Bacteriology & virology > Enterobacteriaceae > Flashcards

Enterobacteriaceae Flashcards

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1
Q

Major pathogenic spp of Enterobacteriaceae

A
  • Escherichia coli
  • Salmonella spp
  • Yersinia spp
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2
Q

Opportunistic pathogens of Enterobacteriaceae

A
  • Klebsiella spp.
  • Enterobacter spp.
  • Proteus spp.
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3
Q

growth of Enterobacteriaceae

A
  • Possess ability to tolerate bile salts
    • Allows them to grow on media like MacConkey
  • generally predominant found in the gut
    • Can be found in the parts of the body & cause a variety of clinical infections in humans
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4
Q

characteristics of Enterobacteriaceae

A
  • gram - rods
  • facultative anaerobes
  • catalase +
  • oxidase -
  • Enteric bacteria
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5
Q

Strains of Enterobacteriaceae

A
  • Most are commensal of host
    • Some strains can acquire resistance & virulence readily, leading to severe infections in both humans & animals
  • Family is extensive, comprising 28 genera & 120 species
    • Only small number are pathogenic
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6
Q

Describe opportunistic infection

A

caused by bacteria that are generally commensal

  • normally live harmlessly within the host but can acquire resistance & virulence & cause severe infections when an opportunity arises
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7
Q

Example of opportunistic infection

A

e.coli often commensal can cause various opportunistic infections

Often involves the bacteria acting as secondary invaders following events such as faecal contaminations or when the host’s defences are compromised
Become terminal invaders in severely debilitated P

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8
Q

major pathotypes of E. coli

A

Commensal
Intestinal Pathogenic
Extraintestinal pathogenic

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9
Q

Describe commensal e coli

A
  • good”
  • part of a healthygut flora
  • Present in high numbers
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10
Q

Describe intestinal pathogenic e.coli

A
  • cause infections primarily in the gut
  • Further divided based on their virulence factors
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11
Q

Primary infections caused by E.coli

A
  • d+ & enteritis
  • ETEC, EPEC, STEC
  • Specialised virulence determinants
  • Adhesins & toxins
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12
Q

What is post weaning d+ caused by

A

primarily caused by ETEC in piglets. particularly during the weaning stage

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13
Q

ETEC what is it

A

Enterotoxigenic E. coli

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14
Q

ETEC in ruminants

A
  • ETEC can cause neonatal colibacillosis or white scours
    • Septica
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15
Q

Mechanism of ETEC causing post weaning d+

A
  1. Ingestion
  2. Attachment
  3. Toxin release
  4. Fluid & electrolyte imbalance
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16
Q

Clinical consequence of ETEC

A

watery + leads to weight loss, dehydration & potentially death in piglets

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17
Q

ingestion of ETEC

A
  1. Animal ingests E.coli
  2. Bacteria then colonise the jejenum & ileum
  3. Colonisation is facilitated by the presence of specific receptors on the intestinal epithelium that match the bacteria’s fimbriae
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18
Q

Attachment of ETEC

A
  1. ETEC possess hair-like structures called fimbriae (aka adhesins) that enable them to attach to receptors on the GIT’s intestinal epithelium
  2. Attachment is crucial for the infection to proceed
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19
Q

Toxin release of ETEC

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A
  1. Once attached, ETEC begins to release toxins
  2. These toxins are coded in the bacterial DNA
  3. The toxins involved are primarily heat labile or heat stable toxins
  4. Toxins do not cause inflammation or cellular changes in the intestinal lining
    1. Cause hypersecretory d+
20
Q

Fluid & electrolyte imbalance caused by ETEC describe

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A
  1. Released toxins lead to the release of H2O & electrolytes out of the intestinal cells
  2. Results in severe watery d+ in the affected piglets
21
Q

primary virulence factors of ETEC

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A

fimbriae & toxins it produces

22
Q

Fimbriae role

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A
  • essential for bacteria to adhere to the intestinal epithelial cells
    • Specific fimbriael types associated with ETEC in different animal species
23
Q

in pigs what are the common fimbrial variants:

