MICRO - GIT Infections Flashcards
gastroenteritis ‘definition’ + Sx
- general disease characterised by N/V/D, abdominal discomfort
diarrhoea ‘definition’ + Sx
- abnormal faecal discharge characterised by frequent and/or liquid stool
- usually small intestine
- usually related to enterotoxin
dysentery ‘definition’ + Sx
- inflammatory disorder (usually large intestine), usually invasive infection with mucosal obstruction
- blood and pus in faeces
- pain, fever, abdo cramps
2 types of salmonella + transmission
- enteric fever: typhi and paratyphi (no animal reservoir - only human-human transmission via contaminated food/water), much easier to become systemic
- non-typhoid: mostly acute but self-limiting diarrhoea, can be invasive (sepsis), have large animal reservoirs - transferred via contaminated food, large infectious dose required
Dx and Tx of salmonella (non-typhoid)
- Dx: culture on selective media or PCR, blood cultures if suspect bacteraemia
- Tx: usually self-limiting, fluid + electrolytes, NO ANTIBIOTICS (doesn’t reduce Sx or illness duration, may prolong excretion of bacteria)
salmonella pathogenesis
- invades M cells and picked up by macrophages in Peyer’s patches
- multiply in the macrophage and end up in bloodstream = bacteraemia and spread to multiple organs
- can also spill out again once they’ve gone to other organs = secondary bacteraemia
enteric fever (typhoid and paratyphoid salmonella) Sx
- fever, malaise, aches
- diarrhoea, constipation
- rose spots are characteristic in half of the Pts
Dx, Tx, prevention for enteric fever (typhoid salmonella)
- Dx: stool AND blood culture
- Tx: immediate antibiotics
- prevention: vaccination
- which E. coli strain is the ‘traveller’s diarrhoea’?
- which strain causes dysentery as opposed to diarrhoea?
- traveller’s diarrhoea: enterotoxigenic E. coli (ETEC)
- enteroinvasive E. coli (EIEC): dysentery
infectious dose required to get E. coli infection
- large dose (>10^5)
shigella (bacillary dysentery)
- aetiology
- transmission
- how infectious
- aetiology: from mild to severe = S. sonnei, S. flexneri, S. boydii, S. dysenteriae
- transmission: faecal-oral route (no animals), primarily paediatric
- VERY infectious (<10 organisms to cause disease)
shigella Sx
- Sx range from mild to severe gastroenteritis depending on species
- watery diarrhoea at first, later contains mucus and blood
- may have lower abdo cramps
shigella pathogenesis
- invades colonic mucosa = inflammation and ulceration
- S. dysenteriae = shiga toxin which can damage glomerular endothelium = kidney failure
Dx and Tx of shigellosis
- Dx: culture or rapid molecular tests
- Tx: rehydration, antibiotics for severe cases
campylobacter jejuni
- transmission
- how infectious is it
- pathogenesis
- transmission: large animal reservoir, transmitted by contaminated chicken, dairy, water
- highly infectious + microaerophilic (doesn’t need lots of oxygen) and thermophilic (grows well at high temps)
- pathophys: invades mucosal surfaces in jejunum, ileum and colon = ulceration and inflamed bleeding. cytotoxins can cause bacteraemia esp. if immunocompromised
Sx and Tx for Campylobacter jejuni
- Sx: diarrhoea
- Tx: usually self-limiting, antibiotics if invasive
cholera
- transmission
- how infectious is it
- Sx
- transmission: spread via contaminated food/water, only human-human transmission (can have asymptomatic carriers)
- high infectious dose needed
- Sx: severe, watery, non-bloody diarrhoea (rice water stool) = massive fluid loss and electrolyte imbalance = high mortality if untreated
cholera pathophys + Dx
- cholera enterotoxin = not very invasive = tricks intestinal epithelium to have a mass exodus of electrolytes
- Dx: culture (selective + differential media) but can also do PCR
cholera Tx
- oral or IV fluids
- antibiotics (e.g. tetracycline, azithromycin) to reduce duration of infection and diarrhoea - if moderate to severe dehydration
- killed whole-cell vaccine (only 50% effective and protective for 3-6 months)
antibiotic-associated diarrhoea
- aetiology
- pathogenesis
- 2 toxins involved
- C. difficile
- pathogenesis: antibiotics disrupts normal flora = C. difficile can multiply
- toxin A (enterotoxin) = increased intestinal permeability and fluid secretion
- toxin B (cytotoxin) = colonic inflammation, haemostasis and colon necrosis
Sx, Dx, Tx of C. difficile infection
- Sx: diarrhoea, abdo pain, fever (after antibiotic Tx)
- Dx: detection of toxin in stool
- Tx: anti-anaerobic (e.g. metronidazole) or oral vancomycin, can also do faecal microbiota transplant (FMT)
food poisoning vs food-borne infections
- food poisoning = consumption of food containing pre-formed toxins, fast onset
- food-borne infections = food is a vehicle for a pathogen to multiply in our bodies once the food is eaten
S. aureus food poisoning pathophys + Sx
- up to 50% of S. aureus produces enterotoxin = heating kills bacteria but not toxin (many ppl carry bacteria on skin and nose)
- Sx: fast onset (<6 hrs) and usually self-limiting vomiting (no diarrhoea)
bacillus cerus food poisoning
- pathogenesis
- 2 forms
- common cause
- produces spores (found in soil and food) which survive cooking and germinate further on cooling
- emetic form: rapid onset vomiting due to preformed toxin in food
- diarrhoeal form: watery diarrhoea due to enterotoxin production in gut
- commonly occurs due to rice not properly stored after cooking