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LCB2 > Immune mediated diseases > Flashcards

Immune mediated diseases Flashcards

1
Q

Give examples of immune mediated diseases with multi-system involvement

A
  • Systemic lupus erythematosus (SLE), very rare

- Sjogren’s syndrome, poorly defined, Cocker spaniels (involves mouth and joints)

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2
Q

Give examples of cutaneous immune mediated diseases

A
  • Canine dermatomyositis
  • Discoid lupus erythematosus
  • Pemphigus pemphigoid complex
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3
Q

Give examples of musculoskeletal/neuromusclar immune mediated diseases

A
  • Polymyositis/polyneuritis
  • Myasthenia gravis
  • Polyarthritis (erosive and non-erosive)
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4
Q

Give examples of haemolymphatic immune mediated diseases

A
  • Immune mediated haemolytic anaemia
  • Immune mediated thrombocytopaenia
  • Immune mediated neutropaenia
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5
Q

Give examples of renal immune mediated diseases

A

Glomerulonephropathies (many)

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6
Q

Give examples of immune mediated diseases of the CNS

A
  • Steroid responsive meningitis/encephalitis

- Grannulomatous meningoencephalitis

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7
Q

Give an example of an immune mediated GI disease

A
  • Inflammatory bowel disease

- Unsure if immune mediated

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8
Q

What causes the development of primary immune mediated diseases?

A
  • MHC class (accounts for some breed predispositions)

- May be true auto-immunity (but not referred to as autoimmune)

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9
Q

Give examples of things that immune mediated disorders may occur secondary to

A
  • Vaccination
  • Neoplasia (esp. lymphoproliferative)
  • Inflammatory disease (pancreatitis, prostatitis)
  • Infection
  • Drugs/toxins (MPS< carprofen, cephalosporins, griseofulvin, zinc)
  • Hormones (oestrogen)
  • Seasonality
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10
Q

Outline the diagnosis of immune mediated disorders

A
  • Recognition of signalment, history and physical examination
  • lab tests and biopsy
  • Fulfilment of specific diagnostic criteria e.g. those for SLE
  • Haematology, biochem and urinalysis as minimum database
  • Diagnostic tests should be carried out before starting therapy
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11
Q

Describe the major signs of SLE

A
  • Skin lesions
  • Polyarthritis
  • Haemolytic anaemia
  • Glomerulonephritis
  • Polymyositis
  • leukopaenia
  • Thrombocytopaenia
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12
Q

Describe the minor signs of SLE

A
  • Fever of unknown origin
  • CNS signs, seizures
  • Oral ulceration
  • Lymphadenopathy
  • Pericarditis
  • Pleuritis
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13
Q

Describe the serology for SLE

A
  • ANA

- Not specific to SLE

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14
Q

Describe the diagnostic criteria for SLE

A
  • Definitely SLE: 2 major signs with positive serology OR 1 major and 2 minor signs with positive serology
  • Probably SLE: 1 major sign with positive serology OR 2 major signs with negative serology
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15
Q

List the potential causes of immune mediated haemolytic anaemia and identify the main one

A
  • Autoantibody to RBC membrane antigen
  • Cross-reacting antibody against infectious agent
  • Antibody against drug adherent to RBC
  • Drug or infection modifies RBC antigen or exposes a hidden antigen
  • Idiopathic (majority of cases in dogs and cats)
  • Alloantibody
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16
Q

Outline the pathogenesis of IMHA

A
  • Phagocytosis of opsonised RBCs mainly in the spleen (extravascular) but also in blood by monocytes (intravascular)
  • Usually IgG, sometimes IgM or C3 complement implicated
  • IgM: intravascular mainly
  • Complement: immediate lysis
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17
Q

Explain how IMHA can cause death

A
  • Thrombus formation
  • DIC
  • Marked systemic immune response
  • Rarely from hypoxia unless limited ability to access blood for transfusion
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18
Q

Outline the signalment for IMHA

A
  • Cocker, Mini Schnauzer, Springer spaniel, poodle, old english sheepdog increased risk
  • Usually youngmiddle aged
  • F>M
  • May be more prevalent in summer
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19
Q

Discuss the approach to vaccination in a patient with IMHA

A
  • Unconfirmed link with vacc
  • Use titre test to identify if need vaccinating
  • If immunity not very robust, discuss with owner re. risk of infection vs risk of immune mediated disease recurrence
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20
Q

Describe the clinical presentation of IMHA

A
  • Variable in severeity and chronicity
  • Lethargy, depression, tachypnoea, tachycardia, weakness, anorexia
  • Collapse, pale MM (>75% of cases)
  • Haemic heart murmur due to altered blood viscosity
  • Jaundice
  • Hepatosplenomegaly
  • may have concurrent IMTP
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21
Q

Explain why jaundice may occur in IMHA and compare the 2 types of IMHA

A
  • Pre-hepatic
  • Increased bilirubin from RBC breakdown, usually from extravascular IMHA
  • Intravascular IMHA usually leads to haemoglobinaemia (red plasma)
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22
Q

Discuss IMTP that is concurrent with IMHA

A
  • = Evan’s syndrome
  • IMTP immune mediated thrombocytopaenia
  • More difficult to stabilise due to bleeding tendency with IMTP
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23
Q

Outlinen the methods for the diagnosis of IMHA

A
  • Haematology and smears
  • Auto-agglutination
  • Coomb’s test
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24
Q

Describe the common findings on haematology/blood smear in a case of IMHA

A
  • Regenerative anaemia (degree depends on magnitude of anaemia)
  • Spherocytes (partial phagocytosis by cells of RES)
  • leukocytosis
  • Hyperbilirubinaemia
  • Elevated liver enzymes
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25
Q

Describe the use of auto-agglutination in the diagnosis of IMHA

A
  • 1-3 drops of saline to one drop EDTA blood, mix by rocking
  • Look for clumping under microscope
  • Must use anticoagulated blood otherwise will mistake normal clotting as abnormal auto-agglutination
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26
Q

Describe the Coomb’s test for IMHA

A
  • Add Coomb’s reagent
  • Anti-canine Fc antibody
  • binds to red cells with antibodies attached leading to agglutination if IMHA
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27
Q

Outline the principles of treatment for IMHA

A
  • aim to induce rapid remission from ongoing haemolysis
  • Slower aim to enable recovery from anaemia
  • halt ongoing immune mediated damage to allow recovery
  • Corticosteroids +/- adjuncts
  • Blood transfusions
  • Oxyglobin
  • Thromboprophylaxis
  • Splenectomy in refractory cases
  • therapeutic plasmapharesis
  • Gastroprotectants
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28
Q

Explain the reasons for the use of corticosteroids in the treatment of IMHA

A
  • reduce egress of inflammatory cells into tissues
  • Reduce inflammatory mediators
  • Suppress macrophage and neutrophil function
  • Lymphocytotoxic
  • Reduce macrophage Fc receptor expression
  • Inhibition of complement
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29
Q

Describe the use of corticosteroids in the treatment of IMHA

A
  • Licensed
  • Some significant side effects, some mild, others less so
  • Rarely may get thromboembolic complications
  • Effects usually see within 24-36hours
  • Dex injectable thought to be more significantly ulcerogenic than prednisolone
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30
Q

Compare the relative immunosuppressive potencies, dose and duration of action of prednisolone, methylpred, dex, betamethasone

A

Pred: 1, 2.0-4.0mg/kg/d, 12-26h
Methyl pred: 1.25, 2.0-4.0mg/kg/d, 12-26h
Dex and beta: 7-10, 0.2-0.5mg/kg/d, >48h

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31
Q

Discuss the use of azathioprine in the treatment of IMHA

A
  • Unlicensed
  • Tablets cannot be split, typically dosed q48h (base frequency so that dose per day works, not dose to make frequency fit)
  • use lowest dose possible and remove as soon as possible
  • Usually well tolerated in dogs
  • Delayed onset of activity, use as adjunct, use early for optimal onset
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32
Q

