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Evolution of enteric pathogens

family Enterobacteriacea. GeneraHuman, animal pathogensSalmonella, Yersinia, Aeromonas, E.coli/ShigellaCommensals/symbionts of animals E.coli, CitrobacterPlant pathogensErwinia Environmental bacteriaAeromonas, KlebsiellaWhy so different?Links to plant-related past?Most grow on plant-deriv

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Evolution of enteric pathogens

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    1. Evolution of enteric pathogens

    2. family Enterobacteriacea Genera Human, animal pathogens Salmonella, Yersinia, Aeromonas, E.coli/Shigella Commensals/symbionts of animals E.coli, Citrobacter Plant pathogens Erwinia Environmental bacteria Aeromonas, Klebsiella Why so different? Links to plant-related past? Most grow on plant-derived sugars Salmonella, E.coli cannot break down pectin. Yersinia, Klebsiella can

    3. Evolution of Salmonella Serovars are differentiated based on antigens O polysaccharide antigen H1, H2 flagella 2,501 serovars are recognized Some (sv Typhimurium, Newport) have a broad host range Gallinarum and Pullorum --> chickens (fowl typhoid) Typhi, Parathyphi --> primates (typhoid fever) Cholerasuis --> pigs (pig paratyphoid) Dublin --> cattle (bacteremia) Other svs are host-adapted Not all serovars are virulent Sv Bongori Sv Sophia Common in chickens in Australia, not known to have caused disease in humans All Salmonella have pathogenicity islands (SPIs)

    4. SPI’s SPI’s = Salmonella pathogenicity islands. Absent in E.coli SPI-1 carries genes involved in epithelial cell invasion. 40-kb, chromosomal mutants are virulent only if delivered by direct injection SPI-2 required for intracellular survival during infection even when injected, mutants are not fully virulent SPI-3 consists of 10 genes required for Mg2+ acquisition and growth in macrophages. Present in some serovars, lost from others SPI-4 carries 18 genes involved in survival within macrophages SPI-5 contains 6 genes, 4 of which are required for enteritis in a calf model

    5. Evolution of Salmonella: relatedness of subspecies

    6. Evolution of Salmonella: relatedness of subspecies

    7. Evolution of virulence in E.coli Normally a commensal in human gut occupies large intestine and lower small intestine the only gut inhabitant using oxygen and thus maintains anaerobiosis virulent and commensal strains do not cluster separately (i.e. many commensal strains have closely related pathogens) some E.coli sv are closely related to different Shigella sp

    8. Virulent E.coli strains Enterotoxigenic plasmid-borne genes for enterotoxins adhesin pili a non-invasive pathogenic E.coli Enteropathogenic. carry LEE island encoding proteins involved in attachment, a protein injection system (Type 3) EAF plasmid with genes for adherence Enterohemorrhagic LEE island carries a phage-encoded Shiga toxin virulence EHEC plasmid Enteroaggregative Enteroinvasive (include Shigella) carry pINV Unlike “typical” E.coli, Shigella can’t utilize lactose, mannitol are non-motile. Most enteroinvasive E.coli have the same deficiencies Uropathogenic

    9. EHEC O157:H7 Discovered in the 1980s Common in cattle. commensal in cattle pathogen in humans Virulence factors LEE stx (Shiga toxin) and EHEC plasmid are possibly recent acquisitions Evolution: gained O157 by recombination, then split into two lineages: sorbital-negative and b-glucuronidase negative both major lineages carry phage-encoded stx genes

    10. How related are E. coli?

    11. Evolution of Yersinia 11 species, only 3 are significant pathogens Y. pseudotuberculosis, Y. enterocolitica food-, waterborne pathogens that cause gastroenterocolitis share virulence factors not found in non-pathogenic isolates escape human immune system thanks to an outer membrane protein encoded by a 70-kB virulence plasmid carry virulence determinants (production of siderophore) on a High Pathogenicity Island (HPI) HPI is highly mobile and was found in other enterics chromosomally encoded virulence factors also present

    12. Evolution of Yersinia Y. pestis causes plague transmitted by fleas a clone of Y. pseudotuberculosis. Indistinguishable by common methods distinct from Y. pseudotuberculosis in its virulence strategy colonizes flea gut. genes on pFra plasmid are involved is transmitted to a host through a bite reverse blood flow during biting due to partial blockage of the flea’s proventriculus. Blood meal is regurgitated. hemin storage genes are found in both Y. pestis and Y. pseudotuberculosis disseminates in blood from the infection site

    13. Population genetics of enterics All bacterial populations are clonal to some extent Recombination important source of variation for enterics, recombination appears more important then mutation frequency differs for different species Neisseria -- frequent, Salmonella -- rare Through recombination clones adapt to specific niches

    14. Conclusions Many virulence determinants are carried on mobile genetic elements Pathogenicity islands, virulence plasmids are shared between clones and species Surface antigen polymorphism O antigen is the main target for immune system and phages (high selective pressure) Gene decay Genes mutate, and loss of function is OK e.g. Shigella is non-motile, can’t utilize lactose or decarboxylate lysine. Occupies a different niche (inside a eukaryotic cell) than commensal E.coli (in the gut of mammals where lactose is found). Making flagella is expensive, flagella is also an antigen

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