Lymphoreticular system Flashcards
Glucocorticoids
Associate with binding proteins - transcortin and albumin
Following dissociation from binding proteins, passively diffuse into cell
Bind to a cytoplasmic receptor (under 3)
Conformational change of receptor unmasks DNA binding domain; associates with GREs following nuclear translocation
Cellular targets:
-Inflammatory cells: eosinophil, T cell, Mast cell, Macrophages, dendritic cell
- Structural cells: epithelium, endothelium, airway smooth muscle, mucus glands
Glucocorticoid - potential adverse effects
Central nervous systen - decreased mentation Musculoskeletal system - muscle wasting GIT Fluid, electrolyte balance Metabolic, endocrine immune systems - secondary infections Cats are more resistance that dogs
Chlorambucil
Rapidly metabolised to phenylacetic acid mustard
Slowest acting, least toxic of all alkylating agents
Myelosuppression generally not observed until administered for > 1 month
Urinary and faecal excretion
Administered without food
Azathioprine
Greater decrease of cellular than humoral immunity
Hepatic metabolism to active 6-mercaptopurine then to 6-thioinosinic, 6-thioguanylic, thiouric acids
Compete with endogenous adenine and guanine -> non-functional nucleic acid strands
Slow immunosuppressive effect
Haematological, gastrointestinal, hepatic +/- neuromuscular toxicity
Vincristine, vinblastine
Bind to tubulin, blocking polymerisation
Also break down pre-formed microtubules - increased release of PLTs from megakaryocytes
Both used in rxl of ITP (usually vincristine)
Can be given as bolus IV or to preload PLTs
Severe extravascular vesicants
Haematological, GI, neurological toxicity
Ciclosporin
Isolated from Cylindrocarpon lucidium and Trichoderma polysporum
Both IV and oral forms
Large volume of distribution: primary hepatic metabolism
Therapeutic drug monitoring - acute and chronic
Ketoconazole may be used to reduce costs
GI, renal, hepatic toxicity; also hirsutism, gingivial hyperplasia, papillomatosis +/- diabetogenic
Pathogenesis of immune-mediated disease
Immune system overeacts to normal body tissues or harmless exogenous proteins - loss of tolerance
Both humoral and cellular mechanisms of tissue damage recognied
Loss of self-tolerance is necessary to perpetuate+/- start disease
Trigger factors:
- release of sequestered antigens
- abnormal immunoregulation
- molecular mimicry
- polyclonal activation of T and B cells
- exposure of cryptic epitopes or haptenisation of foreign molecules to self antigens
Role of infection in immune-mediated disease
- Breakdown of vascular or cellular barriers allowing exposure of self antigens
- Promotion of cell death by necrosis, causing inflammation -> bystander activation
- Polyclonal activation of T cells - bacterial superantigens
- Molecular mimicry -> cross reactivity
Aetiology of immune-mediated disease
Often unclear, likely to be multifactorial
- Genetic, infectious and hormonal influences
Canine examples:
- SLE: genetics (DLA-A7; C4-4), C-type viruses
- IMHA: vaccinal antigens?
- Immune-mediated polyarthritis: vaccinal antigens?
