E. Coli Flashcards

1
Q

What is Enterobacteriacae

A
  • Gram Negative
  • Facultatively anaerobic
  • Rod shaped
  • Ferment glucose to acid and gas
  • May or may not ferment lactose
  • Habitat: GIT, soil, and water
  • 30 genera and >90 species
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2
Q

Which Enterobacteriacae ferment Lactose?

A
  • Escherichia
  • Klebsiella
  • MacConkey Agar turn pink
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3
Q

Which Enterobacteriacae do NOT ferment lactose

A
  • Salmonella
  • Proteus
  • Morganella
  • Serratia
  • Yersinia
  • MacConkey Agar stays yellow
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4
Q

What are the most important Genera of Enterobacteriacae?

A
  • Most Common:
    • Escherichia: E. coli
    • Samonella: S. enterica
    • Klebsiella: K. pneumonia
  • Less Common:
    • Klebsiella aerogenes
    • Proteus mirabilis; P. vulgaris
    • Morganella morganii
    • Serratia marcescens
    • Yersinia:
      • Y. pestis
      • Y. pseudotuberculosis
      • Y. enterocolitica
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5
Q

What are the Coliform Bacteria

A
  • Escherichia coli
  • Klebsiella pneumonia
  • Klebsiella aerogenes
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6
Q

Where is E. coli found?

A
  • Normal inhabitant of the lower intestinal tract
    • Predominant facultative organism
  • Soil and water
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7
Q

What are the Antigenic Characteristics of E. coli?

A
  • Somatic (O) (cell wall)
    • 187 groups
    • lipopolysaccharides
    • Endotoxin production - septicemic infection
  • Capsule (K)
    • Polysaccharide
    • Adhesion, protection against phagocytosis
  • Flagella (H)
    • Protein
    • Motility
  • Fimbrial/Pilus (F)
    • Protein
    • Adhesion
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8
Q

How are the pathotypes/virotypes of E. coli classified?

A
  • Intestinal Pathogenic E. coli (IPEC)
    • AKA: Diarheagenic E. coli (DEC)
  • Extraintestinal Pathogenic E. coli (ExPEC)
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9
Q

What are the categories of IPEC?

A
  • Patterns of attachment on host cells
    • singly or in aggregates
  • Effects on host cells
    • none or destruction
  • Production of toxins
  • Invasiveness
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10
Q

Enteropathogenic (EPEC)

A
  • Attachment is pili mediated
  • Loss of microvilli (effacement)
  • Invasion and structural changes
  • Produce hemolysin
  • Cause diarrhea in hums and animals (pigs)
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11
Q

What hemolysins are produced by E. coli?

A
  • 3 types:
    • Alpha hemolysin (Hly, encoded by hly)
      • produced mainly by ETEC and ExPEC
    • Enterohemolysin (Ehx, encoded by ehx)
      • Produced by STEC
    • Cytolysin A (ClyA, encoded by clyA)
      • Produced by many strains
  • Purpose: obtain Iron from lysed RBCs
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12
Q

What is Shiga toxin-producing E. coli?

A
  • STEC, VTEC, or AEEC
  • Attachment is mediated by a protein intimin (not pili)
  • Loss of microvilli (effacement)
  • Invasion and structural changes
  • Produces Shiga toxin (Stx)
  • ~150 serogroups >400 serotypes
  • associated with outbreaks or sporadic diarrheal diseases in humans
  • Most common is E. coli O157:H7
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13
Q

What is Shiga Toxin (Stx)?

A
  • 2 subunits: A and B (A-B toxin)
  • 2 types:
    • Stx1 (100% homology)
      • Subtypes: Stx1a, Stx1c, and Stxd
    • Stx2 (50% homology)
      • subtypes: Stx2a, Stx2b, Stx2c, Stx2d, Stx2e, Stx2f, Stx2g
  • Stx2e involved in edema disease in swine
  • Stx2 is more cytotoxic
  • Target Cells: Enterocytes and Endothelial cells.
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14
Q

What diseases do STEC infections cause?

A
  • Humans: (O157:H7)
    • Hemorrhagic enteritis
    • Hemolytic and Uremic syndrome (HUS)
    • Food borne
  • Pigs:
    • Edema disease
  • Chickens:
    • swollen head syndrome
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15
Q

What are the serotypes of STEC?

