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One type of Ab mediated disease
1. Evidence of specific Ab in patient’s serum
2. Ag must be identified and characterized
o Ag must be shown to produce immunologic response in the eye of
experimental animals
o Produce similar lesion in animal passively sensitized with serum
from affected animal challenge with specific Ag

The disease can be regard as Ab – mediated
1. Ab to Ag present in high quantity in ocular fluid than serum
2. If abnormal accumulations of plasma cells in ocular lesion
3. If abnormal accumulations of Ig present at site of disease
4. If complement is fixed by Ig at the site of the disease
5. If accumulation of eosinophile is present at site of disease
6. If ocular disease is associated with inflammatory disease elsewhere in the
7. Any parasite infection / fungi / allergi can cause increase in eosinophile

Disease that affect the eyes:
1. Hay fever conjunctivitis:
o Oedema (swelling) and hyperemia (redness) of the conjunctiva and
o Itching and watering of the eyes
o Seasonal incidence (pollens)
o Immunologic pathogenesis
 IgE is attached to mast cells lying beneath conjunctiva
 Contact of Ag with IgE (Ab), the release of vasoactive
amines (histamine) results in vasodilatation
o Two type of mast cells: mucous membrane type and connective
tissue type
o Plasma cell also present in tissue, if present in blood shows
multiple myeloma
o Immunologic diagnosis:


Vernal conjunctivitis: o Seasonal incidence (warms months) o Produce giant papillae of the tarsal conjunctiva o Keratinized epithelium from papillae abrade underlying cornea.  Scrapings of conjunctiva epithelium. stained with Giemsa stains shows many eosinophiles  Scratch tests of skin with extract of pollens show the immediate type of respons  Biopsies of the skin test sites shown of Arthus reaction 2. Atopic keratoconjunctivitis o No specific seasonal incidence o The skin of lids has characteristics dry. Rheumatoid disease affecting the eye: o Uveitis and scleritis o Arthritis affects only one joint (knee) with ocular involve o Immunologic pathogenesis:  Rheumatoid factor (IgM auto – Ab)directed against patient’s own IgG (Ag)  Followed by complement fixation and attraction to WBC  Occlusive vasculitis is cause of rheumatoid nodules 2|Page . Vernal conjunctivitis and atopic keratoconjunctivitis o Itching and lacrimation of the eye o Structural modifications of the lids and conjunctiva 3. giving rise to complaint of foreign body sensations 4. degradation of mast cells  Heavy papillary infiltration by mononuclear cells o Immunologic diagnosis:  Conjunctiva scrapings: large number of eosinophils (Giemsa stain)  Skin testing with extract (pollen) reveals wheal and flare type of reaction within 1 hour of testing 5. scanty appearance o Conjunctiva and cornea may develop scarring in later stage o Immunologic pathogenesis:  Reaginic Ab (IgE) is fixed to sub epithelial mast cells  Ag and IgE interaction.

disease affecting pigmented structure of eye and skin 8. Primary or congenital immunodeficiency o Genetics defects result in increased susceptibility to infections o Bruton’s agammaglobulinemia (cell that produce the gammaglobulin is not present (absent) 2. Sympathetic ophthalmia: o Inflammation in second eye after the other has been damaged by penetrating injury o Accompanied by vitiligo (pigmentation of the skin) and poliosis (whitening) of eyelashes IMMUNODEFICIENCY Immunodeficiency disease: defects in one or more components of immune system that can lead to serious and fatal disorders Aetiology of immunodeficiency: 1. Associated with cell – mediated immunity or delayed type hypersensitivity 7. Secondary or acquired immunodeficiency: o Malnutrition o Disseminated cancers o Treatment with immunosuppressive drugs o Infections of immunocompetent cells with HIV (AIDS) General features of immunodeficiency: 1. Sympathetic ophthalmia:.  Occlusion of vessels (sclera) is responsible for “melting away” of scleral collagen that is characteristics of rheumatoid arthritis  Destruction of acinar cells within the lacrimal gland by circulating Ab result in decrease tear secretion  Combination of dry eye. Increase susceptibility to infection 3|Page . (keratoconjunctivitis sicca) dry mouth (xerostomia) and rheumatoid arthritis known as Sjorgen’s syndrome (systemic autoimmune disease) Cell mediated disease 6.