Signalment of immune-mediated disease
Idiopathic immune-mediated disease over-represented in juvenile to middle-aged patients, through dogs and cats of any age may be affected
Vet examples:
- SLE
- Dogs from 2 months - 13y (GSDs, shelties, collies, beagles, poodles)
- Cats from 1-11y (Siamese, Persian, Persian-related breeds)
History/physical exam of immune-mediated disease
Generally characterised by remission and exacerbation
Lameness, mucocutaneous lesions, lethargy, dyspnoea, weight loss, PU/PD, +/- seizures or behavioural changes
Effusive, painful joints, cutaneous erythema, macules, papules, pustules, erosion etc., pallor +/- petechiae, cardiac arrhythmias
Lymphadenomegaly +/- splenomegaly
Diagnostic tests - CBC/coags
Immune-mediated disease
Anaemia - regenerative (IMHA) or non-regenerative (infection, uraemia, chronic bleeding, attack of precursors)
Thrombocytopaenia - Immune-mediated (I-M) thrombocytopaenia
Leucopaenia? anti-leucocytes antibodies e.g. SLE, I-M neutropaenia
Coagulation abnormalities: increase in APTT, PT,’anti-coagulant antibody’ (SLE), DIC
Diagnostic tests - chemistry panel
Immune-mediated disease
Azotaemia, increased inorganic phosphate - chronic glomerular lesions
Hypoalbuminaemia, hypercholesterolaemia - protein-losing nephropathy (PLN)
Hyperbilirubinaemia - pre-hepatic/haemolysis
Hyperglobulinaemia - inflammatory disease, polyclonal B cell activation
Increased creatine kinase and lactate dehydrogenase - polymyositis and/or myocarditis
Diagnostic tests - urinalysis
Immune-mediated disease
Proteinuria:
- PLN: r/o UTI and occult infection(s) e.g. Dirofilaria immitis, Ehrlichia canis, Anaplasma phagocytophilum, Borrelia burgdorferi, Rickettsia rickettsiae, Bartonella spp.)
Haematuria, pyuria, erythrocyte casts:
- r/o UTI and occult infections
- compatible with membranoproliferative GN
Diagnostic tests - radiography and arthrocentesis
Joint lesions are common in polysystemic IM disease, usually non-erosive pauciarthropathy
Erosive lesions suggest an overlap syndrome
Arthritis is not always clinically obvious
Synovial fluid: increased WBC, increased proportion of neutrophils +/- protein content with decreased viscosity and poor mucin clot formation
Coomb’s test
Immune-mediated disease
If acute IMHA suspected, in-saline agglutination and osmotic fragility tests may be performed
Antibodies associated with the surface of RBCs may also be detected with the Coomb’s test
Primary reagent: polyvalent anti-dog or anti-cat IgG, IgM and C3 antiserum (direct antiglobulin test)
False positive and negative reactions may occur
AChR autoantibodies
Immune-mediated disease
Acquired MG (myasthenia gravis): most common of immune-mediated neuromuscular disorders Various forms described: focal, generalised, acute fulminating, paraneoplastic 'Gold standard' for diagnosis of acquired MG is documentation of nicotinic AChR autoAb by immunoprecipitation RIA False positives v rare; 2% of dogs with generalised MG may be seronegative
ANA - antinuclear antibodies
Immune-mediated disease
Serum ANA - hallmark of human, canine and feline SLE
Indirect immunofluorescence or immunoperoxidase test
Substrate tissues have inc. rat liver, vero and Hep-2 cells; various pattern of staining
False positives and negatives may occur
Von Willebrand’s Factors (vWF)
Produced by endothelium and stored in Weibel Palade bodies
Also produced by platelets
Released early in the haemostatic process
Responsible for platelet adhesion to collagen
Platelets
Small discoid anuclear cells for in circulation
3-5 nanometres and are pale basophilic with small red granules
Derived from the cytoplasm of megakaryocytes in the bone marrow (thrombopoiesis)
Mediated by thrombopoietin
Circulate for 5-9 days in most species
Structure:
- Outer membrane contains receptors important for adhesion and aggregation
- Contain a cytoskeleton with actin and myosin that allows for shape change
- Contain membrane bound granules
Surface receptors:
- Glycoproteins associated with platelet membrane
- GP Ib - binds von Willebrand’s factor
- GP IIbIIa -binds fibrinogen on adjacent platelets and allows platelets to aggregate
- Defects in receptor lead to abnormal platelet function and clot formation
