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SEM3: PATH30200 GI/GU Illness > L3-5: Gastroenteritis > Flashcards

L3-5: Gastroenteritis Flashcards

(79 cards)

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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
Pathogenesis of Camplylobacter
Ingestion of bacilli Attach to and invade GI epithelium No role identified for enterotoxin
26
Clinical Features of Campylobacter?
*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
27
Botulism versus Guillain-Barre Syndrome?
Botulism: Descending parylsysis (botulisism Toxin) Guillain Barre Syndrome: Ascending paralysis
28
Bacteria associated with the immune-mediated development of Guillain-Barre Syndrome and Reactive Arthritis weeks after infection?
Campylobacter
29
Diagnosis of Campylobacter?
*Charcoal-based selective media* Microaerophilic atmosphere See Gram-negative curved bacilli in Flat colonies *Susceptibility Testing* *PCR*
30
Pathogens that cause Enteric Fever (aka. ___________)
Typhoid and paratyphoid fever are caused by: *Salmonella enterica* - typhi *Salmonella enterica* - paratyphi (A, B and C)
31
Pathogenesis of Enteric Fever
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
32
Which condition is associated with hypertrophy of Peyer's Patches?
Enteric Fever (casued by Salmonellae Enterica)
33
Which condition is associated with hypertrophy of Peyer's Patches?
Enteric Fever (caused by Salmonellae Enterica)
34
Clinical Features of Enteric Fever
2 week incubation!! Insidious onset Fever, chills, relative bradycardia Abdominal pain, Diarrhea/constipation * ‘rose’ spots*
35
Diagnosis of Salmonella?
Blood culture (Most Common) Faeces culture bone marrow culture (Only in complicated cases)
36
Treatment of Enteric Fever?
Rehydration Fluoroquinolones (ciprofloxacillin) 3rd gen cephalosporin (meropenem)
37
Pathogens that cause Non-Typhoidal Salmoenlollis?
Salmonella enteritidis Salmonella typhimurium
38
Transmission of Non-typhoidal salmonella?
Peron to Person Contaminated food/water, especially poultry and eggs Exotic pets
39
What is Carriage?
Asymptomatic shedding of organism in faeces
40
When to treat Non-typhoidal salmonellosis?
Treat only if *Severe illness *High risk of invasive disease (age < 1 or > 50, HIV, immunocompromised, cardiac/valvular/joint disease)
41
Selective Media for Campylobacter?
Charcoal Based selective media and microaerophilic atmosphere
42
Diagnosis of non-typhoidal salmonellosis?
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
EHEC/VTEC –verocytotoxin-producing E. coli Epidemiology?
Summer Peak Affects Extremes of age and those w. underlying conditions Outbreaks from wells and in nursing homes
44
VTEC –verocytotoxin-producing E. coli Transmissiion?
*Cattle are the main reservoir of infection* Ground beef (hamburgers) Milk, yoghurt, cheese Apple juice, vegetables Water
45
VTEC Pathogenesis?
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
What Pathogens are responsible for the development of Hemolytic Uremic Syndrome (HUS)?
VTEC –verocytotoxin-producing E. coli S. dysenteriae (Shigellosis)
47
Clinical Features of VTEC
Diarrhoea -may be bloody (25-50%) *Vomiting and fever uncommon* Duration 5-10 days 5-10% may develop *hemolytic uraemic syndrome (HUS) *
48
Treatment of VTEC?
Rehydration Antibiotics not of proven value *Breakdown of E. Coli cells can suddenly release many more toxins => leading to HUS*
49
Shigellosis is also known as ______________
Shigellosis is also known as Bacillary dysentery
50
Shigellosis Pathogenesis?
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
__________ has a potent Shiga toxin that can cause hemolytic uraemic syndrome (HUS)
*S. dysenteriae* (Shigella) has a potent Shiga toxin that can cause hemolytic uraemic syndrome (HUS)
52
Bacterial infections that can cause bloody diarrhea?
VTEC Shigella Campolobacter
53
Bacterial Infections than can cause reactive arthritis?
Camplyobacter S. flexneri
54
Diagnosis of Shigella?
Selective media e.g., XLD- Non-lactose fermenters PCR
55
Chracteristics of Staphylococcus Aureus Gastritis?
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
Characteristics of Bacillus Cereus Gastritis?
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
Characteristics of Clostridioides Perfringes Gastritis?
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
Characteristics of Clostridioides Difficile Gastritis?
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
Characteristics of Clostridioides Difficile Gastritis?
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
C. Diff Risk Factors?
*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
Clinical Features/ Complicaitons of C. Diff Infection?
*Clinical Features* Watery diarrhoea Abdominal cramping/pain Colitis Fever Elevated WCC *Complications* Pseudomembranous colitis Toxic megacolon => Perforation/Death Colonic perforation Death
62
Diagnosis of C. Diff
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
Management of C. DIff
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
Similar efficacy in treating C. DIff to vancomycin but with less recurrence?
Fidaxomycin
65
Monoclonal antibody against C. Diff's toxin B that can lead to reduced recurrence?
Bezlotoxumab
66
Risk Factor's/Treatment Course for Recurrent C Diff infection?
*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
Characteristics/Pathogenesis of Vibrio Cholerae
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
Clinical Features of Cholera?
Abrupt onset Rice-water’ stools, effortless vomiting Excess water excretion=> Dehydration=>Hypovolemia=>Renal failure Cardiac arrhythmia (due to Electrolyte imbalance)
69
Mortality of Cholera?
Untreated 60% Treated <1%
70
What pathogen leads to Rice Water Stools?
Vibrio Cholerae
71
Diagnosis of VIbrio Cholerae?
Culture on selective agar -*TCBS (Thiosulphate Citrate Bile salt Sucrose)* V. cholerae appear as yellow colonies
72
Management of Vibrio Cholerae?
Prompt rehydration: Fluids/Electrolytes Antibiotics reduce toxin production, hasten elimination (Tetracyclines, Co-trimoxazole)
73
Pathogenesis of Entamoeba Histolytica?
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
Protozoal equivalent of a spore? Pathogen that makes use of?
Cyst Entamoeba histolytica
75
Clinical Manifestation of Amoebic Dysentery?
*Caused by Entaoeba Histolytica* Subacute onset –1-3 weeks Diarrhoea, usually bloody Abdominal pain Weight loss (50%) Fever (10-30%)
76
Characteristics of Entamoeba Histolytica
Highest burden in developing countries Exists in cyst and trophozoite forms- cyst present in contaminated food/water *Asymptomatic infection –majority (90%)*
77
Diagnosis of Protozoa?
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
Clinical Manifestation / Diagnosis of Amoebic Liver Abscess?
Returning travelers (8-20 weeks) Right upper quadrant (RUQ) pain- may radiate to right shoulder
79
Treatment of Amoebiasis?
Oral *metronidazole* *Paromomycin* to eradicate intraluminal cysts Liver abscess may require aspiration if risk of rupture

SEM3: PATH30200 GI/GU Illness (5 decks)

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