Week 2

• Enterobacterales general features

  • gram-negative rods
  • Straight, cylindrical, rounded ends
  • Non-sporulating
  • Facultative anaerobes
  • Nitrate to nitrite
  • Motile and non-motile
  • Oxidase
  • Lack cytochrome C oxidase
• Coliforms


  Enterobacteriaceae that ferment lactose
• coliforms used as enteric contamination markers

  • Grow at 42C
  • E. coli is ideal contamination indicator
• Coliforms


  • Escherichia coli
  • Klebsiella spp.
  • Enterobacter spp.
  • Citrobacter spp.
• Pathogenicity


  • Opportunistic- Klebsiella & Proteus spp.
  • pathogenic - E. coli, Salmonella, Yersenia
• Escherichia coli


  Present in the intestine of most animals species
• Virulence factors of E. coli

  • Endotoxin (lipid A)
  • Fimbriae - attachment
  • Enterotoxins (Heat LT, ST, EAST1)
  • Shiga-like toxin, hemolysins
  • Capsule, flagella, siderophores
• Serotyping of E. coli


  • Capsule - K antigen
  • Somatic - O antigen
  • Flagella - H antigen
  • Fimbriae - F antigen
• Diarrheagenic/intestinal E. coli


  • Enterotoxigenic E. coli (ETEC)
  • Enteropathogenic E. coli (EPEC)
  • Enterohemorrhagic E. coli (STEC/VTEC)
• ETEC important pathogens of calves, piglets, & lambs
• Key virulence factors of ETEC

  • Enterotoxins (Heat stable toxin a (STa) - piglets & calves, Heat-stable toxin b (STb) - piglets, Heat labile toxin (LT) - piglets, Enteroaggergative heat-stable enterotoxin 1 (EAST1))
  • Adhesins
• Pathogenesis of ETEC


  1. Adherence step

  2. Presence/absence of fimbriae genes

  3. Expression of fimbriae receptors in intestinal lining

  4. Age dependent (lower expression, over-expression)
• Clinical signs of ETEC

  • Severe watery diarrhea (non-bloody)
  • Dehydration, listlessness, metabolic acidosis, and death
  • Noninflammatory secretory diarrhea
• Age of onset of ETEC

  • Up to 6th week in piglets
  • 1st week in calves
  • Up to first 10 days of life in lambs
• ETEC in piglets- neonatal diarrhea (colibacillosis)


  • newborn to weaning
  • F5, F6, F41, F4
  • Altered equilibrium between maternal immunity and infection pressure (lowering of maternal immunity, increased infectious pressure)
  • High mortality (90-100%)
  • Hemorrhagic infarction of intestines and greater curvature of the stomach
• ETEC in piglets - Post-weaning diarrhea (PWD)

  • F4(a few days after weaning)
  • F18 (2-6 weeks after weaning)
  • Change in intestinal environment in piglets (Alteration of composition of indigenous flora)
  • Yellowish or gray fluid feces, not as watery as neonatal diarrhea, very smelly
• ETEC in bovines- neonatal diarrhea

  • F5, F41
  • STa, EAST1
  • First few days after birth
  • Foul-smelling, pasty to watery feces, pale yellow-white, flecks of blood (occasionally)
• ETEC in dogs


  Associated with cases of diarrhea in young animals
• Treatment


  • Hydration
  • Oral electrolytes
  • Antimicrobial therapy = controversial
  • Prevention
  • Vaccination
  • Separation of sick animals
  • Antibodies (Anti-adhesins, Anti-lipid A)
• ETEc in bovines - neonatal diarrhea & septicemia

  • F17
  • 50% resistant to complement and produce aerobactin
  • 4-21 day old calves
• EPEC


  Enteropathogenic E. coli
• Hostsof EPEC


  • Piglets
  • Lambs
  • Calves
  • Rabbits
  • Pups
• EPEC pathogenesis

  1. Contact gut epithelial cells

  2. Express T3SS and translocate receptor (Tir) and adhesin (intimin)

  3. Cascade of intracellular reactions in host cells to form pedestal under E. coli

  4. Effacement of microvilli

  5. Effectors affect Ca2+ and Cl- concentration, tight junctions, and recruitment of neutrophils
• EPEC in Piglets- Post weaning diarrhea

  • Colonization of small and large intestines
• EPEC in calves

  • Not common
  • 1-8 weeks old
  • Mucoid diarrhea +/- blood
  • Mainly in large intestine
• EPEC in rabbits

  • Only important class of pathogenic E. coli
  • High mortality
  • Principal infectious agent in diarrhea
  • Suckling rabbits - lesions along length of small and large intestine
  • Weaning rabbits - mostly in cecum
• EPEC in pups

  • Not clear association as primary etiological agent of diarrhea
  • Typical lesions in small intestine support association
• Treatmentof EPEC

  1. Hydration

  2. Oral electrolytes

  3. Antimicrobial therapy = controversial
• EPEC Prevention

  1. Vaccination

  2. Separation of sick animals

  3. Antibodies (Anti-lipid A)
• STEC/VTEC


  Enterohemorrhagic E. coli
• Shiga toxin


  • Inhibit protein synthesis following 60s ribosomal subunit interaction
  • Result in cell death
• Edema disease in pigs

  Only animal disease where role of shiga toxin is clear
• Stx2e


  • Produced in intestine
  • Absorbed and carried via bloodstream to target cells
  • Endothelial cells of small arteries
  • Present normally in large intestine of pigs
  • Appear around 5-14 days after weaning
  • F18 receptor
• STEC Clinical signs

  • Sudden death
  • Edema in head and internal organs
  • Neurological signs
  • Anorexia
  • Diarrhea -rare
• STEC Therapy

  1. Fasting

  2. Antimicrobial therapy parenterally

  3. Antimicrobial therapy and acidifiers orally
• STEC Prevention

  1. Reduce stress

  2. Vaccination

  3. Selection of F18- animals

  4. Feed composition
• Cattle


  Reservoirs for STEC/VTEC
• STEC zoonotic importance

  In humans - hemolytic uremic syndrome
• Shiga toxinin humans 


  • Blocks ribosomal peptide elongation
  • Disrupts protein synthesis
  • Cell death
  • Intestinal damage permits Shiga toxin to enter circulation
  • May reach multiple tissues including organs
• Hemolytic uremic syndrome


  • Defined by triad: Acute renal failure, Thrombocytopenia, Microangiopathic hemolytic anemia