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ACVIM > Hematology > Flashcards

Hematology Flashcards

1
Q

Describe prekallikrein or Fletcher factor deficiency in horses.

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 in horses.

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 in horses 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 a 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 in horses.

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 in horses.

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 in horses.

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 in horses.

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.- Fever.- Tacchycardia.- Haemorrhages on MMs.- +/- reluctance to move, colic, epistaxis.
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12
Q

List clinicopathologic findings in cases of PH in horses.

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 horses with 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 in horses.

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 in horses.

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.- Epiphora.- Conjunctivitis.- Rhinitis.- 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 that have a tropisms for neutrophils and eosinophils in horses.
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23
Q

Describe the epidemiology of 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 EGE is unkown as 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 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 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 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 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 in the horse.

A
  • Platelet count
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30
Q

List clinical signs of thrombocytopaenia in the horse.

A
  • Multiple sites of small vessel bleeding –> petechial/ ecchymotic haemorrhage on MMs, nictitans, sclera.-
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31
Q

Outline treatment of thrombocytopaenia causing life-threatening haemorrhage in horses.

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

List causes of thrombocytopaenia in large animals.

A
  • Shortened lifespan most common in LA: DIC, vasculitis.- Hypoplastic anaemia w thrombocytopaenia.- Myelophthisic dz (replacement of BM by neoplastic or inflammatory cells): reported but rare.- IMTP: primary (idiopathic) or secondary (drug admin, infection, neoplasia, other immunologic disorders); reported in horses secondary to EIA, lymphoma, IMHA.- Alloimmune thrombocytopaenia of neonates: horse and mule foals and piglets; severe dec platelets, inc bleeding time, n PT/APTT; definitive dx: inc quantities of platelet-assoc IgG or C3 or anti-platelet activity.
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33
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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34
Q

List clinical signs of DIC in large animals.

A
  • Can vary widely from diffuse thrombosis –> ischaemic organ failure to haemorrhagic diathesis.- Overt bleeding rare in cattle and horses.- MODS more common in cattle and horses.- Renal involvement common.- Colic can occur from GI microthrombi.- Pulmonary involvement –> tachypnoea, dyspnoea.- Cerebral signs uncommon in large animals.- Horses: laminitis, thrombosis of peripheral vv.- Horses may get chronic compensated form –> chronic low-grade pro-coagulant stimulus.
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35
Q

Outline results of coagulation tests in large animals 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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36
Q

Describe the pathophysiology of DIC in large animals.

A

i) 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.ii) Counter-balance fibrinolytic system is activated; liver and spleen overwhelmed and unable to remove FDPs and activated clotting factors from circulation.

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37
Q

Outline treatment of DIC in large animals.

A
  • Treat underlying disease e.g. Sx for strangulated SI, ABs for sepsis.- Combat shock and maintain tissue perfusion: IVFT, flunixin; +/- plasma.- +/- LMWH (controversial).
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38
Q

List the aetiologic agents known to cause Piroplasmosis in horses.

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.
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39
Q

Describe the epidemiology of Equine 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.
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40
Q

List clinical signs of Equine Piroplasmosis.

A
  • Fever, depression, anorexia.- Haemolytic anaemia and haemoglobinuria.- Jaundice.- In-coordination.- Lacrimation.- Mucoid nasal discharge.- Swelling of the eyelids.- Frequent lying down.- Death.
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41
Q

Describe diagnostic test findings in horses with Piroplasmosis.

A
  • CBC: anaemia, parasite in RBCs stained w Giesma stain; T equi may see moncytosis and eosinopaenia.- Haemoglobinuria (may be absent w B. caballi).- Serum: cELISA (official test OIE/USDA).- Whole blood: PCR.
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42
Q

Outline treatment and prognosis for horses with Equine 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.
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43
Q

What bacteria is responsible for most Leptospirosis infections in horses in North America? What is its most common maintenance host? What serovar is considered by some to be the host-adapted species in horses?

