Equine Immunology and Hematology I Flashcards
What are components of Innate immunity?
Nonspecific Acute phase proteins -Fibrinogen Proinflammatory cytokines -IL-1, IL-6, TNFalpha Complement system Lipid mediators -Prostaglandins, leukotrienes Granulocytes, monocytes
Components of Adaptive immunity
Specificity and memory Cellular and humoral (Ab mediated) B cell lymphocytes - Memory cells - Immunoglobulins T-cell lymphocytes -CD8, CD4 -MHC
Neutrophilia causes in the horse
Chronic/established infection
Abscess
Neoplasia, glucocorticoids
Neutropenia causes in the horse
Acute, severe infection (GI)
Septicemia, endotoxemia
- L shift and toxic changes
Endotoxemia is rapid redistribution of N0 to marginal and tissue pools
Lymphopenia causes
Acute viral, rickettsial, or severe bacterial infection
Endotoxemia
Eosinophilia causes
Parasitic
Hypersensitivity
Neoplasia
Basophilia causes
Hypersensitivity
Immunodeficiencies
Primary (rare): genetic Secondary: altered responses of normal immune system - Disease (PPD) - Age - Pregnancy - Drugs - Stressors - Neoplasia - Malnutrition, nutrient deficiencies
Clinical features of immunodeficiency
Onset at young age
Repeat infections, poorly responsive to treatment
Increased susceptibility to organisms of low pathogenicity
Illness or poor immunologic response to vaccination
Persistent abnormalities in leukocytes
Dx of immunodeficiency
Ab mediated immunity: quantitative tests for Ig levels, functional test of response to vax
Cellular immunity: Quantitative CBC, lymphocyte phenotyping, functional test response to vax
Granulocytes, monocytes, M0: quantitative only
Bone marrow: evaluate progenitor cell populations
SCID
Lethal, autosomal recessive condition primarily seen in Arabian foals
- Chromosome 9 mutation
- 8-25% Arabians in US are carriers
T and B cell function absent
- Absence of cell mediated and Ab mediated immunity
Other rare immunodeficiencies
Common variable immunodeficiency - Late onset (6-14yr) no breed or gender disposition - Recurrent bacterial infections IgM dificiency Agammaglobulinemia Transient hypogammaglobulinemia Fell pony syndrome
Lymphoproliferative disorders
Lymphoma
Leukemia
Myeloma
Equine lymphoma basics
Most common neoplasia of the horse
Mean diagnostics 5-10y
CS of equine lymphona
Lymphadenopathy Lethargy, weight loss, fever Others dependent Peripheral lymphadenopathy rare Hematologic abnormalities are variable - Anemia, lymphopenia - Lymphocyte morphology abnormal - Inflammatory leukogram, hyperglobulinemia Paraneoplastic syndromes - Hypercalcemia - Immune mediated Hemolytic anemia or thrombocytopenia Occasional suspect association with EHV 5
Equine lymphoma classification
Morphologic: small cell, large cell, mixed
Cell lineage: immunohistochemical evaluation, T cell rich, large b cell most common
Anatomic distribution: multicentric, generalized, alimentary/intestinal, thoracic, cutaneous
Multicentric lymphoma
Multiple lymph nodes
No extra nodal involvement
Generalized lymphoma
Metastasis to extra-nodal tissues Nonlymphoid tissue involved Spleen most common organ Very poor prognosis Severe clinical signs Leukemia possible
Intestinal lymphoma
CS: malabsorption, PLE, weight loss, edema, abdominal effusion, colic, diarrhea
Neoplastic lesions: diffuse, segmental thickening, focal masses, scattered ulcerative lesions
Dx: US, biopsy, Abd fluid analysis
MOST common neoplasia of GIT
Lymphadenopathy not typical
Thoracic lymphoma
Most common thoracic neoplasia; Mediastinal, thymic, or pulmonary T cell predominates
CS nonspecific: Nasal discharge, adventitial lung sounds, pleural effusion*, ventral thoracic and limb edema, lymphadenopathy
Cutaneous lymphoma
Skin associated lymphoid tissue
Distribution variable; single to multiple firm, SQ, nonpainful masses
