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Year 5 - Pathology > MICRO: GI infections > Flashcards

MICRO: GI infections Flashcards

1
Q

Define gastroenteritis.

A

Rapid onset diarrhoeal illness, lasting <2 weeks with diarrhoea (loose or unformed stool) ≥3/day or ≥200g of stool which is either viral or bacterial in aetiology

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2
Q

Define diarrhoea and the types.

A
  • Loose or watery stool, ≥3 times in 24 hours, acute/chronic/persistent
    • Acute <14 days (may be viral or bacterial)
    • Persistent 14-29 days
    • Chronic >30 days (may be due to parasites and non-infectious aetiology)
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3
Q

How can you distinguish between large and small bowel diarrhoea?

A
  • Small bowel diarrhoea = watery, crampy abdominal pain, bloating and gas; inflammatory cells rare
  • Large bowel diarrhoea = small volume, painful, occur with blood/mucous; inflammatory cells common
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4
Q

Which patients are most vulnerable to GI infections?

A

Infants and the elderly

Other RFs for GI infection:

  • Immunosuppressed patients
  • MSM
  • Haemochromatosis or haemoglobinopathy
  • Outbreak
  • Travel
  • Occupational exposure/iatrogenic
  • Animals and reptiles
  • Institutioon/childcare facility exposure
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5
Q

Why do most diarrhoeal illnesses not present? What is the cause of most?

A

Usually last <48 hours

Viral> bacterial but varies from country to country

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6
Q

Which GI infections are reportable?

A

(Not sure why two different lists were given). Generally all forms of gastroenteritis are notifiable, each trust to notify local health protection unit to help identify outbreaks in areas. Environmental Health Officers may inspect premises and take samples from environment and food.

Reportable Organisms:

  • Campylobacter,
  • Salmonella,
  • Shigella
  • E. coli 0157,
  • Listeria,
  • Norovirus

Notifiable diseases =

  • Campylobacter,
  • Clostridium species,
  • Listeria monocytogenes,
  • Vibrio,
  • Yersinia
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7
Q

Differentiate clinically between the following:

  1. Secretory diarrhoea
  2. Inflammatory diarrhoea
  3. Enteric fever
A
  1. Secretory diarrhoea
    • No/low grade fever
    • No WBC in stool sample (neutrophils)
    • e.g. Vibrio cholerae, ETEC, EAggEC, EPEC, EHEC
  2. Inflammatory diarrhoea
    • Fever
    • WBC in stool sample
    • e.g. Campylobacter, Shigella, Salmonella (non-typhi), EIEC
  3. Enteric fever
    • Fever
    • WBC in stool sample (mononuclear cells)
    • e.g. Typhoidal salmonella, enteropathogenic Yersinia, Brucella spp.
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8
Q

What is the mechanism of secretory diarrhoea?

A

Toxin production

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9
Q

What is the mechanism of diarrhoea in cholera?

A

This causes a secretory diarrhoea

  • Cholera toxin binds to cell plasma membrane and releases subunit A which enters the plasma membrane
  • cAMP opens Cl- channels at the apical membrane of the enterocytes causing an efflux of Cl- to lumen with loss of water and electrolytes à profoundly dehydrated
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10
Q

How do superantigens cause secretory diarrhoea?

A
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11
Q

What are the two components of the pathophysiology of enteric fever?

A
  • Inflammatory (exudative) diarrhoea
  • Enteric fever: interstitial inflammation
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12
Q

What is the average incubation, duration and source of these organism GI infections:

  • campylobacter
  • E coli 0157
  • Shigella
  • Salmonella (non-typhi)
A
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13
Q

What is the average incubation, duration and source of these organism GI infections:

  • Vibrio parahaemolyticus
  • Vibrio cholerae
  • Bacillus cereus
  • Staph aureus
A
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14
Q

Name 2 bacterial GI infections with durations of illness <1 day.

A

Staph aureus (incubation 2-7 hours)

Bacillus cereus (incubation 1-6 hours)

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15
Q
A
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16
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A
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17
Q

Name 2 causes of each.

A
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18
Q

Describe the microbiological features of S. aureus. How does it look when plated?

A

Catalase +ve,

coagulase +ve,

gram +ve

coccus

Appears in tetrads, clusters on gram stain, yellow colonies on blood agar

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19
Q

How is S. aureus transmittted?

A

1/3 of poulation are carrriers and 1/3 transiently carry it

Spread by skin lesions on food handlers

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20
Q

What is the mechanism of S. aureus GI infection? How is it managed?

A

Mechanims:

  • Superantigen production - produces enterotoxin, an exotoxin that can act as a superantigen in the GI tract,
    • release of IL1 and IL2 causevprominent vomiting and watery,
    • non-bloody diarrhoea

Management: none, self-limiting

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21
Q

List 3 gram +ve rods (spore-forming) causing GI infections.

