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Infection > Antimicrobial Chemotherapy COPY > Flashcards

Antimicrobial Chemotherapy COPY Flashcards

1
Q

What are the principles of antivirals?

A
  • All are virustatic, none are virucidal
  • Toxicity to host cell not uncommon: side effects
  • Only used in a minority of viral infections
  • Several stages of the virus life cycle are targets
  • Most targets are intracellular
  • Greater effect on viral replication than on the host cell function
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2
Q

What are most antivirals?

A

Nucleoside analogues that inhibit nuclei acid synthesis

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3
Q

Why are there limited potential targets for antiviral drugs?

A
  • Viruses are obligate intracellular parasites

- They utilise host cell enzymes in order to replicate, hence limited targets for drug

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4
Q

When may virus infection be treated?

A
  • Prophylaxis (to prevent infection)
  • Pre-emptive therapy (when evidence of infection detected, but before symptoms apparent)
  • Overt disease
  • Suppressive therapy (to keep viral replication below the rate that causes tissue damage in asymptomatic infected patient)
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5
Q

Why may suppressive treatment be required following successful treatment of overt infection?

A

Antivirals do NOT eradicate virus from latently infected cells

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6
Q

When are antivirals used in herpes simplex infection

A
  • Mucocutaneous: oral, genital, eye, skin
  • Encephalitis
  • Immunocompromised: any site
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7
Q

When are antivirals used in chickenpox?

A

Those at increased risk of complications

  • Neonate
  • Immunocompromised
  • Pregnant

Immunocompetent adult if begun within 24 hours of onset of rash

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8
Q

When are antivirals used in shingles?

A

Only decreases post-herpetic neuralgia in the immunocompetent host if begun within 72 hours of onset of symptoms

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9
Q

What antivirals are used in HSV and VZV?

A
  • Aciclovir: Oral, IV, eye ointment, cream
  • Valaciclovir: Oral
  • Famiciclovir: Oral
  • Foscarnet: IV
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10
Q

What is the activity of acyclovir in herpes infection?

A

Only active in herpes infected cells, it has low toxicity for uninfected cells

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11
Q

What is the mode of action for acyclovir?

A
  • Aciclovir converted by viral thymidine kinase to ACVMP
  • ACVMP converted by host cell kinases t ACV-TP
  • ACV-TP competitively inhibits and inactivates HSV-specific DNA polymerase
  • Preventing further viral DNA synthesis without affecting the normal cellular processes
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12
Q

When is CMV treated with antivirals?

A
  • Only in life or sight threatening infection as all available drugs have significant toxicity
  • HIV patients with CM retinitis or colitis
  • Transplant patients with pneumonitis
  • May used to treat neonates with symptomatic congenital CMV infection
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13
Q

What antivirals are used in CMV infection?

A
  • Ganciclovir: IV, ocular implant
  • Valganciclovir: Oral
  • Cidofovir: IV
  • Foscarnet: IV
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14
Q

How have antivrials transformed HIV care?

A
  • Restoration of immune function in AIDS

- Decrease in opportunistic infections

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15
Q

What is cART?

A

Combination anti-retroviral therapy

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16
Q

What antivirals are used in chronic hepatitis B?

A

Pegylated interferon alpha (subcut.)

Nucleoside/tide analogues

  • Tenofovir
  • Adefovir
  • Entecavir
  • Lamivudine
  • Emtricitabine
  • Telbivudine
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17
Q

What are the current therapies for chronic hepatitis C?

A
  • Pegylated interferon alpha (subcut.) & ribavirin (oral)
  • Plus protease inhibitor (telaprevir or boceprevir)
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18
Q

What new-directly acting antivirals are there for chronic hepatitis C infection?

A
  • Daclatasvir
  • Sofosbuvir
  • Simeprevir
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19
Q

How long is the therapy regime for chronic hepatitis C?

A

12-48 weeks

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20
Q

How should antivirals be used in influenza A or B?

A
  • Role in both treatment and prophylaxis

- Not always indicated, but if used, should usually start within 48 hours of onset of symptoms/contact.

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21
Q

What antiviral is used in respiratory syncytial virus?

A

Ribavirin (rarely indicated though)

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22
Q

How can resistance to antivirals be tested?

