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Hematology Flashcards

1
Q

Describe prekallikrein or Fletcher factor deficiency.

A
  • 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).
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2
Q

Describe von Willenbrand factor deficiency.

A
  • 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).
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3
Q

Describe the pathophysiology of Glanzmann Thrombasthenia.

A
  • 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.
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4
Q

List the clinical signs and diagnostic test findings with Glanzmann Thrombasthenia.

A
  • 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 mild anaemia secondary to blood loss.
  • Normal PT, APTT, platelet count.
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5
Q

Define vasculitis.

A

Pathologic process involving inflammation and necrosis of blood vessel walls.

Occurs secondary to primary toxic, infectious or neoplastic disease processes.

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6
Q

List aetiologic agents of vasculitis.

A
  • 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).
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7
Q

List clinical manifestations of vasculitis.

A
  • 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.
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8
Q

Describe diagnostic test findings in cases of vasculitis.

A
  • 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.
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9
Q

Describe the pathogenesis of vasculitis.

A

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.

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10
Q

Describe the infectious agents which have been implicated as aetiologic agents in Purpura Haemorrhagica (PH) in horses.

A
  • Strep equi ss equi.
  • Strep equi ss zooepidemicus.
  • Rhodococcus equi.
  • Corynebacterium pseudotuberculosis.
  • Strep equi ss equi vaccination.
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11
Q

List clinical signs of PH in horses.

A
  • 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 +/- reluctance to move,
  • Fever.
  • Tacchycardia.
  • Haemorrhages on MMs.
  • Colic,
  • Epistaxis.
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12
Q

List clinicopathologic findings in cases of PH.

A
  • Anaemia.
  • Neutrophilia.
  • Hyperglobulinaemia.
  • Hyperfibrinogenaemia.
  • Inc CK and AST.
  • Rarely thrombocytopaenia.
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13
Q

Describe typical histopathologic findings in skin biopsies of PH.

A
  • 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.
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14
Q

Describe the pathophysiology of PH.

A
  • 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.
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15
Q

Outline treatment and prognosis of PH.

A
  • 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.
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16
Q

Describe the Equine Arteritis Virus.

A
  • Order: Nidovirales.
  • Family: Arterivirdae.
  • Genus arterivirus.
  • Enveloped RNA virus.
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17
Q

How is the EAV transmitted between horses?

A
  • 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.
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18
Q

List the clinical signs of EAV infection.

A
  • CSx dev 1-10d post-infection.
  • Pyrexia, lethargy, anorexia.
  • Oedema: limbs, periorbital, supraorbital, vetral, mammary gland, scrotal.
  • Stiffness.
  • Rhinorrhea / Rhinitis.
  • Epiphora.- Conjunctivitis.
  • Abortion.
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19
Q

Describe the pathophysiology of EAV infection.

A
  • 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.
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20
Q

Outline methods for diagnosis of EAV.

A
  • Serology: >4x inc 3wk apart.
  • Virus isolation or PCR on sperm, resp secretions, aborted foetus, placenta.
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21
Q

Outline vaccination requirements for EAV.

A
  • 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.
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22
Q

What is the causative agent of Equine Granulocytic Erhlichiosis (EGE)?

A
  • Anaplasma phagocytophilum.
  • Formerly known as Erhlichia equi.
  • Gram negative rickettsial bacteria have tropisms for neutrophils and eosinophils in horses.
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23
Q

Describe the epidemiology of Equine Granulocytic Erhlichiosis (EGE).

A
  • 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.
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24
Q

The pathogenesis of Equine Granulocytic Erhlichiosis (EGE) is unknown at this time, describe the proposed pathogenesis of EGE.

A
  • 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.
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25
Q

List clinical signs of Equine Granulocytic Erhlichiosis (EGE).

A
  • 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.
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26
Q

Outline diagnosis of Equine Granulocytic Erhlichiosis (EGE).

A
  • 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.
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27
Q

Describe necropsy findings in horses that have died from Equine Granulocytic Erhlichiosis (EGE).

A
  • 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.
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28
Q

Outline treatment and prevention of Equine Granulocytic Erhlichiosis (EGE).

A
  • 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.
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29
Q

Define thrombocytopaenia.

