L3-5: Gastroenteritis Flashcards

1
Q

Type of Infectious Gastroenteritis affecting Children vs. Adults?

A

Children: Primarily Viral
Adults: Primarily Bacterial

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2
Q

Classification of Diarrhoea

A

≥ 3 episodes of loose or liquid stool in 24 hours

Acute: <14 Days
Persistent: >14 Days
Chronic: >30 Days

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3
Q

Causes of Viral Gastroenteritis?

A

Rotavirus
Norovirus
Adenovirus

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4
Q

When do cases of viral enteritis peak?

A

Winter

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5
Q

Diagnosis of Viral Enteritis?

A

Direct Visualization: Electron Microscope

Antigen Detection
Lateral Flow
ELISA

Multiplex PCR

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6
Q

Management of Viral Gastroenteritis?

A

Supportive
*Rehydration, oral preferable
*Electrolyte replacement
*Refeeding (in children)

No specific antiviral treatment

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7
Q

Transmission of Rotavirus?

A

Transmitted Fecal-Oral
Sometimes respiratory => URTI kids
Survives on fomites and hands

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8
Q

Pathogenesis of Rotavirus?

A

Infects enterocytes in villous epithelium of jejunum and ileum => cell destruction =>Movement of fluid into intestinal lumen =>Loss of fluid and salt in faeces

May lose ability to digest food, esp complex sugars (lactose intolerance)

Secretory diarrhea caused by enterotoxin

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9
Q

Demographic most commonly impacted by Rotavirus?

A

Most Common in children <2

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10
Q

Diagnosis of Rotavirus?

A

Lateral Flow Test or PCR

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11
Q

Oral Vaccine for this virus given before 6 months => 85% hospital reduction

A

Rotavirus

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12
Q

Characteristics of Norovirus?

A

AKA. Winter Vomitting Virus
Small rounded structured virus (SRSV)
Single Strnaded RNA Virus
Significant Diversity: hard to vaccinate against, immunity short lived

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13
Q

Characteristics of Rotavirus?

A

Reovirus (double stranded RNA
Large amount of virus in faeces

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14
Q

Characteristics of Norovirus?

A

Small rounded structured virus (SRSV)
Single Stranded RNA Virus
LOW infectious dose (18 virus particles)
Significant Diversity: hard to vaccinate against, immunity short-lived

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15
Q

Transmission of Norovirus?

A

Faecal- oral
Airborne droplets- aerosolized by vomiting
Food, water
Contaminated environment, fomites

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16
Q

Pathogenesis of Norovirus?

A

Blunting of villi in jejunum
Epithelial cells not damaged
No enterotoxin has been detected

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17
Q

Clinical Features of Rota Virus

A

Diarrhoea
Vomiting
Fever
Dehydration
+/-respiratory tract symptoms

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18
Q

Clinical Features of Norovirus?

A

Nausea
Vomiting (may be projectile)
Abdominal cramps
Myalgia
Diarrhoea
+/-fever

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19
Q

Diagnosis of Norovirus?

A

PCR- No good Antigen test due to diversity of serotypes

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20
Q

Characteristics of Adenovirus?

A

Double-stranded DNA Virus
Gastroenteritis (serotypes 40 and 41)
Primarily affects kids

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21
Q

Rotavirus – ________
Norovirus– ________

A

Rotavirus – children
Norovirus – adults

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22
Q

Ways that various Bacteria can cause gastroenteritis?

A

Adherence to the intestinal epithelium
Invasion of intestinal cells
Toxin production: Ingestion of pre-formed toxin or Toxin production in GIT

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23
Q

Commonest bacterial pathogen isolated from feces?

A

Camplylobacter

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24
Q

Characteristics of Campylobacter?

A

Commonest bacterial pathogen isolated from faeces
Cases peak in summer
Contanimation with Raw or undercooked foods

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25
Q

Pathogenesis of Camplylobacter

A

Ingestion of bacilli
Attach to and invade GI epithelium
No role identified for enterotoxin

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26
Q

Clinical Features of Campylobacter?

