lecture 9 part two - immunodz Flashcards
1
Q
(Combined Immunodeficiency of Arabian horses)
- failure to produce what?
- due to mutation in what?
- genetics?
- total WBC level?
- dx?
- tx?
A
- B and T lymphocytes (no humoral or cell mediated at all!)
- DNA-dependent protein kinase (lymphoid stem cells don’t differentiate)
- autosomal recessive (25% are carriers)
- low, normal, or high (depends on whether or not 2° is present)
- DNA test
- none! don’t breed two carriers!
2
Q
(selective IgM deficiency of horses)
- humoral immunodeficiency characterized by what?
(three age ranges)
(foals 5-10 months)
- most or least common?
- primary genetic basis suspected in what breeds?
(young horses between 1-2 years)
(adult horses 2-5 yrs)
- usually go on to develop what?
- meaning what?
A
- decreased or absent IgM
(other classes normal or ^)
- most
- arabians and quarter horses
- lymphosarcoma
- immunodeficiency is probably 2°
3
Q
(selective IgM deficiency of horses - cont)
- path?
- dx?
- tx?
A
- unknown (probably not same mech in the three types)
- IgM persistently low (others are normal/high)
- none (abx, supportive, plasma helps short term)
4
Q
(Transient Hypogammaglobulinemia of horses)
- rare humoral immunodeficiency characterized by what?
foals don’t start synth of Ig until when? why?
- mostly what breed?
- dx?
- main diff dx?
- tx?
A
- delayed onset of immunoglobulin synthesis
3 mo (don’t know)
- Arabians
- Demonstration of low serum IgG, IgM, and IgA by RID at 2-4 mo
(Lymphocyte counts and cell-mediated immune responses are normal)
- primary agammaglobulinemia (no B cells ever)
- plasma until Ig prod kicks in
5
Q
(equine agammaglobulinemia)
- primary immunodeficiency characterized by what?
- what horses get?
A
- absence of B cells and Ig
(t cells normal)
- male foals only
6
Q
(common variable immunodeficiency of horses)
not actually common
- occur in young or adult?
- causes what?
- tx?
A
- adult
- progressive B-lymphocyte depletion and hypo- or agammaglobulinemia
- Ig replacement and abx
7
Q
(bovine leukocyte adhesion deficiency)
- genetics?
- what breed?
- affects innate or humoral?
- caused by point mutation in CD18 - a subunit of what?
- how are neutros affected?
- dx?
- tx?
A
- autosomal recessive (hetero are cx normal)
- holstein
- innate
- beta-2 integrins (play role in leukocyte adhesion)
- can’t go into tissues
(see LOTS of neutros)
- genetic testing
- abx work short term (prog grave)