Enteric infections Flashcards
State the symptoms of enteric infection
- Nausea
- vomiting
- diarrhoea
- Non-intestinal manifestations
- botulism
- guillan barre (might seem unusual but campylobacter jejuni is the most common trigger for development of guillan barre syndrome)
Nausea is one of the most common symptoms of gastroenteritis. Voming is actually less common, and when it is the predominant symptom you want to think about certain aetiologies. What might these be
- pre-formed toxin in food - as a resulting of the food cooling, giving change for bacteria to colonise and produce toxins
- Staphy.aureus
- B.cerrus (classic one on rice)
- sudden onset with 6-12hrs of food ingestion
- If not a pre-formed toxin, Norovirus is possible
Define diarrhoea. What in broad terms triggers diarrhoea?
- 3 or more loose or watery stools per day
- usually some kind of irritation to the airway
Small and large bowel diarrhoea will likely present differently. Explain the main differences
Small bowel:
- large volume very watery
- cramps, bloating, wind, weight loss (due to malabsorption)
- fever and blood in stool are rare
- If you see these, you are thinking the pathology is occuring in the small bowel
Large bowel:
- small volumes, more frequently
- painful stool
- fever and blood common
There are 3 broad methods of pathogenicity for diarrhoea. What are they?
- Toxin mediated - can be produced either before or after consumption
- prior - S.aureus, B.cereus
- after - C.difficile, E.coli.
- Pathogen damages intestinal epithelial surface
- Invasion of pathogen across intestinal epithelial barrier
What are the most common infectious aetiologies for Gastroenteritis?
- Campylobacter sp
- Salmonella sp
- Shigella sp
- E.coli 0157. found in beef
LOTS
State the most common viral aetiologies for gastroenteritis
- major one is norovirus
- other less common ones include sorovirus, rotabirus, adenoviruses - these are more common in children than in adults
NSRA - National small bore rifle association
State common parasitic aetiologies of gastroenteritis
- Cryptosporidum - most common in UK - classically in lambing season time - lamb excretes large amounts, can enter water supplies
- Giardira - also common
- Cyclospora
- Isospora
- Entamoeba histolytica
The last 4 are often travel bugs, so important to take a travel history.
3 key tools when assessing the patient for suspected gastroenteritis are:
the History - absolute most important
Stool examination/culture
Enoscopy
What are some of the key things to enquire about when taking a history for gastroenteritis?
- Food history (poultry is big source of many pathogens)
- onset and nature of symptoms - big volume, low volume etc, is it actually diarrhea
- residence - nursing home?
- occupation - sewage works, pipe fitters, livestock?
- travel - tropical?
- pets/hobbies - lizards and snakes - covered in salmonella
- recent hospitlisation/antibiotic use
- co-morbidities; diabetes, heart failure
Stool culture can be used , but it is not particularly sensitive (1.5-5.5% positive stool cultures). What are the main reasons for this?
Furthemore, it is also sometimes not entirely necessary to know, since the illness is self-limiting. You could conversley may the argument that not what the organism is can perhaps help the management of the illness. It may also be in the interest if public health to know what the cause is - for example people who work in particular jobs.
- Many of the infectious agents are viruses and cannot be cultured
- Gut has very specific envrionmental conditions that are difficult to recreate
If you suspect a parasitic cause, you may also have to look at sample using what?
microscope
Endoscopy is rarely needed for gastroenteritis. When would use it?
There are very specific occassions where you would need a biopsy to confirm CMV infection in immunocompromised patients where the patient will not produce sufficient levels of antibodies to test otherwise.
- Basically if you had ruled out that the cause of the patients symptoms is not infectious
Outline treatment options for gastroenteritis
- Is typically self-limiting
- First key one is hydration
- this assumes that the sodium-glucose contransport remains intact
- Water can be reabsorbed if this co-transporter is intact
- IV fluid replacement may be required if patient has been vomiting
- Antibioics
- not always necessary
- reduces symptoms by about 1 day
- in some cases, antibiotics can worsen outcomes - E.coli 0157
What patients should be considered for antiobiotic treatment
- very ill patients
- sepsis or evidence of bacteraemia - some salmoella can invade epithelial surface
- If patient has significant co-morbidities
- diabetes
- Specific aetiologies:
- C.difficile associated diarrhoea - Mentronidazole/vancomycin - these are quite broad spectrum so must be used carefully
Name a drug that can be used to treat diarrhoea as a symptom. Does this improve prognosis?
- Loperamide (Imodium brand name)
- May worsen, since diarrhoea also helps to get rid of the bacteria.
- anything that slows down clearance may allow bacteria more time to colonise, and may let certain bacteria like salmonella to infiltrate GI epithelium.
Other treatments that are not as common for gastroenteritis include probiotics and exclusion diets. Do these work?
- little evidence probiotics actually help treatment - some evidence they they can have preventitive effects of diarrhoea in children
- Exclusion diets doesn’t really work
- exception to this is Giardia infection, which impairs the bodies ability to digest lactose.
Campylobacter infection is usually self-limiting and lasts around ???? days.
It has high resistance rates and develops resistance upon treatment. Antibiotics are rarely indicated unless patient is particularly ill.
What are potential complications of Campylobacter
7
- reactive arthritis
- Guillan-bare
Campylobacter is a gram negative, curved rod or comma shaped bacteria with a double flagellum. Camplybacter Jejuni is most common. They ????? and ?????? epithelial cells in the ???? and ???? bowel, and release toxins to cause diarhoea. The incubation period is 3 days.
- attach and invade epithelial cells
- small and large bowel
What class of drug increases risk of infection by campylobacter (and gastoenteritis in general?)
PPIs
What are the clinical features of campylobacter infection?
- note how the diraahoea presentation has characteristics of small and large bowel diarrhoea
What is the infectious dose of campylobacter?
APPROX 9000 organisms
Salmonella is a commensal bacteria for both chickens and reptiles. It spreads for people. There are typhoidal and non-typhodial species. What is the difference between these?
What is the infectious dose for salmonella?
What drug class increases risk of infection by Salmonella
A dimished gut ????? can also increase risk.
- Typhoidal are serotypes that are strictly adapted to humans
- 10,000 organisms
- PPIs
- microbiome.
very briefly outline pathogenesis of salmonella
Pathogenic salmonellae ingested in food survive passage through the gastric acid barrier and invade the mucosaal enterocytes of the small and large intestine and produce toxins. Invasion of epithelial cells stimulates the release of proinflammatory cytokines which induce an inflammatory reaction. They can also infiltrate the blood causing bacteriaemia.
Illness from Salmonella begnins within ???? hours. The higher the innoculum, the faster the onset.
Symptoms?
Complications?
Antiobiotics?
Lasts for?
72
Nause, cramps, diarrhoea, fever
Can be invasive(5%) and enter the blood. Can also cause secondary infection, Salmonella can stick to many tissues - causing endocarditis, can manifest in the Reactive arthritis
Not for uncomplicted gastroenteritis as it does not have any noticeable effect , but prescribed for bacteraemia.
10 days
E.coli 0157 - Veratoxin producing e.coli.
Commensal of the guy in ruminant animals - animals that have more than one gut; cows, sheep and goats.
Often comes about by meat not been butured properly - especially beef that is destined to be mince. It is however also present on vegetables, such as spinach and beansprouts.
Outline the pathogenesis of E.coli 0157.
- attaches to gut enterocytes
- produces shiga toxin, which is internalised by the cell
- shiga toxin blocks ribosomal peptide elongation, leading to cell death
- Enterocyte death results in release of shiga toxin and other bacterial factors entering systemic circulation, as well as ulceration of the gut mucosa due to cell death - this leads to blood diarrhoea
What is the infectious load of E.coli 0157?
WHat is the incubation period of how long?
Clinical presentation?
As few as 10 organisms
3-4 days
Abdominal pain, bloody diarrhoea, fever is rare
Describe the main complication of haemolytic uraemic syndrome as a result of systemic exposure to shiga toxin
- triad of things
- Microangiopathic haemolytic anaemia - this is where shiga toxin damages blood vessel walls, seems to happen especially in the smaller blood vessels. Meshes of fibrin form, and blood cells passing through get sheared.
- Acute renal railure - the place where most of these tiny blood vessels are, causes the renal circulation to become clogged resulting in renal failure, in addition to the vasoconstriction that occurs due to endothelial damage.
- Thrombocytopenia - because platelet consumption is so high in generating the fibrin meshes.
Management is supportive for E.coli 0157.
Key is ??
Prevention
Clostridioides difficile is primarily a hospital infection. Outline the pathogenesis
- Usually neeeds to be some kind of initial colonic insult that has depeleted the commensal flora - such as antibiotic treatment
- Clostridium spores are activated by bile salts
- The bacteria then adhere to the colonic mucosa
- toxins are released that stimulate inflammation of the colonic lining by inducing cytoskeletal changes that compromise the epithelial barrier and inflammatory cytokine production.
- Disruption of tight junctions allows the toxins to cross the epithelium, where they can further induce inflammatory cytokine production in lymphocytes and mast cells. This leads to escalation of the inflammatory response due to neutrophil and lymphocyte influx, which can lead to pseudomembrane formation
State the risk factors for c.diff infection
Antibiotic exposure is big one
older age > 65 years
PPI use - maybe
hospitalisation
Clinical presentation of c.diff?
- Loose stool and colic
Fever
Leukocytosis
Patients with recurrent lose protein and become malnourished
In the stool, what are the two things that are tested for with regards to C.diff infection?
the antigen
and the toxin i.e. even if bacteria is present it might not be pathogenic.
Treatment for C.diff?
- stop causative antibiotics if possible to allow normal gut flora to recolonise
- Mentronidazole/vancomycin help get c.diff down, then stop them, allowing normal gut flora to come back and prevent furtehr c.diff in colinisation
- in some patients, c.diff comes back before commensal bacteria, so fecal transplant will be necessary via nasogastric tube
Most common viral cause of gastronenteritis?
norovirus - the winter vomiting bug - although it can now be seen all year around
Norovirus is transmitted via facel oral route. Infectious dose is extremely low at 10-100 viruses, and occurs at all months but peaks in winter. Alcohol gel does nothing for norovirus.
State clinical featues:
- Acute diarrhoea, and vomiting - LOTS of both
- 24-48 hours
- No lasting immunity
WASH HANDS!
What is the ultimate go to treatment for enteric infections?
ORAL REHYDRATION