A

Adults have more severe disease
May have a prodromal illness (~ 24 hours)
Abdominal pain
Diarrhea, may be bloody
Fever, Nausea, vomiting

Complications (bloodstream infection): Guillain-Barre Syndrome or Reactive Arthritis

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27
Q

Botulism versus Guillain-Barre Syndrome?

A

Botulism: Descending parylsysis (botulisism Toxin)
Guillain Barre Syndrome: Ascending paralysis

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28
Q

Bacteria associated with the immune-mediated development of Guillain-Barre Syndrome and Reactive Arthritis weeks after infection?

A

Campylobacter

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29
Q

Diagnosis of Campylobacter?

A

Charcoal-based selective media
Microaerophilic atmosphere
See Gram-negative curved bacilli in Flat colonies

Susceptibility Testing
PCR

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30
Q

Pathogens that cause Enteric Fever (aka. ___________)

A

Typhoid and paratyphoid fever are caused by:
Salmonella enterica - typhi
Salmonella enterica - paratyphi (A, B and C)

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31
Q

Pathogenesis of Enteric Fever

A

Ingestion of Salmonellae from contaminated food/water

Penetration of small intestinal epithelium
Proliferation in submucosa –hypertrophy of Peyer’s patches

Disseminate via lymphatic or haematogenous route

Chronic Carriage common

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32
Q

Which condition is associated with hypertrophy of Peyer’s Patches?

A

Enteric Fever (casued by Salmonellae Enterica)

33
Q

Which condition is associated with hypertrophy of Peyer’s Patches?

A

Enteric Fever (caused by Salmonellae Enterica)

34
Q

Clinical Features of Enteric Fever

A

2 week incubation!!
Insidious onset
Fever, chills, relative bradycardia
Abdominal pain, Diarrhea/constipation
* ‘rose’ spots*

35
Q

Diagnosis of Salmonella?

A

Blood culture (Most Common)
Faeces culture
bone marrow culture (Only in complicated cases)

36
Q

Treatment of Enteric Fever?

A

Rehydration
Fluoroquinolones (ciprofloxacillin)
3rd gen cephalosporin (meropenem)

37
Q

Pathogens that cause Non-Typhoidal Salmoenlollis?

A

Salmonella enteritidis
Salmonella typhimurium

38
Q

Transmission of Non-typhoidal salmonella?

A

Peron to Person
Contaminated food/water, especially poultry and eggs
Exotic pets

39
Q

What is Carriage?

A

Asymptomatic shedding of organism in faeces

40
Q

When to treat Non-typhoidal salmonellosis?

A

Treat only if
*Severe illness
*High risk of invasive disease (age < 1 or > 50, HIV, immunocompromised, cardiac/valvular/joint disease)

41
Q

Selective Media for Campylobacter?

A

Charcoal Based selective media and microaerophilic atmosphere

42
Q

Diagnosis of non-typhoidal salmonellosis?

A

PCR- Done first => Culture only done if PCR positive

Selective media e.g., XLD, Salmonella Shigellaagar
Non-Lactose Fermenters+ Hydrogen sulfide production (except S. enterica)

Serotyping

43
Q

EHEC/VTEC –verocytotoxin-producing E. coli Epidemiology?

A

Summer Peak
Affects Extremes of age and those w. underlying conditions
Outbreaks from wells and in nursing homes

44
Q

VTEC –verocytotoxin-producing E. coli Transmissiion?

A

Cattle are the main reservoir of infection
Ground beef (hamburgers)
Milk, yoghurt, cheese
Apple juice, vegetables
Water

45
Q

VTEC Pathogenesis?

A

Low Infective dose (<100)
Ingestion of bacilli => Attachment to large intestinal epithelium => Release of verotoxin (Shiga-like toxins, SHT-I and SHT-II)=> Haemorrhagic colitis and/or Haemolytic uraemic syndrome

46
Q

What Pathogens are responsible for the development of Hemolytic Uremic Syndrome (HUS)?

A

VTEC –verocytotoxin-producing E. coli
S. dysenteriae (Shigellosis)

47
Q

Clinical Features of VTEC

A

Diarrhoea -may be bloody (25-50%)
Vomiting and fever uncommon
Duration 5-10 days
5-10% may develop *hemolytic uraemic syndrome (HUS) *

48
Q

Treatment of VTEC?