Outline the side effects of azathioprine

A
  • Irreversible myelosuppression if used at higher than recommended dose
  • Progressive hepatopathy
  • Metabolites produced in dogs more toxic than those in people
  • Not recommended in cats, rapid lethal bone marrow suppression
33
Q

Discuss the use of ciclosporin in the treatment of IMHA

A
  • Licensed for atopy, not IMHA
  • Suppresses formation of cytokines in innate and adaptive immune system
  • Anecdotally useful
  • Various formulations (microemulsion capsule and liquid preparations)
34
Q

Outline the side effects of ciclosporin

A
  • May increase risk of infection

- Linked with increased incidence of lymphoma

35
Q

Discuss the use of cyclophosphamide in the treatment of IMHA

A
  • UNlicensed
  • Alkylating agent
  • Assocaited with neutral or negative impact on survival in IMHA therefore not recommended use in immune mediated disease
36
Q

Discuss the use of chlorambucil in the treatment of IMHA

A
  • Unlicensed
  • Alkylating agent
  • Slow acting, low toxicity
  • Give on empty stomach as food reduces absorption
  • Can use as adjunct to steroids in IMHA (also IMTP, immune mediated polyarthritis and IBD)
37
Q

Discuss the use of mycophenolate mofetil in the treatment of IMHA (mech of action, use, side effects)

A
  • Unlicensed
  • Antimetabolite agent inhibiting purine synthesis in lymphocytes
  • Steroid adjunct
  • Limited evidence for efficacy, some evidence for IMHA (and myasthenia gravis)
  • Can have GI side effects
38
Q

Discuss the use of IV immunoglobulin in the treatment of IMHA (mech of action, use)

A
  • Unlicensed
  • Purified preparation of polyspecific IgG from human blood donors: ethics
  • Very expensive, inconsistent availability
  • Multiple actions: block Fc receptors, neutralise autoantibodies
  • Used in IMHA, IMTP, some skin diseases as adjunct
  • Variable efficacy
39
Q

Discuss the use of vincristine in the treatment of IMHA

A
  • Use to treat concurrent IMTP

- Stimualtes thrombopoiesis in bone marrow, inhibits platelet phagocytosis by monocytes

40
Q

Outline the monitoring required in a case of IMHA

A
  • Abscence of spherocytes, lack of reticulocytes once PCV normalised, acute phase proteins
  • Check CRP before changing drug dose
  • Monitor steroid neutrophilia
41
Q

What does it indicate if PCV is normal but reticulocytes are high in a case of IMHA?

A

Disease is not under control

42
Q

Outline the general protocol for the of therapy for IMHA

A
  • Start with single agent pred at 1-2mg/kg PO q24h (dogs), cats 2mg/kg q12h
  • Maintain dose until induction of remission (often 3-4 weeks)
  • Once have remission, taper corticosteroids over 3-4 months at 20-25% reduction per month (based on side effects, maintenance of remission, APP concentration, re-check dose 2 weeks after)
  • If poor response after 3-4 weeks, add additional therapy
  • Monitor for recurrence (common)
43
Q

Outline the prognosis for IMHA

A
  • 50-88% survival to discharge from hospital
  • Death/euthanasia due to ongoing IMHA or complications e.g. thromboembolic disease
  • Variable median survival times
  • Relapse common
  • Survive past 14 days most the survive to a year
44
Q

What are the negative prognostic indicators for IMHA?

A
  • Icterus
  • Severe agglutination
  • Thrombocytopaenia
  • Hypoalbuminaemia
  • Elevated urea
45
Q

Explain the cause of immune mediated thrombocytopaenia

A
  • Usually from destruction of circulating platelets
  • Occasionally immune mediated attack at level of precursors in teh bone
  • Mediated by IgG against platelet membrane protein
46
Q

Which breeds are predisposed to immune mediated thrombocytopaenia?