A

Decrease Platelet count

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30
Q

List clinical signs of thrombocytopaenia.

A

Multiple sites of small vessel bleeding
–> petechial/ ecchymotic haemorrhage on MMs, nictitans, sclera.-

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31
Q

Outline treatment of thrombocytopenia causing life-threatening haemorrhage.

A
  • Administration of fresh blood or PRP used immediately.
  • NB do not store blood in glass –> platelet adhesion.
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32
Q

Define Disseminated Intravascular Coagulation (DIC).

A

Secondary disease characterised by widespread fibrin deposition in the microcirculation (–> ischaemia) and development of haemorrhagic diathesis caused by the consumption of pro-coagulants and hyperactivity of fibrinolysis.

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33
Q

List clinical signs of DIC.

A
  • Can vary widely from diffuse thrombosis –> ischaemic organ failure to haemorrhagic diathesis.
  • MODS:
    • Renal involvement common.
    • Colic can occur from GI microthrombi.
    • Pulmonary involvement –> tachypnoea, dyspnoea.
  • Laminitis, thrombosis of peripheral vv.
  • May chronic compensated form –> chronic low-grade pro-coagulant stimulus.
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34
Q

Outline results of coagulation tests with DIC.

A

Results vary; as Dz progresses see following results:

  • Prolonged TT, PT, APTT.
  • Inc D-dimers and FDPs.
  • Fibrinogen and platelet count: WNL or sl dec.
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35
Q

Describe the pathophysiology of DIC.

A
  1. Generation of excessive pro-coagulant factors in the blood or contact of blood w abnormal surfaces –> excessive thrombin prod –> ischaemia e.g. LPS stimulates mono/macro –> prod of pro-coag factors: platelet-activating factor, tissue factor, Pgs, ILs, TNF.
  2. Counter-balance fibrinolytic system is activated; liver and spleen overwhelmed and unable to remove FDPs and activated clotting factors from circulation.
36
Q

Outline treatment of DIC.

A
  • Treat underlying disease e.g. Sx for strangulated SI, ABs for sepsis.
  • Combat shock and maintain tissue perfusion: IVFT, flunixin; +/- plasma.- +/- LMWH (controversial).
37
Q

List the etiologic agents known to cause Piroplasmosis.

A
  • Babesia caballi - intra-erythrocytic parasite similar to B. bigemina, pear-shaped, forms acute-angled pairs.
  • Theileria equi (more pathogenic) - parasite with lymphocytic and erythrocytic stages; intraerythrocyte parasite divides into four cells to form a Maltese cross.
38
Q

Describe the epidemiology of Piroplasmosis.

A
  • Widely distributed through tropics and subtropics; less in temperate areas.
  • Both parasites transmitted by ticks of the genera Dermancentor, Hyalomma and Rhipicephalus.
  • Once infected horses remain chronic carriers.
  • T. equi can be transmitted transplacentally.
  • Incubation period 5-28d.
39
Q

List clinical signs of Piroplasmosis.

A
  • Fever, depression, anorexia.
  • Haemolytic anaemia and haemoglobinuria.
  • Jaundice.
  • Incoordination.
  • Lacrimation, mucoid nasal discharge & Swelling of the eyelids.
  • Frequent lying down.
  • Death.
40
Q

Describe diagnostic test findings in horses with Piroplasmosis.

A
  • CBC: anaemia, parasite in RBCs stained w Giesma stain;
  • T equi may see monocytosis and eosinopenia.
  • Haemoglobinuria (may be absent w B. caballi).
  • Serum: cELISA (official test OIE/USDA).
  • Whole blood: PCR.
41
Q

Outline treatment and prognosis for horses with Piroplasmosis.

A
  • Imidocarb; T. equi more refractory to tx than B. caballi.
  • Good Px if Dx and Tx early.
  • Higher doses of imidocarb can cause transient colic in horses.
  • Control of tick infestations.
42
Q
  • What bacteria is responsible for most Leptospirosis infections?
  • What is its most common maintenance host?
  • What serovar is considered by some to be the host-adapted species in horses?
A
  • Leptospira kirschneri serovar Grippotyphosa in EU & Leptospira pomona kennewick in North America.
  • Skunk is most common maintenance host.
  • L. bratislava is considered by some to be a host-adapted spp in horses while others think it is pathogenic.
43
Q

What disease can be caused by Leptospirosis in horses?

