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gastroenteritis
inflammatory process of the stomach or intestinal mucosal surface, associated with ingestion of contaminated foods, water, poor sanitation/hygiene, most food-related illnesses are easily dealt with due to microbial antagonism, can occur due to infections or intoxications
gastroenteritis infection
pathogen gains entry in GI tract, survive microbial antagonism, there is a delay in appearance of GI symptoms (~1-3 days), while pathogen increases in sufficient numbers to cause damage, associated with fever
gastroenteritis intoxication
associated with ingestion of preformed toxin (exotoxin), characterized by sudden onset of symptoms (~2-10 hours after consumption of toxin), fever rarely a symptom (exotoxins don’t cause fever)
gastroenteritis symptoms
abdominal pain/cramping, diarrhea, nausea and vomiting, dehydration, weight loss (can’t eat), fatigue (disrupted sleep), fever may or may not be present
physician consultation advised in patients with fever (> 38.5C), significant abdominal pain, dehydration, diarrhea persisting more than 7 days, visible blood and mucus/pus in stool
acute diarrhea
increased frequency of stools (more than 3 BM/day), increased stool volume (>200 mL of fluid/day excreted in feces), and stools take shape of their container (not formed) (all 3 criteria must be met)
3 clinical syndromes - non-inflammatory (type I), inflammatory (type II), invasive (type III)
non-inflammatory (secretory) diarrhea
most common in NA, easily dealt with, self-limiting, typically caused by viruses (norovirus, rotovirus), more severe cases caused by bacteria (enterotoxigenic E. coli, vibrio cholerae), associated with some parasites (Giardia intestinalis), characterized by infection leading to large volumes of watery diarrhea
inflammatory diarrhea
typically caused by bacteria that invade intestinal epithelial cells (damage intestinal wall) (ex. shigella spp., salmonella enterica, campylobacter jejuni), characterized by frequent, small volume, loose stools, blood (gross or occult) often present, mucus and/or pus
invasive diarrhea
subset of inflammatory diarrhea associated with increased risk of bacteremia (some salmonella spp., enterohemorrhagic E. coli)
gastroenteritis diagnosis
patient history - focus on disease severity and risk factors for significant disease
symptom duration; fever, abdominal pain, nausea, vomiting, dehydration and fatigue
description of diarrhea important (frequency, volume, visible blood, pus or mucus)
investigate potential for common source outbreak (parties, gatherings, events, restaurants), inquire about friends and relative with similar symptoms
travel history and recent antibiotic use (camping)
short intubation period suggests ingestion of pre-formed toxin
viral infection or food poisoning should be considered when vomiting is dominant symptom
staphylococcal food poisoning (2-4 hours), norovirus (12-48 hours), salmonellosis (8-18 hours), giardiasis (7-10 days), others (1-5/7 days)
risk factors - age over 70, neonates, recent travel or camping, recent antibiotic use, immunosuppression (glucocorticoids, chemotherapy)
physical exam - establish severity, level of dehydration (decreased skin turgor, dry mucus membranes, tachycardia (low blood volume), orthostatic hypotension)
gastroenteritis diagnosis for bacterial infection
cultures and/or multiplex PCR should be performed for patients with severe or persistent disease (>1 week), green cap stool sample container containing preservative, not recommended if patient admitted for > 72 hours (likely C. diff)
gastroenteritis diagnosis for protozoa or helminth infection
studies for ova and parasites (O&P) (and now parasite PCR) indicated in cases of persistent diarrhea despite antibiotic therapy, exposure to infants in daycare centres, international or wilderness travel, immunosuppression, raw fish consumption
3 specimens may need to be collected on 3 separate days for O&P examination (yellow cap containing fixative) (orange cap - sterile)
other causes of diarrhea
acute diarrhea is also associated with other conditions/disease states and may represent the initial presentation of noninfectious and potentially life-threatening disease like IBS, bowel obstruction, GI hemmorhage
medications can also cause diarrhea - metformin, colchicine, diuretics, ACEi, PPIs, magnesium containing antacids, antibiotics
broad differential diagnosis considered upon initial investigation, but more than 90% of cases caused by GI infections or intoxications
