Escherichia Flashcards
E. coli
Gram negative rods, facultative anaerobes, catalase +, lactose +, indole + (from breakdown of tryptophan to indole), flagellated, some have capsules, glucose fermenters, grow on MacConkey, some strains are hemolytic, commensals of GIT (pathogenic strains are not), enteric dz, septicemic dz, non-enteric localized dz (cystitis, pyometra, metritis, mastitis).
What are some predisposing factors that permit pathogenic E. coli to cause disease?
Age, immune status, nature of diet, heavy exposure to pathogenic strains, normal flora not fully established, receptors for ETEC adhesins are present only during the first week of life in calves, stress (cold temps, mixing of animals).
E. coli diagnosis
Clinical signs, age, and species suggests category of disease. Fecal samples, tissue samples (in septicemic cases), mastitic milk, urine, cervical swabs. Blood agar - characteristic smell. MacConkey agar - pink colonies. API tests. Identify virulencce factors: serological (antibodies against virulence factors), molecular (DNA probes, PCR).
E. coli pathotypes
ETEC - enterotoxigenic ETEC - enteropathogenic VTEC/STEC - verotoxigenic/Shiga-like toxin producing EHEC - enterohemorrhagic ExPEC - extra-intestinal pathogenic
What are the factors causing dz in ETEC (enterotoxigenic E. coli)? What is the pathogenesis of this disease?
Enterotoxigenic (ETEC) - enterotoxins LT and ST. These are heat Labile and heat Stable toxins. Particular fimbriae. Toxin introduce into enterocyte, but E. coli stays outside cell. Genes for LT and ST on plasmids. Non-inflammatory, watery diarrhea via disruption of electrolyte balance. Young animals.
How is E.coli (ETEC) different from Salmonella in the way they cause diarrhea?
E. coli (ETEC) - extracellular, non-inflammatory, no damage to villi Salmonella - intracellular, inflammatory, causes damage to villi
How do LT (heat labile) and ST (heat stable) enterotoxins cause diarrhea?
Increase cAMP (LT) or cGMP (ST), which leads to disturbances in electrolyte transport and therefore water absorption = water balance changes from net absorption to net secretion. Genes for these are carried on plasmids.
What are the factors causing dz in EPEC (enteropathogenic E. coli)? What is the pathogenesis of this disease?
Enteropathogenic (EPEC) - pathogenecity island LEE, intimin adhesion molecule, particular fimbriae, Type III injection system. Diarrhea in young. Attachment to enterocyte via adhesin molecule intimin and formation of an “actin Pedestal”, then injection of toxins (little known about the toxins). This leads to destruction of microvilli, atrophy and shedding of enterocyte, and loss of absorbative surface. Type III injection system forms a hollow-like tube structure to which effector proteins are “injected” into host target cells. Genes are also located on LEE. Genes for Intimin are located on LEE. Another secreted protein is inserted onto enterocytes, to which Intimin attaches.
What are the factors causing dz in VTEC/STEC (verotoxigenic/shiga-like toxin producing E. coli)? What is the pathogenesis of this disease?
Verotoxigenic (VTEC) - verotoxins VT!, VT2 Shiga-like toxin producing (STEC) - shiga-like toxins SLT’s. Causes inflammation (unlike ETEC and EPEC). Hemorrhagic colitis (bloody diarrhea), edema, hemorrhage, thrombosis. VT’s/SLT’s damage vasculature of intestines and other tissues as well as enterocytes. They inhibit protein synthesis which kill the cells. Main targets of the toxins are endothelial cells of blood vessels.
What are the factors causing dz in EHEC (enterohemorrhagiic E. coli)? What is the pathogenesis of this disease?
Enterohemorrhagic (EHEC) - as EPEC +VT’s or SLT’s. Believed to be the result of EPEC conjugating with a bacteriophage carrying the SLT/VT. These are VTEC/STEC’s but they cause dz in HUMANS. Carriers (mainly intestines of cattle) don’t become sick = infects meat, other foods, milk. Causes inflammation (unlike ETEC and EPEC). Mediated by VT’s or SLT’s. HUS - hemolytic-uremic syndrome, which results from hemolyic anemia, thrombocytopenia, kideney failure, and uremia. Also as in VTEC/STEC - hemorrhagic colitis, edema, thrombosis.
What are the factors causing dz in ExPEC (extra-intestinal pathogenic E. coli)? What is the pathogenesis of this disease?
Extra-intestinal pathogenic (ExPEC) - hemolysin, cytotoxic necrotizing factor 1 (CNF-1), iron-uptake systems, capsules, particular fimbrae. Mastitis, septicemia, UTI, pyometra(dogs, cats).
What are the two types of siderophores that may be present in E. coli? Which one is important for disease?
Enterochelin and Aerobactin. Enterochelin is bound by albumin which inactivates it, and it stimulates the production of anti-enterochelin antibodies. Aerobactin has a greater affinity for iron than enterochelin at a lower pH.
Why might antibiotics make EHEC dz worse?
The cause of disease in EHEC are the toxins, which are released if the bacteria are killed via antibiotics. The toxins are released into the lumen of the GIT and subsequently absorbed.