A
  • Uveitis and immune-mediated keratitis.
  • Placentitis.
  • Abortion & Stillbirth.
  • Renal disease: tubulointerstitial nephritis, pyuria, rarely ARF.
  • Haemolytic anaemia.
44
Q

List clinical signs of Leptospirosis.

A
  • Fever.
  • Anaemia.
  • Jaundice.
  • Abortions during late-term gestation.
  • Signs of renal or ocular dz.
45
Q

Outline diagnosis of Leptospirosis.

A
  • Serology: microscopic agglutination titre; 1:6400 significant or rising titres over 2-3wk period.
  • Infected tissues: IFAT.- PCR.
  • Histology.
  • Bacterial culture.
46
Q

Outline treatment options for Leptospirosis.

A
  • AMBs: ampicillin, amoxicillin, penicillin, oxytetracycline, doxycycline.
  • Anti-inflammatories if ERU or IMMK.
47
Q

Outline methods for prevention of Leptospirosis.

A
  • Control exposure to shedding hosts, infected animals and contaminated fomites.
  • Infected horses can shed in urine for up to 14wks.
  • Isolate pregnant mares from other horses.
  • In endemic areas isolate horses w titres of 1:6400 or higher.
  • Clean and disinfect contaminated areas.
  • Vaccination on farms w endemic abortions or ERU.
  • Attempts to decrease shedding w AMBs not successful.
48
Q

Describe the Equine Infectious Anaemia (EIA) virus.

A
  • Family: Retroviridae.
  • Genus: Lentivirus.
  • RNA virus.
  • Lentiviruses are integrated into the host’s genome and therefore infection is lifelong.
49
Q

What tests for EIA are approved by the USDA?

A
  • The Coggins test: agar-gel immunodiffusion (AGID).
  • 4 ELISAs: detect Ab directed at the transmembrane glycoprotein (gp45) and/or the p26 Ag.
  • No test based on detection of viral nucleic acid are USDA-approved.
50
Q

Describe clinical signs of EIA.

A
  1. Acute phase:- High fever.- Thrombocytopaenia.- Malaise.- +/- petechial or ecchymotic haemorrhages on MMs.- May go into DIC and die.- Rarely leukoencephalitis and enterocolitis.
  2. Chronic phase:- Similar signs as above interspersed with periods of clinical quiescence due to waves of viraemia.- Periods of stress may precipitate clinical dz.- +/- weight loss, dependent oedema, ill-thrift, anaemia.
  3. Inapparent phase:- Occurs once viraemia is immunologically contained.- No Csx –> inapparent carrier.
51
Q

Describe the pathophysiology of EIA.

A
  • Lentiviruses use an integrated DNA intermediate to usurp host cells, replicate its genome, make viral proteins and assemble proteins into virions that bud from the cell.
  • EIAV can generate several viral variants that differ genetically from previous ones –> escape from neutralising AB and cytotoxic T cell responses and thwarts attempts to develop vaccines.
  • EIAV can replicate in monocytes, dendritic cells. tissue macrophages and endothelial cells (may –> endothelial damage and subsequent thrombosis/vasculitis).
52
Q

Describe clinicopathologic findings in horses with EIA.

A
  • Anaemia due to intra- and extra-vascular haemolysis and BM supression.
  • Thrombocytopaenia and hypofunctional platelets.
  • Hyperglobulinaemia, hypoalbuminaemia, polyclonal B cell proliferation.
53
Q

Describe necropsy findings in horses that have died from EIA.

A
  • Splenomegaly, hepatomegaly & lymphadenitis.
  • Pronounced hepatic lobular architecture.
  • Echymoses of mucosa and viscera.
  • Dependent s/c oedema.
  • Mononuclear cell infiltrate in periportal regions of the liver, spleen, LNs, meninges and lungs.
  • Haemosiderophages in spleen, LNs, liver, BM.
  • Immune-mediated glomerulonephritis.
54
Q

Outline methods for prevention and control of EIA outbreaks.