Humoral immunodeficiency disease 2. Deficiencies in classical pathways components (C1. Prone to certain type of cancers (by oncogenic viruses) 3. and C4) 2. C8. o Deficient in humoral immunity results in increased susceptibility to infections by pyrogenic bacteria o Deficient in cell – mediated immunity lead to infection by viruses and other intracellular microbes 2. C6. Congenital hypogammaglobulinemia o X – linked (Bruton’s) agammaglobulinemia o Common variable immunodeficiency o Selective IgA deficiency 3. Leukocytes adhesion defect: disorders of oxidative metabolism o Myeloperoxidase deficiency (MPO) o Chronic granulomatous disease (CGD) Defects in neutrophil granule formation and function: 1. C7. Deficiencies in regulatory proteins o C1 esterase inhibitors (C1 INH) deficiency (HAE) Disorders of phagocyte function: 1. C2. Chediak Higashi syndrome Disorders of the lymphoid system: 1. Deficiencies in alternative pathway components o Deficient in C3 o Deficient in properdin o Deficient in C5. Patients with IgA deficiencies have compensatory increase of IgM in secretions that may act to protect mucosal surface against potential infections 4|Page . Deficient in immune response result from abnormalities: o Specific immunity abnormal development of T and B cells o Natural immunity are defect in phagocytes and complement Disorders of complement system: 1. and C9 3. Specific granule deficiencies 2.

Caused by human immunodeficiency virus (HIV) type 1 and 2 2. 3 types of virus that usually found is HIV virus. 4. and platelets 5. and cytomegalovirus 4. When screening blood. whole blood) they can become sensitized and develop IgE Ab directed against IgA 5. drug abusers. In blood smear. Upon subsequent exposure to IgA – containing product there is a risk of developing anaphylactic reaction 6. and blood transfusion) o Prenatal transfer 3. Laboratory diagnosis: individual develops Ab against several viral components o ELISA o Western blot assay 5|Page . Pregnant IgA – deficient women developed anti IgG anti IgA Ab that crossed the maternal – foetal barrier and suppressed foetal IgA production T – Lymphocytes and combined T and B lymphocytes disorders: 1. When exposed to blood products that contains IgA (plasma. The disease is acquired by: o Sexual contact with infected individual (homosexual) o Parental administration (intravenous injection. needle stick from infected patient. hepatitis B virus. we can find RBC. Exhibit partial or complete defects in T – cell function o Thymic hypoplasia (DiGeorge’s syndrome) o Cellular immunodeficiency with elevated immunoglobulins (Nezelof’s syndrome) o Combined (cellular and humoral) immunodeficiency (SCID) o Immunodeficiency with thrombocytopaenia and eczema (increase in IgE concentration) – (Wiskott – Aldrich syndrome)  Platelet count increase in chronic myeloid leukaemia but decrease in thrombucytopaenia o Ataxia – telangiectasia (associated with gene disorders – gene associated A-T) – cause loss or impairment of muscular coordination o X – linked lympho-proliferative syndrome (Duncan’s disease) o AIDS (absolute decrease in CD4 concentrations) Acquired immunodeficiency syndrome (AIDS): 1. leukocytes.

During replication. o In peripheral blood CD8 atypical cells are seen. the CD4 lymphocytes are destroyed making the individuals is highly susceptible to infectious agent 6|Page . C3 and C – reactive protein decrease transferring o Polyclonal increased in γ globulin with oligoclonal band. α2. T cells are markedly reduced especially the CD4 cells o Serum reveal acute phase pattern with increased α1. Use of p24 AG testing and polymerase chain reaction (PCR) 6. Pathology / mechanisms: o AIDS virus attaches to a receptor on the membrane of CD4 lymphocytes and fuse with the cell membrane o Viral core then released into cytoplasm of T – lymphocyte o Viral reverse transcriptase converts the viral RNA genome to dsDNA o dsDNA circularizes and transported into the nucleus where it integrates with the host DNA o Viral mRNA is produced and formed into virions.