Enteric Bacteria I & II Flashcards Preview

Infectious Disease: Unit 1 > Enteric Bacteria I & II > Flashcards

Flashcards in Enteric Bacteria I & II Deck (17)
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1
Q

Relationship between genetics and pathogenesis of bacteria

A
  • Plasmids:
    • Encode antibiotic resistance, pili to help with attachment, enterotoxins to mediate fluid changes
  • Bacteriophage conversion:
    • Bacteriophage infecting bacteria & transfer genes coding for toxins (Shiga, cholera)
  • Chromosomal pathogenicity islands:
    • Large segments of foreign DNA incorporated into bacterial genome that aid in its survival
2
Q

Relationship between morphology and pathogenesis of bacteria

A
  • Pili help with adhesion to epithelial cells
  • Some bacteria have flagellum and motility –> thus H antigens
    • Motile: Salmonella, Vibrio, Yersinia, H. pylori
      • Y. enterolitica temperature-based motility threshold
    • Non-motile: Shigella
3
Q

Relationship between metabolism and pathogenesis of bacteria

A
  • Lactose-fermenting: E. coli, Yersinia
  • Non-lactose fermenting: Shigella, Salmonella, Vibrio cholerae
  • H2S producing: Salmonella
  • Non-H2S producing: Shigella
  • Oxidase (+): Vibrio cholerae, Campylobacter jejuni
  • Oxidase (-): Shigella, Salmonella
4
Q

Diagnostic value of major antigenic structures of enteric bacteria

A
  • Antigenic structures help you figure out which bacteria it is!
  • Most have a combination of the following:
    • LPS parts
      • Lipid A
      • Core polysaccharides
      • O antigens: variable within a genus, help identify species
    • “H” antigens –> flagellum
    • “K” antigens –> capsule; associated with increased virulence
5
Q

Non-invasive enteropathogenic bacteria

A
  • Vibrio cholerae
  • ETEC
    • Enterotoxic E. coli
  • EPEC
    • Enteropathogenic E. coli
  • EHEC
    • Enterohemorrhagic E. coli
6
Q

Pathogenicity of Vibrio cholerae

A
  • Non-invasive enteropathogenic bacteria
  • Toxin co-regulated pilus (TCP)
  • Prototype A-B type toxin
    • B subunit binds GM1 subunit on intestinal endothelial cells allowing A to enter
    • A invades –> increased ACh –> increased cAMP –> increased Cl- and Na+ secretion
      • blocks absorption
      • results in net secretion of fluid into gut
10
Q

Pathogenicity of ETEC

A
  • Non-invasive enteropathogenic bacteria
  • Heat-labile enterotoxin
    • Same as cholera
  • Heat-stable toxin
    • Increased cGMP –> increased fluid secretion
11
Q

Pathogenicity of EPEC

A
  • Non-invasive enteropathogenic bacteria
  • Type III secretion system which secretes translocated intimin receptor
    • Causes microvilli destruction pedestal formation
    • Thus term “attaching and effacing” (AE)
12
Q

Pathogenicity of EHEC

A
  • Non-invasive enteropathogenic bacteria
  • AE
  • Shiga-like cytotoxins –> StxI or StxII have same MOA as actual Shiga toxins, similar to V. cholerae
    • B units bind Gb3 sphingolipids of enterocytes and renal endothelial
    • A unit enters subsequently and binds 60S ribosome, destroying cells
    • Can result in HUS
13
Q

Pathogenicity of invasive enteropathogenic bacteria

A
  • Largely target M cells of intestine
    • M = membranous
    • No glycocalyx and very small distance to travel to get to lumen = ideal invasion target
  • Shigella –> same A-B toxins as EHEC
  • Salmonella –> 2 pathogenicity islands
    • One helps with invasion
    • The other helps with macrophage immunity
  • Yersinia
  • Campylobacter
  • Helicobacter pylori
  • EIEC
    • Enteroinvasive E. coli
15
Q

Pathogenicity of Campylobacter

A
  • Invasive enteropathogenic bacteria
  • Flagellum used as corkscrew to enter mucosal intestinal cells
  • LT enterotoxin
  • Cytotoxin
  • Motility, H antigen, chemotaxis all important for colonization of gut, inflammatory response
17
Q

Pathogenicity of H. pylori

A
  • Invasive enteropathogenic bacteria
  • Kag pathogenicity island codes for Type IV delivery system
  • Highly motile to reach epithelium
  • Urease activity makes surroundings more basic
  • Molecular mimicry
19
Q

Pathogenicity of EIEC

A
  • Produces shiga-like toxin
  • Microbe invades intestinal mucosa and toxin causes necrosis and inflammaton
  • Causes dysentery
20
Q

Pathogenicity and stomach acidity + bacterial virulence factors

A
  • More sensitive to acid –> increased infective dose needed to cause disease
    • More likely to be transmitted by food/water
  • Low infective dose more likely to transmit person to person
  • Virulence factors increase pathogenicity
21
Q

Virulence factors and host cell targets of enterotoxigenic bacteria

A
  • A-B toxin
  • Heat-labile and heat-stable toxin
  • Type III systems –> attach and efface (AE) epithelial cells
  • Shiga-like cytotoxins
  • Shiga toxin –> 60S ribosomal subunit leading to epithelial cell death
  • Vacuolating cytotoxin
  • Urease
22
Q

Mechanisms by which type III secretion systems contribute to pathogenesis

A
  • Secretes translocated intimin receptor
  • Initiates characteristic “attaching and effacing” (AE) lesion
    • Microvilli destruction, pedestal formation
  • Probably interferes with absorption leading to diarrhea
  • Found in Shigella and EPEC
23
Q

Classification of enteric bacteria by environment/host range distribution

A
  • All enterics (except Salmonella and Shigella) - normal host flora in GI tract
  • Become pathogenic when they acquire virulence factors
  • Fecal-oral transmission
  • Exceptions:
    • Zoonotic: Salmonella enteritidus, Campylobacter, Yersinia
    • EHEC: often caused by beef, suggests cattle could be a source