summer floods Age <5 , not breastfeeding Older age
pathogenesis of gastroenteritis
Osmotic/Malabsorptive (various mechanisms)
Secretory (toxin mediated)
Intestinal tight junction dysruption (leak-flux)
Inflammatory (mucosal invasion)
Intestinal motility (through the enteric nervous system)
how does diarrhoea happen
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
≥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
diarrhoea
inflammation of the intestine particularly the colon causing diarrhoea associated with blood and mucus
generally associatated with fever, abdominal pain, and rectal tenesmus
dysentry
volume of diarrhoea in large bowel and small?
Large volume tends to be small bowel, large bowel small volume
Yersinia enterocolitica may mimic appendicitis as it may invade mesenteric nodes
what should you ask in a history for gastroenteritis
associated symptoms
exposure history and predisposing factors
travel history
stool appearance
1 to 6 hours
gram positive
from starchy food (reheated Rice)
profuse vomiting
bacillus cereus
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
staphylococcus aureus
investigations for gastroenteritis
stool sample
Blood culture
gram negative rod, nonmotile, anaerobic, enterobacteriaceae
four species
shigella
what are the 4 species of shigella
s. dysenterae (serogroup A), S. flexneri (serogroup B), shigella boydii (C), s sonnei (D)
what species of shigella can cause the hemolytic-uremic syndrome (HUS) and what is it mediated by ?
s. dysenterae 1
and shiga toxin (Stx)
what are the symptoms of a shigella infection
fever abdominal pain mucoid diarrhoea watery/bloody diarrhoea vomiting
what does shiga toxin do
binds to receptors found on renal cells, RBC and others
inhibit protein synthesis
cause cell death
ecoli classes
enteroToxigenic(ETEC)
enteroPathogenic (EPEC)
enteroInvasive (EIEC)
enteroAggregative (EAIC)
how does Ecoli produced toxin
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
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
E Coli 0157
effect of verotoxin (VTEC)
mild to severe (Death)
bloody diarrhoea
haemorrhagic collitis
Haemolytic Ureamic Syndrome (HUS) presentation
abdomen pain fever pallor petechiae oliguria blood diarrhoea under 16 years old
Haemolytic Ureamic Syndrome (HUS) signs
High white cells Low platelets Low HB Red cell fragments LDH>1.5 x normal May develop after diarrhoea stopped
Haemolytic Ureamic Syndrome (HUS) investigations and what treatments should be avoided
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
produces heat liable and heat stable toxin
Heat stable toxin similar to cholera and Yersinia toxins
Travel related
enteroTOXIgenic (ETEC)
Attaching and effacing lesions. No toxin, not invasive
Synthesises, secretes and inserts its own receptor into cell membranes
Non breastfed children
Can be asymptomatic
enteroPATHOgenic (EPEC)
Watery diarrhoea, rare dysentery
Demonstrates invasion
Sereny test
enteroINVASIVE (EIEC)
Travellers diarrhoea
New kid on the block
Cytogenic, secretogenic, proinflammatory
enteroAGGREGATIVE (EAIC)
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
Campylobacter
corkscrew appearance
campylobacter
campylobacter post infectious consequences
Guillain Barré (1-2 weeks after infection) Reactive arthritis ( associated with HLA B-27) Miller-Fischer variant
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
salmonella
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
Listeria monocytogenes
what can invasive listeria monocytogenes causes
meningitis/bacteriaemia
brain abscess, rhomboencephalitis
what are examples of viruses causing viral gastroenteritis
Rotavirus
Norovirus
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
rotavirus
describe the rotavirus vaccine
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!
‘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
norovirus
norovirus symptoms
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
inflammation of lining of stomach, small and large intestine
gastroenteritis
what is the pathophysiology of gastroenteritits
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
what investigations would you do for gastroenterititis
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
what is the treatment for gastroenteritis
usually supporting (oral rehydration + IV fluids) specific C.diff managments
what are the two short incubation (1-6hrs) pathogens
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)
What are the two medium incubation pathogens
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]
what are the two longer incubation pathgogens
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)
management of c.diff
non severe = metrondiazole PO 400 m tds (10 days)
severe = vancomycin 125mg qds PO/NG +/- metrondiazole (10 days) isolate patient
4Cs causing C diff
cephalosporins
clindamycin
ciprofloxacin
co-amoxiclav