gastroenteritis management
rehydration is main focus - fluid and electrolyte replacement
goal is to pass relatively dilute urine every 2-4 hours
oral fluids (water, pedialyte, hydralyte) and table salt (saltines) usually sufficient
IV fluids may be needed in cases of severe dehydration or persistent emesis
patients should eat judiciously until stools are formed (avoid caffeine, high lactose foods due to transient lactose intolerance)
agents to control diarrhea only used for non-inflammatory (secretory) diarrhea - bulking agents, bismuth compounds, anti-motility drugs (loperamide)
antimicrobial therapy reserved for severe infectious cases as they don’t work for toxins and will weaken normal flora
gastroenteritis infection control
transmission through oral route (contaminated hands, food, water), routine practices & contact precautions (pediatric or incontinent), norovirus contact/droplet precautions as it can be transmitted through aerosol vomit
case notification and outbreak notification (reportable disease), source control to prevent new cases
campylobacter jejuni
gram negative, helical shaped bacteria, possess capsule and flagellum, invade and damage intestinal epithelial cells
leading cause of infectious gastroenteritis in NA
~80% of retail chicken contaminated and ~60% of cattle excrete bacterium in feces and milk, found in avian species, dogs, sheep, cattle (milk), and environmental water sources
campylobacter jejuni infection symptoms
fever, abdominal pain and cramping, malaise, blood streaked, inflammatory diarrhea (>10 BM/day), symptoms resolve within 1 week
campylobacter jejuni transmission and infectious dose
transmission: ingestion of contaminated food & water, contact with animal feces
infectious dose: 500-800 microorganisms
campylobacter jejuni treatment and complications
antibiotic treatment in cases of sever illness or those at risk of severe illness and outcomes, associated with post-infection sequelae, Guillain-Barre syndrome and reactive arthritis
campylobacter jejuni infection control
good hand hygiene after handling raw poultry, dog & cat feces, proper refrigeration to prevent increases in bacterial numbers, pasteurization of milk and chlorination of water supply
salmonella enterica
gram negative, bacillus, invades and multiplies within intestinal mucosa, facultative intracellular bacteria
can cause typhoid (enteric) fever (typhi & paratyphi serotypes) and salmonellosis (enteritidis & typhimurium serotypes - most common in Canada)
typhoid (enteric) fever
transmitted from person to person, vaccine preventable, associated with travel
progressively high fevers, stomach pain, diarrhea, rash, headache, muscle aches, chills, cough, loss of appetite
salmonella enterica infection pathogenesis
invades epithelial cells of GI tract by secreting invasins that trigger endocytosis and induces uptake into cells, they multiply within food vesicles, kill host cell, inducing fever, cramps, and diarrhea, salmonella moves into bloodstream causing bacteremia
can travel to liver, spleen, bone and gallbladder within phagocytic cells causing secondary infections; carriers may shed the pathogen for weeks to months
salmonellosis infection symptoms and treatment
abdominal pain and cramps, chills, fever, nausea, loss of appetite, headache, myalgias, malaise, inflammatory diarrhea (usually no blood), symptoms typically resolve within 1 week
require supportive therapy only, antibiotics reserved for sever cases (ex. bacteremia)
salmonellosis transmission
ingestion of contaminated food and water, raw or undercooked meats, eggs, raw fruits and vegetables, seafood
fecal-oral route - people and pets (ex. turtles, iguanas, dogs, cats, small animals)
salmonellosis infection control
good sanitation practices to deter food contamination, proper refrigeration to prevent increases in bacterial numbers, avoid cross-contamination of uncooked foods with raw foods that may contain salmonella enteritidis or salmonella typhimurium, good hand hygiene after handling animals
enterotoxigenic E. coli (ETEC)
gram negative bacillus, produces AB enterotoxin (exotoxin) similar to cholera toxin, disrupts cell function resulting in fluid loss
causes “traveler’s diarrhea”
ETEC infection symptoms and complications
watery, non-inflammatory diarrhea, 4-5 loose watery stools/day, abdominal cramps, bloating, nausea and vomiting, fever (due to infection not exotoxin), symptoms typically resolve in 3-4 days
