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Scid horses
Scid horses




scid horses

  • The most severe form (rare) is a defect in prolymphocytic stem cells that affects both bone-marrow-derived and thymic-dependent lymphocytes.
  • SCID represents a heterogeneous group of entities, each with a different molecular basis the common end result is absence of functional B and T lymphocytes, resulting in impairment of both CMI and humoral immunity.
  • Foals die by five months of age as a result of infection by a variety of pathogens such as equine adenovirus, Pneumocystis carinii, Cryptosporidium parvum and Rhodococcus equi.
  • SCID is the most important equine immunodeficiency with 0.2 to 2.3% prevalence of disease in homozygous foals and a 8 to 26% prevalence in heterozygote Arabian horses and Arabian crossbreeds inherited as an autosomal recessive trait.
  • SCID affects horses, humans, mice, and dogs, and can have an autosomal recessive, X-linked, or sporadic pattern of inheritance.
  • Neutrophils, monocytes, macrophages and natural killer (NK) cells function normally complement levels are normal.
  • SCID is not a specific condition, but a constellation of entities which result in deficiencies in both humoral and cell-mediated immunity (CMI) due to failed production of functional lymphocytes.
  • Pancreas, pancreatic ductal epithelium: Degeneration, necrosis, and hyperplasia, multifocal, moderate, with multifocal moderate fibrosis, multifocal acinar atrophy, edema, and basophilic intranuclear viral inclusion bodies, etiology consistent with equine adenovirus.ĬONDITION: Combined immunodeficiency (CID), severe CID (SCID).
  • Thymus: Lymphoid hypoplasia, diffuse, severe.
  • Spleen, white pulp: Lymphoid hypoplasia, diffuse, severe, Arabian, equine.
  • Multifocally, interlobular septa are expanded by clear space with few ectatic lymphatics (edema).

    scid horses

    Occasionally, pancreatic ductal epithelial cells, including sloughed epithelial cells, contain a round to oval, 15 to 20 um diameter, smudgy, basophilic intranuclear viral inclusion body that marginates the chromatin. Often, ductal lumina contain sloughed epithelial cells admixed with necrotic cellular debris. Often, ductular epithelial cells display one of the following changes: swollen with vacuolated cytoplasm (degeneration), hypereosinophilic cytoplasm with karyorrhexis or nuclear pyknosis (necrosis), or are piled up to four layers with vesiculate nuclei (hyperplasia). Multifocally, pancreatic acini are decreased in size (atrophy). Pancreas: Multifocally, moderate fibrous connective tissue surrounds pancreatic ducts and separates, surrounds, and replaces acinar cells (fibrosis). Hassall’s corpuscles are admixed with moderate numbers of macrophages, eosinophils, and few lymphocytes. There is diffuse lymphoid hypoplasia with lack of a discernible cortex and medulla, and reticuloepithelial cell network is very prominent. Thymus: All thymic lobules are diminutive and are surrounded and separated by abundant adipose tissue. Moderate numbers of neutrophils and a mild increase in macrophages throughout the red pulp vascular spaces. The periarteriolar lymphatic sheaths (PALS) are devoid of resident T lymphocytes and are surrounded by multiple layers of macrophages (PALS collapse) and there is an absence of primary follicles. HISTOPATHOLOGIC DESCRIPTION: Spleen: Diffusely, there is a paucity of white pulp. HISTORY: The foal was normal at birth, but developed respiratory disease at one week of age. 1 = Normal allele 2 = Variant allele.Signalment (86-6580): 7-week-old male Arabian foal Homozygous Normal Females (1-1) and Hemizygous Normal Males (1, only one X chromosome) are not expected to develop signs of Severe Combined Immune-deficiency (X-Linked SCID) and none of their offspring will inherit the disease variant allele. 1 = Normal allele 2 = Variant allele.ġ-1 (Homozygous Normal in Female) or 1 (Hemizygous Normal in Male) Parents, offspring and relatives should also be tested. Heterozygous Carrier Females (1-2) are not expected to develop signs of Severe Combined Immune-deficiency (X-Linked SCID) but each of their offspring has a chance of inheriting a disease variant allele. You may choose to contact us for a consultation on the management of this disease.

    scid horses

    Hemizygous Affected Males (2, only one X chromosome) are expected to develop signs consistent with Severe Combined Immune-deficiency (X-Linked SCID) and only their female offspring will inherit a disease variant allele. Homozygous Affected Females (2-2) are expected to develop signs consistent with Severe Combined Immune-deficiency (X-Linked SCID) and all of their offspring will inherit a disease variant allele. 2-2 (Homozygous Disease Variant in Female) or 2 (Hemizygous Disease Variant in Male)






    Scid horses