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BDS2 - GIT system > GI infections > Flashcards

GI infections Flashcards

1
Q

what is the main infection for the GIT

A
  • clostridium difficile
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2
Q

what are the host defences in the mouth

A
  • flow of liquids
  • saliva
  • lysozyme
  • normal bacterial flora
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3
Q

what are the host defences in the oesophagus

A
  • flow of liquids

- peristalsis

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4
Q

what are the host defences in stomach

A
  • acid pH
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5
Q

what are the host defences in small intestine

A
  • flow of gut contents
  • peristalsis
  • mucus, bile
  • secretory IgA
  • lymphoid tissue
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6
Q

what are the host defences in the large intestine

A
  • normal flora
  • peristalsis
  • shedding and replication of epithelium
  • mucus
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7
Q

what happens to the organisms that don’t die in the mouth

A
  • goe through to the stomach where they are hit with the stomach acid
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8
Q

do microbes increase in amount as you go through the GIT

A
  • yes
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9
Q

why are most microbes good

A
  • selectively inhibit microorganisms
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10
Q

what are ‘good bacteria’ in the body

A
  • 99% of anaerobes

- microbes in the gut produce secondary metabolites which other organisms digest

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11
Q

are drinks such as Yakult any good

A
  • no

- the microbes in these all die in the stomach and so don’t actually do anything

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12
Q

when is C. Dif a problem

A
  • not a problem for healthy people

- only a problem when it is in a susceptible environment such as the hospital

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13
Q

what are some examples of good bacterial flora

A
  • bifidobacterial
  • E. coli
  • lactobacilli
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14
Q

what are bifidobacterial

A
  • the various strains help to regulate levels of other bacteria in the gut
  • modulate the immune response to invading pathogens
  • prevent tumour formation and produce vitamins
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15
Q

what do E. coli do

A
  • several types inhabit the human gut
  • they are involved in the production of vitamin K2 which is needed for blood clotting
  • but some strains can lead to illness
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16
Q

what do lactobacilli do

A
  • beneficial varieties produce vitamins and nutrients
  • boost immunity
  • protect against carcinogens
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17
Q

what are some bad bacterial flora -

A
  • campylobacter
  • enterococcus faecus
  • clostridium difficile
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18
Q

what does campolybacter do

A
  • C jejune and C coli are most commonly associated wit disease
  • infections usually occur through the ingestion contaminated food
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19
Q

what does enterococcus faecaus do

A
  • common cause of post-surgical infections
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20
Q

what does clostridium difficile do

A
  • most harmful following a course of antibiotics when it is able to proliferate
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21
Q

what are some causative agents of GI infections

A
  • bacteria
  • virus
  • protozoa
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22
Q

what is helicobacter pylori

A
  • H. pylori
  • associated with 90% of duodenal ulcers
  • associated with 70-80% of gastric ulcers
  • causes increased risk of gastric cancer = kills
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23
Q

how does H. pylori cause infection

A
  • bugs swim to gastric mucosa
  • cause inflammation of the mucosa
  • then get an ulcer = duodenal or gastric
  • often affects lower part of stomach antrum
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24
Q

what can sever consequences of H. pylori cause

A
  • bleeding ulcers or perforated ulcers

- will cough up blood

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25
Q

what was Koch’s experiment

A
  • showed H.pylori was a bacteria causing cancer
  • give antibiotics to treat
  • he drank H. pylori and then developed gastric ulcers and treated himself and won the Nobel Peace prize
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26
Q

how do H. pylori work

A
  • able to get into the stomach and attach to the epithelial cells and release toxins and then endothelial cells try to kill the bacteria but by doing this they induce inflammatory response that disrupts the barrier and causes ulcers
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27
Q

where is H. pylori most prevalent

A
  • developing world
  • 50-90% are infected in developing world
  • low prevalence in developed world
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28
Q

what is H. pylori associated with

A
  • socio-economic factors
29
Q

what is the mode of transfer of H. pylori

A
  • unknown
  • probably faecal-oral route
  • oral-ora route also implicated
30
Q

what is the pathogenicity of H. pylori

A
  • has the ability to turn acid into ammonia by producing urea
  • ammonia detoxifies the acid so they can survive in stomach
  • can small ammonia on breath of these patients
31
Q

how is H. pylori diagnosed

A
  • pretty easy to diagnose
  • endoscopy and biopsy
  • breath test
  • serology
32
Q

what is the treatment of H. pylori

A
  • proton pump inhibitor
  • bismuth salts
  • antibiotics = amoxicillin, clarithromycin, metronidazole
33
Q

what is gastroenteritis

A
  • is a non-specific term for various pathologic states of the gastrointestinal tract
  • the primary manifestation is diarrhoea, but may be accompanied by nausea, vomiting and abdominal pain
34
Q

what do the definitions of diarrhoea centre on

A
  • frequency, consistency and water content

- disease of the small intestine involving increased fluid and electrolyte loss

35
Q

what alters the gastric mucosa

A

bacteria take sucrose in and take out the things you don’t need

  • toxins released doing this results in altering the gastric mucosa
  • its not the organism itself that is the problem, it is the toxins produced by the organism
36
Q

what are the key viral symptoms of gastroenteritis

A
  • abdominal cramps are number 1
  • vomiting
  • profuse watery stool
  • myalgia
  • fever
  • headaches
37
Q

what are the key bacterial dysentery symptoms in gastroenteritis

A
  • small volume stools
  • fever
  • tenesmus
  • bloody mucoid stools
  • suprapubic
38
Q

what is the main difference between viral and bacterial dysentery gastroenteritis

