Enterobacteriaceae Flashcards
Enterobacteriaceae
- 40 genera, 180 species
- Normal inhabitants of the GI tract
- What do they have in common:
- -Gram-negative rods
- -Facultative anaerobes
- -Oxidase negative
- -Motile (most)
- -Non-spore forming
Coliforms
- Indicative of fecal contamination of water
- Water safety tests screen for coliforms
Features in culture
- Lactose fermentation (MacConkey agar)
- -Selective ingredient: bile salts
- -Differential ingredient: lactose
- –Lactose fermenter = pink
- –Non-lactose fermenter = tan
- Swarming motility
- -Proteus sp.
- Mucoid colonies - due to capsule production
- -Klebsiella and Enterobacter
- Red pigment
- -Serratia marcesens
- H2S production
- -Salmonella sp. on XLT4
E. coli
- First isolated in 1885 by Theodor Escherich (German-Austrian pediatrician and professor)
- Origin name: Bacteria coli
- Name changed to E. coli in 1919
- Most E. coli are commensal
- Can cause a variety of clinical presentations:
- -Gastroenteritis
- -UTIs
- -Septicemia
- -Pneumonia
- -Mastitis
- -Hemolytic uremic syndrome (human)
Serotyping
-Test the isolate against antisera directed toward a specific antigen:
–O = somatic antigen on cell wall surface (LPS)
–H = flagellar protein
–F = fimbrial protein (originally thought to be capsular)
–K = capsular polysaccharide
(Each letter codes for a different part of the antigen)
-E. coli O157:H7 (human)
-E. coli F5 (calf ETEC) (also known as K99)
-E. coli F4 (swine ETEC) (also known as K88)
E. coli - ETEC
Enterotoxigenic
- Colibacillosis - diarrhea of newborn farm animals (calves piglets, lambs)
- -Bovine: <3 days
- –Top differentials for neonatal calf diarrhea:
- —ETEC, rotavirus, coronavirus, and Cryptosporidium spp.
- -Swine: 8-12 weeks
- –Top differentials for neonatal piglet diarrhea:
- —ETEC, TGE virus, Isospora spp., rotavirus, adenovirus, C. perfringens type C, Clostridium difficile
- Clinical presentation: acute, profuse diarrhea
- Control: supportive care, management (vaccination; clean up environment)
- Attachment/entry: fimbriae (F4/K88 in the piglet and F5/K99 in the calf) attach to specific receptors on villous epithelial cells that are only present in neonates; does not invade intestinal epithelial cells (vaccines target the fimbriae)
- Evasion of host defenses: capsule production, survive the acidic pH of the abomasum
- Multiplication/spread: multiplication and formation of microcolonies that cover the surface of the villi, spread proximally
- Damage: produce toxins in SI (heat stable and heat labile) –> disrupt cell homeostasis –> increase in net secretion of fluid and electrolytes (secretion of Cl, inhibition of Na and Cl absorption)–> secretory diarrhea –> dehydration and death
- Transmission: fecal-oral route
E. coli - EPEC
Enteropathogenic (attaching and effacing)
- Human disease
- Rare diarrhea in calves and dogs
- Attachment/entry: attach via Translocated intimin receptor (Tir) interaction –> extensive cellular actin rearrangements in host cell –> pedestal formation
- Evasion of host defenses: capsule production
- Multiplication/spread: colonize the small intestine, disrupt cell-cell junctions via T3SS effectors –> enhance bacterial dissemination
- Damage: pedestal formation –> disappearance of microvilli (enterocyte effacement) –> malabsorptive diarrhea
- Transmission: fecal-oral route
- Process:
1. Initial adhesion
2. T3SS inject Tir
3. Intimate contact via Tir-intimin interaction
4. Cytoskeletal rearrangement and pedestal formation
E. coli - EHEC
Enterohemorrhagic
- Human disease
- -Diarrhea and hemorrhagic colitis
- -Highly fatal hemolytic uremic syndrome (HUS) in children
- Rare hemorrhagic enteritis in calves, usually asymptomatic carriers (not important cause)
- Cattle are an important reservoir of O157:H7
- First recognized as a pathogen in 1982 after two human illness outbreaks
