Salmonella - pathogenesis Ingested orally (acid-labile) 1,000,000-100,000,000 live bacteria for infection (only 1,000 to 10,000 for S. typhi ) Must survive in gastric acid • Lower pH increases number for infection • People on antacids show increased risk
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Salmonella - pathogenesis
Ingested orally (acid-labile)
1,000,000-100,000,000 live bacteria for
infection
(only 1,000 to 10,000 for S. typhi)
Must survive in gastric acid
• Lower pH increases number for infection
• People on antacids show increased risk
Salmonella - clinical syndromes
Gastroenteritis (diarrhea)
• Most common infection seen with Salmonella spp. = salmonellosis
• Invade cells of GI tract
• Loss of water from cells gives rise towatery diarrhea, fever, cramps
• Spontaneous resolution in days to a week
Salmonella - clinical syndromes
Typhoid Fever (S. Typhi)
• Pass through cells into bloodstream
• Picked up by macrophages to liver, spleen,
bone marrow (ulceration, perforation,
endotoxin shock)
• High fever, diarrhea, cramps
ShigellaMedically important species
–S. dysenteriae (most serious)
–S. sonnei (most common in developed)
–S. flexneri (most common in underdeveloped)
Epidemiology
–Human reservoir (fecal-oral through hands)
– Hardy in nature - survives long time on surfaces
– >50% of cases are in children
Shigella - pathogenesis
● Ingested orally - only 200 live bacteria for infection
Acid stable (unlike Salmonella)
Attach to & invade cells & replicate
Spread cell to cell (protected from immunity)
DO NOT spread through bloodstream
Endotoxin causes inflammation
Produces original shiga toxin (Sh. dysenteriae type 1)