Transcript Gastroenteritis

Gastroenteritis
• Inflammation of stomach or intestines
– Inhibits nutrient absorption and excessive H2O and
electrolyte loss
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Bacterial
Viral
Parasites
Poisoning by microbial toxins
– food borne intoxication
• Signs and Symptoms:
– General features: diarrhea, loss of appetite, abdominal
cramps, nausea, vomiting and possibly fever
– Dysentery
– Typically self Limiting
• Enteric fevers
– Systemic with severe headache, high fever, abscesses,
intestinal rupture, shock and death
• Epidemiology
– Occurs worldwide
– Oral to fecal route of transmission
• Water common reservoir
• Overcrowding & poor sanitation are risk factors
• Animals may be source of infection
• Prevention
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Hand washing
Proper food handling and complete cooking
Pasteurization of milk and juices
Adequate sanitation
Safe water supplies
• Treatment
– Rapid replacement of fluids and electrolytes
– Anti-nausea medication
– Antimicrobials may be used in severe cases
Bacterial Gastroenteritis
• 3 groups of gram negative bacteria account for
most bacterial intestinal infections:
– Vibrio cholerae (Cholera)
– Enterics (Salmonella, Shigella, E. coli)
– Campylobacter jejuni
Cholera
• Causative agent: Vibrio cholerae
• High infectious dose
– Bacteria sensitive to stomach acid
– Adheres to small intestine and multiply
– Bacteria don’t enter cells
• Cholera toxin
– Potent exotoxin
– Causes intestinal cells
to rapidly pump out
electrolytes
– Passive osmotic H2O
loss follows
– Metabolic acidosis
– Shock
• Heavy loss of fluid
– “rice-water stool”
• Up to 20L of fluids lost per day
• May discharge 1 million bacteria per ml of feces
• Untreated cases potentially fatal
– Fluid/electrolyte replacement
– Tetracycline reduces toxin production
Shigellosis
• Causative Agent: Shigella sp.
– S. dysenteriae, S. flexneri, S. boydii, S. sonnei
• Low infecting dose
– Bacteria not sensitive to stomach acid
– Characterized by fever and dysentery
•Infects cells of large intestine and
initiates intense inflammatory
response
•Dead cells slough off
•Produces areas covered with
pus and blood
• All species produce enterotoxin and type III
secretion systems
• S. dysenteriae produces powerful endotoxin
– shiga-toxin
• Ciprofloxacin, rifampin or azithromycin may reduce
duration and infectivity
Traveler’s Diarrhea
• Causative Agent: Escherichia coli
– Multiple antigenic strains (O, H, K)
– Virulent strains have fimbriae, adhesions and
multiple toxins
• Enterotoxigenic E. coli
– Enterotoxins
– Type III secretion system
– Typically self limiting
• Enterohemorrhagic E. coli
– O157:H7
– Produce potent Shiga-like toxins and type III secretion
systems
• Antimicrobials cause increase in toxin production
Salmonellosis and Typhoid Fever
• Causative agent: Salmonella enterica
– 2000 strains (serotypes)
– Typhimurium and Enteritidis commonly cause
Salmonellosis
– Typhi and Paratyphi cause Typhoid Fever
• Common intestinal
flora of many animals
• Contaminated animal
products are reservoir
• Reptiles, eggs and
undercooked
poultry
•Virulent strains tolerate stomach
acid and pass to intestines
•Toxin induces phagocytosis in
intestinal cells
•Pathogen reproduces inside
phagosome killing host cell
•Bacteria (Typhi) may pass
through intestinal cells into
bloodstream
• Typhoid fever is an
enteric fever
– Macrophages carry
bacteria to liver, spleen,
bone marrow and
gallbladder
– Treated with ciprofloxacin
or ampicillin
– Surgical removal of
gallbladder
Campylobacteriosis
• Causative agent: Campylobacter jejuni
– Leading cause of bacterial diarrhea in United States
– Estimated 1million cases annually with ~100 deaths
• Associated with poultry
– Low infecting dose
• Virulent strains possess adhesions, cytotoxins
and endotoxin
– Induce endocytosis in cells of intestine and initiate
inflammation and bleeding lesions
• Non-motile mutants are avirulent
• Severe cases treated with ciprofloxacin or
azithromycin
• Guillain-Barré Syndrome
– Tingling of the feet leads to progressive paralysis of the
legs, arms and rest of the body
– 40% of cases preceded by campylobacteriosis
– May be associated with autoimmune response
– 80% recover completely; 5% mortality with treatment
Viral Gastroenteritis
• Common causative agents:
– Rotaviruses and Noroviruses
– Both naked RNA viruses
Star-like Noroviruses
Wheel -like Rotaviruses
• Epidemology
– Infect intestinal cells causing cell death
– Typically self-limiting
– Norovirus epidemics cause 90% of cases
– Rotaviruses responsible for 50% infant cases
of serious diarrhea
• 600,000 worldwide annual fatalities
• Oral vaccine available
Bacterial Food Intoxication
• Staphylococcus aureus
– Halotolerent; grows well in foods at room temp
– Associated with cafeterias and social functions
• 5 heat stable enterotoxins:
– 1000 for up to 30 min
– Stimulate muscle contractions, nausea and intense
vomiting, diarrhea and cramping
– Acute and self limiting
• symptoms begin 4-6 hrs after consumption and
end within 24 hrs
Botulism
• Causative agent:
– Clostridium botulinum
• Obligate anaerobic, Gram +, spore forming bacillus
– Produce 7 different neurotoxins
• One of most deadly toxins known
• Signs & Symptoms
– Dizziness, dry mouth, blurred vision
– Abdominal symptoms include pain, nausea,
vomiting and diarrhea or constipation
– Progressive paralysis
• Paralysis of respiratory muscles most common
cause of death
• 3 forms of botulism:
– Food-borne botulism – progressive paralysis of
all voluntary muscles due to toxin production
– Wound botulism – similar symptoms
– Infant botulism – bacteria grow in the intestines,
producing non-specific symptoms
• “floppy baby syndrome”
• Epidemiology
– Food borne botulism
• Commercial sterilization
• Toxin destroyed by heating foods
– Wound botulism
• deep crushing wounds
– Infant botulism
• Inhalation or ingestion of spores
• Commonly associated with honey
or juices
• Prevention
– Proper sterilization and sealing of canned food
– No honey or unpasteurized juices for infants!!
• Treatment
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Antitoxin
Gastric washing and surgical removal of tissues
Artificial respiration may be required
Anti-microbials given to kill bacteria in infant and wound
botulism