A

Rehydration
Antibiotics not of proven value
Breakdown of E. Coli cells can suddenly release many more toxins => leading to HUS

49
Q

Shigellosis is also known as ______________

A

Shigellosis is also known as Bacillary dysentery

50
Q

Shigellosis Pathogenesis?

A

Ingestion of bacilli => Adherence to/invasion of M cells of Peyer’s patches of large bowel=> Spread to adjacent cells => inflammatory reaction

S. dysenteriae has a potent Shiga toxin that can cause haemolytic uraemic syndrome (HUS)

51
Q

__________ has a potent Shiga toxin that can cause hemolytic uraemic syndrome (HUS)

A

S. dysenteriae (Shigella) has a potent Shiga toxin that can cause hemolytic uraemic syndrome (HUS)

52
Q

Bacterial infections that can cause bloody diarrhea?

A

VTEC
Shigella
Campolobacter

53
Q

Bacterial Infections than can cause reactive arthritis?

A

Camplyobacter
S. flexneri

54
Q

Diagnosis of Shigella?

A

Selective media e.g., XLD- Non-lactose fermenters
PCR

55
Q

Chracteristics of Staphylococcus Aureus Gastritis?

A

Ingestion of pre-formed heat stable enterotoxin
Rapid onset (2-6 hours)
Short-lived (6-12 hours)
Malaise
Nausea, vomiting
Abdominal pain, diarrhoea
NO fever!!

56
Q

Characteristics of Bacillus Cereus Gastritis?

A

Heat-stable, Aerobic spore-forming Gram-positive bacilli

2 enterotoxins:
– emetic toxin (pre-formed)
–diarrhoeal toxin (produced in small bowel)

Emetic syndrome-ingestion of toxin in food (e.g., rice) =>Illness within 1-5 hours, lasts 6-24 hours

Diarrhoeal syndrome –toxin produced in small bowel =>Illness within 8-16 hours, lasts 24 hours

57
Q

Characteristics of Clostridioides Perfringes Gastritis?

A

Food Poisoning
Pre-Cooked meat (Stews/Curries)
Heat-resistant spores
nterotoxin production (spores germinate and enterotoxin produced in the bowel)
Abdominal cramps, Diarrhea
Self Limiting 1-2days

58
Q

Characteristics of Clostridioides Difficile Gastritis?

A

Anaerobic Gram-positive bacillus
Spore forming
Toxin-producing (Toxins A and B)
Toxin mediated colonic inflammation and mucosal damage leading to Intestinal fluid secretion

Present in 60-70% of Healthy infants’ bowels (Not diagnostically useful. Diarrhea likely viral)

59
Q

Characteristics of Clostridioides Difficile Gastritis?

A

Anaerobic Gram-positive bacillus
Spore forming
Toxin-producing (Toxins A and B)
Toxin-mediated colonic inflammation and mucosal damage leading to Intestinal fluid secretion

Present in 60-70% of Healthy infants’ bowels (Not diagnostically useful. Diarrhea likely viral)

60
Q

C. Diff Risk Factors?

A

Antimicrobials -Broad-spectrum penicillins e.g., co-amoxiclav, Clindamycin, Cephalosporins, Fluoroquinolones
Advanced age
Hospitalization
Recent GI surgery or procedure
Immunosuppression
Proton pump inhibitor (PPI)- Reduction in gastric acid => Spores of C. Diff more likely to pass the stomach and make it to the bowel. STOP Patient on PPI if w/ active infection

61
Q

Clinical Features/ Complicaitons of C. Diff Infection?

