Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Ross LAM I > 1 - Immunodeficiencies > Flashcards

1 - Immunodeficiencies Flashcards

1
Q

What is the difference between a primary and secondary immunodeficiency?

A

Primary have a genetic, heritable basis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which is the dominant immunoglobulin in colostrum?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When is colostrum produced?

A

During final weeks of pregnancy

Lasts ~24 hours after birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Is FPT a humoral or cell-mediated immunodeficiency?

A

Humoral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How much colostrum should the foal get?

A

2L of quality colostrum in first 8 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What screening is recommended to prevent FPT?

A

Screen all foals at 24-36 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the etiology of SCID?

A

Primary immunodeficiency - Arabian

Failure to produce functional B and T lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

What are the clinical presentations of selective IgM deficiency?

A
  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
Q

How is selective IgM deficiency diagnosed?

A

Serial measurement of serum Ig - IgM persistently low (all others normal)
Normal lymphocyte counts

27
Q

How is selective IgM deficiency treated?

A

Supportive care - abx, plasma transfusions

Poor prognosis

28
Q

What is the etiology of transient hypogammaglobulinemia?

A

Humoral immunodeficiency - delayed onset of Ig synthesis (until 3-6 months)
Arabians mostly affected

29
Q

What are the clinical signs associated with transient hypogammaglobulinemia?

A

Susceptibility to recurrent infections once maternal Ab wanes

30
Q

How is transient hypogammaglobulinemia diagnosed?

A

RID demonstration of low IgG, IgM, IgA after 2 months
B/T lymphocyte counts and CMI responses normal
(Autologous Ig levels eventually normalize)

31
Q

What are the differential diagnoses for transient hypogammaglobulinemia?

A

FPT

Primary agammaglobulinemia

32
Q

How is transient hypogammaglobulinemia treated?

A

Plasma transfusions and serial Ig testing until autologous Ig production
Management may only be practical in valuable foals

33
Q

What is the etiology of equine x-linked agammaglobulinemia?

A

Primary immunodeficiency - absence of B-lymphocytes and immunoglobulins (will never develop)
Affects male foals (x-linked)

34
Q

How is equine x-linked agammaglobulinemia diagnosed?

A

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
Q

How is equine x-linked agammaglobulinemia treated?

A

Supportive tx only

Grave prognosis, death within 2 years

36
Q

What is the etiology of common variable immunodeficiency (CVI)?

A

Similar to human CVI - group of primary immunodeficiencies
Progressive B-lymph depletion and hypo/agammaglobulinemia
Affects ADULT horses

37
Q

What clinical signs are associated with CVI?

A

Recurrent bacterial infections in adult horses

38
Q

How is CVI diagnosed?

A

Serial testing shows declining B-cell numbers and Ig levels (beginning later in life)
No serological response to vaccination

39
Q

How is CVI treated?

A

Supportive tx only - grave prognosis

40
Q

What is the etiology of bovine leukocyte adhesion deficiency (BLAD)?

A

Inherited autosomal recessive disorder of Holsteins

Causes dysfunction of innate immune system

41
Q

What is the pathogenesis of BLAD?

A

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
Q

What clinical signs are associated with BLAD?

A

Infectious disease with delayed healing in young cattle

43
Q

How is BLAD diagnosed?

A

Marked mature neutrophilia (>40,000 cells/µL)

Genetic testing available (PCR)

44
Q

How is BLAD treated?

A

Supportive only - grave prognosis, death within 1st year

45
Q

How is BLAD prevented?

A

Avoid breeding carriers

Ross LAM I (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions