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
STEC
EHEC is a subset
Large herbivores are reservoir (passed through feces)
Associated with undercooked meat, petting zoo, contaminated produce, raw milk
Low infectious (<100 viable) dose to cause disease
Causes watery then bloody diarrhea
Complication: hemolytic uremic syndrome (toxin mediated, acute kidney failure, thrombocytopenia, microangiopathic hemolytic anemia)
STEC pathogenesis
biofilm formation
Survival at low pH
Attachment using locus of enterocyte effacement (LEE)
Type III secretion system
Intimidating receptor inoculated into host by T3SS
Intimidating on bacterial cell promotes attachment leading to the attaching and effacing histopathology
Shiga toxin 1 (Stx1) and Shiga toxin 2 (Stx2- more potent and more often causes disease)
_ is the critical first step in the pathogenesis of most bacterial infections
Adherence to the host mucosa
STEC treatment
No antimicrobials just support
Antimicrobials increase toxin release which increases risk of HUS
EIEC
Watery diarrhea
Foodborne outbreaks
Pathogenesis similar to Shigella
Plasmid mediated invasion
E Terence into phagocytes
Epithelial cell destruction leading to colonic ulceration
E. coli infection diagnosis
Bacterial culture
PCR recommended (molecular PCR testing)
Due to high sensitivity and ability to differentiate between pathogenic and non pathogenic
Limitations: does distinguish between viable and non viable organism/nucleic acid
Klebsiella species are
Aerobic lactose fermenters
Proteus are
Aerobic lactose non-fermenters
Lower urinary tract infections include
Urethritis
Cystitis
Prostatitis
Upper urinary tract infections include
Pyelonephritis
Perinephrinc abscess
Two mechanisms of UTI pathogenesis
Ascending (most common)
Hematogenous (unusual)
Ascending UTI
Colonization of periurethral area
Urethral colonization migration to the bladder
Bladder entry
Infection with possible ascension
Hematogenous UTI
S aureus
Mycobacterium tuberculosis
Risk factors for uncomplicated UTI
Females
Older age
Younger age
Risk factors for complicated UTI
Indwelling catheters
Immunosuppression
Urinary tract abnormalities
Antibiotic exposure
Top bacteria that cause UTIs
UPEC (uropathogenic E. coli)
K pneumoniae
P mirabilis
Klebsiella pneumoniae
lactose fermenting
Non-motile
Gram - rod
Causes Nosocomial pneumonia, UTI, bacteremia, wound infection, pyogenic liver abscess)
Klebsiella pneumoniae pathogenesis/virulence factors
Capsular serotypes
Hypermucoviscosity phenotype
LPS
Sideophores (allow bacteria to enhance iron uptake)
Pili
Antimicrobial resistance
Klebsiella pneumoniae Capsular serotypes
K1 and K2 most virulent
Polysaccharide matrix coats the cell
Thick mucoid colonies on blood agar (sting test)
Hyoermucoviscosity causes more invasive disease
Dark red currant jelly sputum
Klebsiella pneumoniae resistance genes
encoded on plasmids
CTX-M
KPC
NDM-1
SHV
TEM
OXA-48
resistance to most extended spectrum beta lactamases
Proteus mirabilis causes
UTI
Proteus mirabilis virulence factors
Urease production
Flagella
Swarm cell differentiation
Bacterial adhesion using 4 types of flagella
Hemolysis and IgA protease
Iron aquisition using siderophores
Proteus mirabilis urease production
Hydrolyzes urea into ammonia and carbon dioxide
Ammonia used as a nitrogen source for bacteria
Increase in pH in the bladder leading to precipitation of phosphate carbonate and magnesium which forms Struvite stones 
Proteus mirabilis swarm cell differentiation
Differentiate into elongated highly flagellated cells
Move over solid surfaces inform concentric rings on growth media
Lactose fermenting bacteria are _ on _ agar
Pink
MacConkeys
Salmonella
Bacilli
Aerobic
Lactose non-fermenter
Oxidase -
Salmonella infection requires
A large infectious dose
Typhoid fever
Caused by Salmonella typhi and paratyphi (human serotypes)
Transmitted though human feces
Carrier state within gallbladder colonization
Nontyphoidal salmonella
transmitted though animal feces
Poultry, eggs, dairy products, and food prepared on contaminated surfaces
Salmonella pathogenesis
Attached to an in bed M cells in Pyers patches
Replicate an Endo psychotic vacuoles
Transported across the cytoplasm and released into blood or lymphatic circulation (disseminate hematogenously) 
S. typhi has the _ antigen
VI
Typhoid fever
5-21 day incubation
Abdominal pain, fever, chills, bradycardia
Rose spots
abnormal bowel movements ranging from constipation to bloody diarrhea
Non-typhoidal salmonella
Incubation period 8-72 hours
Diarrhea, nausea, vomiting, fever, abdominal cramping
Bacteremia: endovascular infections, HIV
Osteomyelitis: sickle cell disease
Shigella
Non-motile
Non-encapsulated
Gram -
Rod
47 serotypes grouped into 4 groups (S. Dysenteriae, S. Flexneri, S. Boydii, S. Sonnei)
Shigella pathogenesis
Attached to/transport across the epithelial layer
Engulfed into macrophages where shigella induces apoptosis
Multiply in cytoplasm
Tissue destruction, impaired absorption of water and nutrients, blood and mucus in stool
Shigella toxins
Shiga toxin (Stx) produced by S. Dysenteriae is only major toxin
Shigella epidemiology
Humans and large primates are the only natural reservoir
Outbreaks in daycare centers and men who have sex with men
High communicable with low infectious dose (100 viable cells)
Withstand low pH (acid-stable)
Watery diarrhea to severe dysentery
Diagnosis of Enterobacterales infections
Molecular detection is sample
Cultures
Stool culture on Hektoen enteric agar (Shigella-green, Salmonella-black)
Other enterobacterales are rare in immunocompetent individuals
