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12 Cards in this Set
- Front
- Back
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Factors causing infertility
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-no cycle/abnormal
-already pregnant -tumours -management -lactational aneastrus -presistant cl=abnor. progesterone levels -multiparous oviduct challeneges(blocked oviduct) -pairing -infection=endometritus -morpho. abnormal embryos -hermephrodite -predisposed conformation |
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Endometritis
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-inflamm/degeneration/fibrosis
1)acute=nutrophils employed 2)chronic=lymphocytes=persistant mating 3)chronic degenerative 4)STI *susceptible mare=normal inflam response to semen but a)fails to clear seminal plasma,fluid collct. in uterine lumen=biopsy+culture b)persistant mating=fils to clear uterus Treatment=inseminate=flush uterus/oxytocin,use deep uterine insem. Chronic infectious endo.=antibiotics,remove excess semen |
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Stallion factors
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-planpiniform plexus abnor.
-Cryptorchid=perm/temp/iguinal/uni/bi lateral *congentital=dec. fertility,perm abdominal=infertility as too hot,left one ^ retention |
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Type of immunity
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-Innate=non specific,primary defence
-Acquired=Active=own antibodies-immunsation(artificial) or exposure (natural) -Acquired-passive=maternal or artificial vaccin. |
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Antigen
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Anything bond by antibody ie peptides,chemicals,viruses
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Lymphocytes-receptors for antigens,specific immune response
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B cells-produce antibodies IgG
T cells-have surface receptors related to IgGs,recognise peptide fragments of antigens with surface MHC glycoproteins -glycoproteins encoded by genes in major histocompatibility complex binds frgement of antigens |
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2 types T cell
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-T helper/CD4=MHC class 2,cytokine production,help B cell and cytoxic t cells
-T cytoxic=MHC clss 1,lysis infected cells |
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MHCs
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-MHC identicle regions swap grafts easier
-minor hisocompatibility loci can influence graft survival but are weak -structure=class 1 or 2 -MHC prodcuts manage immune response -T cells recognise antigen as a complex with MHC properties -MHC proteins bind small peptides and show themselves to T cell antigen receptors |
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Epithiliochorial placenta
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-maternal epithilium of endometrium in contact with foetl chorion
-no acquired passive immunity via mother -fetus as allograft=organ/cell transfer from one person to next -immunological recognition=genetic differences sig. as cause incompatibility,high polymorphic -90% maiden mares =cytoxic response to sperm,10% genetically identicle to stallion |
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Why does foetus survive?
(Roberts et al,2006) |
-immune capacity of uterus
-influence of pregnancy (emvryo movement) -trophoblast producing eCG |
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Cellular immune response to trophobast
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-CD4,CD8,T cells surround trophoblst of equine endometrial cups
-endometrial cups=killed via immune response -not immunogically inert but feotus not rejected -allantoantibody does not risk conception |
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Immturity theory
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-main response=MHC1
-atlantochorion = MHC1 -ve so forms barrier -some points do show MHC1 so see lymphocytes from mare -chorionic girdle +ve MHC1 invades maternal epithelium and produce eCG glands -endometrial cups downregulate MHC1 effect so CG theory false as maternal immune response modified by foetus |