A
  • bloody stool

- only in bacterial dysentery

39
Q

how do you know whether you’ve eaten the organism or the toxin is in the food

A
  • if get symptoms quickly then the toxin was in the food (rice)
  • if get symptoms after quite a while then you ate the organism (chicken)
40
Q

what is the causative agent of gastroenteritis

A
  • viral 50-70% = norovirus, calciviruses, rotavirus, adenovirus, parvovirus, astrovirus
  • bacterial 15-20% = salmonella, shigella and campylobacter species
  • parasitic 10-15% = guardia lamblia, entamoeba, cryptosporidium
41
Q

what are invasive infections

A
  • the organism enters the mucosal cells, destroys them, causing diarrhoea usually with blood in the stool
42
Q

what are enterotoxin syndromes

A
  • the organisms do not invade the mucosa, but produce enterotoxins of which act as chemical mediators causing hypersecretion of the fluid
  • little damage to the tissue is done
  • produce proteins that cause physiological response
43
Q

what is the norovirus

A
  • non enveloped RNA virus

- transmitted faecal-oral route

44
Q

how many particles does it take to infect someone with norovirus

A
  • not a lot
  • only 10-100
  • highly contagious and very resilient so need to keep a clean environment
  • aerosolised particles are an issue
45
Q

what is the incubation period of norovirus

A
  • 1-2 days
46
Q

what are the clinical signs of norovirus

A
  • abrupt onset of vomiting and watery diarrhoea
  • possibly a fever and abdominal pain
  • similar to rotavirus
47
Q

what is the chance of recurrence of norovirus

A
  • strain specific immunity only lasts a few months
  • get repeated infections
  • no full immunity to it = can keep getting it
48
Q

when was the first recognised outbreak of c. diff in UK

A
  • 2003
  • 150 cases
  • 12 deaths
  • poor standard healthcare leads to C. diff
49
Q

what are the causes of C. diff

A
  • nosocomial antibiotic-associated diarrhoea

- infectious cause of acute diarrhoeal illness

50
Q

what is C. diff

A
  • the only nosocomial organism that is anaerobic and forms spores = survives up to 5 months and hard to destroy
  • pathogenesis is mainly due to toxins it produces
  • infective dose <10 spores
51
Q

who gets C. diff

A
  • healthy people don’t

- unhealthy also don’t unless on lots of antibiotics

52
Q

what are the risk factors of C. diff

A
  • exposure to antimicrobials for past 2-3 months
  • exposure to healthcare in past 2-3 month
  • old age >64 years
  • underlying illness
  • immunosuppression and HIV
  • chemotherapy
  • tube feeds and GI surgery
  • exposure to gastric acid suppression meds??
  • inconsistent microbiome in gut
53
Q

what is the microbiology of C. diff

A
  • gram positive spore forming bacillus (rods)
  • obligate anaerobe
  • part of the GI flora =1-3% in adult, 70% of children <12 months
  • some strains produce toxins A and B = these cause C. diff infection
  • very resilient
54
Q

what is the mortality of C. diff infection

A
  • 35%
55
Q

how is C. diff transmitted

A
  • faecal-oral route = contaminated hands of healthcare workers, contaminated environmental surfaces
  • person to person in hospitals
  • reservoir = human (colonised or infected), contaminated environment
56
Q

how long can C. diff spores survive in environment

A
  • up to 5 months

- need a very high level of disinfection

57
Q

can you acquire C. diff in hospital

A
  • yes

- if have C. diff spores in colon at some point then can become susceptible

58
Q

what are the clinical manifestations of C. diff

A
  • illness caused by toxin producing strains ranges from
    = asymptomatic carriers
  • mild or moderate diarrhoea
  • pseudomembranous colitis that can be fatal
  • a median time between exposure to onset of CDI symptoms is 2-3 days
  • risk of developing CDI after exposure ranges between 5-10 days to 10 weeks
59
Q

what are the symptoms of C. diff

A
  • watery diarrhoea
  • loss of apatite
  • fever
  • nausea
  • abdominal pain
  • lots of negative consequences
60
Q

what are the 4 steps of pathogenesis of C. diff

A
  • 1 = ingestion of spores transmitted from other patients
  • 2 = germination into growing (vegetative) form
  • 3 = altered lower intestine flora allows proliferation of C. difficile in colon
  • 4 = toxin A and B production leads to colon damage and possibly pseudomembranous colitis
61
Q

what is pseudomembranous colitis

A
  • consequence of immune response
62
Q

what are some antimicrobials that are commonly related to C. diff

A
  • clindamycin
  • ampicillin
  • amoxicillin
  • cephalosporins
  • fluoroqionolones
63
Q

what are some antimicrobials that are less commonly related tonC. diff

A
  • sulfa
  • macrolides
  • carbarenems
  • other penicillins
64
Q

what are antimicrobials that are not related to C. diff

A
  • aminoglycosides
  • rifampin
  • tetracycline
  • chloramphenicol
65
Q

what percentage of hospital patients are colonised with C. diff

A

20%

66
Q

how is C. diff treated

A
  • antibiotics = metronidazole, vancomycin
  • oral rehydration
  • probiotics
  • colectomy
  • faecal transplants
67
Q

what are faecal transplants

A
  • take a sample of someone with a similar gut biome’s stool and inject into the patient
  • best treatment for C. diff
68
Q

how can GI infections be prevented

A
  • use of statutory powers
  • safe food handling and hand washing
  • infection control - enteric precautions for diarrhoea and vomiting
  • surveillance

BDS2 - GIT system (5 decks)

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