A

Cockers, poodes, Old english sheep dogs

- NB CKCS and cairn terriers low platelet count as normal

47
Q

What platelet count would be indicative of IMTP?

A

<30x10^9/l

48
Q

Describe the clinical signs of IMTP

A
  • Spontaneous bleeding
  • Pyrexia prior to thrombocytopaenia
  • Mucosal and skin haemorrhage (petechiae, ecchymoses)
  • Hyphaema/retinal haemorrhage/epistaxis
  • GI haemorrhage (melaena, haematemesis)
  • Death through severe bleeding
49
Q

Why may pyrexia occur with IMTP?

A

Release of pyrogenic cytokines from platelet breakdown

50
Q

Describe the diagnosis of IMTP

A
  • Low platelet count
  • Exclusion of other causes of bleednig
  • Determine between primary and secondary IMTP
  • Severe thrombocytopaenia with absence of disease elsewhere is the main method of diagnosis
51
Q

Give examples of alloimmune haemolytic anaemias

A
  • Neonatal isoerytrholysis in cats and dogs

- Delayed haemolytic transfusion reaction in dogs

52
Q

Describe alloantibodies/isoantibodies

A
  • Specific antibodies directed against erythrocyte antigens from the same species but not from the individual producing the antibody
53
Q

How are alloantibodies produced?

A
  • Occur naturally in cats
  • Produced through sensitisation by birth of foal with mismatched blood group (horses)
  • Produced through sensitisation with mismatched blood transfusion (dog)
54
Q

Describe neonatal isoerythrolysis

A
  • Transfer of maternal antibodies in colostrum against the blood cells of the offspring
  • NI develops several hours to days after colostrum ingestion
  • Natural alloantibodies in cats, sensitisation required in horses
  • Haemolysis is main mechanism of pathogenesis, also agglutinating antibodies
55
Q

Explain how neonatal isoerythrolysis occurs in horses

A
  • Sensitisation to blood antigen with first foal
  • Second and subsequent mismatched foals at risk due to production of alloantibodies to stallion’s blood due to blood leakge through placenta during pregnancy or delivery
  • OR sensitisation occurred prior to pregnancy through blood transfusions or administration of vaccines containing equine tissue products, through which first foal can be at risk
56
Q

Explain feline neonatal isoerythrolysis

A
  • Caused by maternal anti-A alloantibodies in colostrum of blood group B queens
  • Immune mediated haemolysis of type A and type AB erythrocytes
  • Major cause of fading kitten syndrome
57
Q

Outline the proportion of type B queens in different breeds

A
  • UK BSH: high prevalence type B queens

- DSH: low prevalence type B queens

58
Q

Describe the clinical signs of feline neonatal isoerythrolysis

A
  • Within hours of feeding or after a few days
  • Haemoblobinuria
  • Fading kitten syndrome
59
Q

Describe the treatment of feline neonatal isoerythrolysis

A
  • Blood transfusion
  • Fostering type A queen or milk replacer
  • Supportive therapy
  • Rarely successful due to acute disease course
60
Q

Outline the prevention of feline neonatal isoerthrolysis

A
  • Blood typing queen and tom and mating only type B with type B
  • Foster nursing type A and AB kittens born to type B queen
61
Q

Which antibodies are implicated in equine neonatal isoerythrolysis?

A
  • 90% to blood groups Aa and Qa,

- None to Ca

62
Q

Describe the clinical signs of equine neonatal isoerythrolysis

A
  • Progressive lethargy, weakness, depressed
  • Pale mucous membrane, later icteric
  • Severe anaemia, marked haemoglobinaemia and haemoglobinuria
  • Breathing may become shallow, rapid, laboured
  • +/- tachycardia
  • Severe hypoxia can lead to convulsions, coma, death
  • Shock leads to rapid death (within 6-8hrs postpartum)
63
Q

Describe the treatment of equine neonatal isoerythrolysis

A
  • Immediately stop further ingestion of colostrum
  • Supportive care needed until foal recovers
  • IV fluid therapy
  • Transfusions - whole blood if suitable donor available or washed RBCs from dam
64
Q