A
  • Phenotypic: can virus grow in presence of compound, e.g. HSV
  • Genotypic: sequence genome and identify resistance-associated mutations, e.g. HIV
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23
Q

When should resistance be suspected in herpes virus?

A

In immunocompromised if there is no response to appropriate antiviral doses within 7 days

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24
Q

What is usually effect in acyclovir resistant HSV and CMV?

A

Foscarnet

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25
Q

When is HIV resistance testing performed?

A
  • Baseline diagnosis
  • Failing therapy
  • New treatment approach required for other reasons
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26
Q

When do trough and peak levels need to be monitored in acyclovir use?

A

In patients with renal impairment

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27
Q

What are the principles of prescribing antibiotics?

A
  • Indications for antimicrobials
  • Making a clinical diagnosis
  • Patient characteristics
  • Antimicrobial selection
  • Regimen selection
  • Liaison with laboratory
  • Antimicrobial Stewardship
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28
Q

What is empiric antimicrobial therapy?

A

Therapy without microbiology results

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29
Q

What is directed antimicrobial therapy?

A

Therapy based on microbiology results

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30
Q

Give examples of primary antimicrobial prophylaxis.

A
  • Anti-malarial; immunosupressed patients
  • Pre-operative surgical
  • Post-exposure e.g. HIV, meningitis
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31
Q

Give an example of secondary antimicrobial prophylaxis.

A

To prevent a second episode of PJP

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32
Q

What is involved in diagnosis when prescribing antimicrobials?

A

Diagnosis of infection

  • Clinical
  • Laboratory
  • None (no treatment)

Severity assessment

  • ?Sepsis (qSOFA; systolic BP <100, altered mental state, RR>20)
  • ?Septic shock
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33
Q

What patient characteristics contribute to the prescribing of antimicrobials?

A
  • Age
  • Renal function
  • Liver function
  • Immunocompromised
  • Pregnancy
  • Known allergies
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34
Q

What antimicrobial selection/ choice must be made when prescribing?

A
  • Guideline or “individualised” therapy
  • ? likely organism(s)
  • Empirical therapy or result-based therapy
  • Bactericidal vs. bacteriostatic drug
  • Single agent or combination
  • Potential adverse effects
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35
Q

What should antibiotic selection be based on?

A

Known (or likely) organism

36
Q

What bacteria are implicated in soft tissue infections?

A
  • Streptococcus pyogenes
  • Staphylococcus aureus
  • Streptococcus group C or G
  • E. coli
  • Pseudomonas aeruginosa
  • Clostridium species
37
Q

What bacteria are implicated in pneumonia?

A
  • Streptococcus pneumonia
  • Haemophilus influenzae
  • Staphylococcus aureus
  • Klebsiella pneumonia
  • Moraxella catarrhalis
  • Mycoplasma pneumonia
  • Legionella pneumonia
  • Chlamydia pneumonia
38
Q

What are the features of bactericidal antibiotics?

A
  • Example: B-lactams
  • Act on cell wall
  • Kill organisms
  • Indications include neutropenia, meningitis and endocarditis
39
Q

What are the features of bacteriostatic antibiotics?

A
  • Example: macrolides
  • Inhibit protein synthesis
  • Prevent colony growth
  • Require host immune system to ‘mop up’ residual infection
  • Useful in toxin-mediated illness
40
Q

What are the advantages of single therapy?

A
  • Simpler
  • Fewer side effects
  • Fewer drug interactions
41
Q

When is combination therapy used?

A
  • HIV and TB therapy
  • Sever sepsis (febrile neutropenia)
  • Mixed organism (faecal peritonitis)
42
Q

What must be considered when selecting a regime for antimicrobials?

A
  • Route of administration
  • Dose
  • Adverse effects (side effects/toxicity)
  • Duration
  • Intravenous to oral SWITCH therapy
  • Inpatient or Outpatient therapy (outpatient parenteral antimicrobial therapy OPAT)
  • Therapeutic drug monitoring
43
Q

What is oral bioavailability?

A
  • Ratio of drug level when given orally compared with level when given iv
  • Varies widely: flucloxacillin 50-70%, linezolid 100%
44
Q

When is the oral routed used to administer antimicrobials?