A
  • ~150 serogroups and >400 serotypes
  • 7 serogroups are more often involved than others
  • Most common: O157:H7
  • Other major: O26, O45, O103, O111, O121, O145
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16
Q

What is Enteroinvasive E. coli (EIEC)

A
  • Multiply inside the cell
    • Salmonella - like”
  • Invasion and cellular destruction
  • Cause bacteremia or septicemia
  • Mostly seen in poultry (APEC)
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17
Q

What is Enterotoxgenic E. coli? (ETEC)

A
  • ‘Cholera-like’
  • Attach (pili mediated) but do NOT invade
  • Produce enterotoxins
    • Heat labile (LT, 60C or 15 min)
    • Heat stable (ST, 100C for 30 min)
  • LT is Cholera toxin-like
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18
Q

What are the LT toxins?

A
  • Enterotoxin
  • A-B toxin
  • 2 types: LT-I and LT-II
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19
Q

What are the ST toxins?

A
  • Enerotoxin
  • Small 2kDa proteins
  • STa (methanol soluble): fluid accumulation in the intestine
  • STb (methanol insoluble)
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20
Q

What is Enteroaggregative E. coli? (EAggEC)

A
  • New group
  • Form aggregates (stacked brick adherence)
  • Do not invade
  • Produce ST-like (heat stable), called “EAST” and hemolysin-like toxins
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21
Q

What is Cytotoxin Necrotizing Factor Producing E. coli? (CNF-PEC)

A
  • Attach but do not invade the cells
  • Produce a toxin (CNF) that causes necrosis
  • Cause:
    • diarrhea in calves, pigs and humans
    • Mastitis in cows
    • UTI in dogs
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22
Q

What diseases doe Extraintestinal Pathogenic E. coli (ExPEC) cause?

A
  • Septicemia
  • Mastitis in dairy cows
  • Uterus (Metritis)
  • Urinary tract (UPEC)
  • Air sacculitis in chickens and turkeys (APEC)
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23
Q

What are the important Virotypes of E. coli in animals?

A
  • ETEC: Intestinal infections (enterotoxins)
  • EPEC: Intestinal and extraintestinal infections
  • STEC: Edema disease in Pigs (Shiga Toxins)
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24
Q

Who is affected by Intestinal Colibacillosis?

A
  • Piglets
  • Calves
  • Lambs
  • Goat kids
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25
Q

Where does Extraintestinal Colibacillosis occur?

A
  • Septicemic or localized infections in:
    • mammary gland
    • Urinary tract
    • Uterus
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26
Q

What are the modes of infection for E. coli and what do they result in?

A
  • Ingestion: Enteritis
  • Inhalation: Mostly in poultry - Respiratory infection
  • Direct infection: Entry into an organ
    • Teat canal: Mastitis
    • Urethra: UTI
    • Vagina: Metritis
27
Q

What are the 3 forms of Colibacillosis in Swine?

A
  • Neonatal enteritis
  • Post weaning diarrhea (weanling enteritis)
  • Edema disease
28
Q

What is Neonatal enteritis?

A
  • Occurs in the first 3-4 days of life
  • Profuse diarrhea (pale yellow and watery)
  • Mortality almost 90%
  • Death due to dehydration
29
Q

What is Post Weaning Diarrhea?

A
  • Caused by: EPEC, ETEC, and STEC strains
  • Toxins: Enterotoxins (ST, LT, EAST), hemolysin, Stx2e
  • Usually seen within the first week of weaning
  • Affected pigs develop diarrhea, depression, anorexia, and fever
  • Low mortality
30
Q

What is Edema disease?

A
  • Caused by STEC
  • Stx(Stx2e) is major virulence factor
  • 7-10 days after weaning
  • Edema of the submucosa of the stomach and colon and SQ tissues (eye lids)
31
Q

What are the predisposing factors of Edema disease

A
  • Age 7-10 days after weaning
  • Change of feed
  • Rapid growth
  • Diarrhea
32
Q

What are the clinical signs of Edema disease?