A
  • Leptospira pomona kennewick.- 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.
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44
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.
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45
Q

List clinical signs of Leptospirosis in horses.

A
  • Fever.- Anaemia.- Jaundice.- Abortions during late-term gestation.- Signs of renal or ocular dz.
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46
Q

Outline diagnosis of Leptospirosis in horses.

A
  • Serology: microscopic agglutination titre; 1:6400 significant or rising titres over 2-3wk period.- Infected tissues: IFAT.- PCR.- Histology.- Bacterial culture.
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47
Q

Outline treatment options for Leptospirosis in horses.

A
  • ABs: ampicillin, amoxicillin, penicillin, oxytetracycline, doxycycline.- Anti-inflammatories if ERU or IMMK.
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48
Q

Outline methods for prevention of Leptospirosis in horses.

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 ABs not successful.
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49
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.
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50
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.
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51
Q

Describe clinical signs of EIA.

A
  1. Acute phase:- High fever.- Thrombocytopaenia.- Malaise.- +/- petechial or ecchymotic haemorrhages on MMs.- May go in to 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.
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52
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).
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53
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.
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54
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-med glomerulonephritis.
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55
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.
56
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 in large animals) assoc w drug admin, viral, protozoal, bacterial or rickettsial infection, neoplasia or in assoc w other immune-med disorders e.g. lupus.
57
Q

List clinical signs of IMHA in large animals.

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): in horses most commonly PH, lymphoma, other neoplasma, PLE, chronic bacterial infections.
58
Q

Describe clinicopathologic abnormalities in large animals with IMHA.

A
  • Pronounced, progressive anaemia.- Blood smear: may see erythrophagocytosis and autoagglutination.- Ruminants: if >3d see evidence of regenergative response.- May see moderate neutrophilic leukocytosis.
59
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.
60
Q

Describe the pathophysiology of IMHA in large animals.

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).
61
Q

Describe treatment and prognosis of IMHA in large animals.

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.
62
Q

List oxidising agents capable of inducing Heinz body haemolytic anaemia in horses.

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).
63
Q

List clinical signs of Heinz body anaemia in horses.

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.
64
Q

Describe the pathophysiology of Heinz body anaemia in horses.

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.
65
Q

List clinicopathologic abnormalities in horses 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.
66
Q

Outline treatment for Heinz body haemolytic anaemia in horses.

A
  • Remove source of toxicity.- IVFT - reduce chance of ARF.- 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.
67
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.
68
Q

Describe intravascular haemolysis associated with cutaneous burns in horses.

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.
69
Q

List clinical signs of Anthrax in horses.

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.
70
Q

List the aetiologic agent of Lyme Disease in horses.

A
  • Borrelia burgdorferi.- Spirochete.
71
Q

Describe the epidemiology of Lyme Disease in horses.

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.
72
Q

List clinical signs of Lyme Disease in horses.

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.
73
Q

Outline diagnosis of Lyme Disease in horses.

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.
74
Q

Describe treatment of Lyme Disease in horses.

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.
75
Q

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

A
  • Three form: ulcerative lymphangitis, internal abscesses, external abscesses (most common).- Ulcerative lymphangitis: severe cellulitis involving lymphatics in 1 or more limbs –> lameness, fever, lethargy, anorexia; often becomes chronic –> limb oedema, lameness, weakness, weight loss.- 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%.- 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.
76
Q

Describe treatment of C. pseudotuberculosis infection in horses.

A
  • Principles of therapy:i) Allow the abscess to mature.ii) Establish drainage.iii) Collect and properly dispose of infective exudate. iv) 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.
77
Q

In what breeds is Factor XI deficiency reported? What is the mode of inheritance and genetic defect which causes the condition?

A
  • Holstein, Holstein-Friesian and Japanese Black cattle.- Autosomal recessive inheritance.- Mutation of F11 gene.
78
Q

What are the clinical manifestations reported in cattle with Factor XI deficiency?

A
  • Asymptomatic.- Prolonged bleeding.- Decreased resistance to infection.- Increased prevalence of repeat breeding.- Prolonged APTT, normal PT (intrinsic pathway only).
79
Q

In what breeds is Factor VIII deficiency (Haemophilia A) reported? What is the mode of inheritance of this condition?

A
  • Japanese Brown and Hereford cattle; QHs.- X-linked recessive; clinical disease usually occurs in males but is possible in females.
80
Q

What are the clinical manifestations reported in cattle with Factor VIII deficiency (Haemophilia A)?

A
  • Factor VIII conc 5% normal: may see excessive haemorrhage post-trauma.- Prolonged APTT, normal PT (intrinsic pathway only).
81
Q

Does vasculitis occur commonly in cattle? What agents has it been associated with?

A
  • Vasculitis occurs rarely in cattle.- Has been reported secondary to septicaemic diseases incl MCF and Bluetongue.
82
Q

List the aetiologic agent of Bovine Anaplasmosis.

A
  • Anaplasma marginale.- Obligate intraerythrocytic, gram-negative bacteria of the order Rickettsiales, family Anaplasmataceae, genus Anaplasma.
83
Q

Describe the epidemiology of Bovine Anaplasmosis.

A
  • Transmitted by tickes of the ixodid spp, mainly Dermancentor in US and Rhipicephalus in tropical/subtropical climates.- Maintained by asymptomatic carrier state in cattle and possibly in wild ruminants.- Disease occurs in Summer and Spring.- Severity of CSx related to strain virulence, breed resistance, age-related susceptibility (younger).- Incubation period 15-30d.
84
Q

List clinical signs of Anaplasmosis in cattle.

A
  • Fever, lethargy, anorexia.- Dec milk production.- Dec rumination.- Dry muzzle.- MM pallid or icteric if survive first 2-3d.- +/- neuro signs.- +/- constipation w dark brown, mucus-covered faeces.- +/- pollakiuria w dark yellow urine.- +/- abortion if infected during late gestation.- If survive: 3-4wk convalescence; infected for life (–> asymptomatic carrier).
85
Q

Describe diagnostic test findings in cattle with Anaplasmosis.

A
  • Acute: rapid drop in PCV; 5-70% RBCs contain A. marginale morula on Wrights or Giesma stain.- Chronic: regen anaemia: anisocytosis, basophilic stippling, poikilocytosis, polychromatophilia, reticulocytosis.- Serology: cELISA highest sens/spec (OIE/USDA test for carriers) > complement fixation.- PCR on whole blood during acute infection.
86
Q

Describe the pathophysiology of Bovine Anaplasmosis.

A
  • Most commonly ticks transfer to cattle; may be trans by biting flies, dehorning/castration etc equi, blood trans.- Bacteria rapidly replicates in vesicles in RBCs –> 10-90% infected.- Anaemia occurs secondary to splenic and hepatic macrophage phagocytosis of infected and non-infected RBCs.- Immune-reaction: auto-ABs against erythrocyte surface antigens and activation of macrophaghes to enhanve phagocytosis –> remove many but not all bacteria from blood (antigenic variants) –> recurring waves of bacteraemia and immune reactions.
87
Q

Describe findings on necropsy of cattle that have died from Anaplasmosis. What finding differentiates this disease from Bovine Babesiosis, Leptospirosis, Copper toxicity and Clostridial infection?

A
  • No pathognomic findings.- Blood is thin, icterus, splenomegaly, hepatomegaly.- Lack of haemoglobinuria and haemoglobinaemia differentiates from other listed diseases as haemolysis is intravascular in Anaplasmosis.
88
Q

Outline treatment and prevention methods for Bovine Anaplasmosis.

A
  • Tetracyclines NB do not prevent persistent infection.- +/- blood transfusion.- Endemic area: expose cattle when young –> asymptomatic carriers.- Non-endemic areas: live vacc of young cattle (only licensed in California in USA).- Tick spray, fly ear tags.
89
Q

What other names is Babesiosis known by in cattle?