- “Hamburger disease” (cook your hamburger thoroughly)
- Diarrhea:
- -Secretory and malabsorptive (leading to bad dehydration)
E. coli - STEC
Shigatoxigenic
- Edema disease in pigs
- Occurs in rapidly growing weaner pigs (4-12 weeks) following change in diet
- Clinical signs:
- -Sudden death, incoordination, falling, edema of eyelids and face, death within 6-36 hours of clinical signs
- -+/- diarrhea
- Attachment/entry: attach via F18 adherence factor, F18 receptors are present in the intestine of pigs <12 weeks
- Evasion of host defenses: capsule
- Multiplication/spread: nutritional factors and GI stasis –> proliferation in small intestine
- Damage: toxin production (Stx2e) –> absorption of toxin –> carried by bloodstream to target cells (endothelial cells of small arteries) –> damage to vascular endothelium (via Stx2e receptor) –> edema
- Transmission: fecal-oral route
- Colostrum with Stx2e antibodies prevents endothelial and vascular damage
Coliform mastitis
- Opportunists: E. coli, Klebsiella spp. Enterobacter aerogenes
- -Proteus spp. can also cause mastitis, but it is not a coliform
- Transmission: fecal contamination of the environment, contaminated sawdust and shavings bedding, rainfall and high-humidity increase risk of contamination
- Attachment/entry: E. coli binds fibronectin –> adherence to ductular epithelium
- Evasion of host defenses: capsule
- Multiplication/spread: E. coli proliferates in large numbers in the mammary gland
- Damage: upon death or excessive production of cell wall during rapid replication, endotoxin is released –> causes change in vascular permeability –> edema and acute swelling of the gland
E. coli - small animal UTIs
- Top differentials for UTI:
- -Canine: E. coli, Staph, Proteus, Klebsiella, Enterococcus, Corynebacterium, Mycoplasma, and Pseudomonas
- -Feline: E. coli, Streptococcus, Staph, Enterococcus, Klebsiella, Pasteruella, Enterobacter
- Attachment/entry: ascending infection, attach via fimbrial adhesins
- Evasion of host defenses: capsule
- Multiplication/spread: E. coli can invade and form microcolonies within the uroepithelial cells
- Complications: Pyelonephritis, strains that cause pyelonephritis have greater ability to adhere to cells (via fimbriae), flagella facilitates ascent from bladder to kidney, E. coli and Proteus spp. are often implicated in pyelonephritis
E. coli - equine metritis
- Culture report comments: Uterine culture results should be interpreted in light of cytological or histological examination. The following organisms are considered to be equine uterine pathogens: Beta-Streptococci, E. coli, Klebsiella, Pseudomonas, and S. aureus
- Opportunistic, ascending infections
- Adhesins and flagella play a role in pathogenicity
E. coli - septicemia
- Attachment/entry: adherence to intestinal lining (fimbriae), Type IV pilus is important for adherence and invasion
- Evasion of host defenses: capsule, iron uptake systems (siderophores) (host tries to scavenge iron)
- Multiplication/spread: via bloodstream
- Damage: immune response to endotoxin (LPS) –> fever, weakness, depression, tachycardia
- Transmission: typically a complication of fecal-oral acquired infection (exceptions: surgical or catheter), may not transmit from septicemic host
Salmonella spp.
- History
- -Isolated in 1885
- -Dr. Daniel Elmer Salmon
- Potential pathogens
- Environmental contaminant
- > 2400 serotypes
Salmonella nomenclature
S. enterica and S. bongori
- S. enterica ssp. enterica
- -S. serotype Typhimurium
- -S. serotype Enteritidis
- -S. serotype Typhi
- -S. serotype Cholerasuis
- -S. serotype Dublin
- -S. serotype Pullorum
- -S. serotype Gallinarium
- -S. serotype Arizonae
- -S. serotype Brandenburg
- S. enterica ssp. salamae
- S. enterica ssp. arizonae
- S. enterica ssp. diarizonae
- S. enterica ssp. houtenae
- S. enterica ssp. indica