salmonella - pathogenesis
TRANSCRIPT
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)
Enterotoxins (Sh. flexneri)
Shigella – clinical syndromes
Shigellosis
• Starts with watery diarrhea
• Turns grossly bloody with pus
• Severe cramps
• Self-limiting
• Complication: HUS
Miscellaneous Enterobacteriaceae
• Klebsiella pneumoniae– community-acquired pneumonia
– diarrhea
• Enterobacter, Serratia, Citrobacter
– opportunistic pathogens = they cause infections
in patients that are very sick and have weakened
defences
– hospital-acquired infection are primary source
Proteus (UTI), Enterobacter, Citrobacter etc.
Yersinia pestis, enterocolitica,
pseudotuberculosis
• Gram-negative rod
• Intracellular pathogen
• Zoonotic infection
Epidemiology
– World-wide problem
– Usually associated with contact with squirrels &
other urban animals
Yersinia pestis - clinical syndromes
Bubonic Plague
–Flea bite
–Bacilli travel to lymph nodes (multiply in
lymph nodes – can survive within
macrophages)
– Infection results in swelling and pain
–High fever, chills, headache, nausea
Yersinia pestis - clinical syndromes
Septicemic Plague
Can penetrate & invade bloodstream
• All organs infected
• Lungs (secondary pneumonic plague)
50-75% mortality when it goes to
bloodstream• Endotoxin shock primary problem
Yersinia pestis - clinical syndromes
Primary Pneumonic Plague– spread via respiratory droplets
– 1 bacilli can cause disease in patient
– severe hemorrhages
– death in hours
– 100% mortality if untreated or late treatment
Diagnosis and Treatment
– symptoms & patient history key
– must act fast with treatment
Clinically important nonfermentative
GN bacilli
General characteristics of nonfermenters
Oxidative GN bacilli, facultative anaerobes &
microaerophiles
Produce acid from glucose or other carbohydrates only
in the presence of oxygen (nonfermenters)
NOTE: Enterobacteriaceae, Aeromonas and Vibrio are
fermentative & can utilize carbohydrates in the absence
of oxygen
Pseudomonas aeruginosa oxidizes but does not
ferment glucose
Pseudomonas
aeruginosa
(Family Pseudomonadaceae)
Pseudomonas aeruginosa
• GN long & thin rods
• Pigmented growth on agar & distinct odor– usually green or red & smells like grapes or juicy fruit gum
• Ubiquitous in environment, especially in
water– Hospital environment loaded with this pathogen
• Hardy, survive extreme conditions
• Rarely part of normal flora
• Primarily opportunistic pathogen
Pseudomonas aeruginosa
Virulence Factors
– Attachment by fimbriae
– Capsule - anti-phagocytic
– Endotoxin – inflammation
– Exotoxin A
•blocks protein synthesis
•kills cells
•skin or lung damage depends on infection
– Many other toxins & enzymes
Virulence factors associated with
Pseudomonas aeruginosa
Pseudomonas aeruginosa
Epidemiology
– Opportunistic infections
– Require weak defense systems
– Colonize hospitalized patients
• respirators
• solutions
• cut flowers
• instruments
Diverse sites of infection by P. aeruginosa
Pseudomonas aeruginosa
Pulmonary Infections
– Colonization
– Benign bronchitis to necrotic fatal pneumonia
– Cystic Fibrosis
• mucoid encapsulated strains
• exacerbations of disease happen frequently
• invasive pneumonia
– Neutropenic patients
• respiratory equipment is a primary source
• serious pneumonia
Pseudomonas aeruginosa
Skin Infections
– Most common in burn victims
• moist environment
• lack of WBC reaching damaged tissue
• vascular damage
• tissue necrosis
• blood stream invasion
– Folliculitis (hot tubs, whirlpools, pools)
Pseudomonas aeruginosa
Other infections associated with contaminated
water or liquid solutions
– outer ear infections (swimmers ear)
– eye infections (contact lens wearers especially)
– endocarditis (drug abusers)
Treatment challenges
– multiple antibiotic resistance problems
– develops resistance overnight
Diseases Associated with Burkholderia spp.