LECTURE - Extraintestinal E. coli Flashcards
Most common cause of community-acquired UTIs
E. coli
- mainly in females <10 y/o and from 20-40 y/o
Two step process of E. coli UTIs
from colon to perineum and vagina then to urethra
- could invade and hide in bladder cells
- always ascending infections
- genetic factors contribute to recurrent infections
- colon could be a reservoir
E. coli is also a cause of hospital-acquired UTIs
- urinary catheters
- fecal incontinence
- urinary tract abnormalities (kidney stones, enlarged prostate or other obstruction) ex: having a baby
from urethra to bladder UTI (ascending)
cystitis
from bladder to kidney UTI ascending
pyelonephritis (then maybe to bloodstrem)
how do UPEC colonize the colon?
- lactobacilli inhibit UPEC colonization of the vagina; spermicides can kill lactobacilli
- attachment by type I pili and by P pili
type I pili
bind mannose residues on host glycoproteins (eg. in the bladder)
P pili
bind to globobiose (alpha-D-Gal(1,4)- alpha-D-gal) attached to ceramide in KIDNEY cell membranes
What follows attachment ?
invasion of superficial bladder epithelial ‘facet’ cells that are coated with uroplakin protein arrays
Virulence factors of meningitis and disseminated E. coli
- K1 capsule
- S fimbriae bind cellular fibronectin (NOT plasma fibronectin)
- OmpA porin) may facilitate invasion of endothelial cells
- LPS contributes to inflammation and septic shock
- CNF-1 (cytotoxic necrotizing factor 1) can activate Rho GTPase, deregulating cell function
NDM-1
- New Delhi metallo-beta-lactamase
- enzyme produced by certain bacteria = resistant to most beta-lactam antibiotics
- cleaves carbapenem = power beta-lactam antibiotic used for organisms resistant to other antibiotics
Risk factors for aspiration pneumonia with E. coli
doesn’t need an extra pathogenic E. coli; just any
- decreased level of consciousness
- problems with swallowing
- alcoholism
- tube feeding
- poor oral health
UTI pathogenic cascade
- UPEC bind to and invade superficial bladder epithelial cells
- early stages = 3 microm - community doubles in size every thirty mins
- transition to the middle intracellular bacterial-community stage is hallmarked by a decrease in the average bacterial length to 1 microm and a doubling time of 45 mins
- late stages = bacteria return to the typical rod shape; filamentous and late-stage rod-shaped bacteria detach from the community, escape from epithelial cells and either attach to naive epithelial cells or exit host during micturition
- filamentous UPEC are induced intracellularly in the urothelial cells capable of recognizing bacterial LPS
other virulence factors of UPEC
- flagella; motility; can change from peritrichous to polar
- toxins
- LPS contributes to inflammation (synergistically with pili?)
- alpha hemolysin (RTX pore-forming toxin family)
- CNF-1 kills epithelial cells
- iron-acquisition systems = enterobactin, aerobactin, and yersiniabactin, all siderophore binders
- O antigen of LPS O1, O4, O6, and O18
- growth rate in urine
UPEC Pai
- possess auxiliary virulence genes (pap, hly, iron uptake)
- four main types in UPEC - vary in size and can be > one type of strain; inserted in the chromosome of the organisms and there can be more than one type in a strain; they don’t all have all these different pathogenicity islands, but they can have multiple types and each of which encoding either different things or similar things that contribute to the establishment of the organism in the urinary tract and disease production
- have different %G+C content
- possess bacteriophage-like sites (mobilizable)
