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Equine Clinical Immunology > Chapter 8 Serum Sickness > Flashcards

Chapter 8 Serum Sickness Flashcards

1
Q

What is serum sickness?

A

A systemic disease caused by the formation of immune complexes, typically deposited in vessel walls of tissues/organs.

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2
Q

What type of hypersensitivity reaction is serum sickness?

A

Hypersensitivity type III reaction.

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3
Q

Who elucidated serum sickness and in what year?

A

Clemens von Pirquet in 1906.

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4
Q

What are the common tissues/organs where immune complexes deposit in serum sickness?

A

Glomeruli, synovial membrane, lymph nodes, and skin.

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5
Q

What are the common clinical signs of serum sickness in horses?

A

Fever, skin eruptions of purpura, lymphadenopathy, arthralgia, polysynovitis, albuminuria/proteinuria, and acute renal failure.

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6
Q

What is a key historical observation about antibodies in serum sickness?

A

Antibodies, which should protect against disease, are also responsible for disease.

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7
Q

Is there a breed and sex predisposition to serum sickness in horses?

A

No, there is no known breed and sex predisposition.

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8
Q

What is the main immunoglobulin involved in serum sickness?

A

IgG and IgM.

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9
Q

What are the main factors that determine immune complex formation in serum sickness?

A

Quality of antigens and immune-complexes, condition of circulation and vascular beds, antigen-antibody concentration.

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10
Q

What happens in the initial phase of antigen-antibody complex formation in serum sickness?

A

Initially, there is an excess of antigen, leading to small immune complexes that do not deposit or activate complement.

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11
Q

What role do liver sinusoidal endothelial cells play in serum sickness?

A

They clear antigen-antibody complexes from the circulation via Fc-gamma receptor II.

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12
Q

How are large antigen-antibody immune complexes removed from the circulation?

A

By mononuclear phagocyte system (MPS), particularly macrophages in the red pulp of the spleen.

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13
Q

What is the consequence of medium-size immune complex formation in serum sickness?

A

They deposit along the endothelial surface of certain vascular beds, activating complement.

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14
Q

What happens when complement is activated by medium-size immune complexes?

A

It results in an inflammatory cascade with endothelial cell swelling, fibrin deposition, increased vascular permeability, and chemoattraction of neutrophils.

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15
Q

What is necrotizing vasculitis?

A

A condition where neutrophil activation leads to destruction of the basement membrane and surrounding tissues.

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16
Q

What are common etiologic associations of serum sickness in humans?

A

Use of xenogeneic serum to treat toxin-mediated and infectious diseases, administration of antivenoms, anti-toxins, and prevention of allograft rejection.

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17
Q

What are some examples of exogenous immunogenic proteins that can cause serum sickness in horses?

A

Equine polyclonal antibody products, snake antivenins, tetanus, botulinum, Clostrium difficile antitoxins, hyperimmune plasma products, plasma and serum transfusions.

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18
Q

What are the common diagnostic methods for confirming immune complex-mediated diseases in humans?

A

Detection of circulating immune-complexes using radioimmunoassay, enzyme-linked immunosorbent assay, solid phase anti-C3 assay, measurement of C3 and C4 concentrations.

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19
Q

What are the histopathologic findings in immune complex-mediated diseases?

A

Presence of electron-dense deposits in the endothelial basement membrane, immune-complexes, complement and fibrin deposition, necrotizing vasculitis.

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20
Q

What is the main focus of serum sickness management?

A

Removal of the offending antigen, decreasing inflammation, and decreasing antibody production.

21
Q

What is the role of glucocorticoids in treating serum sickness?

A

They decrease inflammation to halt tissue injury.

22
Q

What is a key supportive therapy for serum sickness?

A

Supportive therapy to control clinical signs, particularly renal damage.

23
Q

What is the best prevention strategy for serum sickness?

A

Documentation of the offending antigen and future avoidance of administration.

24
Q

What are immune complexes composed of in serum sickness?

A

Antigen and antibody bound together.

25
Q

How are immune complexes typically cleared from circulation?

A

By the liver sinusoidal endothelial cells and mononuclear phagocyte system.

26
Q

What happens when there is an excess of antigen in serum sickness?

A

Small immune complexes form that do not deposit or activate complement.

27
Q

What is the effect of complement activation in serum sickness?

A

It triggers an inflammatory cascade that includes endothelial cell swelling, fibrin deposition, and neutrophil chemoattraction.

28
Q

What leads to necrotizing vasculitis in serum sickness?

A

Activated neutrophils release proteolytic enzymes and oxidative agents, causing tissue destruction.

29
Q

What are the key components involved in the inflammatory cascade of serum sickness?

A

Complement components such as C3a and C5a, and neutrophils.

30
Q

What is the role of complement component C1q in serum sickness?

A

It initiates the cascade of complement activation.

31
Q

What is the significance of platelet aggregation in serum sickness?

A

It occurs at the site of immune complex deposition, contributing to inflammation and tissue damage.

32
Q

What is the historical context of serum sickness in humans?

A

It was common due to the use of xenogeneic serum for toxin-mediated and infectious diseases.

33
Q

What modern treatments have minimized the immunogenicity of antivenoms and anti-toxins?

A

Use of Fab fragments of immunoglobulins instead of whole immunoglobulins.

34
Q

What are the most common modern causes of serum sickness in humans?

A

Reactions to drugs such as penicillin, cephalosporin, and sulfonamides.

35
Q

What is the importance of detecting C3 and C4 concentrations in diagnosing immune complex diseases?

A

Low values indicate consumption of complement components and suggest immune complex disease.

36
Q

How is histopathologic evaluation used in diagnosing serum sickness in horses?

A

By identifying electron-dense deposits, immune-complexes, and signs of necrotizing vasculitis in tissue samples.

37
Q

What are the primary goals of treating serum sickness?

A

Removing the offending antigen, decreasing inflammation, and controlling antibody production.

38
Q

What is the recommended dose of dexamethasone for treating serum sickness in horses?

A

0.05–0.2 mg/kg IV or PO every 12 or 24 hours.

39
Q

What are the potential side effects of long-term glucocorticoid therapy in horses?

A

Polyuria, polydipsia, laminitis, gastrointestinal ulceration, hepatopathy, and secondary infections.

40
Q

How should glucocorticoid therapy be tapered in horses with serum sickness?

A

Decrease the dose by 10–20% every 24 to 48 hours.

41
Q

What is the role of prednisolone in treating serum sickness?

A

It can be used as an alternative to dexamethasone for long-term therapy.

42
Q

What supportive therapies are crucial for managing renal damage in serum sickness?

A

Maintaining hydration, electrolyte balance, and monitoring renal function.

43
Q

What is the significance of documenting the offending antigen in serum sickness?

A

To prevent future occurrences by avoiding re-administration of the antigen.

44
Q

What are common clinical signs of serum sickness in human patients?

A

Fever, rash, arthralgia, lymphadenopathy, and proteinuria.

45
Q

What is the pathophysiology of serum sickness?

A

Formation and deposition of antigen-antibody immune complexes leading to complement activation and inflammation.

46
Q

Why is it important to monitor horses receiving plasma transfusions for serum sickness?

A

To detect and manage any adverse reactions promptly.

47
Q

What laboratory findings indicate glomerulonephritis in serum sickness?

A

Albuminuria/proteinuria and azotemia.

48
Q

What is the role of Fc-gamma receptor II in serum sickness?

A

It binds the antibody heavy chain constant region, aiding in the clearance of immune complexes.

Equine Clinical Immunology (32 decks)

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