A

Clinical Features
Watery diarrhoea
Abdominal cramping/pain
Colitis
Fever
Elevated WCC

Complications
Pseudomembranous colitis
Toxic megacolon => Perforation/Death
Colonic perforation
Death

62
Q

Diagnosis of C. Diff

A

Test all diarrhoeal stools (> 2 years of age)

First step
ELISA for glutamate dehydrogenase (GDH)
-detects the presence of C. difficile
-does not distinguish between strains that produce toxins and those that do not

OR

PCR
-detects the presence of gene which encodes for toxin
-does not detect presence of toxin

Second step: ELISA for toxin detection

GDH and Toxin present => positive case

63
Q

Management of C. DIff

A

Stop precipitating antibiotics or switch to more narrow spectrum
If on PPI, review indication

Non-severe (WCC <15) –vancomycin po or fidaxomicin po

Severe (WCC >15) –vancomycin po, metronidazole iv, surgical review

VERY Severe: not elligible for surgery, looks like going to die. give intravenous immunoglobulin

64
Q

Similar efficacy in treating C. DIff to vancomycin but with less recurrence?

A

Fidaxomycin

65
Q

Monoclonal antibody against C. Diff’s toxin B that can lead to reduced recurrence?

A

Bezlotoxumab

66
Q

Risk Factor’s/Treatment Course for Recurrent C Diff infection?

A

Risk factors for recurrence
Concomitant antimicrobial use during CDI treatment
027 infection
Elderly

Treatment
1st recurrence –fidaxomycin po
2nd and subsequent recurrences –tapering vancomycin po; fidaxomicin po; consider Fecal Microbiotic Transplant

67
Q

Characteristics/Pathogenesis of Vibrio Cholerae

A

small curved Gram-negative bacilli
Developing countries- Endemic in Asia and Africa (returning travellers)
Contaminated food and water
Person-to-person transmission uncommon-LARGE infectious dose (108 organisms)

Pathogenesis
Binds to specific receptors in small intestine => Enters mucosal cell
Rapid secretion Na+, K+, bicarbonate (Interferes w/ Cyclin AMP)
Virulence factors: Pili, Cholera toxin

68
Q

Clinical Features of Cholera?

A

Abrupt onset
Rice-water’ stools, effortless vomiting
Excess water excretion=> Dehydration=>Hypovolemia=>Renal failure
Cardiac arrhythmia (due to Electrolyte imbalance)

69
Q

Mortality of Cholera?

A

Untreated 60%
Treated <1%

70
Q

What pathogen leads to Rice Water Stools?

A

Vibrio Cholerae

71
Q

Diagnosis of VIbrio Cholerae?

A

Culture on selective agar -TCBS (Thiosulphate Citrate Bile salt Sucrose)

V. cholerae appear as yellow colonies

72
Q

Management of Vibrio Cholerae?

A

Prompt rehydration: Fluids/Electrolytes

Antibiotics reduce toxin production, hasten elimination (Tetracyclines, Co-trimoxazole)

73
Q

Pathogenesis of Entamoeba Histolytica?

A

Ingestion of cyst in contaminated food or water=>Excyst in small intestine to form trophozoites=>Trophozoites invade and penetrate colonic mucosa=>Tissue destruction and increased intestinal secretion

May ascend portal venous system to cause liver abscess

Can Cause Amoebic Dysentery

74
Q

Protozoal equivalent of a spore?

Pathogen that makes use of?

A

Cyst

Entamoeba histolytica

75
Q

Clinical Manifestation of Amoebic Dysentery?

A

Caused by Entaoeba Histolytica
Subacute onset –1-3 weeks
Diarrhoea, usually bloody
Abdominal pain
Weight loss (50%)
Fever (10-30%)

76
Q

Characteristics of Entamoeba Histolytica

A

Highest burden in developing countries
Exists in cyst and trophozoite forms- cyst present in contaminated food/water
Asymptomatic infection –majority (90%)

77
Q

Diagnosis of Protozoa?

A

Don’t Culture- need to visualize

Stool microscopy- Detection of cysts or trophozoites (3 samples from separate days)

Antigen detection- Stool or Serum

Serology - does not distinguish between acute and past infection

78
Q

Clinical Manifestation / Diagnosis of Amoebic Liver Abscess?

A

Returning travelers (8-20 weeks)
Right upper quadrant (RUQ) pain- may radiate to right shoulder

79
Q

Treatment of Amoebiasis?

A

Oral metronidazole
Paromomycin to eradicate intraluminal cysts
Liver abscess may require aspiration if risk of rupture