Primary haemostasis
Damage to the endothelium and exposure of subendothelial collagen
Von Willebrand’s factor is released from damaged endothelium
Platelet adhesion occurs
Platelet bind to collagen via receptor GPIb and vWF from the endothelium
Once platelets have adhered to collagen, they undergo shape change and become spherical with filopodia
Additional receptors for vWF (GPIb) and fibrinogen (GPIIbIIa) are exposed
Secondary haemostasis
Involves activation of the coagulation cascade
Happens simultaneously with formation of the platelet plus because damage to the endothelium releases tissue factor and activates the extrinsic coagulation pathway
Coagulation cascade
Extrinsic system - intiation
Most important in vivo Tissue factor (TF) released from damaged tissue binds and activates FVII in presence of calcium TF_FVII complex activates FX of the common pathway and FIX of the intrinsic pathway
Coagulation cascade
Intrinsic pathway - amplification
FXII is activated by contact with a negatively charged surface (cofactor HMWK)
Activated FXII cleaves and activates FXI which in turn activates FIX (calcium required)
Activated FIX i turn activates FX of the common pathway
Coagulation cascade
Common pathway
Starts with activation of Factor X
Activated FX binds activated Factor V and calcium on the platelet surface
This complex converts prothrombin (FII) to thrombin (FIIa)
Thrombin converts fibrinogen (FI) to fibrin (FIa)
Fibrin crosslinked by activated FXIII
Inhibitors of coagulation
Anti-thrombin III - inhibits thrombin and activated FX
Activity of ATIII increased by heparin from the endothelium
Protein C - inactivates Factors V and VIII
Fibrinolysis (enzymatic breakdown of fibrin by plasmin)
Immune-mediated thrombocytopaenia
Most common cause of thrombocytopaenia
Platelet numbers extremely low (often s syndome - concurrent immune mediated thrombocytopaenia and anaemia
Primary - antibodies produced against platelets antigens
Secondary - many causes (other immune diseases (SLE), drugs or vaccine, neoplasia, infectious)
Diagnosis of exclusion/response to treatment
Disorders of platelet function
Glanzmann’s thrombasthenia - defect in GPIIbIIIa
- Ottermans and Great Pyrenees, Quarter horse
- Defective platelet aggregation and abnormal clot retraction
Canine thrombopathia - abnormal GPIIbIIIa exposure and impaired degranulation - Basset hounds
Bovine thrombopathia - defect not know (Simmentals), mild to severe bleeding
Thrombocytosis
Physiological - transient - epinephrine induced splenic contraction
Reactive (secondary)
- Increased thrombopoietin and possibly IL6
- Inflammation, haemorrhage, iron deficiency
Essential thrombocytemia
- Myeloproliferative disorder
- Marked peristent incerase in platelets
- Bone marrow megakaryocytes increased and may have abnormal morphology
- Function variable - may see petechiae and ecchymoses or thrombosis
Von Willebrand’s disease
Clinical signs: mucosal bleeding (GI, epistaxis, haematuria etc.)
Bleeding may be absent
No petechiae - use to differentiate from other platelet disorders
See prolonged buccal mucosal bleeding time without thrombocytopaenia
Clotting time usually normal but PTT msy be prolonged due to decrease in factor VIII]
Common in dogs (rare in cats and horses)
Von Willebrand’s disease
Type I
All multimers are present but as decreased concentrations
Variable severity of bleeding but not until concentration of vWF are <20%
Most common - 90% cases
Dobermans
Autosomal inheritance so males and females equally affected
Von Willebrand’s disease
Type II
Qualitative abnormalities in vWF structure and function
Often disproportionate decrease in large multimers
Severe and uncommon
Seen in German short haired and wire haired pointers
Autosomal recessive
Von Willebrand’s disease
Type III
Absence of all vWF multimers (<0.1%)
Seen in Scottish Terriers, Chesapeake Bay Retrievers, Shetland Sheepdogs and Dutch Kooiker
Autosomal recessive
Von Willebrand’s disease
Tests
Measure levels of vWF:Ag
- Collect blood into EDTA or citrate
- If using citrate as anticoagulation - dilute blood:citrate at ratio of 1:9
