Infectious Causes of Gastroenteritis 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
2
Q
Diarrhoea of large intestinal origin is
A
frequent, low volume (diseased colon)
3
Q
How much water is reabsorbed in the small intestine?
A
8.5L
duodenum & jejunum = 5.5
ileum = 3.0
4
Q
How much water is reabsobed in the colon?
A
1.4L (plus reserve capacity, ~4-5L)
5
Q
Dysentery is caused by
A
Shigella/EIEC, protozoa (entamoeba histolytica)
6
Q
Non-specific gastro is caused by
A
viruses, bacteria, protozoa
7
Q
Foodborne diarrhoea is caused by
A
- Staph
- Salmonella (typhimurium)
- Clostridium (perfringens)
- Bacillus (cereus)
- Vibrio
- Listeria
- viruses
- ciguatoxin
8
Q
Travellers’ diarrhoea is caused by
A
- ETEC (50%)
- bacteria
- viruses (rota, noro, enteric adenovirus)
- protozoa
9
Q
Antibiotic-associated colitis is caused by
A
C. difficile
10
Q
Haemorrhagic colitis is caused by
A
EHEC
11
Q
Cholera-like diarrhoea is caused by
A
Vibrio cholerae, ETEC
12
Q
Enteric fever is caused by
A
Salmonella typhi, paratyphi
13
Q
Which E. coli use intimin adhesin?
A
EHEC and EPEC
(EHEC evolved from EPEC)
14
Q
The ETEC adhesin is
A
colonisation factor antigens (CFAs)
15
Q
ETEC produce
A
enterotoxins (heat stabile or heat labile)
16
Q
EPEC adhesins are
A
intimin, Bfp (bundle-forming pilli)
17
Q
EPEC produce
A
type 3 secreted effectors (T3S)
18
Q
EHEC adhesins are
A
intimin, Efa
19
Q
EHEC produce
A
shiga toxins
20
Q
EAEC produce
A
Pet, EAST
can acquire ability to producec shiga toxins
21
Q
Shiga toxins are encoded by
A
bacteriphages
22
Q
EIEC (shigella) produce
A
Sen toxin
23
Q
ETEC causes
A
watery diarrhoea in infants from LDCs), travellers
24
Q
EPEC causes
A
non-specific gastro; mainly children in LDCs
25
EIEC causes
dysentery; any age, mainly LDC
26
EHEC causes
haemorrhagic colitis/bloody diarrhoea; any age, developed countries (eg hamburger outbreaks at McD's in US 1980s)
27
EAEC causes
watery diarrhoea; children in LDC most common but occurs everywhere
28
ETEC & cholera invade
1st degree: adhesive to in-tact intestinal mucosa w/o domage
eg ETEC adhering via CFA coli surface antigen 3 (CS3)
29
EPEC invades
2nd degree: adheres to brush border, damages microvilli **but does not invade further**
adhere close to cytoplasm via **intimin**
30
Shigella invades
3rd degree: mucosa
31
Salmonella, Campylobacter, Yersinia invade
4th degree: submucosa and regional lymph nodes; can become systemic if immunocompromised
32
Salmonella typhi and paratyphi invade
5th degree: systemically, they survive in macrophages
33
EPEC & ETEC mainly cause disease
in the small intestine
34
How does EPEC adhere to intestinal mucosa?
* 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
What is a pathogenicity island?
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
What is the LEE pathogenicity island?
Locus for Enterocyte Effacement pathogenicity island
EPEC and EHEC only
37
Which E. coli carry the LEE pathogenicity island?
EHEC & EPEC **only**
38
LEE pathogenicity island encodes for
Type III secretion system
effector proteins (require T3S system)
**Tir & intimin**
39
What is the function of Tir?
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
What is the type III secretion system?
* found only in pathogens
* used to transfer proteins directly from bacterial cytoplasm to host cytoplasm via a syringe-like structure
41
Which species of bacteria encodes shigatoxin in its chromosome?
Shigella dysenteriae
42
Which bacteria produce shiga toxins?
EHEC (all), EAEC (occasionally), Shigella dysenteriae (most)
43
Shiga toxin is associated with what clinical conditions?
haemorrhagic colitis (bloody diarrhoea)
**haemolytic uremic syndrome (HUS)**
44
HUS is caused by which bacteria?
EHEC, EAEC (occasionally), Shigella dysenteriae
## Footnote
**ie species that produce shiga toxin**
45
What is HUS?
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
What determines virulence?
* 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
Laboratory diagnosis of gastroenteritis is based on
* 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
Presence of RBCs and phagocytes in faeces indicates
blood & pus - tf **dysentery**
49
In amoebic dysentery, fewer bacteria are seen in faeces because
the amoebae eat them
50
Giardia lamblia
* 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
rotavirus
52
Norovirus is usually detected with
ELISA or PCR
53
Enteric adenovirus is detected using
ELISA
54
What are the goals of treatment of diarrhoea?
* **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
What do oral rehydration salts contain?
* 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
How does oral rehydration work?
* 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
How is fluid loss reduced in diarrohea?
anti-diarrhoeals and/or antibiotics
58
What are the differnt types of anti-diarrhoeals, and why doesn't Roy like them?
* 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
What is paradoxical about shiga toxin receptors?
* 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
When is antimicrobial (antibiotic) treatment indicated for diarrhoea?
* 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
What antimicrobials were previously recommended to travellers?
* tetracyclines - most organisms nowresisitant, problems with sunlight sensitivity
* ciprofloxacin (fluoroquinone) - most resistant, available OTC tf overused
* azithromycin (macrolide) - resisitance does occur
62
What were the measures taken by WHO to control diarrhoeal disease?
* 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