A
  • Edema: eyelids, facial area, stomach, colon, mesenteric lymph nodes, gall bladder, larynx, etc.
  • Peculiar squeal
  • Neurological: Convulsions, Ataxia
  • Recumbency with paddling of legs
33
Q

What is the mortality rate of Edema disease?

A
  • 65%
  • Death in 1-3 days
34
Q

How can Edema disease be prevented?

A
  • Separation of sick pigs
  • Vaccine (recombinant toxoid)
  • Antibiotic in the Feed (CTC, Enrofloxacin)
35
Q

What is White Scour?

A
  • Colibacillosis in calves
  • During the 1st week of life
  • Severe diarrhea, feces full of gas bubbles
  • Virulence factor: Enterotoxin (STa)
  • Death in 3-5 days from dehydration
36
Q

What is the Septicemic form of Colibacillosis in Cattle?

A
  • Occurs in calves deprived o colostrum
  • Virulence factor: Endotoxin
  • Endotoxic shock and death
37
Q

What is Coliform mastitis?

A
  • Mastitis from E. coli
  • 30-50% of cases
  • Frequently seen in high-producing dairy cows
  • Mostly mild cases
  • Clinical signs: Swelling of the udder, discolored milk, blood clots, loss of milk production
38
Q

What is the Pathogenesis of Choliform mastitis?

A
  • Entry through the teat
  • Adherence to mammary cells
  • Virulence factors: Pili, Endotoxin, CNF
  • Absorption of endotoxin leads to fever, depression, and occasionally death
39
Q

How is Choliform Mastitis treated/prevented?

A
  • Antibiotics: Amoxicillin, Cephalosporins
  • Vaccine: Endotoxin-based (J5 strain)
40
Q

What diseases does Colibacillosis cause in other large animals?

A
  • Neonatal enteritis
    • lambs and kids
    • occasionally septicemic
  • Enteritis in foals
  • Mastitis and metritis in mares
41
Q

What does Colibcillosis cause in Dogs and Cats?

A
  • Diarrhea is NOT common
  • Commonly isolated from genital and urinary tract infections
  • Cystitis and pyometra in bitches
  • Prostatitis in males
42
Q

What are the Virulence factors of UTIs in Dogs?

A
  • Pili: adherance
  • Hemolysin
  • Cytotoxin Necrotizing factor (CNF)
  • Protease enzyme
43
Q

What does colibacillosis cause in Poultry?

A
  • Enteric infection is rare
  • Respiratory infections (air-sacculitis)
  • Cellulitis: Swollen head syndrome
  • Coli-Granuloma (Hjarre’s Disease): chronic rom with granulomatous lesions in the walls of the intestinal tract, liver, and lungs.
  • Localized or systemic (Colispeticemia)
  • Avian strains (APEC) do NOT cause diseases in other animals
44
Q

What is Air-sacculitis?

A
  • Causes:
    • inhalation of fecal dust
    • inhalation of ammonia predisposes to colonization
  • Secondary to viral and mycoplasma infections
  • Pneumonia: pleuropneumonia, pericarditis, etc.
  • Significant economic loss
44
Q

What is Cellulitis?

A
  • Infection of the subcutis
    • seen in lower abdomen and thigh region
  • Swollen Head syndrome:
    • Cellulitis affecting periorbital region
    • Caused by STEC strains
  • Significant economic losses
45
Q

What is the Public Health significance of E. coli?

A
  • Similar serotypes, but animals are not a source of human infection
  • Enterotoxins are similar but pili antigens are different
  • STEC (O157:H7) are zoonotic pathogens
46
Q

How do you Diagnose an E. coli infection?

A
  • Presumptive Diagnosis:
    • Age
    • Clinical signs
  • Isolation from fecal sample
    • Key: interpretation
    • methods:
      • determination of surface antigens and toxins
      • Serology to detect O, K, F antigens
      • Slide agglutination, ELISA, FAb
    • Molecular: PCR for virulence genes
    • Histopathology: Adherent E. coli cells
      • Light and electron microscopy; Fab tech)
47
Q

How do you Treat?

A
  • Antibiotics:
    • Aminoglycosides (neomycin)
    • Tetracyclines
  • Fluid Therapy:
    • Rehydration and electrolyte balance
48
Q

What are Control Measures for Neonatal Enteritis?????

