microorganisms in GI tract part 2 W4 Flashcards
where does Helicobacter Pylori act?
stomach, duodenum
Helicobacter Pylori features?
curved/spiral, gram-negative
widespread
can survive in acid environments
microaerophile (needs very little oxygen)
motility
urease activity
causes inflammation in stomach and duodenum
urease in Helicobacter Pylori?
urease is an enzyme which transforms protein containing urea into ammonia which is alkaline so acts as a H+ buffer
clinical features of Helicobacter Pylori
gastritis (inflammation of stomach)
gastric and duodenal ulcers
gastric carcinoma (due to chronic inflammation)
Helicobacter pylori diagnosis
gastroscopy
biopsy
urea breath test
antigen in stools
rice-water diarrhoea related to which pathogen?
Vibrio cholerae
where does Vibrio cholerae act
jejunum and ileum
how is Vibrio cholerae transmitted
contaminated water or food (seafood)
how is helicobacter pylori transmitted
food and water
Vibrio cholerae features
gram-negative, comma-shaped bacterium, motile with polar flagellum
sensitive to drying out, sunlight and acid (so high bacterial load needed)
virulence factors = pili, toxin
how does vibrio cholerae toxin work
composed of 5 B-subunits surrounding an A-subunit (active part). binds to GM1 ganglioside in gut cell. A-subunit enters cell, transforms ATP to cAMP. this causes:
-increased secretion of chloride
-reduced absorption of sodium
-net flow of water, potassium and bicarbonate into the bowel lumen
leads to diarrhoea.
clinical features of cholerae diarrhoea?
watery diarrhoea = secretory
rice-water stools
severe dehydration
diagnosis of vibrio cholerae
clinical aspects
stool culture
treatment of helicobacter pylori?
antibiotics
treatment of vibrio cholerae?
rehydrate (oral or IV if possible)
antibiotics
Shigella transmission?
contaminated water or food (very low infectious load)
shigella features
nonmotile, facultatively anaerobic, gram-negative, rod shape
four species
invasive: high inflammation of gut epithelium
S. dysenteriae produces shiga-toxin
four species of shigella? which is the main & most severe one?
S. dysenteriae (main and most severe)
S. flexneri
S. boydii
S. sonnei
pathophysiology of shigella?
enters epithelium through M cells. presented to macrophage, kills macrophage. this provokes release of cytokines and large inflammation which kills cells.
M cells?
immune cells on gut epithelium. present bacterial antigen to other immune cells
shigella clinical features
bacterial dysentery (bloody diarrhoea, abdominal cramps, fever)
complications
what is bacterial dysentery
3 main manifestations:
-bloody diarrhoea
-heavy abdominal cramps
-fever
diagnosis of shigella
stool culture
sometimes PCR
treatment of shigella
supportive treatment (painkillers, IV fluids)
antibiotics (ciprofloxacin, azithromycin)
Clostridioides difficile transmission?
environmental pathogen
spores - healthcare facilities
clostridioides difficile features?
gram-positive, anaerobic
motile, spore former (very resistant)
produces toxins
promoted by antibiotic use
combination of direct cellular damage and immunopathology
clostridioides difficile pathophysiology?
antibiotic therapy
-> disruption of colonic microflora
-> C. difficile exposure and colonisation
-> release of toxin A (“enterotoxin”) and toxin B (“cytotoxin”)
-> mucosal injury and inflammation
clostridioides difficile - toxin pathophysiology?
toxins enter cell
glycosylate and inactivate GTP (cytoskeletal regulatory protein)
causes collapse of actin cytoskeleton and cell death
nosocomial?
originating in a hospital
most common cause of nosocomial diarrhoea?
clostridioides difficile
clostridioides difficile clinical features?
spectrum of:
-asymptomatic carriage
-diarrhoea/simple colitis
-pseudomembranous colitis
-fulminant colitis
diagnosis of Clostridioides difficile
clinical features and stool analysis
treatment of clostridioides difficile
very specific antibiotics (metronidazole or vancomycin)
“faecal transplants” (replace microbiota in gut)
immunotherapy
prevention and control of Clostridioides difficile?
infection control - removal of spores in hospital environment via cleaning
antibiotic stewardship - restriction of antibiotics known to cause CDI
UK hyper-virulent strain of Clostridioides difficile?
tcdC gene deletion - normally negative regulator of secretion of toxins.
some strains were hyper toxin producers.
resistant to quinolone antibiotics. when people were treated with quinolone, microbiota killed but not CDI.
take home messages for Clostridioides difficile?
explosive diarrhoea
resistant spores
antibiotic treatment
elderly patients
incontinence