A
  • High-risk states: Texas, Oklahoma, Arkansas, Louisiana.
  • All horses should have at least yearly AGID/ELISA.
  • Horse owners should require negative tests for new arrivals to property and practice good fly control.
  • If a seroreactor is ID all horses on property are quarantined until all are negative on two tests 30-60d apart.
  • Seroreactor (depending on State reg) is either euth or quarantined for life and ID by USDA brand/lip tattoo.
55
Q

Define immune-mediated haemolytic anaemia (IMHA).

A
  • Anaemia associated w prod of autologous Abs against the patient’s own RBCs. Abs combine w complement and Ags on the RBC membrane –> rapid removal of affected cells from circulation and their destruction.
  • Can be primary (idiopathic) or secondary (more common) assoc w drug admin, viral, protozoal, bacterial or rickettsial infection, neoplasia or in assoc w other immune-med disorders e.g. lupus.
56
Q

List clinical signs of IMHA.

A
  • Variable depending on degree of anaemia and animal’s primary dz.
  • Marked anaemia (PCV depression, pale MMs, variable icterus, tachycardia, tachypnoea, intermittent fever).
  • CSx of primary dz (if secondary): most commonly PPH, lymphoma, other neoplasma, PLE, chronic bacterial infections.
57
Q

Describe clinicopathologic abnormalities in IMHA.

A
  • Pronounced, progressive anaemia.
  • Blood smear: may see erythrophagocytosis and autoagglutination.
  • May see moderate neutrophilic leukocytosis.
58
Q

Describe diagnostic tests for IMHA.

A
  • Direct Coombs test: detects presence of anti-erythrocyte Abs and/or complement on the RBC membrane.
  • Indirect Coombs test: detects anti-erythrocyte Ab in the serum.- Positive reaction at cold temp indicates IgM Abs.- Positive reaction at body temp indicates IgG Abs.
  • NB in ppl and dogs 1/3 w IMHA have a neg Coombs.
  • Direct immunofluorescence flow cytometry has been reported to determine classes of Ab bound to erythrocytes in horses and foals.
59
Q

Describe the pathophysiology of IMHA.

A
  • Rarely primary, usually secondary to another dz/drug.
  • Initiating factor unknown but may incl damage to RBC membrane resulting in lack of recognition of RBC as ‘self’ or stimulation of immune system by other source may result in prod of Abs w cross-reactivity w RBCs.
  • Ag-Ab reaction and complement fixation –> structural and functional changes in RBC membrane –> intravascular erythrolysis or (more commonly) rapid removal of RBCs by reticuloendothelial system in liver and spleen.
  • Partial phagocytosis of affected cells may result in spherocyte formation (can be difficult to ID in LAs).
60
Q

Describe treatment and prognosis of IMHA

A
  • Identify and tx underlying cause: e.g. remove drug if drug-reaction, ABs in bacterial infection, no tx if neoplasia/EIA.
  • Interrupt immune response: glucocorticoids e.g. 0.1mg/kg dex 3-5 days then wean over 10-14d; one successful report in a horse w cyclophosphamide and azathioprine.
  • Supportive care: quiet restful enviro, good nutrition, vitamin suppl; blood transfusion only if anaemia is life-threatening and immune response can be controlled.
61
Q

List oxidising agents capable of inducing Heinz body haemolytic anaemia.

A
  • Red (Acer rubrum), sugar and silver maple leaves.
  • Phenothiazines.
  • Wild and domestic onions.
  • Methylene blue.
  • Acetylphenylhydrazine.
  • Brassica family e.g. rape or kale.
  • Lymphoma (single case report).
62
Q

List clinical signs of Heinz body anaemia

A
  • Vary w specific toxin, amount ingested, time course of dz process and secondary complicating factors.
  • Weakness, lethargy, anorexia, exercise intol.
  • MM pale and variably icteric, cyanotic or muddy.
  • Tachycardia and tachypnoea.- +/- colic.- +/- brown discolouration of blood.- +/- decreased urine production.
  • Pigmenturia (haemoglobinuria, methaemoglobinuria, bilirubinuria).
  • May see sudden death.
63
Q

