Professional Documents
Culture Documents
Kuliah Blok 10 TH 2013
Kuliah Blok 10 TH 2013
Enny Suswati
2/3/2014
Gastroenteritis
Gastroenteritis
Inflammation of stomach or intestines
Inhibits nutrient absorption and excessive H2O and electrolyte loss
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Gastroenteritis
Enteric fevers
Systemic with severe headache, high fever, abscesses, intestinal rupture, shock and death
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Gastroenteritis
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Gastroenteritis
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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Bacterial Gastroenteritis
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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Gastroenteritis
Cholera
Causative agent: Vibrio cholerae High infectious dose
Bacteria sensitive to stomach acid Adheres to small intestine and multiply
Bacteria dont 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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Gastroenteritis
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Gastroenteritis
Shigellosis
Causative Agent: Shigella sp.
S. dysenteriae, S. flexneri, S. boydii, S. sonnei
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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
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Travelers 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
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Enterohemorrhagic E. coli
O157:H7 Produce potent Shiga-like toxins and type III secretion systems
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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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Campylobacteriosis
Causative agent: Campylobacter jejuni
Leading cause of bacterial diarrhea in United States Estimated 1million cases annually with ~100 deaths
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Non-motile mutants are avirulent Severe cases treated with ciprofloxacin or azithromycin
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Guillain-Barr 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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Viral Gastroenteritis
Common causative agents:
Rotaviruses and Noroviruses Both naked RNA viruses
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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Botulism
Causative agent:
Clostridium botulinum
Obligate anaerobic, Gram +, spore forming bacillus
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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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