L3-5: Gastroenteritis Flashcards
Type of Infectious Gastroenteritis affecting Children vs. Adults?
Children: Primarily Viral
Adults: Primarily Bacterial
Classification of Diarrhoea
≥ 3 episodes of loose or liquid stool in 24 hours
Acute: <14 Days
Persistent: >14 Days
Chronic: >30 Days
Causes of Viral Gastroenteritis?
Rotavirus
Norovirus
Adenovirus
When do cases of viral enteritis peak?
Winter
Diagnosis of Viral Enteritis?
Direct Visualization: Electron Microscope
Antigen Detection
Lateral Flow
ELISA
Multiplex PCR
Management of Viral Gastroenteritis?
Supportive
*Rehydration, oral preferable
*Electrolyte replacement
*Refeeding (in children)
No specific antiviral treatment
Transmission of Rotavirus?
Transmitted Fecal-Oral
Sometimes respiratory => URTI kids
Survives on fomites and hands
Pathogenesis of Rotavirus?
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
Demographic most commonly impacted by Rotavirus?
Most Common in children <2
Diagnosis of Rotavirus?
Lateral Flow Test or PCR
Oral Vaccine for this virus given before 6 months => 85% hospital reduction
Rotavirus
Characteristics of Norovirus?
AKA. Winter Vomitting Virus
Small rounded structured virus (SRSV)
Single Strnaded RNA Virus
Significant Diversity: hard to vaccinate against, immunity short lived
Characteristics of Rotavirus?
Reovirus (double stranded RNA
Large amount of virus in faeces
Characteristics of Norovirus?
Small rounded structured virus (SRSV)
Single Stranded RNA Virus
LOW infectious dose (18 virus particles)
Significant Diversity: hard to vaccinate against, immunity short-lived
Transmission of Norovirus?
Faecal- oral
Airborne droplets- aerosolized by vomiting
Food, water
Contaminated environment, fomites
Pathogenesis of Norovirus?
Blunting of villi in jejunum
Epithelial cells not damaged
No enterotoxin has been detected
Clinical Features of Rota Virus
Diarrhoea
Vomiting
Fever
Dehydration
+/-respiratory tract symptoms
Clinical Features of Norovirus?
Nausea
Vomiting (may be projectile)
Abdominal cramps
Myalgia
Diarrhoea
+/-fever
Diagnosis of Norovirus?
PCR- No good Antigen test due to diversity of serotypes
Characteristics of Adenovirus?
Double-stranded DNA Virus
Gastroenteritis (serotypes 40 and 41)
Primarily affects kids
Rotavirus – ________
Norovirus– ________
Rotavirus – children
Norovirus – adults
Ways that various Bacteria can cause gastroenteritis?
Adherence to the intestinal epithelium
Invasion of intestinal cells
Toxin production: Ingestion of pre-formed toxin or Toxin production in GIT
Commonest bacterial pathogen isolated from feces?
Camplylobacter
Characteristics of Campylobacter?
Commonest bacterial pathogen isolated from faeces
Cases peak in summer
Contanimation with Raw or undercooked foods
Pathogenesis of Camplylobacter
Ingestion of bacilli
Attach to and invade GI epithelium
No role identified for enterotoxin
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
Botulism versus Guillain-Barre Syndrome?
Botulism: Descending parylsysis (botulisism Toxin)
Guillain Barre Syndrome: Ascending paralysis
Bacteria associated with the immune-mediated development of Guillain-Barre Syndrome and Reactive Arthritis weeks after infection?
Campylobacter
Diagnosis of Campylobacter?
Charcoal-based selective media
Microaerophilic atmosphere
See Gram-negative curved bacilli in Flat colonies
Susceptibility Testing
PCR
Pathogens that cause Enteric Fever (aka. ___________)
Typhoid and paratyphoid fever are caused by:
Salmonella enterica - typhi
Salmonella enterica - paratyphi (A, B and C)
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
Which condition is associated with hypertrophy of Peyer’s Patches?
Enteric Fever (casued by Salmonellae Enterica)
Which condition is associated with hypertrophy of Peyer’s Patches?
Enteric Fever (caused by Salmonellae Enterica)
Clinical Features of Enteric Fever
2 week incubation!!
Insidious onset
Fever, chills, relative bradycardia
Abdominal pain, Diarrhea/constipation
* ‘rose’ spots*
Diagnosis of Salmonella?
Blood culture (Most Common)
Faeces culture
bone marrow culture (Only in complicated cases)
Treatment of Enteric Fever?
Rehydration
Fluoroquinolones (ciprofloxacillin)
3rd gen cephalosporin (meropenem)
Pathogens that cause Non-Typhoidal Salmoenlollis?
Salmonella enteritidis
Salmonella typhimurium
Transmission of Non-typhoidal salmonella?
Peron to Person
Contaminated food/water, especially poultry and eggs
Exotic pets
What is Carriage?
Asymptomatic shedding of organism in faeces
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)
Selective Media for Campylobacter?
Charcoal Based selective media and microaerophilic atmosphere
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
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
VTEC –verocytotoxin-producing E. coli Transmissiion?
Cattle are the main reservoir of infection
Ground beef (hamburgers)
Milk, yoghurt, cheese
Apple juice, vegetables
Water
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
What Pathogens are responsible for the development of Hemolytic Uremic Syndrome (HUS)?
VTEC –verocytotoxin-producing E. coli
S. dysenteriae (Shigellosis)
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) *
Treatment of VTEC?
Rehydration
Antibiotics not of proven value
Breakdown of E. Coli cells can suddenly release many more toxins => leading to HUS
Shigellosis is also known as ______________
Shigellosis is also known as Bacillary dysentery
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)
__________ 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)
Bacterial infections that can cause bloody diarrhea?
VTEC
Shigella
Campolobacter
Bacterial Infections than can cause reactive arthritis?
Camplyobacter
S. flexneri
Diagnosis of Shigella?
Selective media e.g., XLD- Non-lactose fermenters
PCR
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!!
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
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
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)
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)
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
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
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
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
Similar efficacy in treating C. DIff to vancomycin but with less recurrence?
Fidaxomycin
Monoclonal antibody against C. Diff’s toxin B that can lead to reduced recurrence?
Bezlotoxumab
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
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
Clinical Features of Cholera?
Abrupt onset
Rice-water’ stools, effortless vomiting
Excess water excretion=> Dehydration=>Hypovolemia=>Renal failure
Cardiac arrhythmia (due to Electrolyte imbalance)
Mortality of Cholera?
Untreated 60%
Treated <1%
What pathogen leads to Rice Water Stools?
Vibrio Cholerae
Diagnosis of VIbrio Cholerae?
Culture on selective agar -TCBS (Thiosulphate Citrate Bile salt Sucrose)
V. cholerae appear as yellow colonies
Management of Vibrio Cholerae?
Prompt rehydration: Fluids/Electrolytes
Antibiotics reduce toxin production, hasten elimination (Tetracyclines, Co-trimoxazole)
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
Protozoal equivalent of a spore?
Pathogen that makes use of?
Cyst
Entamoeba histolytica
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%)
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%)
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
Clinical Manifestation / Diagnosis of Amoebic Liver Abscess?
Returning travelers (8-20 weeks)
Right upper quadrant (RUQ) pain- may radiate to right shoulder
Treatment of Amoebiasis?
Oral metronidazole
Paromomycin to eradicate intraluminal cysts
Liver abscess may require aspiration if risk of rupture
