JPC SYSTEMIC PATHOLOGY
HEMOLYMPHATIC SYSTEM
April 2018
H-M02

Signalment (86-6580):  7-week-old male Arabian foal

HISTORY:  The foal was normal at birth, but developed respiratory disease at one week of age.

HISTOPATHOLOGIC DESCRIPTION:  Spleen:  Diffusely, there is a paucity of white pulp.  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.  Moderate numbers of neutrophils and a mild increase in macrophages throughout the red pulp vascular spaces.

Thymus:  All thymic lobules are diminutive and are surrounded and separated by abundant adipose tissue.  There is diffuse lymphoid hypoplasia with lack of a discernible cortex and medulla, and reticuloepithelial cell network is very prominent.  Hassall’s corpuscles are admixed with moderate numbers of macrophages, eosinophils, and few lymphocytes.

Pancreas:  Multifocally, moderate fibrous connective tissue surrounds pancreatic ducts and separates, surrounds, and replaces acinar cells (fibrosis).  Multifocally, pancreatic acini are decreased in size (atrophy).  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).  Often, ductal lumina contain sloughed epithelial cells admixed with necrotic cellular debris.  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.  Multifocally, interlobular septa are expanded by clear space with few ectatic lymphatics (edema).

MORPHOLOGIC DIAGNOSIS:  

  1. Spleen, white pulp: Lymphoid hypoplasia, diffuse, severe, Arabian, equine.
  2. Thymus: Lymphoid hypoplasia, diffuse, severe.
  3. 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.

ETIOLOGIC DIAGNOSIS:  

  1. Hereditary lymphoid hypoplasia
  2. Adenoviral pancreatitis

CAUSE:

  1. Homozygous defective DNA-PKcs
  2. Equine adenovirus

CONDITION:  Combined immunodeficiency (CID), severe CID (SCID)

GENERAL DISCUSSION:

PATHOGENESIS:

 TYPICAL CLINICAL FINDINGS:

TYPICAL GROSS FINDINGS: 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

ADDITIONAL DIAGNOSTIC TESTS:  

DIFFERENTIAL DIAGNOSIS: 

Other significant immunodeficiencies in horses:

COMPARATIVE PATHOLOGY:

SCID in other species:

References:

  1. Santagostino SF, Arbona RJR, Nashat MA, White JR, Monette S. Pathology of aging in NOD scid gamma female mice.  Vet Pathol, 2017:54(5):855-869.
  2. Valli VEO, Kiupel M, Bienzle D. Hematopoietic system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 3. 6th St. Louis, MO: Elsevier; 2016: 139-141.
  3. Webb JL, Lattimer KS.   In:  Lattimer, KS.  Duncan and Prasse’s Veterinary Laboratory Medicine Clinical Pathology.  5th Ed. Ames, IA: Wiley-Blackwell; 2011:78-79.
  4. Zachary JF. Pathologic Basis of Veterinary 6th ed. St. Louis, MO: Elsevier; 2017:281-283, 789.

 

 


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