A
  • Piroplasmosis.- Tick fever.- Texas fever.- Redwater.- Tristeza.
90
Q

List the aetiologic agents of Babeiosis in cattle.

A
  • > 6 species of Babesia can cause dz in cattle. - Intra-erthyrocytic protozoa.- USA: i) B. bigemina: big, pale, pear-shaped, acute angle paired inclusions.ii) B. bovis (more virulent): small, pleomorphic, round or pear-shaped, obtuse-angle paired inclusions.
91
Q

Outline the epidemiology of Babesiosis in cattle.

A
  • Tick-bourne dz.- Transmitted by Boophilus spp in USA.- Trans by adults, nymphs, larvae of ticks or mechanical vectors e.g. biting flies, contained dehorning etc equip.- Incubation period: 5d->3wk.- Bos indicus and
92
Q

List the clinical signs of Babesiosis in cattle.

A
  • Fever, depression, anorexia.- Icterus.- Tachypnoea.- Tachycardia.- Haemoglobinaemia and haemoglobinuria.- Abortion.- Death.- +/- central babesiosis (secondary to anoxia): hyperexciteability, opisthotonus, coma, death.- Outcome: death, asymptomatic carrier or persistent infection w recrudescence of infection and death.
93
Q

Describe the pathophysiology of Babesiosis in cattle.

A
  • Babesia enters bloodstream, infects RBCs.- Intravascular haemolysis due to emergency of merozoites from infected RBCs and osmotic fragility of whole (incl uninfected) RBC population.- +/- autoimmune removal of infected RBCs by spleen.- Results in rapid anaemia despite low parasitaemia.
94
Q

How is Babesiosis diagnosed in cattle?

A
  • Blood smear: organisms identified in RBCs following Giesma stain.- IFA or complement fixation.
95
Q

List necropsy findings in cattle with Babesiosis.

A
  • Pallor, icterus.- Enlarged liver.- Distended gall bladder.- Dark red urine (acute).- +/- hydropericardium.- +/- subepi, subendo, GI petechiae.
96
Q

Outline treatment of Babesiosis in cattle.

A
  • Supportive care: blood transfusion, IVFT, prophylactic ABs, minimal handling.- Anti-protozoals: imidocarb (tx and prev), diminazene diacturate, phenamidine diisethionate, amicarbalide diisethionate.
97
Q

Outline prevention of Babesiosis in cattle.

A
  • Young animals: live vaccine.- Older animals: live vaccine + imidocarb.- Sub-unit vaccines may modify severity of dz.- Tick control: acaricide, controlled range burning, cultivation, pasture rest.
98
Q

List causes of Heinz body haemolytic anaemia in cattle which are unique to those reported in horses.

A
  • Grazing selenium deficient pastures.- Grazing rye grass (Secale cereale) pastures.
99
Q

Describe water intoxication as a cause of haemolytic anaemia in cattle.

A
  • Reported in milk-reared calves when first allowed water –> excess water consumption; 4-5mo at highest risk.- Prod marked hypotonicity of body fluids –> intravascular haemolysis due to osmotic lysis of RBCs.- CSx: neuro deficits, resp distress, haemoglobinuria and death in some cases.- Clin path: haemolytic anaemia, hypoproteinaemia, hypochloraemia, hyponatraemia, hyposmolality, haemoglobinuria, hyposthenuria.- Tx: restrict access to water; if profound hyponatraemia may need hypertonic saline, mannitol, corticosteroids.
100
Q

What is the aetiology of postparturient haemoglobinuria?What is the signalment of cows most commonly affected?

A
  • Phosphorus deficiency –> low intracellular phosphate conc interferes w energy metab –> affects cell viability and ability of RBCs to cope w potential haemolysins.- High-producing multiparous cows that dev CSx within one month of calving.
101
Q

Describe the clinical presentation of postparturient haemoglobinuria in cattle.

A
  • Depression, dec feed consumption, dec milk prod.- Haemoglobinuria and icterus.- Marked anaemia w marked regen response after 4-5d.
102
Q

Describe treatment of postparturient haemoglobinuria in cattle.

