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Infection > The immunocompromised host > Flashcards

The immunocompromised host Flashcards

1
Q

Immunocompromised definition

A

State in which the immune system is unable to respond appropriately and effectively to infectious microorganisms

Due to defect in one or more components of the immune system

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2
Q

often failure to recognise and diagnose

A

PID

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3
Q

PID

A

primary immunodeficiency

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4
Q

Age of onset of PID

A

8-12.4

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5
Q

>60% of PID patients will be

A

18 years old and older when diagnosis is made

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6
Q

37% will have

A

permanent tissue/organ damage e.g. bronchiectasis in the lungs

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7
Q

most common type of PID is

A

CVID

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8
Q

CVID

A

(antibody production)- common variable immune deficiency

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9
Q

why is a host immunocompromised: primary immunodeficiency

A
  • Congenital
    • Intrinsic gene defect (275 genes)
      • Missing protein
        • E.g. complement
      • Missing cell
        • E.g. B cells –> no antibodies
      • Non-functional component
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10
Q

Why is a host immunocompromised: secondary immunodeficiency disease

A
  • Due to an underlying disease/treatment
    • HIV
    • Chemotherapy
    • Cancers
  • Decrease in production/ function of immune components
  • Increase or catabolism of immune components
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11
Q

Immunodeficiency is caused by defects of

A

one or more components of the immune system

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12
Q

when to suspect immunodeficiency?

A

SPUR

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13
Q
A
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14
Q

SPUR

A
  • Severe
  • Persistent
  • Unusual e.g. oppertunistic infection
  • Recurrent
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15
Q

Recognition and diagnosis of PID: The 10 warning signs for children

A
  1. four or more new ear infections within 1 year
  2. two or more serious sinus infections within 1 year
  3. two or more months on antibiotics with little effect
  4. two or more pneumonias within 1 year
  5. failure of an infant to gain weight or grow normally
  6. recurrent deep skin or organ abscesses
  7. persistent thrush in mouth of fungal skin infections
  8. need for IV Ax to clear infection
  9. two or more deep-seated infections inc. septicemia
  10. family history of PID
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16
Q

10 warning signs for adults

A
  1. two or more new ear infections within 1 year
  2. two or more serious sinus infections within 1 year in the abscence of allergy
  3. two or more months on antibiotics with little effect
  4. One pneumonias a year for more than 1 year
  5. diarrhoea with weight loss
  6. recurrent vial infections (colds, herpes, warts and condyloma)
  7. recurrent deep skin or organ abscesses
  8. persistent thrush in mouth of fungal skin infections
  9. need for IV Ax to clear infection
  10. infection with normally harmless tuberculosis-like bacteria
  11. family history of PID
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17
Q

Limitations of 10 warning signs

A
  • General use: lack of population base evidence
    • Family history (only in 25% of pt)
    • Failure to thrive
      • T cell defect
    • Diagnosis of sepsis treated with IV antibiotics
  • PID patients with different defects/ presentation
    • T cell, B cell, phagocytes, complements
    • Infection with a subtle presentation
  • PID patients with non-infectious manifestations
    • Autoimmunity
    • Malignancy
    • Inflammatory response
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18
Q

Causes of immunodeficiency

A
  1. Antibody defects
  2. T cell defects
  3. Phagocytic defects
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19
Q

1) Immunodeficiency caused by antibody defects accounts for …….% of all PID

A

65%

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20
Q

1) Immunodeficiency caused by antibody defects due to:

A
  1. Defect in B cell development
  2. Defect in antibody production
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21
Q

Defect in B cell development

A

X-linked agammaglobulinemia (Bruton’s disease)

22
Q

Defect in antibody production

A
  • Common variable immunodeficiency (CVD- most common PID)
  • Selective IgA deficiency
    • If you give IgA via transfusion they may have Anti-IgA antibodies
  • IgG subclass deficiency (IgG2)
  • Hyper- IgM syndrome
    • Missing CD4 ligand on T cell (CD4 T cell)
    • Therefore no maturation of IgM to IgG by B cell
23
Q

2) Immunodeficiency caused by T cell defects account for …..% of all PIDS

A

15%

24
Q

2) Immunodeficiency caused by T cell defects

A
  1. Combined B and T cell defects
  2. T cell defects
    3.
25
Q

Combined B and T cell defects

A
  • Severe combine immunodeficiency (SCID)
  • Wiskott- Aldrich syndrome
  • Ataxia telangetasia
26
Q

