Gastroenteritis

Enny Suswati

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 Inflammation of stomach or intestines
◦ Inhibits nutrient absorption and excessive H2O
and electrolyte loss
 Bacterial
 Viral
 Parasites
 Poisoning by microbial toxins
◦ food borne intoxication

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 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

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 Epidemiology
◦ Occurs worldwide
◦ Oral to fecal route of transmission
 Water common reservoir
 Overcrowding & poor sanitation are risk factors
 Animals may be source of infection

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 Prevention
◦ 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

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 3 groups of gram negative bacteria account
for most bacterial intestinal infections:
◦ Vibrio cholerae (Cholera)
◦ Enterics (Salmonella, Shigella, E. coli)
◦ Campylobacter jejuni

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 Causative agent: Vibrio cholerae
 High infectious dose
◦ Bacteria sensitive to stomach acid
◦ Adheres to small intestine and
multiply
◦ Bacteria don’t enter cells

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 Cholera toxin
◦ Potent exotoxin
◦ Causes intestinal
cells to rapidly pump
out electrolytes
◦ Passive osmotic H2O
loss follows
◦ Metabolic acidosis
◦ Shock

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 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

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 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

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•Infects cells of large intestine and
initiates intense inflammatory
response

•Dead cells slough off

•Produces areas covered with
pus and blood

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 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

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 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

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 Enterohemorrhagic E. coli
◦ O157:H7
◦ Produce potent Shiga-like toxins and type III
secretion systems

 Antimicrobials cause increase in toxin

production

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 Causative agent: Salmonella enterica
◦ 2000 strains (serotypes)
◦ Typhimurium and Enteritidis commonly cause
Salmonellosis
◦ Typhi and Paratyphi cause Typhoid Fever

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 Common intestinal
flora of many
animals
 Contaminated
animal products are
reservoir
 Reptiles, eggs and
undercooked poultry

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•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

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 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

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 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

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 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

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 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

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 Common causative agents:
◦ Rotaviruses and Noroviruses
◦ Both naked RNA viruses

Wheel -like Rotaviruses

Star-like Noroviruses

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 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

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 Staphylococcus aureus
◦ Halotolerent; grows well in foods at room
temp
◦ Associated with cafeterias and social
functions

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 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

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 Causative agent:
◦ Clostridium botulinum
 Obligate anaerobic, Gram +, spore forming
bacillus
◦ Produce 7 different neurotoxins
 One of most deadly toxins known

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 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

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 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”

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 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

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 Prevention
◦ Proper sterilization and sealing of canned food
◦ No honey or unpasteurized juices for infants!!

 Treatment
◦ Antitoxin
◦ Gastric washing and surgical removal of tissues
◦ Artificial respiration may be required
◦ Anti-microbials given to kill bacteria in infant and
wound botulism

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