Describe the prevention of equine neonatal isoerythrolysis

A
  • Avoid mismatched matings
  • Prevent colostrum ingestion until crossmatch performed between mare’s serum and offspring RBC (Jaundice Foal Agglutination JFA test)
  • Feed stored suitable colostrum
  • Once colosturm gone, rest of milk ok
65
Q

Describe the clinical signs of bovine neonatal pancytopaenia

A
  • Calves <1mo
  • Pyrexia
  • Unexplained haemorrahge from nose, gums, ear tag sites, injection sites, GIT etc.
  • Recumbency, pale MM, dyspnoeic, colic, sudden death
  • mortality 90%
66
Q

Describe the aetiology of bovine neonatal pancytopaenia

A
  • Destruction of bone marrow cells
  • Some evidence for immunopathological reaction due to alloreactive antibodies which are transferred to calves via colostrum
  • Greater risk 2nd and 3rd partum cows with multiple vacc (BVD vacc implicated)
67
Q

Describe the diagnosis of bovine neonatal pancytopaenia

A
  • Multiple internal and external haemorrhages
  • Thrombocytopaenia
  • Leukocytopaenia
  • Bone marrow depletion
68
Q

Describe the treatment of bovine neonatal pancytopaenia

A
  • Gentle handling to prevent further haemorrhage/haematoma formation
  • Blood transfusion (whole blood) often only gives transient improvement of clinical signs
69
Q

Describe the prevention of bovine neonatal pancytopaenia

A
  • Avoid use fo pooled colostrum
  • Newborn calves to previous cow with BNP calf should receive colostrum from another cow with no BNP calf
  • No colostrum or blood from cows on farms with BNP history should be used for commercial purposes
70
Q

Describe the aetiology of immune mediated diseases

A
  • Loss of self tolerance, allowing formation of antibodies to subset of normal proteins in the body
  • Lack of regulation leads to development of progressive inflammation and damage
  • Usually not global immunodeficiency
  • Specificity of loss appears to be determined in part by genetic background
  • Role of hormones unclear
  • More common in younger vs older
71
Q

What are primary immunodeficiencies?

A

Inherited defects of innate or adaptive immunity rather than antibodies attacking host cells. Usually global effect of 0 innate immune cells, B and T lymphocytes. Rare, except fell pony immunodeficiency syndrome

72
Q

What is Fell pony immunodeficiency syndrome?

A
  • Autosomal recessive disoder

- Majorly impaired adaptive immune system, molecular basis unknown

73
Q

What condition causes foals to appear normal at birth, but then fail to thrive and die within 3 months, and have prodound anaemia, B-lymphopaenia and fail to produce immunoglobulins?

A

Fell pony immunodeficiency syndrome, autosomal recessive disease common in UK

74
Q

What causes Arab horse SCID?

A

Autosomal recessive disorder leading to no functional B or T cells, no adaptive immunity

75
Q

What condition of horses causes foals to be normally initially, then succumb to opportunistic infections within the first 4-6 months of life?

A

Arab horse SCID

76
Q

Which dog breeds are susceptible to severe combined immunodeficiency?

A
  • Jack Russel terrier

- Basset Hounds and cardigan Welsh Corgi (x-SCID)

77
Q

Which rare condition causes lymphopaenia, agammaglobulinaemia, thymic and lymphoid aplasia in Jack Russel terriers?

A

SCID

78
Q

How does SCID of JRTs cause disease?

A

Defect in DNA dependent protein kinase => blocks gene splicing and recombination of T cell receptors

79
Q

What condition causes stunted growth, increased susceptibility to infection, absence of lymph nodes, and a partially developed thymus in Basset Hunds and Cardigan Welsh Corgis?

A

X-SCID (mutation in common gamma chain, defect of receptors for IL-2, IL-4, IL-7, IL-9 and IL-15)

LCB2 (14 decks)

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