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A

F4, F5, F6, F8 & F41

24
Q

f4 fimbriae variants in pigs

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A
  • F4 fimbriae attach to F4 receptors present in the gut of pigs during the weaning stage
  • Pig industry has even attempted to breed pigs that lack the F4 receptor to prevent F4 infections, sometimes led to increased F18 infections
25
fimbriae in calves describe
In calves, F5 & F41 are key adhesion fimbriae that enable colonisation of the intestinal tract
26
toxins of ETEC
- Toxins (LT & ST) - after attachment, these heat labile(LT) or heat stable(ST) toxins are attached
27
primary role of toxins in ETEC
disrupt ion & water transport across the intestinal cells, leading to excessive secretion of H2O & lytes into the lumen, resulting in the characteristic water d+
28
what is STEC
shiga toxigenic E. coli (STEC)
29
Describe STEC
significant foodborne pathogen does not typically cause severe infection in animals, cattle & sheep often carry these organisms in their gut often through
30
Contamination cycle of STEC
1. ingestion of pathogenic e.coli 2. faecal excretion + contamination of environment 3. contamination of food & water 4. transmission animal to person 5. transmission person to person
31
Describe Animal reservoir & shedding
1. Cattle & sheep commonly carry STEC in their gut as part of normal flora 2. They shed the organism in high numbers into the environment
32
Describe Slaughter process that leads to transmission of STEC
faecal materials from infected cattle & sheep can contaminate the surface of meat
33
Describe high risk meat products that lead to transmission of STEC
Products with a large surface area, such as burgers & sausages are particularly susceptible to contamination if not cooked thoroughly
34
vegetables & water of STEC transmission
1. faecal material can also contaminate water systems 2. If upstream farms have STEC-carrying animals, their manure can enter the water supply 3. Contaminated water can then be used for irrigation in downstream farms, leading to contamination of raw products like sprouts & salads
35
Human Ingestion & transmission of STEC
1. Humans ingest these contaminated products 1. frequently occur when burgers or beef patties are undercooked = bacteria not destroyed 2. Direct contact 1. direct contact with cattle faecal material 3. Human-human/pet to human transmission 1. dynamic strain sharing between humans & pets where human strains can move into cats & dogs vice versa 2. Can lead to clinical infections in dogs & presumably further transmission to humans
36
How STEC ingested & colonisation in humans
1. Humans ingest STEC 2. E.coli then sticks to the intestinal epithelium & proliferates
37
toxin production of STEC in humans
1. Bacteria proliferates, they release Shiga toxins (STX) which are coded within the bacterial DNA, often brought in by phages 2. e.g. O157H7 type: common in US which produces STX2E & intimin genes & O104H4 strain from recent German outbreak
38
Intestinal damage & haemorrhagic disease by STEC in humans
1. toxins damage the cells in the intestinal wall 2. Also get into blood vessels in the intestine, leading to bleeding in the gut 1. the infection causes bloody d+ (hallmark of Enterohaemorrhagic E.coli infection in humans)
39
Systemic spread & kidney failure caused by STEC in humans describe
1. toxins enter bloodstream 2. Once in bloodstream, they dmaage blood vessels throughout the body, particularly those in the kidneys 3. Damage to kdiney blood vessels can lead to renal failure & severe syndrome known as haemolytic uremic syndrome 4. Many P suffering from HUS may require dialsysis for rest of their lives
40
Low importance abx
amoxycillin Erythromycin Penicillin Tetracycline Neomycin Nitrofurantoin
41
Medium importance abx
2nd generation cephalosporins Amoxycillin -clavulanate gentamicin/tobramycin Spectinomycin Trimethoprim-sulphonamide
42
High importance abx
3rd & 4th generation cephalosporins Carbapenems Fluoroquinolones Colistin Amikacin
43
Antimicrobial rankings
have been developed from a human health perspective & require adherence to strict guidelines when used for infection management in food animals
44
main characteristics of E. coli ST131 clone
- multi drug resistant - Extra intestinal pathogen - Global distribution - Strong association with increasing age & health care facilities, complicated infections, UTIs & previous antimicrobial therapy - Urosepsis, wound infections - resistant to fluoroquinolones, trimethoprim-sulpha, ESBL producer - Sticky & present in the gut of healthy people & companion animals - More virulence factors
45
Major typing methods
Serotyping & molecular typing
46
Describe MLST
early molecular method that involved looking at seven housekeeping genes to understand strain evolution
47
How is typing done
- done by creating an antigen-antibody test; antibodies are made by injecting the antigen into an animal (e.g. a rabbit) to produce antiserum. - This antiserum is then used to test a bacterial strain for an antigen-antibody reaction, often visible with latex or other indicators
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