A
  • Sanitation and management
  • Newborn animals should get colostrum
49
Q

Are there vaccinations for E. coli?

A
  • Pilus-based vaccines for neonatal enteritis:
    • F4 (K88), F5 (K99), F6 (987P)
    • Pregnant sows and cows are vaccinated for passive transfer
  • Autogenous bacterins
  • Recombinant Stx toxoid for edema disease
  • J5 vaccine for mastitis (LPS vaccine)
50
Q

Are there vaccinations for E. coli?

A
  • Pilus-based vaccines for neonatal enteritis:
    • F4 (K88), F5 (K99), F6 (987P)
    • Pregnant sows and cows are vaccinated for passive transfer
  • Autogenous bacterins
  • Recombinant Stx toxoid for edema disease
  • J5 vaccine for mastitis (LPS vaccine)
51
Q

What illnesses does STEC cause in humans?

A
  • Diarrhea:
    • mild to severe
    • +/- blood
  • Hemolytic uremic syndrome (HUS)
    • Mostly in children
  • Thrombocytopenic purpura (TPP)
    • mostly in adults
52
Q

What are the most common Non-O157 STEC groups?

A
  • O26 (22%)
  • O111 (16%)
  • O103 (12%)
  • O121 (8%)
  • O45 (7%)
  • O145 (5%)
  • These 6 account for 71% of non-O157 STEC infections
53
Q

How do O157 and non-157 STEC infections compare?

A
54
Q

What is the incidence of STEC illnesses in the US?

A
  • Food born illness is about 66% of STEC illnesses
  • O157 accounts for:
    • 36% of illnesses
    • 89% of hospitalizations
    • 100% of deaths
55
Q

What about STEC in foods?

A
  • E. coli O157:H7 declared an adulterant in ‘94
  • in ‘11 six non-O157 STEC (O26, O45, O1-3, O111, O121, and O145) were also declared as adulterants
  • Testing ground beef by Food Safety Inspection Service (FSIS) began in June 2012
56
Q

Why are STEC infections of Public Health importance?

A
  • Human pathogen, NOT animal pathogens
  • Cattle are major reservoirs
  • Most are food borne:
    • Beef and dairy
    • Fruits and veges
57
Q

E.coli O157:H7

A
  • First recognized in 1982
  • important food borne pathogen
  • Causes:
    • hemorrhagic colitis
    • Hemolytic Uremic Syndrome (HUS) - acute renal failure, hemolytic anemia and thrombocytopenia
  • Present in the GI tract, particularly in the hindgut of cattle
    • Shed in feces
    • highly variable shedding
58
Q

Pathogenesis of E.coli O157:H7

A
  • Colonizes intestinal cells
  • Produces Stx (Verotoxin)
    • Damages endothelial cells, which causes thrombocyte aggregation and capillary damage in the kidney or other organs
  • No enterotoxin
  • NOT invasive
58
Q

Pathogenesis of E.coli O157:H7

A
  • Colonizes intestinal cells
  • Produces Stx (Verotoxin)
    • Damages endothelial cells, which causes thrombocyte aggregation and capillary damage in the kidney or other organs
  • No enterotoxin
  • NOT invasive
59
Q

What is the prevalence of E. coli O157:H7 in cattle?

A
  • Herd level: 80-100%
  • Prevalence in dairy and beef cattle: 10-28%
  • Shedding is seasonal
    • higher in summer and early fall
  • Shedding is <102 per gram of feces
  • Super shedders >103
60
Q

How do carcasses get contaminated?

A
  • During Hide removal
    • physical transfer
    • Aerosol
  • Evisceration
    • gut contents
61
Q

What are some sources of E. coli O157:H7?

A
  • Undercooked ground beef
  • Unpasteurized milk
  • Unpasteurized fruit juices
  • Drinking water and recreational water
  • Contaminated leafy vegetables
62
Q

How is the spread of E.coli O157:H7 prevented?

A
  • Preharvest:
    • management
    • Probiotics
    • Bacteriophages
    • Vaccine
  • Post Harvest:
    • Hide and carcass wash
  • Implementation of Hazard Analysis and Critical Control Points (HACCP) in slaughtering and Meat Processing procedures
  • Adequate cooking (160F for 15 sec)
  • Pasteurization of milk and fruit juices