Enteric Bacteria I & II

Question 1

Relationship between genetics and pathogenesis of bacteria

Answer 1

• 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

Question 2

Relationship between morphology and pathogenesis of bacteria

Answer 2

• 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

Question 3

Relationship between metabolism and pathogenesis of bacteria

Answer 3

• 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

Question 4

Diagnostic value of major antigenic structures of enteric bacteria

Answer 4

• 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

Question 5

Non-invasive enteropathogenic bacteria

Answer 5

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

Question 6

Pathogenicity of Vibrio cholerae

Answer 6

• 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

Question 10

Pathogenicity of ETEC

Answer 10

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

Question 11

Pathogenicity of EPEC

Answer 11

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

Question 12

Pathogenicity of EHEC

Answer 12

• 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

Question 13

Pathogenicity of invasive enteropathogenic bacteria

Answer 13

• 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

Question 15

Pathogenicity of Campylobacter

Answer 15

• 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

Question 17

Pathogenicity of H. pylori

Answer 17

• 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

Question 19

Pathogenicity of EIEC

Answer 19

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

Question 20

Pathogenicity and stomach acidity + bacterial virulence factors

Answer 20

• 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

Question 21

Virulence factors and host cell targets of enterotoxigenic bacteria

Answer 21

• 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

Question 22

Mechanisms by which type III secretion systems contribute to pathogenesis

Answer 22

• 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

Question 23

Classification of enteric bacteria by environment/host range distribution

Answer 23

• 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