A
  • Blood transfusion.- IVFT.- IV sodium acid phosphate followed by oral phosphorus supplementation.- Correct herd dietary imbalances.
103
Q

Describe the effect of bracken fern ingestion of the bone marrow of cattle and the subsequent clinical condition seen after 2-8wks on an affected pasture.

A
  • Bone marrow suppression –> pancytopaenia.- CSx: fever, melena, epistaxis, haematuria, mucosal petechiation, hyphema, bleeding from the eyes and vulva.- CBC: platelet count
104
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.
105
Q

Describe the epidemiology of Anthrax in livestock.

A
  • Found worldwide.- Soils with elevated pH, Mn++, Ca++ and rich in organic material favour spore survival.- Drought followed by heavy rain or earth-disturbing activities often –> outbreak.- Outbreaks usually during warmer part of year.- Bloodsucking insects transfer B. anthracis b/w animals.- Scavengers disseminated bacteria and carcasses of infected animals contaminate the enviro.- Susceptibility: ruminants > horses > pigs.
106
Q

Describe the pathophysiology of Anthrax in livestock.

A
  • Exposure: grazing contaminated pastures (spores), forage grown on contam pastures, animal by-products, insects.- Ingested anthrax spores gross mucosal barriers, phagocytosed by macro, travel to LNs –> convert to vegetative stage and kill host cell –> enter extracellular enviro.- Virulence factors:i) Poly-D-glutamic acid capsule: evade phagocytosis.ii) Three-component toxin: protective antigen - attaches to cell and on of other 2 factors, enters cell by endocytosis and forms pore to let other 2 factors in; lethal factor and oedema factor - interrupt cells immune functions, phagocytic capacity, cAMP prod –> oedema, cell death, expression of pro-inflamm cytokines.- B. anthracis proliferates rapidly in the host –> overwhelming septicaemia –> death due to hypotensive shock and multi-organ failure.
107
Q

List clinical signs of Anthrax in sheep, goats and cattle.

A
  • Typically peracute form –> sudden death.- May see fever, depression, resp distress, MM congestion, convulsions, bloody dxa, haematuria, localised tissue swelling.
108
Q

List clinical signs of anthrax in pigs.

A
  • Most common form: oropharyngeal form w swelling of head, neck, cervical LNs; may obstruct breathing and swallowing.- GI form present as dysentary.- Pregnant sows may abort.
109
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.
110
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.
111
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.
112
Q

Describe C. pseudotuberculosis infection in cattle.

A
  • Sporadic herd problem, doesn’t affect production.- Most common form is cutaneous excoriated granulomas’ mastitis, visceral and mixed infections also reported.- Granulomas: ulcerative, exuding, granulomatous lesions up to 20cm diam that can be excised to leave underlying granulation tissue bed; lesions usually on face, neck, thorax, flanks; spontaneous heal in 2-4wks.
113
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.
114
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.
115
Q

Is Bartonella present in horses in North Carolina? 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.
116
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.
117
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.
118
Q

In what breed of sheep is combined vitamin-K dependent factor (II, VII, IX, X) deficiency reported? What is the mode of inheritance of this disease?

A
  • Rambouillet sheep.- Autosomal recessive.
119
Q

What is the clinical manifestation of combined vitamin-K dependant clotting factor deficiency in sheep?

A
  • Excessive s/c haemorrhage and umbilical bleeding in lambs.- Prolonged APTT and PT (intrinsic and extrinsic pathway involved).
120
Q

What aetiologic agent is responsible for Anaplasmosis in sheep and goats?

A
  • Anaplasma ovis.- Gram negative rickettsial bacteria.- Rarely causes clinical dz, but if it does CSx similar to Bovine Anaplasmosis.
121
Q

List a cause of Heinz body anaemia in sheep that is unique to the causes reported in horses.

A

Low molybdenum formulate diet –> chronic Cu toxicity.

