GIT Pathogens - Bacteria - Invasive Flashcards
Types of invasive pathogens 1) 2) 3) 4) 5)
1) Shigella
2) Salmonella
3) Yersinia enterolytica
4) Campylobacter
5) Vibrio parahaemolyticus
Major serotypes of Shigella 1) 2) 3) 4)
1) Shigella flexneri
2) Shigella dysentariae
3) Shigella boydii
4) Shigella sonnei
Shigella infective dose
10^2 - 10^3 bacteria
Shigella transmission
Human to human. No animal vectors.
Shigella virulence plasmid contents
1)
2)
3)
1) Type III secretion system.
2) Invasion plasmid antigens (ipas).
3) IcsA - Recruits host actin for motility.
Shigella virulence plasmid size
240kb
Shigella host cell, and place of entry
Enterocytes, basal side
Shigella pathogenesis 1) 2) 3) 4) 5) 6)
1) Shigella invades, enters through M cell
2) Enters lamina propria, phagocytosed by macrophage.
3) Induces macrophage apoptosis, releases IL-1, IL-8. This causes enterocytes to become more ‘leaky.’
4) Uses ipa to enter enterocytes.
5) Uses IcsA for transport between enterocytes.
6) Shigella passes between enterocytes without becoming extracellular. Invaded cells die, focal ulcers form.
O Antigen
Fimbriae
H antigen
Flagella
Immune cells that contain shigella infection
Neutrophils
Lab diagnosis of shigella:
1)
2)
3)
1) Lactose non-fermenter
2) No motility
3) O antigens (no H antigen)
4) Desoxycholate agar (DCA)
Pathogenic species of salmonella
Salmonella enteritica
Infectious dose of salmonella
High - salmonella are acid-labile
Role of ipa
Induce membrane ruffling in host cell.
In shigella.
Salmonella pathogenicity island I role
Enter host cell
Salmonella pathogenicity island II role
Survive inside host cell
Salmonella pathogenicity island I contents
Type III secretion system
Sip proteins - induce membrane ruffling
Sip protein role
Induce membrane ruffling in salmonella
Salmonella pathogenicity island II contents
Type III secretion system
Ssa protein - Inactivate elements of innate immune system.
Ssa protein role
Inactivate elements of innate immune system.
Allow salmonella to survive intracellularly.
Salmonella pathogenesis: 1) 2) 3) 4) 5) 6)
1) Invade m cells and enterocytes by inducing membrane ruffling.
2) Uptake mediators induce electrolyte accumulation in the lumen, inflammatory exudate.
3) Transcytose to basal membrane, are phagocytosed, carried to regional lymph nodes.
4) Multiply in regional lymph nodes. Results in reticuloendothelial hyperplasia and hypertrophy.
5) DIsease confined to GIT by neutrophils.
6) Prostaglandins released by neutrophils increase cAMP levels, increase active fluid secretion.
Lab diagnosis of salmonella:
1)
2)
3)
Desoxycitrate agar (DCA).
H2S production
Lactose non-fermenting
Yersinia enterolytica growth temperature
Lower than that of other enteropathogenic bacteria
Yersinia virulence plasmid contents
Yersinia outer proteins (YOP)
Yersinia outer proteins role
Cytotoxic
Injected into macrophages, prevent phagocytosis
Yersinia enterolytica pathogenesis
1)
2)
3)
1) Invade M cells
2) Invade basal layer, kill macrophages attempting phagocytosis. Also inhibit TNF release
3) Local systematic dissemination
Yersinia enterolytica lab diagnosis: 1) 2) 3) 4)
1) CIN agar, ‘bullseye’ colonies
2) Lactose non-fermenting
3) Urease positive
4) Oxidase negative
Foods associated with yersinia
Unpasteurised milk, meat
Campylobacter infective dose
High. Acid-labile
Campylobacter incubation period
2-4 days
Campylobacter transmission
Contaminated milk, meat. Coassociation with amoebae living in water.
Non-pathogenic in chickens.
Campylobacter pathogenesis
Not well understood
Might release a cytolytic toxin
Campylobacter lab diagnosis
CAMP medium
Incubated at 42 degrees C
Microaerophilic conditions
Microaerophilic conditions
5% oxygen
10% carbon dioxide
85% dinitrogen
Salmonella incubation period
8-72 hours.
