Equine Immunology and Hematology II

Question 1

Primary hemostasis covers up to ___ while secondary hemostasis is for ___

Answer 1

Clot formation

Fibrin formation and clot stabilization

Question 2

Differentiate between disorders of Primary and Secondary Hemostasis

Answer 2

Primary: vascular and platelet diseases
- Mucosal bleeding, petechiation, ecchymoses, melena
Secondary: soluble coagulation factors
- Hemorrhage, prolonged bleeding, hematomas

Question 3

Tests of hemostatic function

Answer 3

Activated clotting time: intrinsic
APTT: intrinsic and common
PT: extrinsic and common
Thromboelastometry, thromboelastography
FDPs (lab dependent)
Fibrinogen
Factor assays

Question 4

Coagulopathy

Answer 4

Inherited disorders: coagulation factor deficiency

Acquired: vasculitis, thrombocytopenia, DIC, toxicity (warfarin, sweet clover)

Question 5

Factor VIII deficiency (Hemophilia A)

Answer 5

X linked recessive
Most common deficiency in horses
Abnormal intrinsic pathway: Abnormal APTT with normal PT
Dx: Eval factor VIII activity, hx of hemorrhage
Poor prognosis
There are other inherited; not important

Question 6

Vasculitis (acquired)

Answer 6

Inflammation and necrosis of the vessel walls, causes: infectious, toxic, immune-mediated, neoplastic
CS: Dermal, SQ edema, skin infarction, necrosis, exudation
Skin and MM: hyperemia, petechiae, ecchymosis, ulcers
Cellulitis, laminitis, thrombophlebitis
Additional Dx: Punch biopsy - N0 inflammation, immune complex deposition

Question 7

Vasculitis DDx

Answer 7

Equine purpura hemorrhagica
Equine viral arteritis
Equine infectious anemia
Anaplasma phagocytophila

Question 8

Equine purpura hemorrhagica (EPH)

Answer 8

Strep equi equi after vaccination or exposure
Other less common bateria can cause
Strangles
Vasculitis with edema and hemorrhage - Infarctive syndrome possible = coagulative necrosis of muscle
CS: severe limb edema, mucosal petechiation, fever
Dx: Skin biopsy, Strep equi M protein Ab
Tx: Corticosteroids, antimicrobials (penicillin)

Question 9

Equine viral arteritis

Answer 9

4 clinical syndromes: panvasculitis, abortion, conjunctivitis, neonatal pneumonia
Transmission: Semen of persistently infected stallions, aerosolized virus, fomites
ID of carrier stallions and vaccination crucial for disease control

Question 10

Anaplasma phagocytophila

Answer 10

Vector: Ixodes scapularis
- Late fall, winter, spring
CS: limb edema, fever, petechiation, ataxia, anemia, thrombocytopenia, pancytopenia
Dx: morulae in granulocytes, serum PCR, serum IFA
Tx: Oxytetracycline
Good prognosis

LIMB EDEMA NOT AS SEVERE AS PURPURA

Question 11

Equine infectious anemia

Answer 11

Reportable, USDA regulated
Most infected horses are inapparent carriers
CS: Acute - fever, thrombocytopenia, petechiae, Chronic - anemia, edema, weight loss
Dx: Coggin’s test
- travel, import, competition, change of address or ownership
Mainstay of control is removal of positive horses from population

Question 12

Thrombocytopenia

Answer 12

Platelet count is <100,000/uL
- <30,000 = clinical bleeding
- <10,000 = spontaneous hemorrhage
Causes: decreased production (bone marrow disease, drugs), sequestration (splenomegaly), increased consumption (DIC, hemorrhage), increased destruction (infectious, immune-mediated diseases)
CS: Petechial and ecchymotic hemorrhage, epistaxis, melena, hematuria, hyphema, hematoma, hemorrhage

Question 13

Thrombocytopenia

Answer 13

DDx: EIA, Purpura, anaplasma
Inciting factor often not found (idiopathic, infectious, neoplastic, drug)
Increased platelet surface bound immunoglobulins or complement target normal platelet antigens or “noel” Ag
- Platelet destruction and removal by MPS primarily in spleen or liver

Question 14

Thrombocytopenia Dx

Answer 14

Negative Coggin’s, normal PT PTT, normal to increased megakaryocytes in bone marrow, increased platelet bound Ab
- Platelet C3 test, platelet bound IgG, IgM
Presumptive Dx: thrombocytopenia, normal coag panel, Coggins neg

Question 15

Tx of thrombocytopenia

Answer 15

Stop admin of all exogenous compounds, tx primary dz, corticosteroids, transfusion

Question 16

DIC

Answer 16

Acquired dysfunction in coagulation secondary to severe systemic diseases
- Endotoxemia, sepsis, GIT dz
Pathophysiology: exaggerated activation of coagulation, microthrombi deposition (ischemic organ damage), consumption coagulopathy (hemorrhage)
Clinical forms: MODS or hemorrhagic form

Question 17

DIC Dx

Answer 17

No one test
Thrombocytopenia
Increased procoagulant activation
Consumptive coagulopathy (increased PT and APTT)
Decreased fibrinogen and antithrombin
Increased D dimers or FDPs

Question 18

DIC prognosis

Answer 18

Guarded to grave

Tx typically very expensive

Question 19

DIC Tx

Answer 19

Control underlying dz
Early recognition and treatment
Plasma transfusion and antithrombotics (Heparin)
Supportive care

Question 20

Vit K dificiency

Answer 20

Essential for hepatic synthesis of factors II, VII, IX, X
CS associated with decreased factor VII often seen first
Primary Vit K deficiency rare
Antagonism of vit k more common
- Warfarin, moldy sweet clover
Tx: Vit K1 SQ