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Clinical pathology > Theme 3- part 1 > Flashcards

Theme 3- part 1 Flashcards

1
Q

What are antimicrobials for?

A
  • To increase the likelihood that a person with an infection will make a clinical recovery
  • Inhibit critical process in bacterial/fungal cells – antimicrobial targets-

Enzymes, molecules or physical structures

cell wall

protein synthesis

DNA synthesis

RNA synthesis

-With minimal harm to the patient – selective toxicity

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2
Q

What is an antibiotic?

A

Chemical products of microbes that inhibit or kill other organisms

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3
Q

Whar are types of antibmicrobial agents?

A

Antimicrobial agents (antibacterial, antifungal, antiviral)

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4
Q

What are antimicrobial agents?

A
  • Antibiotics
  • Synthetic compounds with similar effect
  • Semi-synthetic i.e. modified from antibiotics -Different antimicrobial activity/spectrum, pharmacological properties or toxicity
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5
Q

What does a bacteriostatic/fungistatic do?

A

Inhibit growth- Mainly protein synthesis inhibitors

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6
Q

What does a bacteriocidal/ fungicidal do?

A

Cause cell death-Mainly cell wall-active agents

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7
Q

What is minimum inhibitory concentration?

A

Minimum concentration of antimicrobial agent at which visible growth is inhibited

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8
Q

What is minimum bacteriacidal/fungicidal concentration?

A

Minimum concentration of antimicrobial agent at which most organisms are killed

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9
Q

Antimicrobial interactions- what is synergy?

A

A combination is considered to be synergistic when the effect observed with a combination is greater than the sum of the effects observed with the two drugs independently

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10
Q

Antimicrobial interactions- what is antagonism?

A

Activity of two antimicrobials given together is less than the activity of either if given separately

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11
Q

What is the antimicrobial spectrum?

A

Range of bacterial/fungal species likely to be sensitive to a particular antibacterial/antifungal agent

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12
Q

What are broad spectrum antibiotics?

A

Broad spectrum – kills most types of bacteria/fungi encountered

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13
Q

What are narrow spectrum antibiotics?

A

Narrow spectrum – kills only a narrow range of organisms

The narrowest-spectrum antibiotic that is appropriate should be used at all times

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14
Q

What is the cell wall of bacteria made up of?

A

Peptidoglycan (murein)

  • Major structural component of bacterial cell wall
  • Polymer of glucose-derivatives, N-acetyl muramic acid (NAM) and N-acetyl glucosamine (NAG)
  • Oligopeptide crosslinks formed by transpeptidases known as “penicillin binding proteins” (PBPs).
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15
Q

Why are cell wall synthesis inhibitors allow selective toxicity?

A

No cell wall in animal cells

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16
Q

Examples of cell wall synthesis inhibitors?

A
  • β-lactams (beta-lactams, penicillins)
  • Glycopeptides
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17
Q

What do β-lactam antibiotics contain?

A
  • All contain β-lactam ring
  • Four-membered ring structure (C-C-C-N)
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18
Q

Mechanism of action for β-lactam antibiotics?

A

Mechanism of action: Inhibition of PBPs (penicillin binding proteins)

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19
Q

What are types of B-lactam antibiotics?

A

Penicillins, Cephalosporins and Cephalosporins, monolactams

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20
Q

What are examples of penicillins for B-lactam antibiotics?

A

Benzylpenicillin, amoxicillin, flucloxacillin

Relatively narrow spectrum

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21
Q

What are examples of cephalosporins

A

Cephalosporins- better for gram negative

Cefuroxime, ceftazidime etc.

  • Broad spectrum
  • Arranged into ‘generations’- age into clinical use

Cephalosporins Meropenem, imipenem

Extremely broad spectrum

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22
Q

What are examples of monobactams?

A

MonobactamsAztreonam

  • Gram-negative activity only
  • And has slightly different ring structure
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23
Q

What are examples of glycopeptides?

A

Vancomycin, teicoplanin

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24
Q

What do glycopeptides do? Are they able to penetrate gram-negative of postive?

A

Large molecules, bind to terminal amino acids on NAM pentapeptides- Inhibit binding of transpeptidases and thus peptideoglycan cross-linking

Gram-positive activity- Unable to penetrate Gram-negative outer membrane

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25
Q

What is the mechanism for bacterial protein synthesis inhibitors?

A

Protein synthesis takes place on the bacterial ribosome- inhibit this stop the growth

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26
Q

What are examples of bacterial protein synthesis inhibitos?

