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MBChB3 > Infection In Immunocompromised Patients > Flashcards

Infection In Immunocompromised Patients Flashcards

1
Q

List the innate defence mechanisms of the body

A
  • skin
  • resident flora (colonisation resistent)
  • complement
  • lysozyme
  • acute phase reactants
  • phagocytes (macrophages, neutrophils)
  • spleen
  • NK cells
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2
Q

List the adaptive immune mechanisms of the body

A
  • humoural B cells (neutralisation, C1 activation, opsonisation)
  • cellular T cells (help macrophages + B cells, kill virus infected cells)
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3
Q

What are the different types of immunodeficiency?

A

Primary (rare):
- inherited
- exposure in utero to environmental factors

Secondary (common):
- due to underlying disease state
- requires treatment for disease
- common

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4
Q

What developments in healthcare have had a detrimental effect on immunodeficiency?

A
  • improved survival at extremes of life
  • improved cancer treatment
  • development in transplant techniques
  • developments in intensive care
  • management of chronic inflammatory conditions
  • steroids
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5
Q

Describe the pathogenesis of neutropenia

A
  • caused by things like cytotoxic chemotherapy/therapeutic irradiation (reduction in chemotaxis, phagocytic activity + intracellular killing)
  • leads to decrease in proliferation of haemopoietic progenitor cells (responsible for forming neutrophils)
  • depletion of marrow reserves (normally high turnover)
  • neutropenia = <0.5x10^9/L
    (Relative neutropenia = <1x10^9/L + falling)
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6
Q

What pathogens can take advantage of neutropenia?

A
  • gram positive cocci (S. aureus, CoNS, S. viridans, enterococci)
  • anaerobes (bacteriodes spp, clostridia spp)
  • gram negative bacilli (E.coli, P.aeruginosa, klebsiella pneumoniae, enterobacter spp)
  • fungi (candida spp, aspergillus spp.)
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7
Q

Describe features of chronic granulomatous disease

A
  • inherited disorder (X-linked)
  • defect in gene which codes for NAPDH oxidase (reduction in production of oxygen radicals leading to defective intracellular killing)
  • recurrent bacterial + fungal infections
  • abscesses in lung, lymph nodes, skin
  • inflammation = widespread granuloma formation
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8
Q

What pathogens can take advantage of chronic granulomatous disease?

A

Pulmonary infection:
- aspergillus spp
- S. aureus
- nocardia spp (unique to this condition)

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9
Q

List the things that suppress cellular immunity

A
  • DiGeorge syndrome (primary deficiency)
  • malignant lymphoma
  • cytotoxic chemotherapy
  • extensive radiation
  • immunosuppressive drugs
  • allogenic stem cell transplant (esp if GVHD)
  • infections (HIV, mycobacterial, measles, EBV, CMV)
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10
Q

List the immunosuppressive drugs which can affect immunity

A
  • corticosteroids
  • cyclosporin (used to prevent organ rejection)
  • tacrolimus (more potent form of ^)
  • alemtuzumab (anti-CD52 monoclonal)
  • rituximab (anti-CD20 monoclonal)
  • purine analogues
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11
Q

Describe conditions which affect humoral immunity

A
  • bruton agammaglobinaemia (primary loss of mature B cells)
  • lymphoproliferative disorders (decrease antibody production) = CLL, multiple myeloma
  • radio + chemotherapy will cause hypogammaglobinaemia
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12
Q

Describe the function of the spleen in defence

A
  • splenic macrophages eliminate non-opsonised microbes (esp encapsulated bacteria)
  • site of primary immunoglobulin response (specific opsonising antibody required for phagocytosis of encapsulated bacteria)
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13
Q

What pathogens can take advantage of humoral deficiency/splenectomy/hyposplenism?

A
  • S. pneumoniae
  • H. Influenza type B
  • N. Meningiditis
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14
Q

Describe the aspects of the skin which helps it as defence

A
  • dry (pathogens like wet environment)
  • pH = 5-6
  • temperature = 5 or lower
  • secretory IgA in sweat (protects)
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15
Q

Describe the pathogenesis of mucosal barrier injury + colonisation resistance

A
  • injury/altered microbiome (antibiotics, diarrhoea etc)
  • mucositis
  • pain, dysphagia, xerostomia, ulceration
  • impaired GI function, alteration in permeability (pathogens from gut to blood)
  • altered nutritional status
  • possible secondary infection to catheter
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16
Q

What defines severe nutritional deficiency?

A
  • <75% ideal body weight/rapid weight loss
  • hypoalbuminaemia
17
Q

Describe how impaired nutritional status affects immunity

A
  • results in mucositis and metabolic derangements
  • compromises host defences
  • iron deficiency reduces microbicidal capacity of neutrophils and T cell function
18
Q

Describe how organ dysfunction + concurrent illness can affect host defences

A
  • eg. Tumours can cause local organ dysfunction (eg. Blockage of bile duct leading to inflammation and infection)
  • lung is susceptible
  • CNS tumours = spinal cord suppression (loss of cough/swallow reflex, incomplete bladder emptying)
  • reduction in removal of pathogens from system
  • concurrent illness = diabetes (reduces T cell function), diabetes (reduces opsonisation and chemotaxis)
19
Q

How is infection risk reduced in solid organ transplants?

A
  • optimal tissue typing
  • donor evaluation
  • organ procurement
  • surgical technique
  • tailored immunosuppressive regimen
20
Q

What is a unique aspect of infection in solid organ transplants?

A
  • they do not present the same as in immunocompetent people
  • inflammatory responses are impaired
  • symptoms are diminished
  • muted clinical and radiological signs
21
Q

What community acquired pathogens are individuals at risk of following a solid organ transplant?

A
  • pneumococcus, listeria, salmonella, legionella
  • viruses: influenza, parainfluenza, RSV
22
Q

What nosocomial infections are individuals at risk of following a solid organ transplant?

A
  • resistant gram positive and gram negative bacteria
  • C. Diff
  • fungi
23
Q

What types of infection are we trying to avoid following solid organ transplants?

A
  • community acquired
  • nosocomial
  • donor-derived infections (latent/active)
  • reactivation of infections (eg. TB/HSV)
  • opportunistic pathogens (eg. Aspergillus)
24
Q

Where can neutropenic fever arise from?

A
  • solid tumours receiving cytotoxic chemotherapy
  • non-leukaemic haematological malignancies
  • acute leukaemias receiving induction chemotherapy
25
Q

Describe the pathogenesis of neutropenic fever

A
  • neutropenia
  • abnormal antibody production
  • T cell defects
  • organ dysfunction
  • deficient nutritional status
  • affect on IV access devices
  • concurrent illness

MBChB3 (100 decks)

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