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Management of Infection > Lecture 22 - Antimicrobial Resistance (Global Challenges) > Flashcards

Lecture 22 - Antimicrobial Resistance (Global Challenges) Flashcards

1
Q

What are the main causes of resistance?

A

poor compliance

inadequate treatment and diagnosis

poor health care infrastructure

lack of education and knowledge

global location causes severe logistical issues

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2
Q

How many deaths annually does tuberculosis cause?

A

1.5 million

> 40 million deaths in the next 20 years

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3
Q

How is tuberculosis spread?

A

from inhaling droplets from a cough or sneeze by an infected person

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4
Q

What is there a strong epidemiological co-existance between?

A

HIV and TB as patients who are immunocompromised easily catch TB

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5
Q

What is the structure of the TB cell wall?

A

very complicated

have long fatty acids called mycolic acids

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6
Q

What is very unique with TB?

A

persistance - after you become ill with TB bacteria can lie dormant in the body

you can be infected with TB but never full develop the disease

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7
Q

Why is treatment of TB difficult?

A

the disease causes many complex systems

mycobacterium tuberculosis has a very complex cell wall

reactivation of dormant or persistent bacteria

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8
Q

Bacterial persistence of TB?

A

after treatment a small % may remain in a dormant state in macrophage

these can become reactivated many years later

patients can show no symptoms - carriers

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9
Q

What is the % of risk of reactivation to secondary TB?

A

2-23% lifetime risk

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10
Q

What is risk of reactivation increased by?

A

10% if immunosuppressed

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11
Q

What are the 2 phases of treatment?

A

initial phase and the continuation phase

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12
Q

What is the initial phase of TB treatment?

A

4 drugs given together daily

isoniazid

rifampicin

pryazanimide

ethambutol

(first 3 as rifater)

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13
Q

How long is the initial phase?

A

2 months

can be extended until sensitivity testing is complete

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14
Q

What is the initial phase for?

A

to reduce the bacterial population as rapidly as possible

prevents resistance

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15
Q

What is pyrazinamide used for?

A

helps to reduce the chance of reactivation

PZA is only active during the initial phase

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16
Q

Why is PZA only active during the initial phase?

A

due to host immune response lowering pH in macrophages

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17
Q

What is the continuation phase of TB treatment?

A

rifampicin and isoniazide used together as Rifinah

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18
Q

How long is the continuation phase?

A

4 months

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19
Q

What does the continuation phase do?

A

helps destroy remaining bacteria left from initial phase

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20
Q

When is the treatment of TB extended?

A

for meningitis or resistant TB

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21
Q

What is directly observed treatment?

A

necessary for patients who cannot comply with their regime

ensures the best chance of fighting the infection

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22
Q

What needs to be changed in DOT?

A

regime and doses

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23
Q

How often is supervision given in DOT?

A

3 times per week

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24
Q

Why is treatment of TB so critical?

A

because of the complex nature of TB all drugs need to be taken and the treatment must be completed

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25
Q

How is the treatment of TB designed?

A

it is old and designed due to the complex pathology of the mycobacteria

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26
Q

What are bacteriostatic drugs?

A

inhibit growing bacteria

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27
Q

What are bactericidal drugs?

A

kill bacteria outright

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28
Q

What is the distinction of drugs relative to?

A

the environment

29
Q

When is PZA bactericidal?

A

against TB at low pH but bacteriostatic against growing bacteria

30
Q

What do the first line TB drugs have?

A

superior efficacy with acceptable toxicity

31
Q

What do second line TB drugs have?

A

less efficacy and/or worse side effects

32
Q

What is isoniazide?

A

(1952)

isonicotinic acid hydrazide

33
Q

How does isoniazide work?

A

targets the ketoenoyl-reductase enzyme InhA in cell wall mycolic acid biosynthesis

34
Q

What is isoniazide activated to?

A

a binding complex with InhA

35
Q

How does rifampicin work?

A

prevents protein synthesis binding to DNA-dependent RNA polymerase b-subunit

36
Q

Spectrum of rifampicin?

A

broad spectrum bactericidal activity

37
Q

What does rifampicin help sterilise?

A

persistors and active mycobacteria

38
Q

What is pyrazinamide bactericidal against?

A

persisting slow growing mycobacteria

39
Q

Mode of action of pyrazinamide?

A

unclear but it is a prodrug

40
Q

What is pyrazinamide converted to?

A

the acid form pyrizinoic acid

41
Q

What does pyrazinamide require?

A

low pH macrophage environment (intracellular)

42
Q

How does resistance of TB occur?

A

rapidly when single drug is used so combination therapy is the standard

43
Q

What is the mechanism of resistance?

A

via efflux or mutation at the target enzyme or the enzyme which activates the prodrug to the active form

44
Q

MDR-TB?

A

INH and RIF with/out 2nd line drugs

45
Q

XDR-TB?

A

INH, RIF at least one second line injectable aminoglycoside and any fluoroquinolone

46
Q

What is XDR-TB?

A

extremely drug resistant TB

47
Q

What do future TB drugs need to be?

A

more efficacious, reduce bacterial population faster, combat MDRTB and be less prone to inducing resistance

destroy persistant bacteria and prevent cross resistance

reduce duration of therapy and increase compliance, need to be cheap

suitable for infants

48
Q

What to TB drugs need to be compatible with?

A

rifampicin

this increases the rate of metabolism of antiviral drugs

49
Q

Estimated annual deaths of malaria?

A

1-2 million

50
Q

Malaria infections annually?

A

500 million

51
Q

What increases the pool of infection of malaria?

A

global warming and ease of international travel

52
Q

What is the malaria vector?

A

female anopheles mosquito

53
Q

What species transmit malaria?

A

plasmodium vivax, falciparum malariae, ovale

54
Q

What are the most prevalent species of plasmodium?

A

vivax and flaciparum (95% of infection)

55
Q

What do tissue schizontocides do?

A

inhibit the growth of the pre-erythrocytic stages of the parasite in the liver

sometimes called casual prophylactics

56
Q

Examples of tissue schizontocides?

A

sulfafioxine, pyrimethamine, dapsone, proguanil

57
Q

Type I tissue schizontocides?

A

anti-folates
inhibits dihydrofolate production

sulfadioxine
dapsone

58
Q

Type II tissue schizontodices?

A

anti-folates

inhibit dihydrofolate reductase

pyrimethamine
proguanil

59
Q

What are hypnozoitocides?

A

only used to eradicate the dormant liver stage of vivax infections

disrupts the REDOX process in the pentose-phosphate pathway

60
Q

Example of a hyponozoitocide?

A

primaquine (UK)

61
Q

What are blood schizontocides?

A

act rapidly and only on the erythrocytic stage of the infection

some used prophylactically but mainly for treating established malarial infection

62
Q

What do blood schizontocides prevent?

A

hemozoin formation leading to cell death by binding to heme in the parasite

63
Q

Examples of blood schizontocides?

A

chloroquine

quinine

64
Q

How have new antimalarials been found?

A

through nature or by making analogues of natural products

65
Q

What are examples of new antimalarials?

A

mefloquine

artemisinin

66
Q

What is malarial resistance caused by?

A

mutation as active site or pro-drug activation in the chromosome

preventing cellular uptake of the drug

67
Q

What is resistance of malaria mainly due to?

A

plasmodium falciparum

68
Q

What varies with destination?

A

chemoprophylaxis guidelines and the treatment of infection due to resistance

Management of Infection (36 decks)

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