A

If not vomiting, normal GI function, no shock or organ dysfunction

45
Q

When is the IV route used to administer antimicrobials?

A

For severe or deep-seated infection and when oral route is not reliable

46
Q

What types of allergic reactions can occur with antimicrobials?

A

Immediate hypersensitivity
-Anaphylaxis

Delayed hypersensitivity
-Rash, drug fever, serum sickness, erythema nodosum, Steven’s Johnson syndrome

Most occur with penicillin’s and cephalosporins

47
Q

What gastrointestinal adverse effects can occur with antimicrobials?

A
  • Nausea, vomiting, diarrhoea

- C. diff infection

48
Q

What neurological adverse effects can occur with antimicrobials?

A
  • Ototoxicity - gentamicin, vancomycin
  • Optic neuropathy - ethambutol (TB)
  • Convulsions, encephalopathy - penicillins, cephalosporin
  • Peripheral neuropathy - isoniazid (TB), metronidazole
49
Q

What haematological adverse effects can occur with antimicrobials?

A
  • Marrow toxicity

- Megaloblastic anaemia (folate metabolism) co-trimoxazole

50
Q

What types of antibiotics are most likely to cause candida (thrush)?

A
  • Broad spectrum penicillins

- Cephalosporins

51
Q

What drugs can have an adverse effect on the liver?

A
  • All drugs, particularly tetracyclines, TB drugs

- More likely if pre-existing liver disease

52
Q

What drugs can have an adverse effect on the renal system?

A
  • Gentamicin, vancomycin

- More like if pre-existing renal disease or on nephrotoxic meds

53
Q

When does liaison with the laboratory take place?

A

Sending appropriate specimens
-Culture / direct detection/ serology

Receiving results

  • Preliminary culture results
  • Sensitivity results
  • Final results

Monitoring

  • Disease activity
  • Therapeutic drug monitoring
54
Q

What is antimicrobial stewardship?

A

-Making the best use of our current antimicrobials

55
Q

Who is involved in antimicrobial stewardship?

A

Antimicrobial management team

  • Antibiotic pharmacists
  • Infectious diseases
  • Acute medicine
  • Medical microbiology
  • Infection prevention and control
  • General practice
  • Public partner
56
Q

What is the role of the antimicrobial management team?

A
  • Produce antimicrobial guidelines and policies
  • Audit of quality of antimicrobial prescribing
  • Education
57
Q

What are the 4C antibiotics implicated in CDI?

A
  • Co-amoxiclav
  • Ciprofloxacin
  • Ceftriaxone
  • Clindamycin
58
Q

Give examples of antimicrobial classes.

A
  • Penicillins (β-lactams)
  • Cephalosporins (β-lactams)
  • Aminoglycosides
  • Macrolides
  • Quinolones
  • Glycopeptides
  • Others
  • Antifungals
  • Antivirals
59
Q

What are the 3 main mechanisms of action of antibiotics?

A
  • Inhibition of cell wall synthesis
  • Inhibition of protein synthesis
  • Inhibition of nucleic acid synthesis
60
Q

Give examples of antibiotics which inhibit cell wall synthesis.

A

B-lactams
-Penicillins and cephalosporins

Glycopeptides
-Vancomycin and teicoplanin

61
Q

Give examples of antibiotics that inhibit protein synthesis.

A
  • Aminoglycosides: gentamicin
  • Macrolides: clarithromycin
  • Tetracyclines: doxycycline
  • Oxazolidinones: linezolid
62
Q

Give examples of antibiotics that inhibit nucleic acid synthesis.

A
  • Trimethoprim
  • Sulfonamides: sulfamethoxazole
  • Quinolones: ciprofloxacin
63
Q

Give examples of classes of antifungals.

A
  • Azoles
  • Polyenes
  • Echinocandins
  • Terbinafine
64
Q

Give example of azole antifungals.

A
  • -Fluconazole: Candida, some resistance
  • Itraconazole: Candida & Aspergillus
  • Voriconazole: Candida & Aspergillus
65
Q

Give examples of polyene antifungals.

A
  • Amphotericin: candida and aspergillus

- Nystatin: candida

66
Q

Give examples of echinocandin antifungals.

A

Caspofungin, anidulafungin, micafungin : candida, aspergillus

67
Q

What is terbinafine used for?