A
  1. Bacillus cereus
  2. Clostridia (botulinum, perfringens, difficile)
  3. Listeria monocytogenes
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22
Q

What are the clinical features of Bacillus cereus infection?

A

Presentation and complications:

  • Watery non-bloody diarrhoea;
  • Self-limiting
  • Rare cause of bacteraemia in vulnerable population
  • Can cause cerebral abscesses
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23
Q

What toxins are produced by bacillus cereus?

A

Produces 2 types of toxins:

Heat stable toxin: spores germinate in reheated fried rice (not destroyed by reheating)

Heat-labile diarrhoeal toxin: food is not cooked to a high enough temperature

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24
Q

Which gram +ve anaeobes cause GI infections?

A

Clostridia

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25
Q

What is the source, mechanism and treatment of clostridium botulinum?

A

Source: canned or vacuum-packed food (honey in infants)

Mechanism: Ingestion of preformed toxin (inactivated by cooking). Blocks ACh release from peripheral nerve synapses –> paralysis/botulism

Treatment: with antitoxin

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26
Q

What is the source, mechanism and presentation of clostridium perfringens infection?

A

Source: reheated food (meat)

Mechanism: superantigen/enterotoxin affects normal flora of colon but not small bowel, where the enterotoxin acts (superantigen). Incubation is 8-16hrs.

Presentation: Watery diarrhoea, cramps, vomiting lasting 24hrs (suspect GI necrosis if persists)

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27
Q

What is the % of C. difficile carriage in community vs hospital?

A

3% of general population, 30% of hospitalised patients

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28
Q

Which toxins are produced by C. difficile? Which is more dangerous?

A

Produces 2 toxins – Toxin A and Toxin B

  • Toxin A = enterotoxin = inflammation
  • Toxin B = cytotoxin = virulence factor (more dangerous than A)
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29
Q

Which antibiotics precipitate C.difficile? What is the management?

A
  • Any but mainly cephalosporins, cipro, clindamycin and co-amoxiclav
  • Any antibiotic other than an aminoglycoside

Management:

  • Infection control – isolation and hand-washing.
  • PO metronidazole +/- vancomycin
  • Stop offending agent/antibiotics
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30
Q

Describe the microbiolgical characteristics of Listeria monocytogenes?

A

ß-haemolytic, aesculin positive with tumbling-weed motility

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31
Q

Who is most at risk of Listeria monocytogenes infection? What is the source, presentation and management of listeria monocytogenes infection?

A

Can have complications on foetus so dangerous in pregnancy.

  • Source: refrigerated food (“cold-enhancement”), unpasteurized dairy, vegetables (grows at 4ºC)
  • Symptoms: Watery diarrhoea, cramps, headache, fever, little vomiting
  • Treatment: amoxicillin
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32
Q

List 4 types of E coli infections and the associated syndrome. What is the management?

A
  • ETEC; toxigenic , main cause of traveller’s diarrhoea
  • EPEC; pathogenic, infantile diarrhoea
  • EIEC; invasive, dysentery
  • EHEC; haemorrhagic, O157:H7 EHEC: shiga-like verocytotoxin causes HUS

Management: supportive care/resuscitation, avoid antibiotics (can exacerbate condition by unknown mechanism)

33
Q

What is the most common cause of traveller’s diarrhoea?

A

E coli - mainly from food/water contaminated with human faeces

34
Q

What are the microbiological features of E coli?

A
  • Gram -ve rod
  • Facultative anaerobes,
  • glucose/lactose fermenters (LF),
  • oxidase-negative
35
Q

What is shown? What are its microbiological features?

A

Salmonella

  • Gram -ve rod
  • Non-lactose fermenters coliform, H2S producer (black colonies),grown on TSI agar or XLD agar or selenite F broth
  • Antigens:
    • Cell wall O (groups A-I)
    • Flagellar H
    • Capsular VI (virulence, antiphagocytic)
36
Q

Which animals can transmit Salmonella?

A

Particularly spread by reptiles; suspect if recurrent.

37
Q

What are the three species of salmonella causing GI infection? How are they classified?

A
  1. S. typhi (and para-typhi) cause typhoid (enteric) fever
  2. S. enteritidis
  3. S. cholerasuis

Distinguished by disease caused

38
Q

What is the pathophysiology of Salmonella typhi/parathyphi infection? True or false?: S. typhi/parathypic is only transmitted by humans.

A

Mechanism: Multiplies in Peyer’s patches, spreads ERS (endoreticular system)

True

39
Q

What are the clinical features of S. typhi/paratyphi?

A
  • Slow onset,
  • fever and constipation,
  • splenomegaly,
  • rose spots,
  • anaemia, leucopaenia,
  • bradycardia, haemorrhage
40
Q

What investigation is diagnostic? What is the management?

