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enteric infections Flashcards

1
Q

repeat enteric infections can lead to

A

malnutrition
growth stunting
cognitive impairment
impaired immunity (with vaccine hyporesponsiveness)

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2
Q

definition of diarrhoea

A

increased stool water causing

  • an increase in stool frequency
  • the passage of soft stools
  • the passage of greater than 3 stools per day or stool volume of greater than 200mls
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3
Q

acute diarrhoea

A

lasting less than 2 weeks

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4
Q

chronic diarrhoea

A

lasting more than two weeks

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5
Q

small intestine

A 
6m ling in adult human 
short duodenum 
jejunum 40% of length 
ileum 60% of length 
absorbs 
- all amino acids 
- all sugars 
- most lipids 
- 80% of water
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6
Q

surface area of the small intestine is increased by

A

mucosal folds
villi and crypts
microvilli and enterocytes

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7
Q

large intestinal structure

A

lacks folds or villi
has crypts
site of water absorption
dependant on Na absortoin

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8
Q

water flux in the intestine

A

inputs 9L
reabsorbs 8.8L
excretes 0.2L in stool

even a small disturbance in flux can result in diarrhoea

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9
Q

water in the intestine follows

A 
osmotic gradients 
osmotically active molecules include 
- electrolytes 
- sugars 
- amino acids
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10
Q

secretion in the small intestine

A

to distinct processes establish as osmotic gradient which pulls water into the small intestine lumen

  • digestion of food into small molecules of high osmolarity
  • active secretion of electrolytes by crypt enterocytes
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11
Q

active secretion of electrolytes by crypt enterocytes

A

cyclic AMP activates the transmembrane chloride channel.

chloride is pumped into the lumen

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12
Q

how is water reabsorbed from the lumen

A

sodium dependant hexose transporter
coupled transport of Na+ and glucose into the enterocyte
high sodium concentration is largely responsible for absorption of water in the small intestine

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13
Q

oral rehydration solutions

A

goal is to increase presence of sodium and glucose in enterocyte cell

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14
Q

mechanisms of diarrhoea production

A
  1. increased active secretion of electrolytes and thus water
  2. damage to brush border resulting in malabsorption of nutrients and electrolytes
  3. damage to brush border, loss of disaccharide activity, increase osmolarity of stool
  4. altered motility, less time for water absorption
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15
Q

4 classifications of diarrhoea

A
  • inflammatory
  • secretory
  • osmotic
  • motility related

type of diarrhoea is dependant upon the virulence factors expressed by the pathogen

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16
Q

main virulence factors

A
  1. those enabling adhesion
  2. those enabling invasion
  3. those having toxins
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17
Q

types of toxin production

A
  • enterotoxins - work on the enterocyte (don’t damage it)
  • cytotoxins - damage the enterocyte
  • neurotoxins - stimulate the smooth muscle of the bowel
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18
Q

enterotoxins

A

interfere with the salt and water transport without damaging the enterocyte itself
result sin net loss of water
can use rehydration solutions in these cases

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19
Q

cytotoxins

A

cause damage to the cells of the intestin

20
Q

neurotoxins

A

central or loval nervous system stimulation causing increased intestinal motility

21
Q

preformed toxin disease

A

by already be present in the food before it is eaten

disease usually has short incubation period

22
Q

heat labile toxins

A

are destroyed by cooking (preformed)

23
Q

heat stable toxins

A

not destroyed by cooking (preformed)

24
Q

vibrio cholerae

A

curved gram negative rod
some strains produce a powerful enterotoxin
produce watery diarrhoea
sever dehydration, may cause death within hours in malnourished, debilitated hosts

25
ingested vibrios
more likely to be killed by stomach acids | those that survive adhere to small intestinal enterocytes and secrete cholera toxin
26
cholera toxin
has 2 subunits the B subunit binds the toxin to specific reception on the enterocytes the A subunit enters the enterocyte
27
the A subunit of the cholera toxin
enters the cytoplasm and alters molecules which enhance adenyl cyclase activity causes overproduction of cyclic AMP more chloride pumped into the lumen - overstimulation of transmembrane chloride channel Na and other electrolytes follow chloride massive amounts fo water follow the sodium and chloride ions enterocytes are not damaged by this process, allowing effective therapy of ORS
28
ORS
oral rehydration solution presenting extra Na and glucose to the sodium dependant hexose transporter pumps into the cell pulling water with it
29
shigella
gram negative rod, member of the enteroacteriaceae
30
four spaces of shigella
S sonny S dysenteriae S flexneri S boydii
31
shigella causes
bacterial dysentery | inflammatory diarrhoea
32
bacterial dysentery
diarrhoea illness with blood and pus in the stool | inflammatory colitis
33
how does shigella cause diarrhoea
M cells exist in the intestine as part of the immune system in the payer's patches shigella stimulates parasite directed endocytosis M cell engulfs and internalises the bacteria
34
virulence plasmids of shigella
virulence plasmids encode invasion plasmid antigens (4 types - called Ipas) upon contact with host cell, Ipas are secreted and enter the host cytoplasm stimulate the actin (protein forming cytoskeleton) to push out and form filopods and engulf the bacteria allowing the bacteria to enter the cytoplasm in vacuoles normally vacuoles destroy pathogens but shigella can survive in them
35
what happens once shigella is engulfed into the M cell
it enters the cytoplasm in vacuoles vacuoles normally kill pathogens but shigella can survive in them is carries through to the submucosal surface and released into the submucosal tissues where macrophages engulf them shigella kills the macrophage, causing the macrophage to release interleukin-1 IL-1 draws polymorphonuclear leukocytes into the area
36
what does shigella do once engulfed by macrophages
kills the macrophage but causes the macrophage to release IL-1 in doing so IL-1 draws polymorphonuclear leukocytes into the area PMNLs cause inflammation of the mucosa causing damage and allowing more shigella bacteriums to enter
37
what does PMNL do
causes inflammation and damage to the mucosa allowing more bacteriums to enter shigella have other plasmid genes that encode outermembrane proteins
38
outer membrane proteins (icsA)
cause condensation of host cell actin behind the bacterial cell that propel the bacterium through the cytoplasm and into adjoining cells causes cell membrane to break down
39
lateral invasion of shigella
outer membrane proteins (icsA) cause cytoskeleton to push shigella bacterial cells through outermsmbrane and destroy the membrane causing bleeding this leads to damage and inflammatory diarrhoea blood and pus in stool
40
faeces in shigella infection
dystentery | white blood cells and red cells in stool
41
dehydration from shigella
damaged intestinal cells fail to reabsorb water causing excess water in stool
42
symptoms of shigella infection
- prodromal upper intestinal watery diarrhoea - frequent scanty dysenteric stools - blood - pus - mucus - tenesmus - constant feeling of wanting to pass stool despite not passing stool - significant protein less, malnutrition and impaired immunity
43
tenesmus
constant feeling of wanting to pass stool
44
mode of action of neurotoxins
action on autonomic nervous sytem, increased motility
45
mode of action of enterotoxin
increased fluid secretion without mucosal damage
46
mode of action of cytotoxin
damage to intestinal mucosal cells
47
mucosal invasion
penetration and destruction of mucosal intestinal cells

microbiology 2 (26 decks)

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