- vWF levels will be decreased by clots in the sample and by haemolysis but are inaffected by lipaemia
- Separate plasma immmediately, freeze and ship overnight
ELISA: quantative measurement of vWF using specific antibodies -<50% considered decreased
Immunoelectrophoresis: used to separate relative amounts of different multimers - required for diagnosis of type II
Genetic test to detect carriers
Von Willebrand’s disease
Treatment
Transfusion to supply vWF
Cryoprecipitate best - concentration of vWF 5-10x greater than in plasma - give at dose of 1 unit/10kg
Plasma can be given at 6-12 ml/kg if cryoprecipitate nto available
Whole blood if animal is anaemic
Desmopressin (DDAVP)as a pre-op prophylaxis for dogs with type I vWD
Causes release of vWF from endothelium
Give dose of 1 nanog/kg SQ 30 min prior to surgery
Intranasal preparation
Vitamin K deficiency
Factors II, VII, IX and X are produced in the liver
Are activated by a vitamin K dependent carboxylase - this step requires reduced vitamin K
Production of reduced vitamin K requires the action of vitamin K reductase
Vitamin K reductase is inhibited by coumarin - type redenticides
This leads to a lack of active factors II, VII, IX and X and a coagulopathy
Extrinsic, intrinsic and common pathways affected
Factor VII has the shortest half life so will decrease 1st
PT is often prolonged 1st in early vitamin K deficency
Main clinical sign: haemorrhage
Test results: elevation in PT and PTT, platelet numbers and buccal mucosal bleeding time should be normal but mild thrombocytopaenia is possible - due to consumption associated with haemorrhage, FDP’s may also be elevated
Vitamin K deficiency - Treatment
Emetics, cathartics, activated charcoal if ingestion of rodenticide is recent
Transfusions of whole fresh blood or fresh frozen plasma to replace coagulation factors
May also need packed red cells if severe anaemia is present
Vitamin K therapy:
- Can be given orally or parenterlly (SQ)
- Loading dose of SQ and then lower dose 8h later
- Same dose can be given orally with a fatty meal
Inherited coagulation defects - treatment
Factor VII deficiency, Haemophilia A - factor VIII deficiency, Haemophilia B - factor IX deficiency, factor XI deficiency, Factor XII deficiency
Transfusions of whole blood or plasma to replace factor deficiency and red cells
Use of fresh or frozen plasma will give a small amount of factor
Administration of cryoprecipitate - 10x more factor VIII vs plasma
Disseminated intravascular coagulation (DIC)
Mixed haemostatic defect
Results when excessive coagulation leads to widespread thrombosis
Haemorrhage eventually results as all coagulation factors are consumed
Not a primary event but secondary to other underlying disease (neoplasia, liver disease, immune mediated diseases, infectious diseases)
May be chronic or acute
Haemostatic abnormalities: thrombocytopaenia, prolonged PT and PTT, elevated FDP’s, decrease fibrinogen, decreased antithrombin III
DIC - Treatment
Stop the coagulation process Heparin (different regimes) Transfusion of whole blood, plasma or cryoprecipitate as source of antithrombin III Aspirin to stop platelet activation Correct other underlying abnormalities Prognosis - poor
FeLV
Family Retroviridae, subfamily Oncovirinae, genus Gammaretrovirus
Replicates in many tissues, non-cytopathic
Prevalence of 1-2% in ‘healthy’ cats in UK, 20% in symptomatic cats
Transmission: shed in saliva, nasal secretions, faeces, urine, milk, short survival outside of body
- Intimate prolonged contact
- Neonates (in utero, nursing)
- Blood transfusions
Persistent viraemia, transient viraemia, latent infection, localised infection
FeLV
Clinical signs
Inappetence Weight loss, wasting Poor coat condition Lymphadenopathy Persistent fever Pale mm Ocular disease Gingivitis Stomatitis Infections of skin, urinary bladder, upper resp tract Persistent diarrhoea Seizures, behavioural changes and other neuro disorders Queen's - abortions
FeLV
Secondary infections
Immunosuppression - most common manifestation of FeLV
Depletion of interference with function of lymphocytes +/- neutrophils
Susceptible to co-infection - common for FeLV+ cats to have concurrent infection (opportunistic pathogens)