Describe the pathophysiology of Heinz body anaemia

A
  • Heinz bodies are formed by precipitation of oxidatively denatured Hg.
  • Normal Hg undergoes oxidative stress; protective mech incl prod of reduced forms of NADPH and glutathione.
  • Pathogenic process (e.g. gallotannins in RBC which are potent oxidising agents, or Se defic –> dec glutathione peroxidase anti-oxidant) –> RBC reductive capacity overwhelmed –> oxidative damage to RBCs –> RBCs less deformable than n –> removed by RES in spleen.
  • Gallic acid in red maple leaves also causes methaemoglobinaemia i.e. oxidative change of Hg iron to non-functional ferric state –> loss of O2 carrying capacity of RBCs.
64
Q

List clinicopathologic abnormalities with Heinz body haemolytic anaemia.

A
  • Acute and profound anaemia.
  • Blood smear: Heinz bodies (round, oval to serrated, refractile granules at RBC margin or protruding from cells; best seen w New Methylene Blue or Crystal Violet); eccentrocytes; anisocytosis w regeneration.
  • Inflammatory leukogram.
  • Coombs test: negative.
  • Methaemoglobinaemia (red maple tox).
  • Hyperbilirubinaemia.- +/- haemoglobinaemia, haemoglobinuria, azotemia.
65
Q

Outline treatment for Heinz body haemolytic anaemia

A
  • Remove source of toxicity & IVFT (reduce chance of AKI).
  • Whole blood transfusion - if indicated clinically.
  • NSAIDs to manage pain.
  • InO2 if poor oxygenation.
  • Red maple: methylene blue and corticosteroids assoc w death; vitamin C - not associated w impr survival.
66
Q

What is the prognosis for horses with red maple toxicity?

A
  • Guarded, Mortality rate: 60-65%.
  • Potential complications of hypoxia, hypoperfusion and inflammation: ARF, colic, laminitis, pyrexia.
67
Q

Describe intravascular haemolysis associated with cutaneous burns.

A
  • Reported in horses with burns of >25% body SA.
  • Plasma shows haemolysis along w abnormal RBC morphology, inc osmotic fragility, haemoglobinuria, azotemia and pigment nephropathy.
  • Suspected to be assoc w prod of hydroxyl radicals by complement-activated neutrophils.
  • In humans early tx w free-radical scavengers and fluid therapy, together w supportive and wound care, control of pain and inflamm and sepsis prophylaxis have proven beneficial.
68
Q

List clinical signs of Anthrax

A
  • Acute intestinal form: colic, diarrhoea, fever, depression, fatal septicaemia.
  • Localised form may occur following insect trans: massive oedema in the neck followed by ventral oedema.
69
Q

List the aetiologic agent of Lyme Disease

A
  • Borrelia burgdorferi.
  • Spirochete.
70
Q

Describe the epidemiology of Lyme Disease

A
  • Tick-bourne infection; Ixodes scapularis > I. pacificus.
  • Tick feeds on wild animal reservoir incl white-footed mouse, California kangaroo rat, dusky-footed wood rate, then transmit to horses, humans, dogs, cats.
  • Exposure/infection rates high (50%) in horses in NE US, Midwest, Texas and California.
71
Q

List clinical signs of Lyme Disease.

A
  • Non-specific incl fever, stiffness, lameness in >1 limb, muscle tenderness, hyperaesthesia, swollen joints, behavioural change.
  • A. phagocytophylum and B. burgdorferi can co-exist in Ixodes ticks –> concurrent infection in horse.
  • Experimental exposure has not proven dz but has proven seroconversion and shedding and seroconversion of in contact controls.
72
Q

Outline diagnosis of Lyme Disease.

A
  • Serology: ELISA, IFA, Western Blot; dx of active or recent infection: titres >300 kinetic ELISA units.
  • Culture from blood, urine, CSF difficult.
  • PCR on skin, LNs, fascia, sk muscle, organs.
73
Q

Describe treatment of Lyme Disease.

A
  • Tetracycline, doxycycline or ceftiofur for 3-4 wks.
  • If CNS dz IV penicillin and ceftriaxone have been used.
  • Recommendations for vacc in clinical setting are lacking.
74
Q

Describe the clinical presentation of C. pseudotuberculosis infection (‘Pigeon Fever’).