A
  • Aminoglycosides (e.g. gentamicin, amikacin)
  • Macrolides (e.g. erythromycin, clarithromycin) and lincosamides (clindamycin)
  • Tetracycline, doxycycline
  • Linezolid – Gram-positive infections
  • Mupirocin – topical agent for staphylococcal/streptococcal infection
  • Fusidic acid (not used very much)
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27
Q

What are examples of DNA synthesis inhibitors?

A

trimethoprim and sulfonamides

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28
Q

What do trimethoprim and sulfonamides inhibit?

A

Both agents inhibit folate synthesis

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29
Q

What does trimethoprim treat?

A

Commonly used to treat urinary tract infections

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30
Q

What is co-trimoxazole?

A

Co-trimoxazole (trimethoprim-sulfamethoxazole)

Treats Antibacterial, antifungal (Pneumocystis jirowecii) and antiparasitic (Toxoplasma gondii)

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31
Q

What is a DNA synthesis inhibitor?

A

fluoroquinolones

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32
Q

What does fluoroquinolones inhibit?

A

Inhibit one or more of two related bacterial enzymes

  • DNA gyrase and topoisomerase IV
  • Involved in remodelling of DNA during DNA replication
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33
Q

fluoroquinolones examples?

A

Ciprofloxacin, levofloxacin

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34
Q

What is an RNA synthesis inhibitor?

A

Rifampicin

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35
Q

What is the mechanism for rifampicin?

A
  • RNA polymerase inhibitor
  • Prevents synthesis of mRNA
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36
Q

What are examples of gram-negative cell membrane agents?

A

Colistin/polymyxin E (Gram-negatives)

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37
Q

What are examples of gram positive cell membrane agents?

A

Daptomycin (Gram-positives)1

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38
Q

Mechanism of cell membrane agents?

A

Destruction of outer membrane or cytoplasmic membrane

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39
Q

Summary of antibacterial mechanisms

A
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40
Q

Pathogenic fungi divided into what?

A

filamentous fungi and yeasts

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41
Q

What is the structure of a fungal cell?

A
  • Fungal cell has cell membrane, cell wall and protein synthesis apparatus within it.
  • Fungal cell membrane ergosterol which has the same function as cholesterol in cell membranes.
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42
Q

What is the fungal cell wall made of?

A

β-1,3-glucan

No cell wall in animal cells- Ideal potential for selective toxicity

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43
Q

What are antifungal cell wall inhibitors?

A

Echinocandins (antifungal)

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44
Q

What is the mechanism of antifungal cell wall inhibitors?

A

Inhibit β-1,3-glucan synthase

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45
Q

Examples of Antifungal cell wall inhibitors?

A
  • Anidulafungin
  • Caspofungin
  • Micafungin
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46
Q

Antifungal cell membrane agents examples?

A
  • Azoles
  • Terbinafine
  • Amphotericin B (and nystatin)
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47
Q

What are examples of azoles?

A

Azoles (eg clotrimazole, fluconazole, voriconazole)

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48
Q

What is the mechanism for terbinafine?

A

Inhibit synthesis of ergosterol

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49
Q

What is the mechanism for Amphotericin B (and nystatin)?

A

Bind to ergosterol causing physical damage to the membrane

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50
Q

Antifungal RNA/DNA synthesis inhibition- what agent is used?

A

5-fluorocytosine

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51
Q

What is the mechanism for Antifungal RNA/DNA synthesis inhibition?

A

Transported into fungal cells by a fungal enzyme-Cytosine permease

Metabolised into inhibitory molecules- Mainly 5-fluorouracil

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52
Q

Summary of antifungal mechanisms

A
53
Q

What are the steps for use of antimicrobial agents?

A

Empiric therapy- based on predicted susceptibility of likely pathogens and local antimicrobial policies

Targeted therapy- predicted susceptibility of infecting organisms

Susceptibility-guided therapy- based on susceptibility testing results

54
Q

What is empiric therapy?

A

Empiric therapy – initial selection of antimicrobial agent(s) of broad enough spectrum to cover the range of organisms likely to be causing the patient’s infection

55
Q

What is targeted therapy?

A

Targeted therapy – use of narrowest-possible spectrum agent(s) based on the ID and sensitivities of the causative organism(s)

56
Q

Choice of empiric therapy stages?

A
  • Know the likely organisms – based on site of infection, patient’s immunological status and microbiological history
  • Identify what antimicrobial/combination is likely to have a spectrum that covers the organisms identified in (1)
  • Select an antimicrobial/combination from (2) that is appropriate for the patient and the site of the infection – taking into account any history of antibiotic allergy, availability at different body sites, drug interactions and adverse effects
57
Q

What does a virus consist of?