FeLV
Haematological disorders
Bone marrow suppression: viral infection of haemopoietic stem cells and stromal cells
- Anaemia: non-regenerative, aplastic anaemia, regenerative (10%)
- Thrombocytopaenia
- Granulocytopaenia
Myelodysplasia -> myelodysplastic syndrome
Leukaemia (all cell lines susceptible)
FeLV
Lymphoma
FeLV+ cats, >60x increased risk of lymphoma
Expect to develop in 25% of FeLV+ cats within two years of diagnosis
Most often mediastinal (thymic) and multicentric
Some cats with lymphoma test FeLV- but have virus in tumours
FeLV
Diagnostic tests
Immunoassay - screening (ELISA)
Immunofluorescent antibody test (IFA) - confirms
Polymerase chain reaction (PCR) - confirms
Viral culture - gold standard confirms
Antibody tests - not for diagnosis
FeLV
Treatment
Systemically well:
- General preventative helath care
- Neuter and confine indoors
Sick:
- Supportive care
- Treat secondary illness
- Confine indoors
FIV
Family Retroviridae, genus Lentivirus, RNA virus, five subtypes - similar to HIV, not zoonotic
Clinical findings: stomatitis, neoplasia, ocular inflammation (uveitis, chorioretinitis), anaemia and leucopaenia, opportunistic infections, renal insufficiency
FIV
Diagnosis
CBC: neutropaenia, anaemia common, thrombocytopaenia, co-infection with Mycoplasma haemofelis - haemolytic anaemia Serum biochemical profile: no particular abnorm, +/- polyclonal gammapathy Tests: - Antibody test - develop with 60d - IFA - detects antibodies - Western blot - confirms - PCR - Viral isolation
FIV
Treatment
Supportive therapy: - antibiotics (aerobes) - cautious use of glucocorticoids in combo with antibiotics (gingivitis, stomatitis) - lactoferrin - possibly in stomatitis Antiviral therapy: - Zidovudine - Reduce plasma load - Generally well tolerated but check for Heinz body haemolytic anaemia and non-regenerative anaemia
FIV
Prevention of infection
Prevent exposure to virus Virus readily killed but disinfectants, dies within a few hours in environment Low risk transmission by social contact Do not breed fro FIV+ queens If FIV+ queen, hand rear kittens
FeLV
Subgroups
Subgroup A:
- present in almost all FeLV-infected cats
- transmitted cat-cat
- basis from production of other subgroup
- least pathogenic
Subgroup B:
- recombination of subgroup A with endogenous FeLV proviral sequences
- oncogenic
Subgroup C:
- arises from mutation of subgroup A
- non-regenerative anaemia
FIP
Fatal disease, domestic and non-domestic cats
Causative agent: feline coronavirus, enveloped, ssRNA virus
Replicates in cytoplasm
FIP in 5-10% of FCoV infections
Vasculitis, complement activation, excessive cytokine formation
Clinical signs: consequences of vasculitis and secondary organ damage
Incubation period: weeks - months
Onset: sudden or insidious
Feline enteric coronavirus (FECV)
Present in large portion of healthy cat population
Oronasal transmission
Virus replicates in enterocytes
Clinical signs mild/inapparent - V and D, upper resp signs
Feline infectious peritonitis virus (FIPV)
FCoV may undergo mutations to FIPV
Infects macrophages -> systemic infection
FIP = clinical disease syndome result from ineffective immune reponse
FIP
Clinical signs
Early:
- Pyrexia
- Inappetence/anorexia, weight loss
- Diarrhoea
- Listlessness, dehydration
- Jaundice (icterus)
Effusive vs non-effusive form (sometimes mixed)
- Effusive: abdominal, pleural, pericardial effusions
- Non-effusive: dry or granulomatous form, predisposition to eye, brain and CNS, kidney, liver, localised regions of intestine
FIP
Diagnosis
Often difficult AM (esp dry form)
CBC: Lymphopaenia, neutrophilia with mild left shift, mild non-regenerative anaemia, may also be normal
Serum biochem: Hyperglbulinaemia (polyclonal increase in gamma globulins, albumin:globukin ratio <0.5) hyperbilirubinaemia, usually not azotaemic, may also be normal
Fluid analysis: clear, straw - yellow colour, high protein content, viscous, cellularity variable
FIP
Treatment/prognosis
Grave prognosis - no cure usually, palliative treatment
Options:
- Suppotive/palliative care - Abx, SQ fluids, nutrition, rest, thoracocentesis
- Immune modulators
- Glucocorticoids +/- chlorambucil
- Aspirin?