Predominantly T cell rich large B cell
Often aggressive - may progress
Often responsive to corticosteroids, sx excision
Best one to get
Lymphoma Dx and Tx
Antemortem Dx difficult Excisional biopsy, fluid analysis Bone marrow Other Tx: Corticosteroids, immunomodulation, antiviral medication, chemo (transient remission possible, recurrence typical) Long term prognosis poor
Equine leukemia basics
Primary originats from bone marrow
Secondary is leukemic phase of lymphoma
Myeloid or lymphoid cell lineage
Leukemic: profound leukocytosis
Subleukemic: blast cells, low/normal WBC
Aleukemic: abnormal bone marrow only
Grave prognosis
Equine leukemia CS
Weight loss anorexia lethargy Pyrexia Lymphademopathy if secondary to lymphoma
Equine leukemia hematologic changes
Anemia Thrombocytopenia Marked leukocytosis Pancytopenia - Neutropenia, lymphopenia Increased blast or atypical cells in blood Hyperproteinemia Hyperfibrinogenemia
Equine leukemia Dx
Bone marrow aspirate
Flow cytometry
IHC, immunophenotyping
Equine myeloma
Plasma cell proliferation Primary: bone marrow Secondary: extramedullary - LN, spleen, kidney, liver Multiple myeloma: bone marrow and tissues
Equine myeloma CS
Weight loss, fever, lethargy
Pale MM
Limb edema
Recurrent infection
Equine myeloma Dx
Bone marrow: plasmacytosis
Hematology: anemia, hyperproteinemia (globulins), Pancytopenia (myelopathies), hypercalcemia, monoclonal immunoglobulinemia
Poor prognosis, rapid deterioration
Equine erythron
Variable PCV - ~30% circulating equine RBC in spleen - Excitement/pain - transient increase in PCV - alpha 2 agonists - transient decrease in PCV Rouleau Peripheral reticulocytes extremely rare Howell Jolly Bodies - Basophilic nuclear remnants
Clinical evaluation of erythron
Coomb’s test: detect Ig or complement on erythrocyte surface
- Agglutination = positive
- Useful with IMHA
RBC fragility
Bone marrow eval: Aspirate or core biopsy, characterize anemia (Regen, nonregen, NO circulating reticulocytes), myeloid:erythroid (
Anemia
Decreased O2 carrying capacity of blood secondary to RBC loss - hypoxia
Causes: blood loss, hemolysis, impaired RBC production
CS vary: tachycardia, tachypnea, depression, mucosal pallor/icterus, hemoglobinuria, lethargy, weakness
Anemia Dx
Hx PE CBC Urinalysis Bone marrow aspirate
Acute blood loss: hemorrhage
Causes: trauma, Sx, guttural pouch mycosis, hemorrhage into body cavity, peripartum hemorrhage, coagulopathy, neoplasia
CS: Hypovolemic shock, colic and abd distension, dyspnea, braced stance, epistaxis
Acute blood loss Dx
PCV/TP decrease over 12-24h, with IMHA TP shouldn’t decrease
Blood lactate increases secondary to tissue hypoxia
US
Abdominocentesis, thoracocentesis
Acute blood loss Tx
Stop hemorrhage Address hypovolemic shock Judicious use of sedation Replace blood loss With internal hemorrhage body can reuse blood components- avoid removal if posiible
Blood transfusion basics
Transfused RBC last 2-4d in adult horse
Cross match
-Major: donor RBC- recipient serum alloAb
- Minor: dono serum Ab - recipient RBC
If cross match not possible Qa, Aa neg geldings or maiden mares
Blood transfudsion strategy
Replace 20-40% of total loss
Can safely remove 5-10L from donor
Avoid adverse rxn to transfused RBC (start slow)
CS of adverse rxn: tachycardia, urticaria, dyspnea, pyrexia, colic, diarrhea, anaphylaxis, pulmonary edema, hemolysis, DIC
Causes of chronic blood loss
GI or urogenital/renal dz: neoplasia, EGUS, RDC, Hemostatic dysfunction
Physiologic adaptation to gradual onset of tissue hypoxia secondary to anemia
Iron stores may become depleted: low serum iron, decreased bone marrow iron stores, increased total iron binding capacity, hypochromic, microcytic anemia
