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CP > antibiotic resistance > Flashcards

antibiotic resistance Flashcards

1
Q

how do you identify resistance?

A

antibiotic sensitivity and susceptibility testing (growing the organisms in the presence of antibiotics, if it grows in the presence of a high concentration it is resistance and if lower is sensitive
low MIC = sensitive
detection of antibiotics resistance genes - see if the genes are present in the organism

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2
Q

how do you carry out antibiotics sensitivity testing?

A

on a liquid media microtitre plate - add antibiotics to wells in doubling dilutions and add microorganisms. Ensure that there is one row without AB and one without microorganisms. Incubate to make microorganisms grow and look at the colour change. see the concentration of the AB that is sufficiently high to kill bacteria and find MIC and compare to find breakpoint

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3
Q

what is the breakpoint?

A

it is the MIC value whereby if the MIC is lower than or the same then the organism if sensitive to the antibiotics

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4
Q

why are there different breakpoints?

A

concentration of different antibodies to human body is different

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5
Q

what is disc sensitivity testing?

A

it is on a solid media where you add organisms to an agar plate and use a swab dipped into culture to spread evenly. You add antibiotics of known concentrations and incubate overnight, Compare the zones against the published breakpoint sizes and interpret and report

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6
Q

how do you detect antibiotic resistance genes?

A

nucleic acid amplification tests such as PCR - can be applies to any sample type

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7
Q

what are the advantages an disadvantages of the antibiotic resistance genes tests?

A

they are sensitive and fast

they are expensive and the presence of the gene does not necessarily mean resistance

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8
Q

what are the resistance mechanisms?

A

innate or acquired

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9
Q

what is innate resistance?

A

it is a fundamental property of a bacteria or antibiotics or combination that is usually to do with the entry into a cell or permeability to ABs

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10
Q

what are examples of innate immunity?

A

gram positives - glycopeptides, daptomycin
gram positives - aztreonam or colistin
anaerobes/streptococci - aminoglycosides

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11
Q

why wont aminoglycosides work in an anerobic bacteria?

A

they are taken into the cell to work which is aerobic meaning that they do not work in anaerobic

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12
Q

what is meant by acquired resistance?

A

acquisition of a gene that encodes a resistance mechanism

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13
Q

what are examples of acquired resistance?

A

horizontal transfer, new mutation - usually an antibiotic modifying enzyme or a target alteration

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14
Q

why might antibiotics not work?

A

wrong type, enzymatic degradation, target alteration so cannot bind or decreased permeability

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15
Q

what are examples of decreased permeability?

A

vancomycin - gram negative bacilli have an outer membrane that is impermeable to it
gentamicin - anaerobes - uptake of aminoglycosides is O2 dependent

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16
Q

what are examples of the target modification?

A

flucloxacillin - MRSA has an altered penicillin binding protein meaning that beta lactams cannot bind
trimethoprim - gram negative bacilli have mutations in the dihydrofolate reductase genes
vancomycin - VRE has altered peptide sequence in gram negative peptidoglycan meaning that they binding of vancomycin is reduced 1000 fold

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17
Q

what are examples of enzymatic degradation?

A

penicillins and cephalosporins - there are extended spectrum beta lactamases, penicillinases and carbapenamases
other enzymes will inactivate aminoglycosides and chloramphenicol

18
Q

what are examples of drug efflux?

A

multiple antibiotics, especially in gram negatives, antifungal triazoles and candida spp

19
Q

what are the main reasons for development and spread of resistace?

A

horizontal and vertical transfer, single genes encoding resistance and resistance genes encoded in plasmids

20
Q

what are examples of single gene resistance?

A

antibiotic modifying or altered targets

21
Q

what are plasmids for in resistance?

A

these are circular DNA sequences that are transmitted within and between species mainly bhy conjugation

22
Q

what role does horizontal transfer play in resistance?

A

enabled by transponons and integrons, DNA sequences are designed to be transferred from plasmid to plasmid or to chromosome/genome between or within species - often contain cassettes with multiple resistance genes

23
Q

what role does vertical transmission play in resistance?

A

chromosomal or plasmid borne resistance genes transferred to daughter cells on bacterial cell division - binary fission

24
Q

what are the causes of resistance?

A

bacteria are subject to constant spontaneous mutations that may confer a survival advantage that favours the growth and propogation of the mutant strain. If the organisms is growing in the presence of a sub-inhibitory concentration of ABs then the development of the resistance gene will confer an advantage, out compete and produce a new strain therefore making it more likely to reinfect

25
Q

how can bacteria get into humans?

A

can enter the microbiome through direct or environmental contact - fomites

26
Q

what is the result of a microbiome?

A

it will be a mix of resistant and sensitive bacteria - resistance may pass on to other species and sensitive will die and result in a dominant strain

27
Q

what are the two distinct ways that antibiotic resistance is conferred?

A

exposure to antibiotics and transmission of resistant organisms - spontaneous mutation and natural selection

28
Q

how is resistance managed?

A

through minimal use of ABs and through effective infection prevention and control

29
Q

if you remove antibiotics why do resistant strains die out?

A

resistance mutations usually affect bacterial cell functions such as DNA synthesis and therefore these are less fit than sensitive bacteria. If remove ABs then exposure is ceased and no longer advantageous gene meaning they will be outcompeted

30
Q

what is difficult about AB development?

A

everytime a new AB is produced a new mutation appears

31
Q

what is the antibiotic era?

A

it is the time period when antibiotics were readily available

32
Q

what is the post antibiotic era?

A

term used to describe time after the widespread antibiotic resistance has reduced the availability of antibiotics to treat infection

33
Q

what are the practical consequences of resistance?

A

bacterial infections become resistant to the antibiotics that usually treat them - MRSA, vancomycin/glycopeptide resistant enterococcci, extended spectrum beta lactamase enterococci, carbapenamase producing enterobacteriaceae, extremely resistant and multidrug resistant TB

34
Q

what is enterobacteriaceae resistant to?

A

resistant to amoxicillin, ciproflaxacin, gentamicin and carbapenems

35
Q

what are pseudomonas resistant to?

A

ceftazidime, and carbapenems

36
Q

how is resistance applied?

A

empiric therapy - do not want under treatment but do not want broad spectrum, targeted therapy - toxic, expensive and last line

37
Q

how do we monitor antibiotic resistance?

A

through local, national and international surveillance

38
Q

how do we do local surveillance?

A

alert organism surveillance for individual cases to trigger immediate interventions and do longitudinal data collection to work out trends in resistance and inform local AB policies

39
Q

how do we do national surveillance?

A

submission of isolated of particular concern to reference labs and collection of longitudinal data to inform national antibiotic policies

40
Q

what is the epidemiology of resistance?

A

variation throughout the globe - south europe is highest and there are hotspots such as the indian subcontinent for carbapenem resistance

CP (38 decks)

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