References

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3. Laver, WG et al. Virol 59 (1974) 230.

4. Powell, DG et al. Vet Rec 94 (1974) 282.

5. Pereira, HG et al. Bull Wld Hlth Org 47 (1972) 465.

6. Heuschle, WP. Proc 25th Ann Mtg Am Assoc Eq Pract, 1979. p 31.

7. Burrows, R and Goodridge, D. Proc 3rd Int Conf Eq Infect Dis, 1972. p 306.

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DISEASES OF THE IMMUNE

SYSTEM by R.A. Mansmann

Types of Immune Reactions¹

Type I (Reagin-Dependent)

In this type of immune reaction, an extrinsic antigen reacts with fixed antibody on the sur­face of mast cells, causing the release of chem­ical mediators, such as histamine, serotonin and slow-reacting substance of anaphylaxis. Release of mediators in turn causes broncho-constriction, edema and eosinophilia. Comple­ment is not a major part of this type of reaction. The antigen involved may be inhaled pollen, in respiratory disease, or toxins from an insect bite, as in dermatologic disorders. The fixed an­tibody, IgE (reaginic antibody), is bound to mast cells located in the mucosae and dermis, and is found in only very low concentrations in serum. Although the exact role of IgE in horses has not been determined, this immunoglobulin probably mediates allergic diseases and may be involved in immunity to parasites, such as ascarids.

Type-I immunologic diseases include Queens­land itch, which is a reagin-mediated hyper-sensitivity to insect bites, and some types of chronic obstructive pulmonary disease.²³

Type II (Autoimmune)

In this type of reaction, the antigen is an al­tered endogenous protein that stimulates au-toantibody formation. During embryonic life, lymphocytes develop the ability to differen­tiate endogenous ("self) antigens from exoge­nous antigens. If, in later life, endogenous proteins are altered by infection or other events, lymphocytes respond to the presence of these altered endogenous proteins by production of autoantibodies. Organs and tissues are de­stroyed by combination of the cellular protein (antigen), complement and autoantibodies.

Type-II reactions include autoimmune dis­eases, such as autoimmune hemolytic anemia. Autoimmune hemolytic anemia has been ob­served in horses with lymphomatosis and pur-pura hemorrhagica.⁴⁵ Clinical signs included marked anemia, fever, weakness, dependent edema and a positive Coombs test.

Type III (Immune Complex)

Type-Ill reactions are caused by extrinsic an­tigens reacting with circulating antibodies, usually of the IgG type. The antigen, IgG and complement combine to form an immune com­plex that attracts neutrophils. Lysozymes re­leased by neutrophils cause the lesions related to type-Ill reactions.

Diseases associated with type-Ill reactions include equine infectious anemia, viral arteri-tis, herpesvirus-1 myelitis, hypersensitivity pneumonitis, and possibly purpura hemor­rhagica following sensitization to Streptococ­cus equi. In the type-Ill reaction, the animal is continuously exposed to antigen and produces increasing levels of antigen-specific IgG and IgM. Immune complexes form and are trapped in capillary basement membranes and attract neutrophils, which release lysozymes that cause vasculitis.

428

Type IV (Cell-Mediated)

In type-IV reactions, an exogenous antigen reacts with lymphocytes, which release media­tors, such as lymphokines and migratory-in­hibitory factor. Cell-mediated reactions are associated with diseases, such as tuberculosis, systemic mycoses, neoplasia and contact der-matis from tack or insecticides.