A
  1. Ulcerative lymphangitis: severe cellulitis involving lymphatics in 1 or more limbs –> lameness, fever, lethargy, anorexia; often becomes chronic –> limb oedema, lameness, weakness, weight loss.
  2. Internal abscess: 50-60% had previous external abscesses; liver > lungs, mesentery, mediastinum, kidneys, diaphragm, spleen, pericardium, blood, uterus; anorexia, lethargy, fever, tachycardia, wt loss +/- colic, pale MMs, ventral/limb oedema, ventral dermatitis, ataxia, haematuria, nasal discharge, abortion; fatality 30-40%.
  3. External abscess: >50% cases firm, painful swelling –> thick capsule, deep abscess, hard to drain; once draining est usually heal in 10-14d; fever 25% cases, non-healing wounds, lameness, ventral dermatitis > depression, anorexia, other prob; 91% completely resolve –> immunity; 9% last >1y or recur.
75
Q

Describe the treatment of C. pseudotuberculosis infection.

A

Principles of therapy:

  1. Allow the abscess to mature.
  2. Establish drainage.
  3. Collect and properly dispose of infective exudate.
  4. Lavage the wound with an antiseptic solution.-

Do not tx w ABs prior to drainage of external abscesses.-
Internal abscesses: min 4-6wk ABs (susceptible to nearly all, but consider intraceullular location).
NSAIDs to control pain and inflammation.

76
Q

Describe the bacteria responsible for causing Anthrax.

A
  • Bacillus anthracis.
  • Vegetative form: large, rectangular-shaped, gram positive rod.
  • Vegetative form predominately found in infected animal tissues but can exist in enviro.
  • Forms spores under nutritionally limited conditions (aerobic process) –> stable in enviro for decades.
77
Q

Describe findings on necropsy of animals that have died from Anthrax.

A
  • Carcass decomposes rapidly.- May see bloody exudates from body cavities and blood may not clot.- Spleen enlarged with ‘blackberry jam’ consistency.- LNs and internal organs may be oedematous and haemorrhagic.- Localised exposure may result in enteritis, regional LN involvement, peripheral tissue oedema.- Histo: large numbers of bacilli in affected tissues.
78
Q

Outline diagnostic test findings in Anthrax cases.

A
  • DO NOT OPEN CARCASS!!! –> sporulation of vegetative cells and contam of enviro; use PPE!!!- Dx based on microscopic exam of blood or tissue smears, bacterial culture; NB warn lab personnel (zoonotic risk).- Samples: blood, AQ, whole eye; LN if localised dz.- B. anthracis cells are destroyed during decomp, so take samples early.- Large, gram pos, square-ended rods found singly or in chains of 2-4; polychrome methylene blue (M’Faydean stain) identifies capsule surrounding the organism.
79
Q

Describe measures for treatment and control of Anthrax in large animals.

A
  • Report suspected case to local/state vet ASAP.- Tx often unrewarding/not possible due to peracute nature of dz; can try penicillin or oxytet for at least 5 days.- Carcasses should not be opened or moved; burn carcass and contam bedding/soil > deep burial.- Premise quarantined; clinically normal animals vaccinated w live acapsular vacc, vaccinate neighbouring herds, control insects and scavengers to limit spread.- Endemic areas: vacc 4 weeks prior to turning out on pasture where previous outbreak has occurred; rpt in 2-3 weeks if heavily contam area; goats and llamas may have severe adverse reactions to vaccine!- Ideally do not graze contam areas.
80
Q

What plant, in addition to red and silver maples and wild onions, has been reported to cause Heinz body anaemia and methaemoglobinaemia in horses?

What is the toxic agent in this plant and what body fluid can it be detected in?

A
  • Pistachio trees (Pistacia spp)
  • Pyrogallol or gallic or tannic acids (converted to pyrogallols in the equine GIT).
  • Urine pyrogallol concentration.

Ref: J. Vet. Intern. Med. 2015;29:410–413.

81
Q

Do concurrent hyperglycaemia and endotoxaemia result in more severe coagulation abnormalities in horses than endotoxaemia alone?