A

Consist of:

  • Nucleic acid (DNA or RNA)
  • Protein (coat - structural, enzymes-non-structural)
  • +/- Lipid envelope

Obligate intracellular parasites

58
Q

Virus infections that are acute are caused by what?

A

Acute (RNA viruses)

59
Q

What are examples of acute viruses?

A

Influenza, measles, mumps, hepatitis A virus

60
Q

What are chronic viruses caused by?

A

Chronic (generally DNA viruses)

61
Q

What are examples of latent chronic viruses?

A

Latent with (or without) recurrences

Herpes simplex, Cytomegalovirus

62
Q

What are examples of persistent chronic viruses?

A

HIV, HTLV, Hepatitis B virus, Hepatitis C virus

63
Q

What are non-vesicular rashes from?

A
  • Measles
  • Rubella
  • Parvovirus
  • Adenovirus
  • HHV6
64
Q

What are vesicular rashes?

A

red raised rashes but then become fluid filled

65
Q

What do you get vesicular rashes from?

A
  • Chickenpox (HHV3)
  • Herpes simples (HHV1/2)
  • Enterovirus
66
Q

Respiratory infection examples?

A
  • Influenza A/B
  • Respiratory Syncytial Virus
  • Parainfluenza virus
  • Human Metapneumovirus
  • Rhinovirus
  • Coronavirus (including SARS)
67
Q

Gastroenteritis examples?

A
  • Rotavirus
  • Norovirus
  • Astrovirus
  • Sapovirus
  • Adenovirus (group F)
68
Q

Neurological Disease examples?

A

Encephalitis/Meningitis

  • HSV
  • Enteroviruses
  • Rabies
  • Japanese encephalitis virus
  • Nipah Virus
69
Q

Blood-borne viruses examples?

A
  • Hepatitis viruses
  • Retroviruses
70
Q

Example of Hepatitis viruses?

A
  • HBV
  • HCV
71
Q

Retroviruses examples?

A

HIV

72
Q

When to use antivirals?

A
  • Acute infections in general population
  • Chronic infections
  • Infections in immunocompromised
73
Q

What are infections in immunocompromised?

A
  • Post-transplant
  • Individuals receiving immunosuppressive therapies
  • Patients with primary immunodeficiencies
74
Q

What is the treatment of HSV?

A

Aciclovir

75
Q

What does aciclovir treat?

A

Treat invasive disease

  • encephalitis
  • disseminated HSV (immunocompromised and neonates)
76
Q

What is treatment of primary oral-labial or genital herpes?

A

Primary oral-labial or genital herpes- don’t require treatment but are given prophylaxis (treatment that prevents disease)

Prophylaxis if frequent reactivations- to prevent

77
Q

What is the treatment of chickenpox and shingles (VZV)?

A

Treat with aciclovir

Treat all adults with chickenpox

Treat shingles

  • >60 (reduce incidence of post-herpetic neuralgia- affects nerve fibres and skin causing burning pain)
  • involves eye
  • immunocompromised
78
Q

Treatment of influenza?

A

Neuraminidase inhibitors oseltamivir (oral) and zanamavir (inhaled)

79
Q

Who is the treatment of infleunza?

A

Treat high risk patients

  • Chronic neurological, hepatic, renal, pulmonary and chronic cardiac disease
  • Diabetes mellitus
  • Severe immunosuppression
  • Age over 65 years
  • Pregnancy (including up to two weeks post-partum)
  • Children under six months of age
  • Morbid obesity (BMI ≥40)
80
Q

Treatment of chronic virus infections- how long do you give treatment for?

A

Usually has to be given lifelong – for DNA and retroviruses

81
Q

What virus is not treated with lifelong medications that is a chronic virus?

A

Exception is HCV which is caused by an RNA virus but can get a chronic infection so is treated with antivirals

82
Q

What are the steps for virus replication?

A
  1. Virus attachment to cell (via receptor)
  2. Cell Entry
  3. Virus Uncoating
  4. Early proteins produced – viral enzymes
  5. Replication
  6. Late transcription/translation – viral structural proteins
  7. Virus assembly
  8. Virus release and maturation- some released by killing the cell, others are released by reverse endocytosis out of the cells

If antivirals affect any steps in this process will inhibit viral replication. Cytotoxic T cells kill viral cells. Immunocompromised don’t make good cytotoxic T cells.

83
Q

Eukaryotes and DNA viruses use polyemerases to produce DNA to what?

A
  • DNA to DNA
  • DNA to RNA (mRNA)
84
Q

RNA viruses can produce what using polymerases?