122
Q

Copper is an essential trace mineral for ruminants, however it has a narrow therapeutic window. List ruminants in order from most to least susceptibility to copper toxicity.

A
  • Lambs > adult sheep and goats > cattle > horses.- Dietary requirements for growing sheep: 4-6 ppm.- Toxicity occurs at 10-20 ppm.
123
Q

Describe normal copper metabolism in ruminants.

A
  • Ingested Cu is absorbed through enterocytes by carrier proteins and transported to blood bound to Alb and AAs.- 20% of total plasma copper is ionised copper; 70-90% of this is internalised by hepatocytes –> bile –> packaged in lysosomes in protein complexes or used for formation of ceruloplasmin.- Hepatic storage buffers Cu intake initially but eventually become saturated.
124
Q

Describe the pathophysiology of copper toxicity in ruminants.

A
  • Hepatocytes saturated w copper die spontaneously or in response to envrio stress/diet change –> release large amount of Cu into circulation.- Cu is an oxidant –>– Lipid peroxidation and oxidative denaturation of proteins within RBCs –> Heinz body formation and methaemaglobinaemia –> intra-/extra-vascular haemolysis.– Vitamin E is denatured –> enhances cellular susceptibility to further oxidants.- Sources of excess copper: minerals designed for other species (e.g. cattle mineral given to sheep), inapprop form grain mixtures, chicken litter, Cu-containing fungacides, palm kernel oil, Cu pipes, overdose of C salts.- Low Mb (soil high in sulfates, Cu:Mb > 6:1) –> Cu tox as Mb binds Cu in rumen making it insoluble and non-absorbable.
125
Q

List clinical signs of copper toxicity in ruminants.

A
  • Asymptomatic for weeks until onset of hepatic necrosis.- CSx are of co-existing anaemia, myopathy, neuro, hepatic and renal dz.- Inappetence, lethargy, weakness, recumbency, pallor, cool extremities, grey MMs.- Marked tachycardia, low BP, tachypnoea, hypothermia.- Dark red urine; dark or yellowish faeces.- +/- petechiation of conjunctival mucosa.- +/- abortion; ewes tend to have dystocia if survive.- Death.
126
Q

Describe findings on necropsy of animals that have died from copper toxicity.

A
  • Tissues are pale and icteric w petechial and ecchymotic haemorrhages on serosal surfaces.- Liver often pale and yellow.- Kidneys black w metallic sheen due to Hg.- Urinary bladder filled w serosanguinous urine.- Histo: tubular nephrosis, necrosis of splenic follicles and hepaticytes; biliary duct proliferation and cholangitis; spongy degeneration of pons and brainstem.
127
Q

List diagnostic test findings in ruminants with copper toxicity.

A
  • Plasma copper conc 2.4-20ug/mL diagnostic.- Normal plasma conc may occur with toxic liver levels.- Hepatic Cu conc 16mmol/kg DM are threshold for haemolytic crisis; renal conc 15 ppm dry weight.- Changes occur 24h prior to haemolytic crisis –> inc cytosolic hepatic enzymes and sharp rise plasma Cu.- Acute crisis: haemoglobinaemia, Heinz body formation, methaemoglobinaemia, anaemia, inc bilirubin, AST, GGT, ALP, CK, creatinine, BUN, plasma ceruloplasmin; urine dark brown to black w protein, blood, Hg casts.
128
Q

Outline treatment of copper toxicity in ruminants.

A
  • Acute haemolytic crisis: InO2, Vit E, packed RBCs, D-penicillamine (inc urinary Cu excretion), anhydrous sodium sulphate (bind rumen C) and ammonium molybdate (binds rumen Cu, enhances biliary excretion of Cu).- IV ammonium tetrathiomolybdate + xylazine –> reduced cytosolic and lysosomal hepatic Cu, inc Cu excretion in bile, transient inc blood Cu.
129
Q

Describe the aetiology and clinical signs of copper deficiency in ruminants.

