Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology > 11 - E. coli > Flashcards

11 - E. coli Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q
  1. What type of bacteria is E. coli?
  2. Does E. coli ferment lactose?
  3. Is E. coli indole positive or negative?
  4. Does E. coli have flagella?
  5. Does E. coli have capsules?
  6. Is E. coli capable of hemolysis and if so, what type and on what type of medium?
A
  1. Gram negative rod.
  2. Yes
  3. Positive
  4. Most strains have flagella
  5. Some strains have capsules
  6. Some strains undergo beta hemolysis on blood agar. Most strains that cause septicemia are often beta hemolytic.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  1. E. coli are commensal bacteria. Where are they typically located?
  2. Explain the genomic difference between commensal and pathogenic strains of E. coli.
A
  1. Commensals of mammalian gut.
  2. Pathogenic strains are only 40% similar to commenal strains. They have a number of extra genes that give them pathogenicity.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. Name 5 types of general diseases caused by E. coli in many different species.
  2. Name a disease in pigs.
  3. Name 2 diseases in man.
  4. Name a disease in lambs.
A
  1. Neonatal and post-weaning diarrheaNeonatal septicemiaMastitisUTIsInfection of existing wounds (abscesses)
  2. Edema disease
  3. Hemorrhagic colitis (HC)Hemolytic uremic syndrome (HUS)
  4. Watery mouth.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Several groups of E. coli are responsible for causing intestinal infections. Define the following group types and name the species they infect.

  1. ETEC
  2. EPEC
  3. AEEC
  4. VTEC
A
  1. Enterotoxigenic E. coli - animals, humans
  2. Enteropathogenic E. coli - animals, humans
  3. Attaching and effacting E. coli - animals, humans
  4. Verotoxigenic E. coli - animals, humans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Several groups of E. coli are responsible for causing intestinal infections. Define the following group types and name the species they infect.

  1. STEC
  2. EHEC
  3. EAEC
  4. DAEC
  5. EIEC
A
  1. Shigella-like toxin E. coli - animals, humans
  2. Enterohemorrhagic E. coli - animals, humans
  3. Enteroaggressive E. coli - humans
  4. Diffusely adherent E. coli - humans
  5. Enteroinvasive E. coli - humans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  1. Define ExPEC and state 4 types of diseases it causes.
  2. Generally E. coli strains are host specific and are not zoonotic. What strain of E. coli is the exception to this?
A
  1. Extraintestinal Pathogenic E. coli - causes disease in animals and humans:
  • UTIs
  • Mastitis
  • Septicemia
  • Meningitis
  1. E. coli O157
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

List the virulence factors associated with the following E. coli pathotypes:

  1. ETEC
  2. EPEC
A
  1. Enterotoxigenic E. coli
  • Heat labile enterotoxin (LT)
  • Heat stable enterotoxin (ST)
  • Host-specific fimbriae
  1. Enteropathogenic E. coli
  • Pathogenicity island
  • Locus of enterocyte effacement (LEE)
  • Type III secretion system (TTSS)
  • Intimin
  • Host-specific fimbriae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

List the virulence factors associated with the following E. coli pathotypes:

  1. EHEC
  2. ExPEC septicemia and UTI strains
A
  1. Enterohemorrhagic E. coli
  • Pathogenicity island (LEE)
  • Type III secretion system (TTSS)
  • Intimin
  • Host-specific fimbriae
  • Vero toxins (VT)
  • Shiga-like toxins (SLT)
  1. Extracellular pathogenic E. coli
  • Hemolysin
  • Iron uptake systems
  • Capsules
  • Host-specific fimbriae
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. What virulence factors are associated with strains of E. coli that cause mastitis?
  2. How are E. coli pathotypes and virulence factors determined?
A
  1. Trick question - no particular virulence factors have been identified in strains that cause mastitis. The infection may be an opportunistic situation.
  2. Send sample to reference lab - test methods:
  • Serological - antibodies against virulence factors
  • Molecular - DNA probes, PCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List the major diseases caused by E. coli in the following species:

  1. Cattle
  2. Pigs
  3. Dogs and cats
  4. Poultry
A
  1. Cattle
  • Mastitis
  • Septicemia
  1. Pigs
  • Mastitis
  • Septicemia
  1. Dogs and cats
  • UTI
  • Pyometra
  • Septicemia
  1. Poultry
  • Air sacculitis
  • Septicemia
  • Cellulitis
  • Yolk sac infection