A
  • Investigations: Blood cultures are positive
  • Treatment: ceftriaxone
41
Q

What is the pathophysiology of S. enteritidis enterocolitis?

A
  • Source: Transmitted from poultry, eggs, meat
  • Mechanism: Invasion of epi- and sub-epithelial, tissue of small and large bowel
42
Q

What are the clinical features of S. enteritidis infection?

A
  • Presentation: Bacteraemia infrequent, no fever, just diarrhoea.
  • Management: No investigations required as by the time they come back usually resolved. (Stool +ve). Self-limited non-bloody diarrhoea, usually no treatment
43
Q
A

Positive blood cultures

Constipation

44
Q

What are the microbiological features of shigella?

A
  • Gram -ve rod
  • Non-lactose fermenters,
  • non H2S producers,
  • non-motile
  • Antigens:
    • Cell wall O antigens
    • Polysaccharide (groups A-D): S. sonnei, S. dysenteriae, S. flexneri (MSM)
45
Q

What is the most effective enteric pathogen (lowest infectious dose)?

A

Shigella - infectious dose is 10-100 organisms

46
Q

How is Shigella transmitted? How does it present?

A
  • Transmission:
    • Human –> human only
    • No carrier states
  • Presentation and mechanims:
    • Causes dysentery
    • Invading cells of mucosa of distal ileum and colon
    • Producing enterotoxin (Shiga toxin)
47
Q

What is the management of shigella?

A

Avoid antibiotics (ciprofloxacin if required)

48
Q

What are the microbiological features of vibrio?

A
  • Gram -ve rod
  • Curved, comma shaped,
  • late lactose fermenters,
  • oxidase positive
49
Q

Which vibrio cholerae group causes epidemics?

A
  • Classification:
    • O1 group: epidemics, biotypes El Tor, Cholerae and serotypes Ogawa, Inaba, Hikojima
    • Non O1 group: sporadic or non-pathogens
50
Q

Name 3 vibrio species.

A
  1. Vibrio cholerae
  2. Vibrio parahaemolyticus
  3. Vibrio vulnificus
51
Q

What is the mechanism of vibrio cholerae infection?

A

Mechanism: Colonisation of small bowel and secretion of enterotoxin with A and B subunit, causing persistent stimulation of adenylate cyclase

52
Q

How is vibrio cholerae transmitted and how does it present? How is it managed?

A
  • Transmission: Faeco-oral inc. shellfish, oysters, shrimp
  • Presentation: Causes massive diarrhoea (rice water stool) without inflammatory cells
  • Management: treat the losses: electrolytes and fluids
53
Q

How does vibrio parahaemolyticus spread? What is the management?

A
  • Transmission: Ingestion of raw or undercooked seafood (i.e. oysters). Major cause of diarrhoea in Japan or when cruising in the Caribbean
  • Management: Treat with doxycycline or self-limited for 3 days
54
Q

What are the growth conditions for vibrio parahaemolyticus and why is this important?

A

Have to suspect it and mimic growth conditions i.e. grow in salty 8.5% NaCl

55
Q

How does vibrio vulnificus present? What is the management?

A
  • Presentation: Cellulitis in shellfish handlers and fatal septicaemia with D+V in HIV patients
  • Management: doxycycline
56
Q

What are the microbiological characteristics of campylobacter?

A
  • Gram -ve rod
  • Curved, comma or S shaped;
  • Microaerophilic (doesn’t need much oxygen)
  • C. jejuni grows at 42 ºC
  • Oxidase positive,
  • Motile
57
Q

How does campylobacter present? How is it managed?

A

Presentation:

  • Self-limiting but symptoms can last for weeks (20 days). Watery, foul smelling diarrhoea, bloody stool, fever and severe abdominal pain

Management: Only treated in immunocompromised. Treat with erythromycin (macrolide) .

58
Q

What is the pathophysiology of campylobacter infection?

A
  • Transmission: via contaminated food and water with animal faeces (poultry, meat, unpasteurised milk)
  • Mechanism: Enterotoxin (watery diarrhoea) with invasion (+/- blood)
59
Q

What are 3 complications of campylobacter infection?

A
  1. GBS,
  2. reactive arthritis,
  3. Reiter’s
60
Q

What are the microbiological characteristics of yersinia enterocolitica? What growth conditions does it prefer?

A
  • Gram -ve rod
  • Non-lactose fermenter,
  • prefers 4ºC “cold enrichment”
61
Q

How does Yersinia enterocolitica present and how is it transmitted?

A

Transmitted via food contaminated with domestic animal’s excretions

Presentation:

  • Enterocolitis,
  • Mesenteric adenitis
  • associated reactive arthritis, Reiter’s
62
Q

What are the risk factors for mycobacteria-associated GI infection? How is this diagnosed?

