BASICS
- Lymphocyte count in peripheral blood less than the lower limit of the laboratory reference interval; usually <1500 cells/µL
- Lymphocyte count can change rapidly owing to physiologic influences, disease, or administration of drugs
- Lymphopenia can be caused by corticosteroids, acute infectious disease, increased loss, or decreased production
Hereditary (primary) immunodeficiencies have breed, age, and sex predilections but other causes of lymphopenia have none.
- Endogenous (stress) or exogenous corticosteroids predictably induce lymphopenia
- Mechanism involves redistribution of circulating lymphocytes (predominantly T cells) with transient sequestration in lymphoid tissues or bone marrow
- Prolonged high doses of corticosteroid administration may cause lympholysis of thymic cortical lymphocytes and uncommitted lymphocytes in lymph nodes; effector B and T cells are resistant
Acute Inflammation and Infection
- Viral infections, e.g. equine influenza, equine herpesvirus, equine coronavirus
- Bacterial diseases, e.g. bacteremia, peritonitis, pleuropneumonia; mechanisms may involve endogenous corticosteroid release (stress), sequestration of lymphocytes in lymphoid and other tissues, and trapping of recirculating lymphocytes in lymph nodes
- Rickettsial infections, e.g. Anaplasma phagocytophilum, Neorickettsia risticii (Potomac horse fever)
- Protozoal infections, e.g. equine piroplasmosis (Theileria equi and Babesia caballi)
- Hereditary (primary) immunodeficiencies
- Cytotoxic chemotherapeutic agents (e.g. azathioprine, cyclophosphamide, cyclosporine (ciclosporin), and tacrolimus) suppress clonal lymphocyte proliferation
- Radiation kills rapidly dividing cells
- Copper and vitamin A deficiencies
- Iron toxicity is associated with multifocal lymphoid necrosis
- Protein-calorie malnutrition induces T-cell lymphopenia; B-lymphocyte function and humoral immunity unaffected
- Neoplasia (e.g. lymphoma) disrupting lymph node architecture
DIAGNOSIS
TREATMENT
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS