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Microbiology > The rise of Multi-Drug Resistant Non-Fermenting Gram-Negative Bacilli > Flashcards

The rise of Multi-Drug Resistant Non-Fermenting Gram-Negative Bacilli Flashcards

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Biology 101 flashcards
1
Q

What is the size cut off for nutrient access in porins

A

Generalls about 600Da

Many antibiotics are larger than this

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2
Q

How can porins convey resistance

A

Some bacteria ntaurally have less porins or may lose/downregulate them e.g. in Klebsiella
NFGNBs are an example of this

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3
Q

Why are NFGNBs intrinically resistant to lots of antibiotics

A

They are environmental organisms which are relatively impermeable due to the harsh environmental conditions
But his also decreases nutrient uptake hence are slow growing

They are generally etherefore will only affect immunocompromised for there to be an infection

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4
Q

What are the A-D types of antibiotic efflux pumps

A

A- porins
B - Single component pumps i.e. SMR, MFS, ABC or MATE type
C - Tripartite RND Pump
D - Tripartite transports, MFS or ABC type

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5
Q

Name antibiotics that need to be in the cytoplasm to work

A

Aminoglycosides

Fluoroquinolones

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6
Q

What type of pump is the AcrAB-TolC Pump

A

An RND transported

The wings in the AcrA allows substrates to be pumped from the periplasm as well as the cytplasm

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7
Q

What is the main mechanism of MDR in P. Aeurginosa

A

MexAB-OprM Pump

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8
Q

What does the MexAB-OprM Pump convey resistance to

A 
Quinolones
Trimethoprim
Triclosan
Chloramphonical
Beta lacktams
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9
Q

What are the 3 main regulators of the MexAB-OprM pump

A

MexR, NalD, NalC

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10
Q

Action of MexR

A

Transcriptional repressor of MexAB-OprM

Inactivated by point mutation or insertional inactivation with an IS element of binding site mutations

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11
Q

Action of NalD

A

NalD is another rpressor of MexABoprM –> need inactivation of both MexR and NalD to give high levels of resistance

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12
Q

Action of NalC

A

NalC transcriptionally suppresses PA3719/20

PA3719/20 enocodes a protein that can bind and sequester MexR

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13
Q

Why are there so many mechanisms that can regulate mexABoprM pump expression

A

As the pump is so broad spectrum it has to be able to respond to many different chemicals and signals

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14
Q

Why are NFGNBs worrying for HCAIs

A

As they have high intrinsic resistance, and the ability to gain lots of resistance

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15
Q

What do NFGNBs predominantly cause

A

Bacteraemia or resp infection

Wound infections depending on the skin

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16
Q

What predisposes you to NFGNBs

A

Prior antibiotic therapy and prolonged hospital stay

However they are usually unable to colonise patients

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17
Q

What are the resistance levelss if NDGNBs

A

They are generally variable –> this is due to high genetic variability with unique strains that aren’t generally transmissible hence it is hard to predict the reponse to treatment.

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18
Q

What is the most common NFGNB in HCAI

A

P. Aeruginosa –> causes 3000 bactaraemias per year in england and wales

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19
Q

What is the most virulent NFGNB

A

P. aeurginosa –> produces signifcant virulence factors e.g. elastase and can form biolfilms

Patient to patient transmission has also be seen

20
Q

What is resistance like in P. Aeurginosa

A

25% of HCAI strains shown to be MDR
Pan resistance has emerged –> colisitn is last line but colisitn is also emerging

Resistance has arisen throguh a combination of increase efflux, intrinsic ezymes, decreased permeability and acquired enzymes e.g. VIM and IMP_

21
Q

What does Acinobacter generally cause

A

More wound infections than P. Aeruginosa and also problematic

22
Q

What is the genetic variability like in acinobacter

A

Highly genetically variable but some cloens are emrging in the UK i.e. OXA-23 mediated carbapenemase resistance !

23
Q

Where does acinobacter survive well

A

Highly tolerant of disinfectant and tolerant of dessication

Caused lots of problems in the Gulf war

24
Q

What is MDR like in acinobacter

A

MDR is generally less of a problem as less intrinsic resistance (less efflux and more permisability)

But still resistant to carbapenems, aminoglycosides and fluoroquinolones

25
Q

What disease do strenotrophomonas Maltophilia cause

A

Mainly bactaraemia and respiratory infections

Up to 50% mortality rates

26
Q

Is What is the genetic variability l ike in strenotrophomonas maltophilia lke

A

Highly genetically variable

Patient to patient spread is rare

27
Q

What generally causes transmission of strenotrophomonas maltophilia

A

Contaminated water supply

28
Q

what is stenotrophomonnas maltophilia resistance like

A

THE MOST INTRINISCALLY RESISTANT OF ANY HUMAN CAUSING ORGANISM!

