Enterobacterales Flashcards
Enterobacterales is
The largest collection of medically important gram - rods (ex. E. coli, Klebsiella pneumoniae, Klebsiella oxytocin, Proteus mirabilis, Salmonella serovar Typhi, Salmonella nonthyphoidal Serotypes, Shigella flexneri)
Enterobacterales are found
Soil, water, vegetation, normal intestinal flora
Main Enterobacterales caused infections
Bacteremias
UTIs
intestinal infections
Enterobacterales that are always pathogenic
E. coli
Klebsiella pneumoniae
Proteus mirabilis
Enterobacterales pathogenesis
Spread from animal reservoir (Yersinia, nontyphoidal Salmonella)
From human carrier (Shigella)
endogenously (E Coli)
Acquire virulence (E Coli)
Enterobacterales structure
Non spore forming
Gram - rods
Flagella for motility (except Klebsiella, Shigella, and Yersinia)
Pili for attachment
Common Enterobacterial antigen (polysaccharide core)
Facultative anaerobe that grow on both selective and non selective media
Enterobacterales metabolism
Simple nutritional requirements
Ferment glucose
Reduce nitrate to nitrite
catalase +
Oxidase -
LPS
Major cell wall antigen consisting of 3 components
O polysaccharide (classification of strain)
Polysaccharide core (classification as enterobacterales order)
Lipid A- responsible for endotoxin activity, important virulence factor
Epidemiological classification is based on 3 major antigens
O polysaccharide (part of LPS)
H antigen (part of flagella)
K antigen (part of capsule)
Enterobacterales that ferment lactose on MacConkeys agar
E. coli
Klebsiella
Enterobacter
Serratia
Citrobacter
Enterobacterales virulence factors
Endotoxin- Lipid A component, causes fever and shock (hypotension)
Capsule (repels hydrophobic phagocytic cell surface
Antigenic phase variation (can turn expression of O, H, and K antigens on or off to protect from antibody-mediated cell death)
Type III secretion system (Salmonella, Shigella, EPEC)-effector systems for delivering virulence factors into targeted eukaryotic cells
Antimicrobial resistance- transferable plasmids
Escherichia Coli
Commensal residen of GI trace
Most common Gram - rod associated with sepsis
Most common cause of community acquired UTI
Causes bacterial gastroenteritis
Commensal infections caused by E. coli
Bacteremia
Peritonitis
Specialized E. coli infections
UTI (uropathogenic E. coli- UPEC)
Meningitis (neonatal meningitis-associated E. coli- NMEC)
Gastroenteritis (Enterotoxigenic-ETEC, Enteropathogenic-EPEC, Enteroaggregative-EAEC, Shiga toxin producing/enterohemorrhagic EHEC, Enteroinvasive- EIEC)
Normally sterile sites
Blood
CSF
Pleural fluid
peritoneal fluid
Pericardial fluid
Bone
Synovial fluid
Internal body sites (lymph node, brain, heart, liver)
UTI
Ascending infection
Colonization in bladder mediated by pili and adhesions
Neutrophil infiltration
Biofilm formation
Epithelial damage by bacterial toxin
Ascension into kindness
Colonization of kidneys
Bacteremia
Hemolysis HlyA lyses erythrocytes leading to cytokine release and inflammation
Neonatal meningitis due to E. coli (NMEC) pathogenesis
K1 capsular antigen helps evade host
E. coli caused gastroenteritis
Transmitted by contaminated food
5 major patho types cause diarrhea
Enterotoxigenic (ETEC) acute watery diarrhea (pili, ST/LT enterotoxins)
Enteropathogenic (EPEC) infantile watery diarrhea (pili, effacement of intestinal microvilli)
Shiga toxin producing (STEC) and Enterohemorrhagic (EHEC) bloody diarrhea due to HUS, foodborne outbreaks (Stx1, Stx2)
Enteroinvasive (EIEC) foodborne outbreaks, invade and destroy colonic epithelium
ETEC
Acute, self limited watery diarrhea
Travelers and infantile diarrhea in resource limited countries
Ingestion of contaminated food or water
ETEC Pathogenesis
Colonization factors (CFA/I, CFA/II) used to attach to small bowel epithelium
Produces two enterotoxins (Heat stable-ST and Heat labile-LT) interacts with cyclase receptors leading to increased cAMP and hypersecretion into gut
ETEC treatment
supportive care
Antimicrobial for those with sever diarrhea, prolonged symptoms, or immunocompromised hosts)
EPEC
Severe diarrhea in children <2 in resource limited settings
Rapid onset watery diarrhea
From contaminated food or water
EPEC pathogenesis
Virulence genes called locus of enterocyte effacement (LEE)
Forms attaching and effacing (A/E) lesions
EAEC
Acute and chronic watery diarrhea in both resource limited and rich areas
Spread by contaminated food and water
EAEC pathogenesis
autoagglutination in “stacked-brick” arrangement in epithelium of small intestine leading to epithelial barrier dysfunction