A

RNA to RNA - RNA viruses can produce RNA from RNA so require RNA polymerase

85
Q

RNA use polymerases to DNA in what diseases?

A

RNA to DNA - take RNA to make DNA to insert into host genome

Retroviruses (HIV)

Hepatitis B virus

86
Q

Nucleoside Reverse Transcriptase Inhibitors (NRTI) inhibit what?

A

inhibit reverse transcriptase

87
Q

What are examples of NRTIs?

A
  • AZT (azidothymidine)
  • HIV NRTIs
  • HBV NRTIs
88
Q

What are examples of HIV NRTIs?

A

Pyrimidine analogues

  • Thymidine analogues-Zidovudine
  • Cytosine analogues-Lamivudine

Purine analogues (Adenosine and Guanosine)

  • Abacavir
  • Tenofovir
89
Q

What do Nucleoside Reverse Transcriptase Inhibitors (NRTI) treat?

A
  • HIV NRTIs
  • HBV
90
Q

What are Herpesvirus polymerase inhibitors?

A
  • Guanosine
  • Acyclovir- HSV and VZV
  • Ganciclovir- CMv, HHV6 (as well as HSV and VZV)
91
Q

HCV RNA polymerase nucleotide inhibitor example?

A

Sofosbuvir- prodrug

92
Q

Non-Nucleotide Reverse Transcriptase inhibitors (NNRTIs)- what do they do?

A

inhibit different parts of the enzyme

93
Q

Non-Nucleotide Reverse Transcriptase inhibitors examples?

A
  • Efavirenz
  • Nevirapine
94
Q

Protease Inhibitors (PIs) mechanisms?

A

All cells have proteases- they clip the proteins to make shorter lengths which then fold to bind to the protein- virus do this by make their own proteins and then make their own enzymes

95
Q

What do protease inhibitors treat?

A

HIV and HCV

96
Q

What are the types of PIs that treat HIV?

A

Atazanavir

Darunavir

Ritonavir- boost levels of other PIs

97
Q

What are the types of PIs that treat HCV?

A
  • Paritaprevir
  • Grazoprevir
98
Q

HIV drugs- Entry inhibitor?

A
  • Enfuviritide
  • Maraviroc
99
Q

HIV integrase inhibitors?

A

Integrase Inhibitors (retroviruses)

  • Raltegravir
  • Dolutegravir
100
Q

What is highly active antiretroviral therapy (HAART)?

A
  • 2 NRTIs + NNRTI
  • 2 NRTIs + boosted PI or integrase inhibitor
  • Often use fixed drug combinations (more than one drug in pill)- this is because there are high levels of replication, single agent won’t treat it as much. Also, viruses can adapt quickly so having more than one drug stopping viral resistance
  • Aim to switch off virus replication
  • Require lifelong treatment
  • For treating some chronic virus infections multiple antivirals are used to drive down viral loads and avoid development of antiviral resistance (eg HIV and HCV).
101
Q

RNA viruses can become chronic in immunocompromised individuals due to lack of what?

A

RNA viruses can become chronic in immunocompromised individuals due to lack of an adequate cytotoxic T-cell response.

102
Q

In acute viral infection antivirals only improve recovery if what?

A
  • In acute viral infection antivirals only improve recovery if started early during the illness (typically <48hrs of onset).
  • Therefore, antivirals are only generally used to treat acute infections where individuals are at higher risk of significant morbidity or mortality.
103
Q

Mutations occur quicker in RNA or DNA?

A

This may happen quickly for RNA viruses but can be slower for DNA viruses such as herpesviruses. Inadequate dosing of antivirals can promote antiviral resistance.

104
Q

What are tests done for infection?

A
  • Full blood count, Inflammatory markers (CRP, ESR, procalcitonin) Lactate, Blood gases
  • LFTs (biliary sepsis) U&Es (severe sepsis, urinary tract infection)
  • Serology
  • PCR
  • Microscopy, culture, sensitivity testing
  • Chest and bone x-rays, CT scans and FDG-PET/CT scans
105
Q

Symptoms suggestive of infection can be “system specific” or “non-specific”. What is the difference?

A

System specific e.g.

  • Cough (*respiratory)
  • Neck stiffness (*CNS)
  • Bony pain (*orthopaedic)
  • Skin pain/redness (*SST)
  • Dysuria (*urinary)

SST = skin and soft tissue; CNS = central nervous system

Nonspecific e.g.

  • Fever “burning up”
  • Shaking episodes/chills
  • Sweating/night sweats
  • Feeling muddled/confused
106
Q

Examination findings can also be “system specific” or “non-specific” what is the difference?

