Infection And Immunity Flashcards

1
Q

What is an infection?

A

Invasion of a host’s tissues by microorganisms which case disease through microbial multiplication, release of toxins/virulence factors and/or the host response to infection

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2
Q

Name 3 modes of horizontal transmission of infection (3)

A
  • Contact (direct, indirect, vectors)
  • Inhalation (droplets, aerosols)
  • Ingestion (faecal-oral)
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3
Q

Which mode of transmission is ‘mother to child’ known as?

A

Vertical transmission

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4
Q

Describe the 5 stages of how a microorganism establishes within a host (5)

A
  • Exposure (patient, environmental)
  • Adherence (stick to body surfaces)
  • Invasion (through skin/soft tissue)
  • Multiplication (colonisation)
  • Dissemination (spread of infection throughout body)
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5
Q

Name 2 ways in which microorganisms can cause damage to the host (2)

A
  • Release of virulence factors (endo/exotoxins)

- Host cellular damage (local inflammation and immune response can damage normal tissue)

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6
Q

What is a virulence factor?

A

Substance produced by microorganism which can either be secreted (exotoxin) or released during microbial breakdown (endotoxin) which can stimulate host biological pathways

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7
Q

Name 4 ways you could get an infection from the environment (4)

A
  • Water
  • Air
  • Food
  • Surfaces
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8
Q

Give 5 disease determinants between patient and pathogen which may lead to disease (5)

A
Pathogen:
- Antimicrobial resistance
- Inoculum size
- Virulence factors
Patient:
- Site of infection
- Comorbidities
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9
Q

What questions would you consider to determine whether a patient has an infection? (4)

A
  • Is there an infection? Any symptoms that suggest this?
  • Where is the infection?
  • What is the cause of infection?
  • What are the best treatment options?
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10
Q

Name the 5 steps you would take to determine if a patient had an infection and how you would treat it

A
  • History (symptoms, potential exposures)
  • Examination (organ dysfunctions)
  • Specific investigations (microbiological)
  • Supportive investigations (aid diagnosis e.g. FBC, CRP)
  • Baceteriology/Virology (take sample, MC&S, antigen/NA detection)
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11
Q

What are the stages of investigation in bacteriology? (4)

A
  • Specimen sample (swab, tissue biopsy)
  • Microscopy (inc. gram stain), culture and antibiotic susceptibility (MC&S)
  • Antigen detection
  • Nucleic acid detection
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12
Q

Name 3 virulence factors other than toxins which contribute to bacterial pathogenesis (3)

A
  • Enzymes e.g. Collagenase (invasiveness)
  • Pili/Fibri (adherence)
  • Polysaccharide capsule (host entry)
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13
Q

Name 2 ds envelopes viruses and 2 ds non-enveloped viruses (4)

A
  • Non-enveloped: adenovirus, HPV

- Enveloped: Herpes viruses, hepatitis B

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14
Q

What is a bacteriophage?

A

Virus which parasitises bacteria and uses their machinery to reproduce and replicate

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15
Q

Give 2 examples of parasites: one single cellular and one multicellular (2)

A
  • Single cellular: Protozoa e.g. Plasmodium falciparum

- Multicellular: Helminths e.g. Schistosoma mansoni (fluke)

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16
Q

Give 2 examples of fungi: one single cellular and one multicellular (2)

A
  • Single cellular: Yeasts e.g. Candida

- Multicellular: Moulds/dermophytes e.g. Ringworm

17
Q

Define bacteraemia and explain how this differs from sepsis (2)

A
  • Bacteraemia is the presence of bacteria in the blood

- Sepsis is a serious life threatening response to infection

18
Q

What is septic shock?