A
  • RF: immunosuppression, associated lymphadenopathy
  • Ix: biopsy of gut, will appear as gram variable
63
Q

List 3 protozoal infections which can cause GI infection, and name their microbiological features.

A
  • Entamoeba histolytica
    • Motile trophozoite in diarrhoea; Non-motile cyst in non-diarrhoeal illness,** **4 nuclei, killed by boiling
  • Giardia lamblia
    • Trophozoite “pear shaped”; 2 nuclei, 4 flagella and a suction disk
  • Cryptosporidium parvum
    • Oocysts seen in stool by modified Kinyoun acid fast stain
64
Q

What is the pathophysiology of entamoeba histolytica infection? What are the symptoms?

A

Ingestion of cysts –> trophos in ileum which colonize cecum and colon –> causing a “flask shaped” ulcer. No animal reservoir

Symptoms:

  • dysentery,
  • flatulence,
  • tenesmus
  • in chronic form: weight loss +/- diarrhoea, liver abscess
65
Q

How is Entamoeba histolytica diagnosed and treated?

A

Diagnosis

  • Stool microbiology (wet mount, iodine and trichrome)
  • Serology in invasive disease

Treatment: metronidazole and paromomycin in luminal disease

66
Q

What is the pathophysiology of giardia lamblia? What are the symptoms?

A

Mechanism:

  • Ingestion of cyst from faecal-contaminated water and food
  • Excystation at duodenum, tropho attaches, no invasion but malabsorption of protein and fat
  • RFs: Travellers (cruise), hikers, day care, mental hospitals, MSM

Symptoms:

  • Foul smelling non-bloody diarrhoea,
  • cramps
  • flatulence,
  • no fever
67
Q

How is Giradia lamblia diagnosed and treated?

A

Diagnosis:

  • ova, cysts and parasites(stool micro),
  • ELISA,
  • “string test” (trophozoites attach to a string)

Treatment: metronidazole

68
Q

What is the pathophysiology of Cryptosporidium parvum?

A
  • Mechanism:
    • Infects the jejunum
    • Severe diarrhoea in the immunocompromised (can cause outbreaks)
69
Q

How is Cryptosporidium parvum diagnosed and treated?

A
  • Diagnosis: Oocysts seen in stool by modified Kinyoun acid fast stain
  • Treatment: no treatment, and usually self-limiting.
70
Q

List 3 viruses that can cause GI infection. Name a microbiological feature of each.

A

Norovirus - G2.4 is the predominant strain

Rotavirus - dsRNA “wheel like”

Adenovirus - Types 40/41 cause non-bloody diarrhoea usually <2yrs of age. Any type in immunocompromised

71
Q

Which viral gastroenteritis has the largest economic burden worldwide? Which one causes outbreaks?*

A

Economic burden globally - Rotavirus

Outbreaks - Norovirus

72
Q

Give 3 reasons for why norovirus outbreaks can easily occur.

A
  • Low ID load (18-1000 viral particles) – lick lips on an infected ward is enough!
  • Environmental resilience (0-60 degrees)
  • No long-term immunity
73
Q

What are the clinical features of rotavirus infection?

A

Mechanism = replicates in mucosa of small intestine

Presentation:

  • Secretory diarrhoea, no inflammation
  • Watery diarrhoea by stimulation of enteric nervous system
  • By age 6 most children worldwide have antibodies to at least one type - exposure to natural infection twice confers lifelong immunity
74
Q

What are the clinical features of adenovirus infection?

A

Non-bloody diarrhoea usually <2yrs of age (type 40/41 or any type in immunocompromised)

Diagnosed by stoom EM, antigen detection or PCR

Transmitted via faeco-oral route but main presentation from other systems

75
Q

List the vaccines which help prevent GI infection.

A

Cholera: against serogroups O1 (when going to certain regions), O139

Campylobacter: military, infants, traveller, candidate vaccines exist

ETEC: inactivated and live vaccines in trials

Salmonella typhi: Vi capsular PS (IM) and (PO) live

Rotavirus

  • Rotarix: live attenuated human strain monovalent, 2 (PO) doses
  • Rotateq: pentavalent, 3 (PO) doses, one bovine and four human strains
  • Rotashield and intussusception (8-20 weeks)
  • Age of vaccine is 6-12 weeks
76
Q

What type of vaccine is the cholera vaccine? What components does it include?

A
  • Inactivated, whole cell, contains all above + B subunit of toxin (PO)
  • Live attenuated (PO) not recommended
77
Q

What are the extra-intestinal manifestations of gastroenteritis?

A
78
Q

Which of these is a extraintestinal manifestation of Salmonella infection?

  • Erythema nodosum
  • Aortitis
  • Abscess formation
A

Aortitis

Year 5 - Pathology (89 decks)

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