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GI Microbiology > Infectious Causes of Gastroenteritis > Flashcards

Infectious Causes of Gastroenteritis Flashcards

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Biology 101 flashcards
1
Q

Diarrhoea of small intestinal origin is

A

infrequent or the same frequency as large bowel but much more watery and a greater volume

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2
Q

Diarrhoea of large intestinal origin is

A

frequent, low volume (diseased colon)

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3
Q

How much water is reabsorbed in the small intestine?

A

8.5L

duodenum & jejunum = 5.5

ileum = 3.0

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4
Q

How much water is reabsobed in the colon?

A

1.4L (plus reserve capacity, ~4-5L)

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5
Q

Dysentery is caused by

A

Shigella/EIEC, protozoa (entamoeba histolytica)

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6
Q

Non-specific gastro is caused by

A

viruses, bacteria, protozoa

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7
Q

Foodborne diarrhoea is caused by

A
  • Staph
  • Salmonella (typhimurium)
  • Clostridium (perfringens)
  • Bacillus (cereus)
  • Vibrio
  • Listeria
  • viruses
  • ciguatoxin
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8
Q

Travellers’ diarrhoea is caused by

A
  • ETEC (50%)
  • bacteria
  • viruses (rota, noro, enteric adenovirus)
  • protozoa
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9
Q

Antibiotic-associated colitis is caused by

A

C. difficile

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10
Q

Haemorrhagic colitis is caused by

A

EHEC

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11
Q

Cholera-like diarrhoea is caused by

A

Vibrio cholerae, ETEC

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12
Q

Enteric fever is caused by

A

Salmonella typhi, paratyphi

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13
Q

Which E. coli use intimin adhesin?

A

EHEC and EPEC

(EHEC evolved from EPEC)

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14
Q

The ETEC adhesin is

A

colonisation factor antigens (CFAs)

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15
Q

ETEC produce

A

enterotoxins (heat stabile or heat labile)

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16
Q

EPEC adhesins are

A

intimin, Bfp (bundle-forming pilli)

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17
Q

EPEC produce

A

type 3 secreted effectors (T3S)

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18
Q

EHEC adhesins are

A

intimin, Efa

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19
Q

EHEC produce

A

shiga toxins

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20
Q

EAEC produce

A

Pet, EAST

can acquire ability to producec shiga toxins

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21
Q

Shiga toxins are encoded by

A

bacteriphages

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22
Q

EIEC (shigella) produce

A

Sen toxin

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23
Q

ETEC causes

A

watery diarrhoea in infants from LDCs), travellers

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24
Q

EPEC causes

A

non-specific gastro; mainly children in LDCs

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25
Q

EIEC causes

A

dysentery; any age, mainly LDC

26
Q

EHEC causes

A

haemorrhagic colitis/bloody diarrhoea; any age, developed countries (eg hamburger outbreaks at McD’s in US 1980s)

27
Q

EAEC causes

A

watery diarrhoea; children in LDC most common but occurs everywhere

28
Q

ETEC & cholera invade

A

1st degree: adhesive to in-tact intestinal mucosa w/o domage

eg ETEC adhering via CFA coli surface antigen 3 (CS3)

29
Q

EPEC invades

A

2nd degree: adheres to brush border, damages microvilli but does not invade further

adhere close to cytoplasm via intimin

30
Q

Shigella invades

A

3rd degree: mucosa

31
Q

Salmonella, Campylobacter, Yersinia invade

A

4th degree: submucosa and regional lymph nodes; can become systemic if immunocompromised

32
Q

Salmonella typhi and paratyphi invade

A

5th degree: systemically, they survive in macrophages

33
Q

EPEC & ETEC mainly cause disease

A

in the small intestine

34
Q

How does EPEC adhere to intestinal mucosa?

A
  • via bundle-forming pili (functionally the same as CFAs in ETEC)
  • stage 1: plasmid-mediated
    • initial adherence, to intact microvilli via Bfps
  • stage 2: chromosomal
    • late adherence, causing attachment effacement (thinning) via intimin
35
Q

What is a pathogenicity island?

A

block of genes found on the chromosome of pathogens that are missing from non-pathogens of the same species

eg normal flora E. coli vs EPEC, EHEC

36
Q

What is the LEE pathogenicity island?

A

Locus for Enterocyte Effacement pathogenicity island

EPEC and EHEC only

37
Q

Which E. coli carry the LEE pathogenicity island?

A

EHEC & EPEC only

38
Q

LEE pathogenicity island encodes for

A

Type III secretion system

effector proteins (require T3S system)

Tir & intimin

39
Q

What is the function of Tir?

A

translocated intimin receptor

pumped into mucosal cell cytoplasm from E. coli cytoplasm (EHEC, EPEC) to be expressed on our cells as a receptor for intimin

(occurs via Type III secretion system forming a syringe-like structure to the host cell)

40
Q

What is the type III secretion system?

A
  • found only in pathogens
  • used to transfer proteins directly from bacterial cytoplasm to host cytoplasm via a syringe-like structure
41
Q

Which species of bacteria encodes shigatoxin in its chromosome?

A

Shigella dysenteriae

42
Q

Which bacteria produce shiga toxins?

A

EHEC (all), EAEC (occasionally), Shigella dysenteriae (most)

43
Q

Shiga toxin is associated with what clinical conditions?

A

haemorrhagic colitis (bloody diarrhoea)

haemolytic uremic syndrome (HUS)

44
Q

HUS is caused by which bacteria?

A

EHEC, EAEC (occasionally), Shigella dysenteriae

ie species that produce shiga toxin

45
Q

What is HUS?

