microorganisms in GI tract part 2 W4

Question 1

where does Helicobacter Pylori act?

Answer 1

stomach, duodenum

Question 2

Helicobacter Pylori features?

Answer 2

curved/spiral, gram-negative
widespread
can survive in acid environments
microaerophile (needs very little oxygen)
motility
urease activity
causes inflammation in stomach and duodenum

Question 3

urease in Helicobacter Pylori?

Answer 3

urease is an enzyme which transforms protein containing urea into ammonia which is alkaline so acts as a H+ buffer

Question 4

clinical features of Helicobacter Pylori

Answer 4

gastritis (inflammation of stomach)
gastric and duodenal ulcers
gastric carcinoma (due to chronic inflammation)

Question 5

Helicobacter pylori diagnosis

Answer 5

gastroscopy
biopsy
urea breath test
antigen in stools

Question 6

rice-water diarrhoea related to which pathogen?

Answer 6

Vibrio cholerae

Question 7

where does Vibrio cholerae act

Answer 7

jejunum and ileum

Question 8

how is Vibrio cholerae transmitted

Answer 8

contaminated water or food (seafood)

Question 9

how is helicobacter pylori transmitted

Answer 9

food and water

Question 10

Vibrio cholerae features

Answer 10

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

Question 11

how does vibrio cholerae toxin work

Answer 11

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.

Question 12

clinical features of cholerae diarrhoea?

Answer 12

watery diarrhoea = secretory
rice-water stools
severe dehydration

Question 13

diagnosis of vibrio cholerae

Answer 13

clinical aspects
stool culture

Question 14

treatment of helicobacter pylori?

Answer 14

antibiotics

Question 15

treatment of vibrio cholerae?

Answer 15

rehydrate (oral or IV if possible)
antibiotics

Question 16

Shigella transmission?

Answer 16

contaminated water or food (very low infectious load)

Question 17

shigella features

Answer 17

nonmotile, facultatively anaerobic, gram-negative, rod shape
four species
invasive: high inflammation of gut epithelium
S. dysenteriae produces shiga-toxin

Question 18

four species of shigella? which is the main & most severe one?

Answer 18

S. dysenteriae (main and most severe)
S. flexneri
S. boydii
S. sonnei

Question 19

pathophysiology of shigella?

Answer 19

enters epithelium through M cells. presented to macrophage, kills macrophage. this provokes release of cytokines and large inflammation which kills cells.

Question 20

M cells?

Answer 20

immune cells on gut epithelium. present bacterial antigen to other immune cells

Question 21

shigella clinical features

Answer 21

bacterial dysentery (bloody diarrhoea, abdominal cramps, fever)
complications

Question 22

what is bacterial dysentery

Answer 22

3 main manifestations:
-bloody diarrhoea
-heavy abdominal cramps
-fever

Question 23

diagnosis of shigella

Answer 23

stool culture
sometimes PCR

Question 24

treatment of shigella

Answer 24

supportive treatment (painkillers, IV fluids)
antibiotics (ciprofloxacin, azithromycin)

Question 25

Clostridioides difficile transmission?

Answer 25

environmental pathogen
spores - healthcare facilities

Question 26

clostridioides difficile features?

Answer 26

gram-positive, anaerobic
motile, spore former (very resistant)
produces toxins
promoted by antibiotic use
combination of direct cellular damage and immunopathology

Question 27

clostridioides difficile pathophysiology?

Answer 27

antibiotic therapy
-> disruption of colonic microflora
-> C. difficile exposure and colonisation
-> release of toxin A (“enterotoxin”) and toxin B (“cytotoxin”)
-> mucosal injury and inflammation

Question 28

clostridioides difficile - toxin pathophysiology?

Answer 28

toxins enter cell
glycosylate and inactivate GTP (cytoskeletal regulatory protein)
causes collapse of actin cytoskeleton and cell death

Question 29

nosocomial?

Answer 29

originating in a hospital

Question 30

most common cause of nosocomial diarrhoea?

Answer 30

clostridioides difficile

Question 31

clostridioides difficile clinical features?

Answer 31

spectrum of:
-asymptomatic carriage
-diarrhoea/simple colitis
-pseudomembranous colitis
-fulminant colitis

Question 32

diagnosis of Clostridioides difficile

Answer 32

clinical features and stool analysis

Question 33

treatment of clostridioides difficile

Answer 33

very specific antibiotics (metronidazole or vancomycin)
“faecal transplants” (replace microbiota in gut)
immunotherapy

Question 34

prevention and control of Clostridioides difficile?

Answer 34

infection control - removal of spores in hospital environment via cleaning
antibiotic stewardship - restriction of antibiotics known to cause CDI

Question 35

UK hyper-virulent strain of Clostridioides difficile?

Answer 35

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.

Question 36

take home messages for Clostridioides difficile?

Answer 36

explosive diarrhoea
resistant spores
antibiotic treatment
elderly patients
incontinence