- Oral polyprenyl immunostimulant
FIA (feline infectious anaemia)
Haematropic mycoplasmas:
- Mycoplasma haemofelis: anaemia, pleiomorphic (rods, rings or spherical), gram negative, young entire males
- Candidatus Mycoplasma haemominutum:
- Candidatus Mycoplasms turicensis
Pathogenesis:
- Mycoplasmas attach to RBC -> immune-mediated destruction
- Concurrent diseases, immunosuppression -> enhanced disease
- If recover from infection -> chronic infection fro variable time
FIA
Transmission
Fleas
Blood transfusion
Female cats to neonates - in utero, nursing
Fighting? Oral?
Experimentally: IP, IV and PO infected blood, urine and saliva not thought to be infective
M. haemofelis
Clinical signs
Acute: lethargy, inappetence/anorexia, fever (39-41), anaemia, splenomegaly, icterus
Chronic: normal to subnormal temperature, weakness, depression, weight loss/emaciation, icterus and splenomegaly less likely
M. haemofelis
CBC
Regenerative anaemia: varies in severity (PCV 15-18%), reticulocytosis, regenerative morphology, if acute onset may be pre-regenerative
Erythrophagocytosis and autoagglutination may be present
Leucocyte count variable:
- Leucocytosis with monocytosis in acute forms
- Normal counts in chronic forms
- Leucopaenia in moribund cases
M. haemofelis
Treatment
Doxycycline: 5-10mg/kg orally bid for 14-21d
Potentially adverse effects: GIT effects, abdominal discomfort, vomiting, inappetence/anorexia, oesophagitis, oesopharyngeal stricture formation
Flea control
Supportive care: blood transfusion, immunosuppresive therapy (pred)
M. haemofelis
Prognosis
No treatment - 1/3 with uncomplicated acute disease die
Regeneration - destruction + immune response to organism -> recovery
Clinical signs of farm animal anaemia
Pallor Lack of exercise intolerance Weakness Haemic murmur Red urine Jaundice Dependent oedema Black faeces Swollen udder
Causes of haemorrhagic anaemia
Farm animals
Caudal vena caval syndrome Enzootic haematuria Ruptured uterine artery Ruptured aorta Haemonchosis Fasciolosis Lice, mites and ticks Pyelonephritis Abomasal ulcer Intraluminal intestinal haemorrhage Gastric ulceration in pigs Proliferative haemorrhagic enteropathy in pigs (PIA)
Causes of haemolytic anaemic
Farm animals
Leptospirosis Postparturient haemoglobinuria Bacillary haemoglobinuria Protozoa (Babesia, Eperythrozoon) Chronic copper poisoning Cold water ingestion Brassica spp poisoning (rape, kale, cabbages) Drug induced Blood transfusion Autoimmune haemolytic anaemia
Depressed erythrocyte production
Farm animals
Deficiency of cobalt or copper Iron deficiency Acute bracken poisoning (enzootic haematuria) Faciolosis Lymphosarcoma Chronic renal disease (amyloidosis, pyelonephritis) Anaemia of inflammatory disease Radiation damage
Enzootic haematuria
Clinical signs:
- Haematuria with blood clots
- Freq urination
- Thickened bladder may or may not be palpable per rectum
- Other signs of chronic progressive anaemia
- Internal bleedings
Diagnosis:
- Most common cause of haematuria in cattle
- Pyelonephritis also causes haematuria but not necessarily anaemia
Abomasal ulcer
Sand, DA, 'stress' Diagnosis: - Occult blood in faeces/black stinking dung - Free air in the abdomen - Abdominal pain
Chronic copper poisoning
Farm animals
Species and breed variation in susceptibility
