Kuliah Blok 10 Th 2013
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Transcript of Kuliah Blok 10 Th 2013
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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
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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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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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Cholera
• 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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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
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•Infects cells of large intestine and
initiates intense inflammatoryresponse
•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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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
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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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Salmonellosis and Typhoid Fever
•
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 floraof 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 intobloodstream
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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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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
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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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Viral Gastroenteritis
•
Common causative agents: – Rotaviruses and Noroviruses
– Both naked RNA viruses
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Star-like NorovirusesWheel -like Rotaviruses
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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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Bacterial Food Intoxication
• 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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Botulism•
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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