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Gastroenteritis

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					                Gastroenteritis
• Inflammation of stomach or intestines
    – Inhibits nutrient absorption and excessive H2O and
      electrolyte loss
•   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
  –   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
  –   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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posted:10/25/2011
language:English
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