NB: causes septicemia and UTIs in all species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  1. Where are strains of E. coli that cause extraintestinal infections (ExPEC) carried in the host?
  2. Where are strains of E. coli that are pathogens of the GIT carried in the host?
  3. What are the 4 virulence factors associated with ExPEC strains?
A
  1. They are are carried in the GIT but do not cause pathology in the GIT. Strains that cause septicemia, UTIs, etc. originate from the gut and get transferred to other sites in the body where they cause pathology.
  2. They are not carried in the GIT - they are transferred from animal to animal, human to human during disease.
  3. ExPEC virulence factors
  • Capsule
  • Fimbriae (host-specific)
  • Siderophore
  • Toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. What is the role of the capsule in pathogen survival?
  2. Why are fimbriae important? What particular disease are they particularly important in?
  3. What two toxins are important in ExPEC strains?
  4. What two compounds are associated with siderophores in ExPAC strains?
A
  1. Capsular polysaccharides prevent phagocytosis and interfere with complement - enhance survival in the tissues. It is the K antigen.
  2. They are important for attachment. In ExPECs that are important for adherence in UTI’s in all species.
  3. Toxins
  • Hemolysin - lyses both RBCs and WBCs
  • CNF-1 - cytotoxic necrotizing factor 1, causes tissue damage
  1. Siderophore compounds:
  • Enterochelin (enterobactin)
  • Aerobactin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. What strains of E. coli produce enterochelin? Where are the genes for the compound located?
  2. What strains of E. coli produce aerobactin? Where are the genes for the compound produced?
  3. How doe the affinity for iron differ between enterochelin and aerobacin?
  4. Why is there a need for both enterochelin and aerobactin?
A
  1. Enterochelin is produced by all E. coli strains - the genes are located on the chromosome.
  2. Not produced by all strains - generally produced by septicemic strains, genes are usually located on a plasmid - if the bacteria loses the plasmid, it becomes avirulent.
  3. In vitro, affinity of iron: enterochelin > aerobactin
  4. Need for both because:
  • In serum, enterochelin bound by albumin and is inactivated, prevents Fe uptake by bacteria
  • Stimulates the production of anti-enterochelin antibodies - prevents Fe uptake by bacteria
  • At lower pH, e.g. in urinary tract, affinity for iron: aerobactin > enterochelin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  1. Are ETEC invasive or non-invasive?
  2. What is the primary disease in animals caused by ETEC?
  3. What species are affected?
  4. What diseases are caused by ETEC in humans? Are the strains the same?
  5. Are ETEC zoonotic?
A
  1. Non-invasive; sit on mucosal surface and do not invade tissues tf non-inflammatory
  2. Non-inflammatory, watery diarrhea - is acute and can be life threatening - potentinal to die from dehydration
  3. Young animals of many species - pigs, cattle, sheep, etc.
  4. Children’s diarrhea, travellers diarrhea - caused by different strains.
  5. No. Human and animal isolates have different O groups and do not cross species.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  1. Virulence is often multifactorial. What is meant by this?
  2. What two genes are responsible for virulence of ETEC?
  3. Where are they located?
  4. What virulence factor(s) do they produce?
  5. What happens if one of the ETEc virulence factors is removed?
A
  1. Not just one virulence factor is required for disease - often more than one, or several, are required.
  2. Tox and K88
  3. On plasmids
  4. K88 produces fimbriae and Tox produces toxins that cause disease.
  5. If fimbriae are removed, no attachement to host cells and may get slight diarrhea. If no toxins are produced, the host will not get diarrhea.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  1. For review, what are the 3 virulence factors associated with ETEC?
  2. What is the pathogenesis of ETEC?
  3. How does the structure of fimbriae make them host specific?
A
  1. LT, ST and host-specific fimbriae
  2. Pathogenesis:
  • The bacteria colonize the gut and attach to host cells via fimbriae.
  • The bacteria then produces toxins that cause disease
  • Water absorption into the gut is prevented and is also secreted.
  • Result is disruption of electrolyte balance and water diarrhea.

3, Sugar molecules at the tip of the fimbriae recognize sugars on the surface of the host cell. These are different for each host and also each cell type they bind to.

17
Q
  1. Discuss the action of ETEC’s heat labile toxin (LT) in causing diarrhea.
  2. Discuss the role of ETEC’s heat stable toxin (ST) in causing diarreha.
A
  1. Action of LT:
  • LT binds to a Gs receptor on the cell membrane and along with NAD causes constitutive activation of adenylate cyclase
  • Incresed adenylate cyclase = increased cAMP = increased production of protein kinase A
  • PKA causes channels to open in the cell membrane - leaks fluid out and prevents absorption of water
  1. Action of ST:
    * ST activates guanylate cyclase which increases cGMP in the cell - leads to prevention of water absorption
18
Q
  1. What is the end result of the action of LT and ST in the GIT?
  2. Which of the two toxins is immunogenic?
A
  1. Acute watery diarrhea and electrolyte imbalances - water balance in the gut changes from net absorption to net secretion
  2. LT is highly immunogenic while ST is non-immunogenic
19
Q

Compare diarrheal disease caused by ETEC and Salmonella.

