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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
diagnosis and treatment of campylobacter
Clinical + stool culture, antibiotics
26
How is non-typhi Salmonella transmitted
Zoonotic ⇒ asssociated with poultry/ eggs
27
Pathogenic mech, diagnosis and treatment of Salmonella and symtpoms
Similar to Campulobacter But symptoms slightly different , - Often serious ⇒ fever, diarrhoea, vomiting
28
Is vibrio cholerae infective or intoxicative
Intoxicative
29
Transmission of V cholerae
contaminated water or food(seafood)
30
Virulence factors of cholera
- 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
Pathogenic mechanism of V cholerae
Toxins triggered in jejunum and ileum
32
Clinical features of V cholerae
- Water diarrhoea (secretory) - Rice-water stools - Severe dehydration ⇒ only water and a bit of protein but no blood, no protein, no WBC
33
diagnosis and treatment of cholera
- Diagnosis - Clinical aspects - Stool culture Treatment - REHYDRATE - ORS - IV even better - May give antibiotics
34
What pathogen is likely to have caused suden onset of severe diarrheoa and fever, with greenish, liquid and smelly stools while in hospital??
C.dif
35
Name a gram positive anaerobe that causes diarrhoea
C. dif
36
How is c dif spread
forms very resistant spores, - Environmental pathogen - Found in soil, water, meats - Spores in health care facilities
37
What pathogen can cause pseudomembranous colitis
C dif
38
Pathogenic mechanism of C dif
Produces toxins in **colon** (not invasive)
39
How do the toxins produced by c dif work?
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
Which toxins are more important for C dif
Can have the disease with only B toxins but not A toxin
41
dignosis of cdif
- Clinical features (+ history ⇒ typically have been on antibiotics) - Stool analyses - Greenish, smelly diarrhoea - Antigen - Toxins - Bacteria (enzyme) - Culture
42
How to treat c dif
- 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
Aerotolerant, gram +ve rod
Clostridium perfringens
44
What forms endospores
Clostridium perfringens
45
Pathogen associated with bulk cooking of mear
Clostridium perfringens Warm food- contamination by spores which will germinate
46
Pathogenic mechanism of c perfringens
- 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
Symptoms of c peringens
watery fever
48
diagnosis of c peringens
stool culture and detection of toxins
49
Treatment of c peringens
Supportive, no antibiotics usually
50
Clostridium botulinum pathophysiology Toxins produced where? Are spores formed? aerobic??
- 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
Where is c botulinum found
Soils, lake sediments, veg, GI tract of mammals, birds and fish, home-canned or fermented foods
52
Pathogenic mechanism of c botulinum
Toxins attack the small intestine, primarily in jejunum and ileum
53
Symptoms of c botulinum
Watery, +/- fever, similar to perfirngens
54
Diagnosis of c botulinum
Stool culture and detection of toxins
55
Treatment of c boutlinum
Supportive, anti toxins
56
Does staph aureus form spores
NO
57
where is it usually found and where does it contaminate
Usually found on skin, contaminates salted food and dairy produce
58
PM of Staph aureus
Forms toxins in SI, toxins anre heat stable
59
What does s aureus cause
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
Symptoms of S A
Water +/- fever
61
Diagnosing S aureus
Not necessary, simply based on symptoms
62
Treatment of s aureus
Supportive
63
Pathophysiology of bacillus cereus
Spore forming, looks like clostridium but nit anaerobic
64
How is bcereus spread
spores germinate in warm cooked rice, resists exteme temps and forms biofilms
65
Pathogenic mechanism of B cereus
Spores ingested ⇒ vegetative cells in SI⇒ toxins
66
Symptoms of b cereus
Water +/- fever
67
Diagnosis of b cereus and treatment
Not neccessary, supportive treatment
68
How are EHEC/EPEC/EIEC transmitted
- Food borne (faecal contamination) - Faecal-oral - Environmental contamination by domestic animals
69
Physiopathology of EHEC and EPEC
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
Pathophysiology of Norovirus
- 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
Pathogenic mechanisms
May have invasive patterns but also produces toxins in SI
72
Symptoms of norovirus
- Vomiting, diarrheoa, low-grade fever - Watery +/- fever
73
Diagnosis of norovirus + treatment
Clinical + PCR (outbreak), supportive treatment
74
what bacteria can cause bloody fever
Shigella Campylobacter Non-typhi salmonella EIEC/EHEC c perfringens

Y2 NnD (10 decks)

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