E. coli Overview (Ditki Notes)

• E. coli are common members of the colon microbiome and reside in the intestines of animals and humans, classifying them as "enteric" bacteria.
• E. coli can cause endogenous infections upon transfer to new anatomical niches and exogenous infections through ingestion of pathogenic strains found in soil and water due to fecal contamination.
• E. coli utilize pili for adhesion and biofilm formation, flagellar motility for movement, grow rapidly, and have simple nutritional needs.
• E. coli are facultative anaerobes, catalase-positive, oxidase-negative, reduce nitrate, and ferment glucose and lactose, classifying them as coliforms that are Gram-negative enteric lactose fermenters.
• Selective media like Eosin methylene blue agar and MacConkey's agar inhibit Gram-positive bacterial growth and indicate acid production from lactose fermentation, used to identify coliforms.
• EMB agar indicates lactose fermentation and strong acid production through a greenish hue, while MacConkey's agar indicates E. coli lactose fermentation via a pinkish-purple color.
• Virulence factors in E. coli are acquired via horizontal gene transfer of plasmids, bacteriophages, and pathogenicity islands.
• E. coli endotoxin, a heat-stable lipopolysaccharide, triggers inflammatory responses, disseminated intravascular coagulation, and hypovolemic shock via its A-antigen.
• The core polysaccharide of E. coli endotoxin is common to all Enterobacteriaceae, while the O-antigen classifies E. coli serotypes.
• Exotoxins in E. coli promote cell death or fluid loss, and adhesins are present on pili, fimbriae, or strain-specific surface antigens.
• Type III secretion systems in E. coli inject virulence effector proteins into host cells, promoting attachment, invasion, and cell destruction.
• Phase variation alters the expression of O, K, and flagellar H antigens and pili in E. coli, allowing immune evasion and energy expenditure adjustment.
• Antibiotic resistance in E. coli is rapidly spread via HGT, making treatments difficult, while siderophores acquire iron for bacterial growth, and polysaccharide capsules repel phagocytes to avoid serum killing.
• Extraintestinal pathogenic E. coli (ExPEC) are commensals that act as opportunistic pathogens in new anatomical sites.

Urinary Tract Infections

• Uropathic E. coli (UPEC) causes most urinary tract infections through Type 1 and P pili and Dr fimbriae attaching to urothelium
• Hemolysin A in UPEC causes cell damage, facilitating bacterial movement, while strains lacking these virulence factors are easily removed in urine.

Neonatal Meningitis

• E. coli is the second most common cause of bacterial neonatal meningitis
• Neonatal Meningitis-causing E. coli (NMEC) have special virulence factors enabling translocation across the blood-brain barrier, including Type I pili and Outer Membrane Protein A (OmpA) attaching to brain microvascular endothelial cells.
• Ibe proteins, CNF1, and other mediators facilitate NMEC invasion of the blood-brain barrier, while K1 capsular antigens are thought to prevent lysosome fusion, allowing live bacteria to move across the barrier.

Septicemia

• Septicemia occurs when urinary or gastrointestinal tract infections spread to the blood, potentially occurring due to abdominal trauma.

Gastroenteritis

• Intestinal Pathogenic E. coli (IPEC) infection follows ingestion of contaminated food or water potentially from human or animal feces.
• The pathotypes can affect the small and/or large intestine; Enteropathogenic and Enterotoxigenic E. coli for the small intestine, Enteroaggregative E. coli for both, and Enteroinvasive E. coli for the large intestine.
• Shiga toxin-producing E. coli virulence factors affect each pathotype determine the pathogenesis of infection.