1 - Immunodeficiencies Flashcards

(45 cards)

1
Q

What is the difference between a primary and secondary immunodeficiency?

A

Primary have a genetic, heritable basis

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2
Q

How can the humoral immunity be evaluated?

A
  1. CBC for lymphocytes
  2. Serum Ig concentrations
  3. Vaccination (watch response)
  4. Phenotyping studies (measure B-cells in blood/lymphoid tissues)
  5. In vitro B-lymphocyte proliferation test (function)
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3
Q

How can the CMI be evaluated?

A
  1. CBC for lymphocytes
  2. Phenotyping studies (measure T-cells in blood/lymphoid tissues)
  3. In vitro T-lymphocyte proliferation test
  4. Intradermal injection of PHA (in vivo test of function)
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4
Q

Which is the dominant immunoglobulin in colostrum?

A

IgG

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5
Q

When is colostrum produced?

A

During final weeks of pregnancy

Lasts ~24 hours after birth

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6
Q

How is colostrum absorbed by foals? When is it most efficiently absorbed

A

Specialized enterocytes bind colostral Ig
Transfer across epithelium to lymphatics and capillaries
Best absorption during first 6 hours

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7
Q

Is FPT a humoral or cell-mediated immunodeficiency?

A

Humoral

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8
Q

What clinical signs are associated with FPT?

A

D/t secondary infection (doesn’t always occur)
Umbilical infections
Bronchopneumonia
Enteritis
Bacteremia and septicemia (injected, pale, or muddy mms; tachycardia; hypoperfusion)
DIC (petechiation, hemorrhage, thrombosis)

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9
Q

How is sepsis diagnosed in the foal?

A
  • Maintain high index of suspicion in any sick neonatal foal!
    1. Sepsis score sheet (>11)
    2. Radial immunodiffusion (RID) to measure IgG
  • gold standard, but pricey and time-consuming
    3. ELISA-based tests
  • IgG >800 = adequate
  • IgG <400 = complete FPT
    4. SNAP test
  • color of blue dot indicates strength of IgG
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10
Q

What are the indirect indicators of passive transfer? Are they used in the foal?

A

Plasma TP, colostrum-derived serum GGT

Both NOT used in foals

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11
Q

If a foal has IgG levels 400-800 mg/dL and is clinically normal, should it be treated for FPT?

A

Not necessarily

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12
Q

How should a FPT foal <8-12 hours be treated?

A

PO 2L high quality colostrum (or 2-3 bottles Seramune)

SG >1.060 (colostrometer) / SG >23% (sugar refractometer)

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13
Q

How should a FPT foal >12-24 hours be treated?

A

1-2L plasma transfused IV

+/- flunixin pretreatment to reduce risk of adverse rxns

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14
Q

How much colostrum should the foal get?

A

2L of quality colostrum in first 8 hours

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15
Q

What screening is recommended to prevent FPT?

A

Screen all foals at 24-36 hours

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16
Q

How is FPT screened for/diagnosed in the bovine?

A
  1. Direct - FPT = IgG <1000mg/dL
  2. Indirect - TP (refractometer) <5.0 g/dL
    (ONLY run on healthy calves with good hydration)
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17
Q

How much colostrum should the calf get?

A

100g IgG within 6 hours of birth (SG >1.050)
Dairy cows - 4L
Beef cows - 2L

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18
Q

What is the etiology of SCID?

A

Primary immunodeficiency - Arabian

Failure to produce functional B and T lymphocytes

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19
Q

What is the pathogenesis of SCID?

A

Mutation in DNA-dependent protein kinase
Lymphoid stem cells fail to differentiate
Dysfunctional B and T lymphocytes
Complete deficiency in both CMI and humoral immunity

20
Q

What clinical signs are associated with SCID?

A

Affected foals normal for 2-3 months (until maternal Ab wanes)
Susceptible to opportunistic infections
Die within 5 months

21
Q

How is SCID diagnosed?

A

Severe and persistent leukopenia
Low to absent levels of autologous Ig

PCR test identifies normal, heterozygous, or homozygous

22
Q

How is SCID treated?

A

NO treatment. Grave prognosis

23
Q

How is SCID prevented?

A

Avoid breeding carriers to one another

24
Q

What is the etiology of selective IgM deficiency?

A

Equine specific

Humoral immunodeficiency characterized by persistently low IgM (other classes normal)

25
What are the clinical presentations of selective IgM deficiency?
1. Young foals (most common) Recurrent infections, grave prognosis, death within first year Primary genetic basis suspected (Arabians/Quarters) 2. Horses up to 1-2 years Hx of chronic recurrent infections, stunted growth Death before 2 years 3. Adults 2-5 years Associated with lymphosarcoma, recurrent infections are rare Likely secondary immunodeficiency
26
How is selective IgM deficiency diagnosed?
Serial measurement of serum Ig - IgM persistently low (all others normal) Normal lymphocyte counts
27
How is selective IgM deficiency treated?
Supportive care - abx, plasma transfusions | Poor prognosis
28
What is the etiology of transient hypogammaglobulinemia?
Humoral immunodeficiency - delayed onset of Ig synthesis (until 3-6 months) Arabians mostly affected
29
What are the clinical signs associated with transient hypogammaglobulinemia?
Susceptibility to recurrent infections once maternal Ab wanes
30
How is transient hypogammaglobulinemia diagnosed?
RID demonstration of low IgG, IgM, IgA after 2 months B/T lymphocyte counts and CMI responses normal (Autologous Ig levels eventually normalize)
31
What are the differential diagnoses for transient hypogammaglobulinemia?
FPT | Primary agammaglobulinemia
32
How is transient hypogammaglobulinemia treated?
Plasma transfusions and serial Ig testing until autologous Ig production Management may only be practical in valuable foals
33
What is the etiology of equine x-linked agammaglobulinemia?
Primary immunodeficiency - absence of B-lymphocytes and immunoglobulins (will never develop) Affects male foals (x-linked)
34
How is equine x-linked agammaglobulinemia diagnosed?
Total lymphocyte counts normal, but B-lymphs absent Serum Ig (all classes) persistently low or absent once maternal Ab wanes No serological response to vaccination CMI normal
35
How is equine x-linked agammaglobulinemia treated?
Supportive tx only | Grave prognosis, death within 2 years
36
What is the etiology of common variable immunodeficiency (CVI)?
Similar to human CVI - group of primary immunodeficiencies Progressive B-lymph depletion and hypo/agammaglobulinemia Affects ADULT horses
37
What clinical signs are associated with CVI?
Recurrent bacterial infections in adult horses
38
How is CVI diagnosed?
Serial testing shows declining B-cell numbers and Ig levels (beginning later in life) No serological response to vaccination
39
How is CVI treated?
Supportive tx only - grave prognosis
40
What is the etiology of bovine leukocyte adhesion deficiency (BLAD)?
Inherited autosomal recessive disorder of Holsteins | Causes dysfunction of innate immune system
41
What is the pathogenesis of BLAD?
Point mutation in the gene encoding CD18 (subunit of beta-2 integrins) Beta-2 integrins = cell surface proteins important for leukocyte adhesion to capillary endothelium Neutrophils do not express these adhesion molecules - cannot migrate into tissues
42
What clinical signs are associated with BLAD?
Infectious disease with delayed healing in young cattle
43
How is BLAD diagnosed?
Marked mature neutrophilia (>40,000 cells/µL) | Genetic testing available (PCR)
44
How is BLAD treated?
Supportive only - grave prognosis, death within 1st year
45
How is BLAD prevented?
Avoid breeding carriers