A
  • Copper deficiency due to inadequate copper in soil or milk, excess molybdenum or dietary zinc/sulphur imbalances.- Cu is co-factor in wide variety of enzymatic reactions, therefore –> mulitple CSx in young, growing animals incl red growth rate, rough and depigmented hair, diarrhoea, osteoporosis w spontaenous fractures and anaemia.- Enzootic ataxia/swayback in lambs: demyelinating dz assoc w Cu deficiency.
130
Q

Describe the pathophysiology of copper deficiency-associated anaemia in ruminants.

A
  • Cu plays an important role in transport of iron from the GIT to the BM and incorp of Fe into heme molecule.- Anaemia is moderate, slowly progressive, microcytic, hypochromic.- BM aspirate differentiates from true iron deficiency as revealed sideroblasts (intracellular iron acumm).- Dx by measuring serum Cu as ceruloplasmin, erythrocyte superoxide, dismutase or Cu content of hair, liver or kidney.
131
Q

Describe Corynebacterium pseudotuberculosis.

A
  • Gram positive, intracellular, non-motile, pleomorphic, rod-shaped, facultative anaerobic bacteria.- Two biotypes: small ruminant strains are nitrate negative, strains from horses are nitrate positive, strains from cattle are both.
132
Q

Describe epidemiology of Corynebacterium pseudotuberculosis infection in large animals.

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.- Year-round infection in small ruminants; spread via infected exudates (wounds), long incubation.- Horses: spread by flies, vectors, contam-soil; highest incidence ext abscess Autumn, internal Winterl incubation period 3-4 weeks.- Cattle: spread by flied or fomites; spring and summer.- Bacteria enters via wounds/abrasions –> s/c of submucosal lymphatics –> phagocytosed by macro –> survive intracellulary and can survive lymphatic necrosis and thrombosis.
133
Q

Describe clinical signs of C. pseudotuberculosis infection (‘Caseous Lymphadenitis’) in sheep and goats.

A
  • Two forms: internal (sheep > goats) & external (g > s).- Cause of loss of production, premature mortality/culling.- Charac by suppuration and necrosis of LNs –> thick, inspissated pus (sheep - white, goats - green).- External LNs most commonly involved: mandibular, parotid, prefemoral, prescapular.- Internal abscesses can be found in lungs, kidneys, LNs: mediastinal, bronchial, mesenteric, lumbar –> wt loss +/- signs localised to affected organs.- Prevalence 5-10% in endemic areas.
134
Q

Outline diagnostic test results in sheep and goats with Caseous Lymphadenitis.

A
  • CBC: leukocytosis, anaemia of chronic dz, inc fibrinogen.- Serum ELISA for detection of cell wall antigens.- Synergistic haemolysis inhibition test (SHI) measures IgG response to exotoxin in patient’s serum; 1:128 indicates exposure, 1:512+ indicates active infection; false negatives occur due to acute onset of infection, rapid maturation of abscess prior to dev Ig response, thick capsule isolating org and preventing Ig resp, consumption of Ig during active infection.- Definitive dx: culture of organism from abscess/draining wounds.
135
Q

Describe treatment and prevention of Caseous Lymphadenitis in sheep and goats.

A
  • Drainage alone does not result in resolution; can lavage abscesses w iodine.- Drainage not recomm as may spread dz to other ruminants.- Complete excision of affected LNs is recommended.- Prevention: isolate infected animals, fly control, good sanitation, careful shearing practices, disinfection of contaminated fomites, careful disposal of bedding.- Depopulation may be most economic option.- Vacc: dec number of infected sheep and number of abscesses per sheep; reg for sheep and goats in US.
136
Q

Describe C. pseudotuberculosis infection in camelids.

A
  • Caseous lymphadenitis has been reported in young alpacas in Nth and Sth America.- Presented w abscessed LNs in cervical and submandibular area and adj to eye.- Alpacas were not systemically ill and abscess excision was curative.
137
Q

M. haemollamae

A

…

ACVIM (11 decks)

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