Pashu Sandesh, 13 December 2021

Sonali Mishra1 and Kunal Pandit2

  1. M.V.Sc. Veterinary Pathology (ICAR-IVRI) Assistant Professor, Department of Veterinary Clinical Complex, DGCN COVAS CSKHPKV Palampur H.P.
  2. M.V.Sc. Veterinary Anatomy (GBPUAT Pantnagar) Veterinary Officer, Department of Animal Husbandry H.P. 


Autoimmune disorders are actually the conditions where the immune system of the body accidentally starts attacking our own body cells as foreign invader cells. So the tissue injury is caused by auto-antibodies or cell-mediated immune response to self-antigens. There is no specific cure to these disorders but treatment focuses more on bringing down inflammation, by controlling the overactive immune system. 

These disorders usually run in families as hereditary disorders thus proper selection and tracing back history before selection is useful.

The mechanism of developing autoimmune disorders can be :

  •   Sequestrated or hidden antigens –exposure to antigens that are not exposed early to T cells during the development process in the thymus for eg. brain’s myelin basic protein, lens antigen, sperm antigen etc.
  • Inappropriate expression of MHC class- the expression of MHC II molecules on the pancreas, thyroid epidermal cells, etc. makes them behave as foreign therefore leading to IDDM, thyroiditis etc.
  • Neo antigens: due to physiological, chemical and biological changes.
  • Cross reacting antigens or molecular mimicry: when common epitopes are shared between body cells and antigen, for eg: streptococcal M protein shares common epitopes with the heart muscles (myosin). Trypanosoma cruzi shares some common epitopes with the heart and CNS etc.
  • Loss of immunoregulation: failure of regulation of B and T cells eg. failure of maintenance of central and peripheral tolerance.


Autoimmune diseases are broadly categorised into organ-specific and systemic disorders 

A. Organ-specific autoimmune disorders:

1) Autoimmune Thyroiditis

Autoantibodies are generated against thyroid antigens (thyroglobulins).  It is characterized by lymphocytic infiltration of the thyroid. Animals suffering from disease shows dullness, depression, fatty bodies due to hypothyroidism, inactive animals, myxoedema, dryness of coat etc.

2) Diabetes Mellitus Type 1:-Diabetes mellitus type 1 is a form of diabetes mellitus that results from autoimmune destruction of insulin-producing beta cells of the pancreas and particularly glutamic acid decarboxylase is targeted. The subsequent lack of insulin leads to increased blood and urine glucose. The symptoms are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss.

 3) Adrenalitis: Autoantibodies are generated against the adrenal cortex. It is seen in humans and dogs characterized by depression, weak pulse, vomiting and diarrhoea.

4) Pemphigus: it is an autoimmune dermatological condition, characterized by vesicle and blister formation. In Pemphigus Vulgaris (prototype) blisters are formed within the deepest layers of the epidermis. The second pemphigus group includes entities causing blisters confined to the superficial epidermis, of which, pemphigus foliaceus (PF) is the most common.

5) Equine Polyneuritis: antibodies are produced against myelin protein 2 in the brain causing neurological signs of seizures, tremors and loss of consciousness. 

6) Multiple Sclerosis: autoantibodies are produced against the myelin coating of nerve axons and this causes hardening of CNS and brain.

7) Uveitis:  It is caused because of antigenic mimicry of interphotoreceptor binding protein (epitope) as Leptospira interrogans shows some similarity with the corneal antigens. This causes blepharospasms, lacrimation and photophobia. 

8) Myasthenia Gravis: It can be congenitally due to a deficiency in the receptors of acetylcholine or it can be acquired due to the autoantibodies production. Muscle weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction, inhibiting the excitatory effects of the neurotransmitter acetylcholine on nicotinic receptors at neuromuscular junctions, causing muscle weakness and fatigue.

B) Systemic autoimmune disorders:

  1. Primary immune-mediated hemolytic anaemia (IMHA)

Primary immune-mediated hemolytic anaemia (IMHA) is the result of a spontaneous autoimmune response directed against antigens expressed on the surface of erythrocytes. Antibodies may facilitate direct intravascular lysis of red blood cells or phagocytosis and extravascular destruction by cells of the monocyte-phagocyte system in the liver and spleen. The clinical signs include haemoglobinuria, splenomegaly, hepatomegaly and lymphadenopathy.  Microscopically, spherocytosis, nucleated RBCs, Anisocytosis are seen in blood smears.

2) SLE: Systemic lupus erythematosus (SLE) is a complex disease characterized by the appearance of autoantibodies against nuclear antigens and the involvement of multiple organ systems, including the kidneys. 

3) Rheumatoid Arthritis: RF is the ab formed against the altered self-antigen (IgG) due to which there is swollen joints, pain and stiff gait. Clinical signs include lameness, due to joint erosions. Pannus formation in the joints causes the release of proteases that eat away the articular cartilage.

4) Sjogren's Syndrome: autoantibodies are produced against lacrimal glands and salivary glands, leading to xerostomia ie. dry mouth and KCS, causing dryness of eyes, laceration and ulcer formation.


Smith, D.A. and Germolec, D.R., 1999. Introduction to immunology and autoimmunity. Environmental health perspectives107(Suppl 5), p.661. 

Katelaris, C.H. and Peake, J.E., 2006. 5. Allergy and the skin: eczema and chronic urticaria. Medical Journal of Australia185(9), p.517. 

Simons, F.E.R., Ardusso, L.R., Bilò, M.B., El-Gamal, Y.M., Ledford, D.K.,    Ring, J., Sanchez-Borges, M., Senna, G.E., Sheikh, A. and Thong, B.Y., 2011. World allergy organization guidelines for the assessment and management of anaphylaxis. World Allergy Organization Journal4(2), p.1. 

McGavin, M.D. and Zachary, J.F., 2006. Pathologic basis of veterinary disease. Elsevier Health Sciences.

Bernal-Cano, F., Joseph, J.T. and Koralnik, I.J., 2007. Spinal cord lesions of progressive multifocal leukoencephalopathy in an acquired immunodeficiency syndrome patient. Journal of neurovirology13(5), pp.474-476.

F Estelle R Simons et al, World Allergy Organization Journal,  2011, 4:13-37.