A
  • 6 horses LPS-saline infusion vs 6 horses glucose-LPS infusion; measured PT, APTT, TAT and thromboelastometry (clot characteristics).
  • Minor alterations in coagulation parameters identified for each group were most likely not clinically relevant.
  • Observed differences between groups do not suggest that concurrent hyperglycemia and endotoxemia are associated with greater coagulation abnormalities in horses.

Ref: J. Vet. Intern. Med. 2013;27:347–353.

82
Q

Is Bartonella present in horses?

What is the best method for testing?

A
  • 47 healthy horses, 15 sick foals, 22 horses with musculoskeletal manifestations, and 8 horses w colic were tested for Bartonella.
  • Methods: IFA serology and PCR before and after BAPGM (Bartonella alpha-Proteobacteria Growth Medium) enrichment blood culture.
  • Results: 0 positive IFA; 3 Bartonella species, B. henselae, B. vinsonii subsp. berkhoffii (genotypes I and III), and a Bartonella species with closest homology to Candidatus Bartonella volans, were PCR-amplified and sequenced from blood or BAPGM enrichment blood culture samples from 1/47 healthy horses, 3/15 sick foals, 5/22 horses with musculoskeletal disease, and 0/8 horses with colic.
  • Based upon the IFA assays used in this study, serology was not useful in establishing prior exposure to or infection with a Bartonella sp.

Ref: J. Vet. Intern. Med. 2012;26:1408–1412.

83
Q

List blood and clinical examination changes that occur in horses after experimental infection with Bartonella.

A
  • 3/4 B. henselae-inoculated horses seroconverted, whereas only 1/4 B. bovis-inoculated horse was weakly seropositive.
  • B. henselae was amplified and sequenced from BAPGM blood culture as well as a subculture isolate from 1 horse, blood from a 2nd horse, and BAPGM blood culture from a 3rd horse although a subculture isolate was not obtained.
  • CSx: mild to moderate limb oedema, mild cervical LN enlargement, 1 horse mild medical colic; no fever.
  • Detection of Bartonella sp. in blood after experimental inoculation supports bacteremia and seroconversion.
  • Culture with BAPGM may be required to detect Bartonella sp.
  • Although mild clinical signs followed acute infection, no long-term effects were noted for 2 years post-inoculation.

Ref: J. Vet. Intern. Med. 2012;26:377–383.

84
Q

Does storage of equine blood affect the result of cross-matching testing?

A
  • Blood samples collected and cross-matching performed on fresh blood and blood stored for 1-4wks.
  • Cross-match was repeated on 6 fresh samples from each horse to testing repeatability.
  • Equine blood crossmatching is repeatable using fresh blood.
  • Decreased apparent compatibility after storage makes exclusion of compatible donors more likely than mistaken administration of incompatible blood.
  • These data suggest that fresh samples should be collected from potential donors before crossmatching equine blood.

Ref: J. Vet. Intern. Med. 2012;26:662–667.

85
Q

Describe Corynebacterium pseudotuberculosis.

A
  • Gram positive, intracellular, non-motile, pleomorphic, rod-shaped, facultative anaerobic bacteria.
  • Two biotypes: strains from horses are nitrate positive, (small ruminant strains are nitrate negative, strains from cattle are both).
86
Q

Describe epidemiology of Corynebacterium pseudotuberculosis infection.

A
  • Infection occurs worldwide.
  • Natural cross-species trans doesn’t appear to occur.
  • Different genotypes cause infection in diff US states.
  • Soil-bourne org, survives months to years.
  • Spread by flies, vectors, contam-soil; highest incidence ext abscess Autumn, internal Winter incubation period 3-4 weeks.
87
Q

Differential for nonregenerative anemia in horses

A
  • Iron deficiency
    • chronic hemorrhage
    • nutritional deficiency
  • Chronic disease
    • Chronic infection / inflammation (pneumonia, peritonitis, endocarditis, viral-EIA)
    • neoplasia
    • Endocrine diorders
  • Bone Marrow failure
    • Myelopthisis
    • Myeoloproliferative dss
    • Bone Marrow toxins (PBZ/ Chloramphenicol)
    • Radiation
    • Idiopatic pancitopenia
  • Miscelaneous conditions
    • hEPO
    • Chronic Renal / Hepatic Dss
    • Recent Hemorrhage/ Hemolysis

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