Particularly to beta lactams, aminoglycosides and macrolides

29
Q

What is the treatment of strenotrophomonas maltpphilia

A

Trimethoprim/Sulphamethoxazole –> resistance is rare BUT this bone marrow suppressive. Problematic as most of the patients are immunocompromised

30
Q

Why is CF carrier status so high

A

As one copy of the allele decreases susceptibility to certain bacteria adhering to the gut wall e.g. cholera

31
Q

What do mutations in CFTR cause

A

Defective CFTR Processing so CFTR doesnt reach the apical membrane of epithelial cells –> impairs chloride transport across the epithelial cells

32
Q

Why do aiways become infected repeatedly in CF

A

Increaesd GM-1 in cells –> increases pseudomonas binding to it
Decreased Cl- secretion and Increased Na+ and water reabsoprtion, this leaves less water in airways, decreased depth of the ASL and hence bacteria become trapped in the mucus
Also mutant CFTR = less NO which is a primary innate repsonse to bacterial contamination

33
Q

What organisms commonly infect young CF patients

A

S. aureus - in first year. cotinues for life in 30% of patients
H. Influenzae - closely follows Staph Aureus but then mostly cleared by 10 years

34
Q

What organisms commonly infect older teens CF patients

A

P. Aeruginosa –> colonises 70% of patients.
Burkholderia Cepacia –> also a NFGNB and is very serious ! causes a rapid decline in lung function
Stenotrophomonas Maltophilia –> 30% serious if it colonises children and in adults if co-colonising with P. Aeurginosa
Achromobacter Xylosidas

35
Q

What organisms commonly infect patients in later life

A

Non-tuberculous ycobacteria

Aspergillus

36
Q

Why is p. aeurginosa hypermutable in CF

A

Ozygen free radicals are generated in the inflammatory response
Oxygen free radicaly cause DSB and mutations causing hypermutability
This hypermutability can activate efflux and aliginiate production –> ALIGINATE MAKES THE CELLS GLOOBY AND GET BIOFILM FORMATION

37
Q

what stage do we try and keep patient in with CF

A

In transient colonisation

38
Q

What is the Liverpool strains

A

LIverpool strain is a MDR strain of P. Aureginosa that has increasing clonal spread

Capable of causing super infection and replacing infection in the host of non-epidemic P. Aeurginosa strains.

Clinical state can worse when P. Aeurginosa infection becomes established

39
Q

What is cepacia syndrome

A

A fatal decline over short period when infected with BCC

40
Q

Is BCC antibitoic resistance

A

High levels –> not as high as P. Aeruginosa BUT if co-colonise with p. aeruginosa than the biofilm can protect it

41
Q

What are the 2 main types of BCC

A

B. multivorans and B. cenocepacia

42
Q

What makes B Cenocepacia particularly transmissible

A

Has the cbl gene which encodes the major structural subunit of unique cable pili
This mediates binding to mucin components and respiratory epithelial cells
This also possessses the B Cepacia epidemic strain marker

43
Q

What is the difference between B multivorans and B Cenocepacia

A

B multiborans has less of a clnical impact as less stransmissionle, less likely to cause chornic colinisation and lower morbidity and mortality

44
Q

Which si there more clonal spread of b multivorans or cenocepacia

A

Cenocepacia

In one manchester study all multivorans straisn were unique but 88% of cenocepacia were a single strains

45
Q

What is the treatment of NFGNBs

A

Respiratory quinolones - levofloxacin
Beta lactams with betalactams inhibitors - piperacillin with tazobactam
Trimethorpim/sulphamethoxazole
New tetracycline derivatives e.g. tigecycline!

infection control measures are important to try and rpeven the transmission of MDR organisms

46
Q

Why is hard to test NFGNBs in vitro

A

As they dont grow well in agar

Also clnical response often doesnt correlate to in vitro studies

47
Q

What may be important in the future treatment of NFGNBs

A

Efflux Pump Inhibitors
Antimicriobial peptides
New Beta Lactamase Inhibitors

Microbiology (14 decks)

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