in severe cases patients experience dehydration, bloody stools, persistent vomiting, and high fever (>38.9C) - antibiotic treatment reserved for severe cases
ETEC transmission
ingestion of food, water and ice contaminated with human or animal feces
ETEC infection control
avoid consuming non-sterile sources of water, “boil it, cook it, peel it, or forget it”, oral vaccine (Dukoral) contains killed and attenuated cholera enterotoxin (looks like ETEC), confers 3 months of protection from ETEC and cholera for people going on trips
enterohemorrhagic E. coli (EHEC)
E. coli 0157:H7 most common strain in Canada
produces verocytotoxin (aka shiga toxin) that damages intestinal mucosa, causing lesions and bleeding, microbe can attach to neutrophils and then travel throughout the bloodstream
EHEC infection symptoms
low-grade fever (30% of patients), abdominal cramping, pain and tenderness, inflammatory diarrhea (>10 BM/day), infection progresses to hemorrhagic colitis in 40-60% of patients within 24 hours, in healthy adults symptoms resolve in 1 week
EHEC transmission
contaminated raw milk, water, fruit (skin) juice, undercooked ground beef, and produce (spinach, sprouts), person to person (fecal-oral)
EHEC infection control
avoid consuming non-sterile sources of food and water, observe public health notifications related to contaminated foods and proper cooking of contaminated meats
EHEC and hemolytic uremic syndrome (HUS)
symptoms: fever, abdominal pain, pale skin tone, fatigue and irritability (signs of low hemoglobin), unexplained small bruises or bleeding from nose and mouth, decreased urination, swelling of face, hands, and feet, destruction of RBCs, low platelets, acute kidney injury
prevalence: occurring in 5-15% of cases (extremes of age most vulnerable) 5-10 days after onset, leading cause of AKI in children, most cases resolve with no long-term sequelae
pathogenesis: toxin (verocytotoxin/shiga) damages endothelial cells of small vessels in the kidneys; triggers clot formation and obstruction of the glomeruli resulting in AKI
treatment: risk aggravated by anti-motility drugs and antibiotics (worsen disease from toxin overproduction), IV fluids/electrolytes, RBC and platelet transfusions, kidney dialysis (50% of patients) used to treat
shigella spp
gram negative bacillus, closely related to E. coli, produce invasins, and an enterotoxin similar to cholera toxin
S. Sonnei most common in NA, children most susceptible
causes shigellosis
shigella spp infection pathogenesis
shigella attaches to epithelial cell, secretes invasins and triggers endocytosis, shigella multiplies in cytosol, contains actin fibres for motility, shigella invades neighbouring epithelial cells evading immune defences, mucosal abscess forms as epithelial cells are killed by infection, shigella that enters the blood is quickly phagocytized and destroyed, no bacteremia
shigella spp transmission and infectious dose
contaminated food and water, person to person (fecal-oral), associated with poor hygenic conditions (institutions) and overcrowding
infectious dose: 10-100 organisms
shigellosis infection symptoms
inflammatory diarrhea, often bloody and watery, but main contain pus and mucus, abdominal cramps, rectal pain, fever, nausea, symptoms typically resolve in 2-3 days (carrier status 4 weeks), antibiotics reserved for severe cases only
shigellosis infection control
good sanitation practices to reduce food contaminants and proper hygiene
shigella dysenteriae
severe purulent (mucus and pus) bloody stools, produces shiga toxin/verocytotoxin similar to EHEC, most common in low-middle income countries, antibiotic therapy required
clostridioides difficile
gram positive anaerobic, endospore-forming bacillus, part of intestinal microbiome in 5% of adults, 20-25% of older adults, and 50% of newborns
produce exotoxins that cause inflammation of the colon accompanied by increased fluid secretion and permeability of intestinal mucosa
enterotoxin (toxin A) - diarrhea and inflammation
cytotoxin (toxin B) - induces cell damage and facilitates lesion formation
clostridioides difficile transmission
transmission through fecal-oral route, typically associated with hospitals and nursing homes, but community cases increasing, suspect in any client with diarrhea associated with broad-spectrum antibiotic exposure (< 3 months of disease onset), including clindamycin, cephalosporins, broad spectrum penicillins, and fluoroquinolones
clostridioides difficile infection symptoms
3-10+ watery stools in a 24 hour period, mild lower abdominal cramping and fever, 15% recover spontaneously with discontinuation of causative antibiotic, can advance to pseudomembranous colitis
pseudomembranous colitis
life-threatening complication associated with declining host factors, > 10 blood stools/day (pus often present), intestinal lesions (connective tissues, dying leukocytes, dead cells), on colonoscopy, the inflamed colonic mucosa contains small, raised, yellowish plaques
clostridioides difficile infection treatment and complications
discontinuation of implicated antimicrobial agent and supportive therapy, vancomycin to treat C. diff if symptoms don’t resolve, relapse in 20-30% if patients, for those that fail 2 rounds of antibiotic therapy, fecal microbiota transplant may be beneficial
complications include toxin megacolon (gross distension of colon causing bowel wall to dilate and thin, increasing risk of rupture) and bowel perforation (due to damage to intestinal wall)
clostridioides difficile infection control
contact precautions and single room with dedicated bathroom preferred, do not share equipment, ensure consistent environmental cleaning and disinfection, hand washing with soap and water preferred, due to absence of sporicidal activity in waterless antiseptic handwashes
viral gastroenteritis symptoms
secretory diarrhea, abdominal cramping, nausea & vomiting, fever, chills, clammy skin, weight loss, lack of appetite, symptoms commonly appear within 24 hours of infection and resolve within 12-60 hours after symptom onset
viral gastroenteritis pathogenesis
viruses infect epithelial cells of the intestinal tract where they undergo lytic replication, as host cells die, normal function of GI tract is lost, once epithelial layer is destroyed, replacement cells grow and function is restored (self-limiting)
viral gastroenteritis transmission
contaminated food and water (fecal-oral), person to person, aerosols from vomit
rotavirus
incubation period: 2-3 days
most common in children between 6 months and 2 years, infected children shed ~1000 organisms/g of stool (highly infectious)
symptoms persist (high fever, vomiting, diarrhea) for 1 week
peak incidence: Feb-May
infection control: routine practices & contact precautions
vaccine: oral rotarix (2 doses at 2 and 4 months)
norovirus
leading cause of viral gastroenteritis; seasonality (Nov-April)
transmission: fecal-oral route via direct or indirect contact through contaminated fomites, food and water, transmission via aerosolized vomit
incubation period: 12-48 hours
infectious dose: ~10-100 viral particles
patients can shed asymptomatically for up to 14 days post resolution of symptoms
PCR-based diagnostic panels available for clinical diagnosis
norovirus symptoms and treatment
secretory diarrhea, nausa & vomiting, stomach cramps, fatigue, low grade fever, chills, headache, symptoms persist for 1-3 days, treatment is supportive
norovirus infection control
can live on hard surfaces for as long as 3 weeks, resistant to many disinfectants, in hospital routine practices and contact precautions, cohort affected patients to separate airspaces and toilet facilities, in public good hand hygiene is critical, wash hands with soap and water, hand sanitizer does not work well against norovirus
intoxications
associated with the ingestion of preformed enterotoxin
enterotoxigenic strains of Staphylococcus aureus most common cause in Canada
referred to as “food poisoning”
sudden onset of nausea, vomiting, abdominal cramps and diarrhea, in the absence of fever, suggests food poisoning, especially if symptoms present within 1-16 hours after exposure and resolve in less than 24 hours
spread through colonized food handlers shedding the microbe from their skin and into food during preparation
commonly associated foods: boiled and fried rice, undercooked meat and poultry dishes, soups, sauces (gravy), processed meats, custard pastires, potato salad, inappropriately stored leftovers
self-limiting illness
treatment: fluid replacement (oral rehydration usually sufficient) in cases of mild dehydration, antiemetic drugs
Staphylococcus aureus
gram positive cocci-shaped bacteria, strains produce an enterotoxin that is heat stable and can survive ~30 minutes of boiling, once toxin is formed it cannot be destroyed (even if food is reheated), takes ~2 hours for bacteria to grow and secrete toxin in food, causes no obvious sign of spoilage or change in food taste