T cell defects

A
  • Di George syndrome (thymus)
  • MHC class II deficiency
27
Q

3) Immunodeficiency caused by phagocytotic defects: around …..% of all PIDs

A

10%

28
Q

3) Immunodeficiency caused by phagocytotic defects

A
  • Defects in respiratory burst
  • Chronic granulomatous disease (CGD)
  • Defects in fusion of lysosome/ phagosomes
  • Defect in neutrophil production and chemotaxis
29
Q

age of symptom onset <6 months suggests

A

T cell or phagocyte defect

(antibodies from mothers breast milk)

30
Q
A
31
Q

age of symptom onset >6 months and <5 year suggests

A

B-cell - antibody or phagocyte defect

32
Q

age of symptom onset >5 year suggests

A

a B-cell /antibody/complement or secondary immunodeficiency.

33
Q

Most SID caused by

A

malnutrition

34
Q

with clinical cases you need to consider

A

o SPUR infections (10 warning signs)

o Age- at presentation (sex)
o Site(s) of infection(s)
o Type of microorganism(s)
o Sensitivity and type of treatment (surgery)

o Secondary causes of immunodeficiency
o Family history

35
Q

clinical case 1

A
  • T cell or phagocyte (6 months old)
  • T cell- viral infections (not just bacterial)
  • Weak antibody response
    • T cell and B cell respond
  • SCID
36
Q

clinical case 2

A
  • >6 Months= B cell antibody or phagocyte defect
    • Protected in first 6 months by maternal IgG
  • No fungal or viral infections – B cell
  • Antibody deficient
  • Family history- X linked – Bruton’s disease
37
Q

clinical case 3

A
  • Age= <6 months
    • T cell or phagocytes (granulocyte)
      • Abscesses on the chest, skin, face and buttock requiring surgical incision and antibiotics)
  • Chronic Granulomatous Disease (CGD)
38
Q

clinical case 4

A
  • 40 years old
    • But had problems since a child
  • Repeated bacterial infection
    • B cell/ antibodies
  • Mother and sister also had poor response to vaccine
  • CVID- chronic variable immunodeficiency
39
Q

presentation of chronic granulomatous disease (CGD)

A
40
Q

management fo PID: supportive treatment

A
  • Infection prevention (prophylactic antimicrobials)
  • Treat infections promptly and aggressively (passive immunization)
  • Nutritional support (vitamin A/D)
  • Use UV-irradiated CMVneg blood products only
  • Avoid live attenuated vaccines in patients with serve PIDs (SCID)
41
Q

management of PID: Specific treatment

A

Regular immunoglobulin therapy (IVIG or SCIG)

SCID: haematopoietic stem cell therapy (HSCT, 90% success)

42
Q

treatment for comorbidities

A
  • Autoimmunity and malignancies
  • Organ damages (lung function assessment)
  • Avoid non-essential exposure to radiation
43
Q

IRT

A

immunoglobulin replacement therapy

44
Q

patients with haematological malignanies are at

A

increased susceptibity to infections

45
Q

why are patients undergoing chemotherapy at increased susceptibility to infection

A
  • Chemotherapy-induced neutropenia
    • Treat febrile neutropenia as a acute medical emergency and offer empiric antibiotic therapy immediately
    • Assess patients risk of septic complications
  • Chemotherapy induced damage to mucosal barriers
    • Vascular catheters
    • Hickman line (Staph Epidermis)
46
Q

goal of IRT

A

Serum IgG> 8g/l

Life long treatment

47
Q

conditions that IRT is appropriate for

A

CVID

XLA (brutons)

Hyper IgM syndrome

48
Q

secondary immune deficiencies are due to

A
  1. Decreased production of immune components
  2. Increased loss of immune components
49
Q

Decreased production of immune components

A
  • Malnutrition
  • Infection (HIV)
  • Liver disease
  • Haematological malignancies
  • Therapeutic treatment (corticosteroids, cytotoxic drugs)
  • Splenectomy
50
Q

Increased loss of immune components

A

Protein-losing conditions (nephropathy, enteropathy)

Burns

Infection (36 decks)

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