Copper is stored and accumulated in the liver
Some centrilobular necrosis occurs as liver copper concentrations rise
Sudden release of copper from the liver - acute fatal syndrome develops
Chronic copper poisoning
Farm animals - Diagnosis
Clinical signs: jaundice, pallor, haemoglobinuria, depression, death (24-48h)
Clinical path: Blood copper elevated, liver copper elevated, increased plasma AST
Necopsy: swollen yellow liver, swollen gunmetal kidneys, jaundice everywhere
Chronic copper poisoning
Farm animals - Treatment
Treatment:
- Ammonium tetrathiomolybdate (ATM) 2.7 mg/kg IV 2-3d intervals 3-6 treatments
- Ammonium molybdate 100mg + sodium aulphate 1g oral daily
- Sodium calcium edetate 70mg/kg IV 2d
- Somnulose 10ml IV
Chronic copper poisoning
Farm animals - prevention
Dietary copper < 10 ppm
Cu absorption inhibitors (Mo, Zn, Fe and soil)
Avoid prolonged feeding of concentrates
Physiology of colostrum - calves
Starting 4-6 weeks before calving there is transfer of immunoglobulins (Ig) into the udder
IgG1 is actively transferred into colostrum
Following ingestion of colostrum by the calf, Ig is absorbed by the epithelial cells of the SI and passes via the lymphatic system to the peripheral blood circulation
Systemic production in the calf by IgG and IgM
Local protection of intestine by:
- re-secretion of IgG into the gut lumen
- passage of IgA in colostrum (and milk) through the gut lumen
Immune mediated haemolytic anaemia - Eqine
Primary - uncommon
Secondary - antibodies attach to RBC membranes:
- Alterations in RBC membrane produced by primary infectious, neoplastic or other immune-mediated disease process
- Antigen-antibody complex deposition on RBC surface
- Drugs that cause immunoproteins to react indirectly with RBCs
Oxidative damage to RBCs (Heinz body anaemia)
Equine
Heinz bodies are precipitations of oxidatively denatured haemoglobin on RBC membrane
Can be caused by rarely used drugs (methylen blue, phenothiazine) or plants (onions, Brassica spp: rape, kale)
Exception: red maple leaf toxicity
Equine infectious anaemia
Exotic, Equine infectious anaemia virus (lentivirus)
Persistent infection: no treatment, lifelong carriers
Anaemia of chronic disease
Equine
Most common cause Mild-moderatre regenerative anaemia Pathogenesis: - Iron sequestration - anti-bacterial mechanism - Defective erythropoietin - Decreased RBC lifespan
Failure of passive transfer - foal
Lack of colostrum/poor quality
Failure to nurse
Failure of absorption
Measure IgG conc - <12-18h oral colostrum unless foal has system disease process
- or IV plasma - 1l = 2g in blood (2l usually required)
- Repeat measuring/transfusions as necessary
Neonatal isoerythrolysis - foals
Destruction of foal’s RBC by antibodies present in colostrums directed against foal’s RBC antigens
Blood group incompatibility between mare and foal
Clinical signs:
- First 4d of life
- Weakness, lethargy, increased hr and rr, icterus, pale mm
Diagnosis on clinical signs and haemolytic cross match
Treatment:
- 24-48 hours - prevent further colostrum intake
- Over that, supportive care
- Blood transfusion: mare’s washed red cells (not plasma) or typed donor
Sever combined immunodeficiency - horses
Arab foals - autosomal recessive inheritance
Lack of functional T and B lymphocytes
Fatal by several months of age
Can test for SCID gene