A

Persistent hypotension due to sepsis which requires treatment to maintain blood pressure despite fluid resuscitation

19
Q

Name 3 ways you could recognise sepsis (3)

A
  • Patient is acutely unwell and/or has a raised EWS
  • Clinical features suggesting source e.g. meningitis, pneumonia
  • Red Flag Signs - immediate action required (high RR, low BP, unresponsiveness)
20
Q

How would you treat a patient with sepsis? (6)

A

WITHIN THE HOUR:

  • Give: high flow O2, antibiotics, IV fluids
  • Take: blood culture, urine sample, serum lactate
21
Q

Explain 2 ways in which sepsis can affect the coagulation cascade. What are the consequences of this? (3)

A
  • Release of endotoxins from bacteria leads to the release of cytokines from inflammatory cells (namely macrophages)
  • Cytokines stimulate production of thrombin which activates the clotting cascade. They also inhibit fibrinolysis (breakdown of clots) which can lead to microvascular thrombosis and organ ischaemia
  • Results in shock/multi-organ failure
22
Q

What would be your first choice for an antibiotic to treat meningitis and why? (2)

A
  • CEFTRIAXONE

- Able to penetrate into the CSF

23
Q

Give 3 life threatening complications of sepsis (3)

A
  • Irreversible hypotension (may lead to cardiac arrest)
  • Acute kidney injury
  • Organ ischaemia/necrosis
24
Q

What is the effect of a polysaccharide capsule on bacteria?

A

Prevents phagocytosis of bacteria by inflammatory cells

25
Q

Which bacterium is mainly responsible for causing meningitis? What would its appearance be microscopically? (2)

A
  • Neiserria meningitidis

- Gram -ve (red stained) diplococci (mainly serogroup B) visible in CSF

26
Q

Give 2 preventative measures for meningitis (2)

A
  • VACCINATION (meningococcal C conjugate, serogroup B etc.)

- ANTIBIOTIC PROPHYLAXIS (people in close contact)

27
Q

How is meningitis spread?

A

Aerosols/nasopharyngeal secretions

28
Q

Give 2 consequences of disseminated intravascular coagulation (DIC) (2)

A
  • Tiny clot formation throughout the cardiovascular system which may lead to organ ischaemia
  • Inability to clot when required (as clotting factors are used up) which may lead to bleeding
29
Q

Describe the general classification of Antimicrobials (4)

A
  • Antibacterials
  • Antivirals
  • Antifungals
  • Antiprotozoal
30
Q

Give 3 ideal properties of antimicrobials which can increase patient compliance (3)

A
  • Ease of administration e.g. oral/IV (normally both)
  • Few adverse side effects
  • Long half life (infrequent dosing)
31
Q

Why is it ideal that antimicrobials are ‘selectively toxic’?

A

Minimally toxic to host but very toxic to pathogens

32
Q

What are the main mechanisms of action of antimicrobials? (4)

A
  • Target cell wall synthesis
  • Target cell membrane function
  • Target nucleic acid synthesis
  • Target protein synthesis
33
Q

Explain 3 mechanisms of resistance to antibiotics by bacteria (3)

A
  • Production of drug inactivating enzymes
  • Altered uptake of drug (decreased permeability or increased efflux)
  • Altered targets e.g. target enzyme has a lower affinity for drug
34
Q

Describe 2 ways in which the gene for antimicrobial resistance can be spread to other bacteria (2)

A
  • Chromosomal mutation (bacteria with mutation will multiply asexually so entire population has the mutated gene)
  • Horizontal gene transfer (through conjugation, transduction or transformation)
35
Q

Describe 3 methods of horizontal gene transfer in bacteria (3)

A
  • Conjugation (fusion via sexual contact and transmission of genetic material)
  • Transduction (through bacteriophage)
  • Transformation (free DNA passed directly through cell wall)
36
Q

Describe 2 methods of measuring antibiotic activity (2)

A
  • Disc sensitivity testing (discs soaked in various antimicrobials are placed on a agar; larger circumference=more effective)
  • Minimum inhibitory concentration
37
Q

Explain the pathogenesis of infections in surfaces (4)

A
  • Adherence of pathogen to host cell or prosthetic surface
  • Biofilm formation
  • Invasion and multiplication
  • Host response (pyrogenic, granulomatous etc.)
38
Q

What structure on bacteria allow adherence to surfaces?

A

Pili/fimbriae