A

Tinea and fungal nails

68
Q

What emerging resistance to pathogens is of global interest?

A
  • MRSA
  • MDR
  • VRE
  • Acinetobacter baumannii
  • Clostridium difficile
69
Q

What contributes to the propagation of MRSA in the UK?

A
  • Re-admission of MRSA carriers from community
  • Bed/staff shortage
  • Lack of isolation facilities
  • Poor hygiene, cleaning and disinfection
  • Antibiotic mis-use
  • Standard precautions
70
Q

Give examples of causes of increased pathogenicity of MRSA when exposed to antibiotics.

A
  • Biofilm formation
  • Small colony variants
  • Efflux
  • Hypermutation
  • Skin/RT colonization leads to transmissibility
  • Fibrinonectin-binding protein
  • Toxin production eg x, TSST-1
  • SOS response leads to horizontal gene transfer
  • Phage induction
  • Quorum sensing
  • agr expression
  • Autolysis
  • Intracellular persistence
71
Q

What factors contribute to MRSA colonisation?

A
  • Poor infection control
  • MRSA colonization pressure
  • MRSA in the environment
  • Length of stay, medical devices
  • Antimicrobial consumption
72
Q

What factors contribute to MRSA infection?

A
  • Exposure to fluoroquinolones,
  • ß-lactams - selection,
  • Increased adhesion
  • Increased virulence
  • Patient risk factors, etc.
73
Q

What is the problem with antimicrobial resistance?

A

Patients with infections caused by drug-resistant bacteria are generally at increased risk of worse clinical outcomes and death, and consume more healthcare resources than patients infected with the same bacteria that are not resistant

74
Q

What accelerates the emergence of drug-resistance?

A

The use and misuse of antimicrobials

75
Q

What is the UK 5 years antimicrobial resistance strategy?

A
  • Improve knowledge & understanding of AMR
  • Conserve and steward the effectiveness of existing treatments
  • Stimulate the development of new antibiotics, diagnostics and novel therapies
76
Q

What do the Scottish antimicrobial prescribing group (SAPG) do?

A

Co-ordinates & delivers a national framework for antimicrobial stewardship to enhance the quality of antimicrobial prescribing & management in Scotland

77
Q

What are the current HEAT targets for hospital prescribing?

A
  • Indication for antibiotic is documented and compliant with local policy
  • Duration of oral antibiotics is documented and compliant with local policy
78
Q

What are NHS Grampian’s strategies for reducing AMR?

A
  • Policies and guidelines
  • Audits and feedbacks
  • Surveillance date
  • Education
79
Q

What acute policies and guidelines do NHS Grampian have to prevent AMR?

A
  • Empirical guidelines
  • Documentation & review/stop date
  • IVOST policy
  • Penicillin allergy
  • Alert Antimicrobials
  • Gentamicin
  • Vancomycin
80
Q

When should you consider switching a patient from IV to oral antibiotics?

A

After 48 hours provided that:

  • The patient is improving clinically
  • Is able to tolerate an oral formualtion
81
Q

What criteria should be met before switching a patient from IV to oral antibiotics?

A
  • Able to swallow and tolerate fluids
  • Temp. 36-38°C for at least 48 hours
  • Heart rate < 100bpm for previous 12 hours
  • WCC between 4 and 12x109L
82
Q

What are alert antimicrobials?

A
  • For restricted use only under the authorisation of a microbiologist, or infectious diseases (or other relevant) specialist eg meropenem
  • Administered according to approved indications within local guidelines/policies e.g. ceftriaxone allowed for meningitis
83
Q

What measures are in place in primary care to help prevent AMR?

A
  • Empirical Guidelines
  • Delayed prescriptions
  • ‘Non-Prescription’ Pad
  • Patient information leaflets on management of self-limiting upper respiratory tract infections and cystitis
84
Q

How can healthcare workers tackle AMR?

A
  • Practicing effective infection prevention & control
  • Prescribing and dispensing antibiotics only when truly needed
  • Prescribing & dispensing the right antibiotic(s) for the right duration to treat the illness
85
Q

How can the public tackle AMR?

A
  • Use antibiotics only when prescribed
  • Complete the full course
  • Never share antibiotics or use leftover prescriptions

Infection (15 decks)

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