A

haemolytic uremic syndrome

haemolysis (breakdown of RBCs in circulation ie intravascular) + uremia (buildup of urea in blood causing renal failure) + thrombocytopaenia (low platelet count)

46
Q

What determines virulence?

A
  • adhesins
    • fimbriae (CFAs, Bfp)
    • non-fimbriate (intimin, invasin)
  • invasive ability (degree of invasion)
  • exotoxins
    • cytotonic (activating): cholera toxin, LT & ST of ETEC
    • cytotoxic (poisoning): shiga toxin (inhibits protein synthesis)
  • ability to resist killing
    • by serum (extracellular bacteria in the blood)
    • by phagocytes (eg Salmonella typhi living in macrophages)
47
Q

Laboratory diagnosis of gastroenteritis is based on

A
  • macroscopic appearance of faeces
  • microscopy
    • for host cells (inflammatory and red cells), parasites and parasitic forms (eg Giardia, Cryptosporidium), viruses (if exhausted other aeitiological possibilities; seen in low numbers, cannot be grown in lab)
  • culture (bacteria only)
  • antigen detection (mainly for viruses, but also for parasites and toxins)
  • detection of nucleic acid
    • viruses, bacteria, protozoa
  • most labs do microscopy, culture, sometimes Ag or NA detection for more common viruses (eg rotavirus, norovirus, enteric adenovirus)
48
Q

Presence of RBCs and phagocytes in faeces indicates

A

blood & pus - tf dysentery

49
Q

In amoebic dysentery, fewer bacteria are seen in faeces because

A

the amoebae eat them

50
Q

Giardia lamblia

A
  • lives in proximal SI in duodenum
  • attaches to epithelium and replicates
  • detach and move through gut
  • form cysts (passed in faeces, infect others, esp kids)
  • can be asymptomatic
  • presence in faeces does not indicate cause of diarrhoea
    *
51
Q
A

rotavirus

52
Q

Norovirus is usually detected with

A

ELISA or PCR

53
Q

Enteric adenovirus is detected using

A

ELISA

54
Q

What are the goals of treatment of diarrhoea?

A
  • replace fluid and electrolytes
    • IV if can’t drink
    • oral rehydration salts
  • reduce fluid loss (secondary, ORS can actually make diarrhoea worse but this can expel the pathogen)
55
Q

What do oral rehydration salts contain?

A
  • sodum chloride
  • potassium chloride (a lot of K+ is lost)
  • sodium bicarbonate (dairrhoea can cause metabolic acidosis, especially in babies)
  • glucose (or sucrose)
    • co-transported with Na+, tf induces take up of water by secondary enteric transporters
56
Q

How does oral rehydration work?

A
  • in acute diarrhoea, mature enterocytes are not being made (decreased absorption)
    • tf Na+/CL- transport is inhibited, and water does not get reabsorbed
      • NaCl normally sets up a concentration gradient that passively drags water into the blood with it
  • the secondary system that normally does not contribute is still active
    • relies on small, low MW compoud eg glucose to be absorbed with Na+
    • Na+ absorbtion draws water out of the lumen and into the blood
57
Q

How is fluid loss reduced in diarrohea?

A

anti-diarrhoeals and/or antibiotics

58
Q

What are the differnt types of anti-diarrhoeals, and why doesn’t Roy like them?

A
  • anti-motility agents:
    • reduce peristalsis, which is increased in diarrhoea as a protective mechansim
    • do not stop fluid loss into the lumen, just out of the body (not targeting the true problem and fixing the dehydration)
  • anti-secretory agents:
    • they don’t work
  • binding agents:
    • don’t stop diarrhoea, just improve appearance of stool
59
Q

What is paradoxical about shiga toxin receptors?

A
  • they are on every cell in the body except the gut
  • therefore they enter gut cells directly, without being processed, which is why we get so sick, and why the infection can become systemic
  • animals eg cattle with the receptors in the gut don’t get as sick
  • basis for shiga-toxin bidning agents, receptor (Gb3) stuck to silica to absorb the shiga toxin
    • doesn’t really work because by the time they are sick enough to need it the toxin has already gotten in
60
Q

When is antimicrobial (antibiotic) treatment indicated for diarrhoea?

A
  • Cholera - public health issue, shortens period of excretion of the organism (and duration of the illness, slightly)
  • systemic infections eg typhoid fever - use 3rd gen cephalosporins
  • immunocompromised patients - prone to septicaemia (eg Salmonella in malnourished babies)
  • severe Shigella infections (S. dysentariae)
  • protozoal infections, even asymptomatic (Giardia, Entamoeba, not Cryptosporidium) using metronidazole (anaerobes)
  • pseudomembranous colitis (C. difficile) - metronidazole, vancomycin
61
Q

What antimicrobials were previously recommended to travellers?

A
  • tetracyclines - most organisms nowresisitant, problems with sunlight sensitivity
  • ciprofloxacin (fluoroquinone) - most resistant, available OTC tf overused
  • azithromycin (macrolide) - resisitance does occur
62
Q

What were the measures taken by WHO to control diarrhoeal disease?

A
  • to reduce diarrhoea-associated mortality by:
    • introducing and educating about oral rehydration therapy
  • to reduce incidence of diarrhoea by:
    • education on hygiene, food preparation, water-borne contamination, importance of breast-feeding for as long as possible
    • immunisation eg rotavirus vaccine
  • over ~40 years, deaths in children under 5 brought down from ~5 million to ~750,000 per year

GI Microbiology (3 decks)

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