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Y2 NnD > GI Infections > Flashcards

GI Infections Flashcards

1
Q

What are commensals

A

Microorganisms living in the body in health ( do not cause disease)

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2
Q

What are opportunistic pathogens and example

A
  • Commensals while contained within GI tract ⇒ won’t cause harm while inside
  • Become pathogens when they cause diease
    • But causing disease is not required for their survival
    • Disease only caused because not contained or because protective mechanisms not working anymore

Eg.- Escherichia coli ⇒ to urinary or resp tract
- Bacteriodes fragilis
- Enterococcus faecium/faecalis

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3
Q

What are obligate pathogens

A
  • DO NOT need host defences to be distrupted, unlike opportunistic pathogens
  • Need to cause disease to transmit between hosts → evolutionary survival
  • Can produce asymptomatic infection but not commensal
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4
Q

What is severe diarrheoa

A

> 3 days, >= 5 stools a day, T>38, bloody diarrhoea

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5
Q

DIfference in small bowel and large bowel gastroenteritis

A

Small - watery diarrheoa, abdominal cramping, bloating, gas
Large- water or bloody diarrhoea, low abdominal pain, fever

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6
Q

what pathogens are more likely to cause water fever diarrhoea

A

Viruses mainly but also bacteria that secrete toxins

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7
Q

Rice water diarrheoa, no fever

A

Vibrio Cholera

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8
Q

Clinical manifestation of Diarrhoea

A

> 3 x a day, liquid more than 80% of water, > 300 g/ 24 hr

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9
Q

Secretory diarrhea

A

Causes secretion or lack of reabsorbtion of water and electrolytes

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10
Q

Epigastric pain waning and waxing for a few hours, better after eating, worse 2-3 hrs later, resolved fo a while with Gaviscon and cessation of symptoms after PPI inhibitor but relapse after 2 weeks - what pathogen?

A

H. Pylori

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11
Q

How is H. pylori transmitted

A

Shed in stool contaminates water and food, colonises human stomach

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12
Q

pathogenic mechanism of H. pylori

A

Inflammation in stomach and duodenum

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13
Q

GLod standard for H. pylori infection vs first line

A

Gold standard is gastroscopy and biopsy, and histology/culture, however - However first lines are:
- Urea breath test (radioactively marked protein transferred to ammonia )
- Antigen in stools

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14
Q

Shigella symptoms

A

pale, sweating, abdomen soft but diffuse pain,

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15
Q

How is shigella transmitted

A

contaminated water or food (or mosquitoes), very low infectious load

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16
Q

What bacteria can cause dysentery

A

Shigella dysenteriae

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17
Q

How does shigella work

A

Invades colon and causes massive inflammation of gut epithelium

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18
Q

Clinical features of shigella and complications

A
  • Bacterial dysentry
    • Blood diarrhoea (+pus/mucus)
    • Abdominal cramps
    • Fever
  • Local ⇒ Toxic megacolon (colon is inflating and starts to secrete a lot of cytokines)
  • Systemic ⇒ Autoimmune diseases like GBS
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19
Q

Diagnosis of shigella

A

May use PCR but mainly stool culture

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20
Q

Treatment for shigella

A

Supportive
- IV fluids and painkillers
Antibiotics
- Ciprofloxacin
- Azithromycin

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21
Q

Most common cause of diarrhoea in developed world

A

Campylobacter spp

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22
Q

How is Campylobacter transmitted

A

Zoonotic ⇒ Associated with Poultry (frozen), wild birds and other animals, milk and water

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23
Q

Symptoms of campylobacter

A

Symptoms ⇒ Blood fever → may be bloody, no fever or watery fever eventually

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24
Q

Pathogenic mechanism of Campylobacter
What disease may it cause??

A

Infective and invasive, acts on small bowel or large colon, however can also lead to GBS as it secretes toxins

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25
Q

diagnosis and treatment of campylobacter

A

Clinical + stool culture, antibiotics

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26
Q

How is non-typhi Salmonella transmitted

A

Zoonotic ⇒ asssociated with poultry/ eggs

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27
Q

Pathogenic mech, diagnosis and treatment of Salmonella and symtpoms

A

Similar to Campulobacter
But symptoms slightly different , - Often serious ⇒ fever, diarrhoea, vomiting

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28
Q

Is vibrio cholerae infective or intoxicative

A

Intoxicative

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29
Q

Transmission of V cholerae

A

contaminated water or food(seafood)

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30
Q

Virulence factors of cholera

A
  • Pili ⇒ adherence to mucosae
  • Toxins triggered in small intestine
    A subunit is active, causes ATP to become cAMP, increases secretion of Cl- ions and reduced absorbtion of Na+
31
Q

Pathogenic mechanism of V cholerae

A

Toxins triggered in jejunum and ileum

32
Q

Clinical features of V cholerae

A
  • Water diarrhoea (secretory)
    • Rice-water stools
  • Severe dehydration ⇒ only water and a bit of protein but no blood, no protein, no WBC
33
Q

diagnosis and treatment of cholera

A
  • Diagnosis
    • Clinical aspects
    • Stool culture

Treatment
- REHYDRATE
- ORS
- IV even better
- May give antibiotics

34
Q

What pathogen is likely to have caused suden onset of severe diarrheoa and fever, with greenish, liquid and smelly stools while in hospital??

A

C.dif

35
Q

Name a gram positive anaerobe that causes diarrhoea

A

C. dif

36
Q

How is c dif spread

A

forms very resistant spores,
- Environmental pathogen
- Found in soil, water, meats
- Spores in health care facilities

37
Q

What pathogen can cause pseudomembranous colitis

A

C dif

38
Q

Pathogenic mechanism of C dif

A

Produces toxins in colon (not invasive)

39
Q

How do the toxins produced by c dif work?

A

They get into the cell and glycosylate and inactivate GTP which normally inactive Rho, which leads to increased production of Rho that leads to collapse of actin skeleton.
Cytotoxicity also causes neutrophil chemotaxis and immune activation

40
Q

Which toxins are more important for C dif

A

Can have the disease with only B toxins but not A toxin

41
Q

dignosis of cdif

A
  • Clinical features (+ history ⇒ typically have been on antibiotics)
  • Stool analyses
    • Greenish, smelly diarrhoea
  • Antigen
    • Toxins
    • Bacteria (enzyme)
  • Culture
42
Q

How to treat c dif

A
  • Antibiotics (very specific)
    • Metronidazole or vancomycin
    • Fidaxomicin (not used much in UK)
  • Faecal transplants for microbiota
    • Help to prevent attachment
  • Immunotherapy
    • Antibodies to work on toxins (nut so far no good outcomes in trials )
  • Prevention and control
43
Q

Aerotolerant, gram +ve rod

A

Clostridium perfringens

44
Q

What forms endospores

A

Clostridium perfringens

45
Q

Pathogen associated with bulk cooking of mear

A

Clostridium perfringens
Warm food- contamination by spores which will germinate

46
Q

Pathogenic mechanism of c perfringens

A
  • Toxins in small intestine
    • Culture of vegetative bacteria is ingested
    • Bacteria sporulate in small intestine (becomes infective) and produce an enterotoxin after germination
  • Destruction of villus tips with resultant pain and diarrhoea
  • May have myonecrosis or necrotising fascilitis ⇒ necrosis of skin and all the tissue between skin and muscles
47
Q

Symptoms of c peringens

A

watery fever

48
Q

diagnosis of c peringens

A

stool culture and detection of toxins

49
Q

Treatment of c peringens

A

Supportive, no antibiotics usually

50
Q

Clostridium botulinum pathophysiology
Toxins produced where? Are spores formed? aerobic??

A
  • Anaerobic, spore forming, toxin types A-G
  • Toxins produced in the food in which it was produce
    • Botulism⇒ toxin mediated paralytic illness, reaches peripheral nerves and attacks NMJ
51
Q

Where is c botulinum found

A

Soils, lake sediments, veg, GI tract of mammals, birds and fish, home-canned or fermented foods

52
Q

Pathogenic mechanism of c botulinum

A

Toxins attack the small intestine, primarily in jejunum and ileum

53
Q

Symptoms of c botulinum

A

Watery, +/- fever, similar to perfirngens

54
Q

Diagnosis of c botulinum

A

Stool culture and detection of toxins

55
Q

Treatment of c boutlinum

A

Supportive, anti toxins

56
Q

Does staph aureus form spores

A

NO

57
Q

where is it usually found and where does it contaminate

A

Usually found on skin, contaminates salted food and dairy produce

58
Q

PM of Staph aureus

A

Forms toxins in SI, toxins anre heat stable

59
Q

What does s aureus cause

A

acute vomitting response followed by diarrhoea
- Staph enterotoxins are bacterial superantigens ⇒ can over stimulate immune system and cause toxc shock syndrome ⇒ whole body in sepsis
- Can cause pneumonia or UTI, or osteitis in bones and endocarditis

60
Q

Symptoms of S A

A

Water +/- fever

61
Q

Diagnosing S aureus

A

Not necessary, simply based on symptoms

62
Q

Treatment of s aureus

A

Supportive

63
Q

Pathophysiology of bacillus cereus

A

Spore forming, looks like clostridium but nit anaerobic

64
Q

How is bcereus spread

A

spores germinate in warm cooked rice, resists exteme temps and forms biofilms

65
Q

Pathogenic mechanism of B cereus

A

Spores ingested ⇒ vegetative cells in SI⇒ toxins

66
Q

Symptoms of b cereus

A

Water +/- fever

67
Q

Diagnosis of b cereus and treatment

A

Not neccessary, supportive treatment

68
Q

How are EHEC/EPEC/EIEC transmitted

A
  • Food borne (faecal contamination)
  • Faecal-oral
  • Environmental contamination by domestic animals
69
Q

Physiopathology of EHEC and EPEC

A

Attach to brush border of the epithelium, injects toxins and products into the cell and efface micro-vili.
WIll have pedestal formation due to accumulation of polymerized actin.
Destruction of micro-villi
Absorbtive epithelium will become secretory and non efficient

70
Q

Pathophysiology of Norovirus

A
  • xtremely stable to heat and cold
  • Spread directly usually (faecooral or vomit droplets) but can be spreak via shellfish ( filter-feeders and sewage contamination)
  • Can lead to immunocompromise in small children
71
Q

Pathogenic mechanisms

A

May have invasive patterns but also produces toxins in SI

72
Q

Symptoms of norovirus

A
  • Vomiting, diarrheoa, low-grade fever
  • Watery +/- fever
73
Q

Diagnosis of norovirus + treatment

A

Clinical + PCR (outbreak), supportive treatment

74
Q

what bacteria can cause bloody fever

A

Shigella
Campylobacter
Non-typhi salmonella
EIEC/EHEC
c perfringens

Y2 NnD (10 decks)

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