A

ETEC:

  • Bacteria are extracellular
  • Diarrhea is non-inflammatory and watery - no WBCs seen in fecal samples

Salmonella

  • Bacteria invade cells
  • Diarrhea is inflammatory - WBCs seen in fecal samples
  • Blood may also be seen
20
Q
  1. What does an EPEC infection cause and in what species?
  2. What lesion is characteristic of an EPEC infection?
  3. For review, what are EPEC’s virulence factors?
  4. Which virulence factor is responsible for the lesion in #2?
  5. Where is the virulence factor in #4 located?
A
  1. Diarrhea in young animals (lambs, calves, piglets, puppies) and children (different serotypes, not zoonotic)
  2. AEEC - attaching and effacing lesions.
  • Attachment = actin pedastels that appear underneath the bacteria
  • Effacement = disappearance of microvilli - highly localized, only seen where bacteria attaches
  1. Pathogenicity island, locus of enterocyte effacement (LEE), type III secretion system (TTSS), intimin, host-specific fimbriae
  2. TTSS is responsible for the actin pedastels
  3. TTSS is located on a pathogenicity island - LEE
21
Q
  1. Why are some E. coli named VTEC?
  2. Why are some E. coli named STEC?
  3. Is there a difference between VTEC and STEC?
  4. So how does EHEC relate to all of this?
  5. What the heck?
A
  1. They produce verotoxin - is toxic to Vero cells in vitro.
  2. They produce shiga-like toxin - a toxin similar to that produced by Shigella spp.
  3. Nope - vertoxin is also referred to as shiga-like toxin.
  4. Some human strains of VTEC/STEC cause hemoorhagic diarrhea - these strains are referred to as enterohemorrhagic E. coli - EHEC.
    * NB - All EHEC are VTEC/STEC but not vice versa
  5. Remember VTEC/STEC = animals and EHEC = humans.
22
Q

Verotoxins/shiga-like toxins are compounds made up of A and B units.

  1. How does the A unit contribute to disease?
  2. How does the B unit contribute to disease?
A
  1. The A unit is enzymatic:
  • Inhibits protein synthesis - kills cells
  • It prevents binding of tRNA to the ribosome
  1. The B unit is responsible for binding:
  • Main target = endothelium of blood vessels
  • Results in
    • Edema
    • Hemorrhage
    • Thrombosis
23
Q

Name the two major diseases caused by EHEC and list their clinical signs.

A
  1. Hemorrhagic Colitis - HC
  • Acute severe cramps and abdominal pain
  • Bloody diarrhea
  • Nausea and vomiting
  • Little to no fever
  1. Hemolytic Uremic Syndrome - HUS
  • Hemolytic anemia
  • Thrombocytopenia
  • Renal failure
24
Q
  1. What nasty E. coli type results in HUS 15% of the time?
  2. Should we treat HUS with antibiotics?
  3. How many E. coli specified in #1 are required to infect 50% of people?
A
  1. E. coli O157:H7 - children and adults
  2. Nope - antibiotics may make the infection worse. Bacterial lysis by the antibiotic causes a massive release of toxins, which makes the disease worse.
  3. 100 - i.e., not that many :(
25
Q
  1. What animals are reservoirs for E. coli O157:H7?
  2. Does it make their hosts sick?
  3. How does meat become contaminated with it?
  4. What other food product may be contaminated?
A
  1. Found mainly in the intestine of cattle but also in:
  • chickens
  • deer
  • sheep
  • pigs
  1. Nope
  2. During slaughter
  3. Milk via bacteria on cow’s udders and on milking equipment.
26
Q

E. coli O157:H7 is like an EPEC that produces VT.

  1. Where did the VT come from?
  2. How many types are typically present? What are they called?
  3. How homologous are they to the toxins produced by Shigella spp and to each other?
  4. Which type is associated with severe disease?
A
  1. The VTs were acquired from infection with bacteriophages - genes were incorportated into the host chromosome.
  2. Two - VT1 and VT2
  3. VT1 is nearly 100% homologous with Shigella and VT2 is 56% homologous to VT1.
  4. VT2
27
Q

Describe the pathogenesis of EHEC.

A
  • The bacteria adheres to GIT mucosa - causes AE (attaching and effacing) lesions - pedestal, etc.
    • Causes diarrhea
  • VTs are introduced into the cell and cross through to the blood stream
    • Causes HC or HUS
28
Q
  1. What are the virulence factors associated with edema disease?
  2. Where do symptoms occur?
  3. Is there evidence of enteritis?
  4. Is it zoonotic?
A
  1. ST/VT and fimbriae - no LEE
  2. Edema in
  • Forehead
  • Stomach
  • Large bowel
  • Mesentary
  1. Nope
  2. Nope
29
Q

There was an E. coli outbreak in 2011 - 4000 people were affected, 20% developed HUS and 48 died. All of the patients visited northern Germany.

  1. What was the strain of E. coli implicated in the outbreak?
  2. Why was it such a big deal?
  3. Is it found in animals/zoonotic?
A
  1. E. coli O104:H4
  2. It is a strain believed to be a hybrid of 2 pathotypes - enteroaggressive E. coli with VT genes
    * VT genes presumably acquired from a phage
  3. Nope and nope - possible infection due to human feces contaminating a food source. Ew.

Microbiology (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions