Equine - Haemolymphatic Dz Flashcards
Describe prekallikrein or Fletcher factor deficiency in horses.
- Inherited disorder of Miniature and Belgian horses.
- Required for activation of factor XII in intrinsic pathway, therefore important in thrombosis.
- Asymptomatic but bleed in response to trauma.
- Prolonged APTT, normal PT (intrinsic pathway only).
Describe von Willenbrand factor deficiency in horses.
- vWBF is required for platelet adhesion.
- Reported in one QH filly with haemorrhage from mucosal surfaces post-trauma.
- Prolonged APTT, normal PT (intrinsic pathway only).
Describe the pathophysiology of Glanzmann Thrombasthenia.
- Inherited platelet defect caused by change in the platelet glycoprotein IIb-IIIa complex (integrin alpha-2B-beta-3), the receptor that binds fibrinogen and mediates platelet aggregation.
- Reported in 6 horses of different breeds, all only had abnormality of alpha-2B subunit.
List the clinical signs and diagnostic test findings in horses with Glanzmann Thrombasthenia.
- Intermittent epistaxis.
- Petechial and ecchymotic haemorrhages in the nasopharynx.
- Prolonged gingival bleeding time, prolonged clot retraction, impaired platelet aggregation in response to agonists.
- May see a mild anaemia secondary to blood loss.
- Normal PT, APTT, platelet count.
Define vasculitis.
Pathologic process involving inflammation and necrosis of blood vessel walls. Occurs secondary to primary toxic, infectious or neoplastic disease processes.
List aetiologic agents of vasculitis in horses.
- Equine Viral Arteritis virus.
- Purpura Haemorrhagica (most often secondary to Strep equi ss equi infection).
- Equine Infectious Anaemia virus.
- Equine Granulocytic Ehrlichiosis (Anaplasma phagocytophylum infection).
List clinical manifestations of vasculitis in horses.
- Skin and mucous membranes most commonly affected.
- Well-demarcated areas of dermal or s/c oedema that may progress to skin infarction, necrosis and exudation.
- Hyperaemia, petechial/ecchymotic haemorrhages, ulceration of mucous membranes.
- Secondary cellulitis, thrombophlebitis, laminitis, pneumonia reported.
- May occur as primary problem in any organ –> lameness, renal dz, colic, ataxia, dyspnoea.
Describe diagnostic test findings in cases of vasculitis in horses.
- Skin histo: neutrophilic infiltration of venules in the dermis and s/c tissue with nuclear debris in and around vessels and fibrinoid necrosis.
- CBC/chem: may be WNL or may see anaemia, neutrophilia, hyperglobulinaemia, hyperfibrinogenaemia, normal platelet count, inc CK, inc creatinine.
Describe the pathogenesis of vasculitis in horses.
Immunologic mechanism suspected e.g. Ag-Ab deposition in vessel walls w subsequent complement activation and chemoattractant prod –> neut/macro release proteolytic enzymes –> vessel wall necrosis –> haemorrhage, oedema and infarction of tissues.
Describe the infectious agents which have been implicated as aetiologic agents in Purpura Haemorrhagica (PH) in horses.
- Strep equi ss equi.
- Strep equi ss zooepidemicus.
- Rhodococcus equi.
- Corynebacterium pseudotuberculosis.
- Strep equi ss equi vaccination.
List clinical signs of PH in horses.
- Most often in young to middle aged horses.
- Develops acutely within weeks of resp infection.
- Well demarcated s/c oedema of the limbs.
- Anorexia.
- Lethargy.
- Fever.
- Tacchycardia.
- Haemorrhages on MMs.
- +/- reluctance to move, colic, epistaxis.
List clinicopathologic findings in cases of PH in horses.
- Anaemia.
- Neutrophilia.
- Hyperglobulinaemia.
- Hyperfibrinogenaemia.
- Inc CK and AST.
- Rarely thrombocytopaenia.
Describe typical histopathologic findings in skin biopsies of horses with PH.
- Diagnostic finding: acute leukocytoclastic or non-leukocystoclastic vasculitis with vessel necrosis.
- Dermal and s/c haemorrhage, protein rich oedema, dermal infarction, arteries infiltrated by neutrophils +/- hyaline thrombi.
Describe the pathophysiology of PH in horses.
- Type III hypersensitivity reaction.
- Strep equi: primarily IgM or IgA to Strep M protein; Ag-Ab complexes lodge s/c vessels or throughout the body.
- May see infarcts in kidneys, GI walls, skeletal muscle, spleen in addition to skin lesions.
Outline treatment and prognosis of PH in horses.
- Address primary cause e.g. Strep –> penicillin at least 2wk.
- Suppress immune response: prolonged corticosteroid therapy.
- Hydrotherapy, limb bandaging, walking.
- +/- IVFT and nutritional support.
- Prognosis fair with early and aggressive therapy.
- Potential complications: skin sloughing, laminitis, cellulitis, pneumonia, diarrhoea.
Describe the Equine Arteritis Virus.
- Order: Nidovirales.
- Family: Arterivirdae.
- Genus arterivirus.
- Enveloped RNA virus.
How is the EAV transmitted between horses?
- Maintained in accessory organs of the male repro tract in stallions (ampulla, vas deferens).
- Transmitted in fresh or frozen semen from asymptomatic carriers via natural service or AI.
- Aerosol from respiratory, urinary or repro tract secretions from acutely infected individuals.
- Fomites.
List the clinical signs of EAV infection.
- CSx dev 1-10d post-infection.
- Pyrexia, lethargy, anorexia.
- Oedema: limbs, periorbital, supraorbital, vetral, mammary gland, scrotal.
- Stiffness.
- Rhinorrhea.
- Epiphora.
- Conjunctivitis.
- Rhinitis.
- Abortion.
Describe the pathophysiology of EAV infection.
- Virus rapidly localised in LNs and macrophages –> various tissues –> localised in vessels in endothelium, medial myocytes, pericytes.
- Causes vasculitis with fibroid necrosis of tunica media, vascular and perivascular lymphocytic infiltration, loss of endothelium, dev of fibrinocellular thrombi.
Outline methods for diagnosis of EAV.
- Serology: >4x inc 3wk apart.
- Virus isolation or PCR on sperm, resp secretions, aborted foetus, placenta.
Outline vaccination requirements for EAV.
- Must submit serum to the USDA prior to vacc to prove seronegative status, as serology does not distinguish between vaccination and natural exposure.
- MLV vaccine; isolate post-vacc in case of shedding.
What is the causative agent of Equine Granulocytic Erhlichiosis (EGE)?
- Anaplasma phagocytophilum.
- Formerly known as Erhlichia equi.
- Gram negative rickettsial bacteria that have a tropisms for neutrophils and eosinophils in horses.
Describe the epidemiology of EGE.
- Reported in USA, Canada, Israel, Europe.
- Most cases Autumn to Spring.
- No latent/carrier state in horses.
- Vectors: Ixodes pacificus and I. scapularis (USA) or I. ricinus (Europe).
- Potential reservoir hosts: mice, chipmunks, deer, wood rats, cervids, lizards, birds.
The pathogenesis of EGE is unkown as this time. Describe the proposed pathogenesis of EGE.
- Tick bites horse.
- A. phagocytophilum enters blood or lymph stream then infects and replicates in neutrophils and eosinophils.
- Cytolysis, inflammation, cell sequestration/destruction/ consumption –> pancytopaenia.
- Both CM and humoral IR develops with immunity persisting >2y.
List clinical signs of EGE.
- Reluctance to move.
- Fever.
- Tachycardia.
- Lethargy.
- Decreased appetite.
- Limb oedema.
- Petecchiation.
- Icterus.
- Weakness.
- Ataxia.
- Recumbency.
- Dz is self-limiting and non-fatal so long as secondary complications do no occur e.g. bacterial, viral or fungal infections.
Outline diagnosis of EGE.
- CBC: anaemia, granulocytopaenia, lymphocytopaenia, thrombocytopaenia.
- Blood smear: stain w Wrights stain –> org turns blue; min 3 morulae (granular aggregates) in cytoplasm.
- PCR is buffy coat.
- Serum IFA titre: >4x inc in paired titres.
Describe necropsy findings in horses that have died from EGE.
- Petechiae and ecchymoses of the s/c tissues.
- Oedema of the ventrum, limbs, prepuce.
- Proliferative and necrotising vasculitis, thrombosis and perivascular cuffing in the s/c, fascia, kidneys, heart, brain, lung, ovaries, testes.
Outline treatment and prevention of EGE.
- Oxytet/doxycycline for 5-7d –> rapid response.
- May be self-limitng if un-tx and resolve in 2-3wk.
- Px excellent if no secondary complications.
- Prevention: tick control.
Define thrombocytopaenia in the horse.
- Platelet count
List clinical signs of thrombocytopaenia in the horse.
- ## Multiple sites of small vessel bleeding –> petechial/ ecchymotic haemorrhage on MMs, nictitans, sclera.