A

System specific e.g.

  • Lung crackles (*respiratory)
  • Meningism (*CNS)
  • Bony tenderness (*orthopaedic)
  • Skin erythema (*SST)
  • Loin tenderness (*urinary)

Non specific e.g.

  • Pyrexia
  • Witnessed rigor/chills
  • Sweating
  • Confusion

SST = skin and soft tissue; CNS = central nervous system; *clinical infection lecture

107
Q

What does Hb tell us about infection?

A

Haemoglobin (Hb) Not much help diagnosing infection – but anaemia of chronic disease (normocytic, normochromic) can be caused by infection

108
Q

What happens to WBC in infection?

A

White blood cell count (WCC) can be raised in infection, but other conditions too (poor specificity). Severe sepsis can lower WCC

109
Q

What are inflammatory markers?

A
  • C-reactive protein
  • Procalcitonin
110
Q

When do C-reactive protein and procalcitionin increase?

A
  • C-reactive protein <5mg/L- will go up in bacterial infections, not as much in viral
  • Procalcitonin <0.5µg/L (different centres use different cut-offs)- increases in bacterial infections and less so in viral infections
111
Q

Blood lactate and blood gases are tests for what?

A

Blood lactate and blood gases are tests that can help to identify severe sepsis and respiratory failure

112
Q

What is the tool to test for pneumonia?

A

CURB-65 (risk prediction tool for pneumonia)

113
Q

Methods of microbiological diagnosis?

A
  • Culture
  • Direct detection
  • Immunological tests
114
Q

What do blood cultures show us?

A

Identification-Immediate or by further testing

Typing-To establish organism relatedness

Sensitivity testing-To direct antimicrobial therapy

115
Q

What are false positives and negatives from in blood cultures?

A

False positives- from contamination

False negatives- not inoculating enough blood

116
Q

What is a gram stain?

A

Chemical process that distinguishes between bacterial cell walls that retain crystal violet, and those that do not, when stained and washed with acetone.

117
Q

Gram positive and gram negative stains after dye?

A

Gram positive- purple

Gram negative- pink

118
Q

What do Gram positive and negative cocci look like?

A

Gram positive cocci- long chains or clusters

Gram negative cocci- very small

119
Q

What do gram positive and negative bacilli look like?

A

Gram positive bacilli- chunky

Gram negative bacilli- very small

120
Q

What is sensitivity testing?

A
  • Culture of micro-organism in the presence of antimicrobial agent
  • Work out if the concentration of antimicrobial that will be available in the body is high enough to kill the micro-organism
  • Solid or liquid media
121
Q

What does sensitivity testing require?

A

Requires viable micro-organisms

Usually bacteria or fungi

122
Q

What is empirical therapy?

A

Initial treatment is with “empiric” therapy- based on experience from clinician

123
Q

What is targeted therapy?

A

Subsequent treatment is “targeted”

Requires

  1. Isolation of micro-organism
  2. Antimicrobial susceptibility testing- determines which antibiotics a bacteria or fungi is sensitive to
124
Q

Uses and limitations of cultures?

A
  • Establishes the presence of a micro-organism at a particular site
  • Cultivable organisms only
  • Allows the use of empiric and targeted antimicrobial therapy
  • Provides epidemiological and typing information
  • Is usually slower than direct detection
125
Q

What is direct detection?

A

Detection of whole organism- Microscopy

Detection of component of organism

  • Antigen
  • Nucleic acid (DNA or RNA)
126
Q

Direct detection - uses and limitations?

A

Establishes the presence of a micro-organism at a particular site

  • Cultivable and non-cultivable organisms

Allows the use of appropriate empiric antimicrobial therapy

Does not give any information on:

  • Antimicrobial susceptibility
  • Typing

Is usually the fastest diagnostic method

127
Q

Immunological tests function?

A

Detection of immune response to infectionAntibody detection

  • IgM detection
  • Seroconversion- Change from negative to positive result from one test to a subsequent test
  • Fourfold rise in titre- Rise in concentration of antibody from one test to a subsequent test

Other immunological tests- IFN-γ release assays in tuberculosis

128
Q

Antibody testing uses and limitations?

A
  • Confirms exposure to a specific micro-organism-Cultivable and nun-cultivable organisms
  • Is restricted to patients with a detectable antibody response
  • Is retrospective- Often too late to inform antimicrobial therapy decisions
129
Q

Should culture tests be taken before or after antibiotics are given?

A

Culture tests should be taken before antibiotics are given

Clinical pathology (8 decks)

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