Cats infected with tuberculosis respond poorly to intradermally injected tuberculin and, as a result, the tuberculin test is unsatisfactory in this species. They do not respond with delayed hypersensitivity reactions to proteins such as bovine serum albumin. Nevertheless, cats can develop a good delayed skin response to dinitrochlorobenzene, to viral antigens and to BCG vaccine, although these delayed hypersensitivity reactions are not as intense or as consistent as in other species, such as the guinea pig. Despite this lack of skin reactivity, the granulomatous reactions to tuberculosis in the cat are indistinguishable from those seen in other mammals.
Feline major histocompatibility complex (MHC) molecules
The feline histocompatibility (FLA) system has been unusually difficult to study because the conventional approach of generating lymphocytotoxic antibodies by transfusion, multiple births or skin grafting does not work well. (Only about 25% of cats rejecting allografts produce lymphocytotoxic antibodies.) It may also be difficult to produce substantial mixed lymphocyte culture reactivity between some unrelated feline cells. Although it is possible that this may be due to a lack of FLA polymorphism, it is more likely to be due to a relatively low level of MHC expression on cat mononuclear cells. Thus genetic analysis indicates that the FLA system contains 10-20 class I gene loci, of which only two are expressed. Cats also possess five class II gene loci, of which only three are expressed. Feline class I antigens display 81-82% sequence identity with the human and 73-79% identity with the mouse homologs. Analysis of the histocompatibility antigens of other felids suggests that their MHC has a similar structure. Cat class I and class II MHC genes are located on chromosome B2.
The lack of MHC polymorphism in the cat may help to account for the ease of bone marrow transplantation in this species. The success rate of bone marrow allografts in cats previously treated with X-radiation or cyclosporine is high and graft-versus-host disease is not a major problem.
Cats possess all the major complement components at levels comparable to those in other species of mammal. Cat complement is, however, not as hemolytic as rabbit, dog or guinea pig complement when using rabbit antibodies and sheep erythrocytes as antigens.
The lungs are the primary target organ for anaphylactic shock in the cat, and serotonin release from mast cells is probably the most important mediator of anaphylaxis. Flea-bite dermatitis is the most common allergic reaction in cat skin, whereas allergic-rhinitis is rarely encountered. Food hypersensitivity has been described in the cat.
There are only two feline blood group antigens, called A and B. The prevalence of each of these two antigens varies according to geographical region. Thus, in the USA, 99% of cats are group A and only 1% are group B. In contrast, in Australia, 73% of cats have group A erythrocytes, while the rest are group B. Blood group B tends to be found in more exotic breeds of cats rather than in the common domestic shorthair. Very rare AB (0.4%) cats have been described. About 20% of group A cats possess natural anti-B with titers ranging from 16 to 512. Group B cats invariably contain anti-A at high titer. Agglutination and hemolysis can be used for feline blood typing.
Neonatal isoerythrolysis has been recognized in the cat. It may be induced artificially by immunization of queens with vaccines containing feline blood components. It has also been reported to occur spontaneously when sires of blood group A are bred repeatedly to females of blood type B. The antibodies are transferred from the mothers to the kittens through their colostrum. These then cause massive erythrocyte destruction and profound anemia.
Several spontaneous autoimmune diseases have been described in the cat, including hyperthyroidism, hemolytic anemia, thrombocytopenic purpura, pemphigus vulgaris, pemphigus foliaceous, systemic lupus erythematosus, myasthenia gravis and arthritis.
Feline hyperthyroidism is recognized as an important clinical entity in older cats. The presence of autoantibodies against thyroid microsomes has been demonstrated by immunofluorescence in about one-third of these cases, while lymphoid infiltration is found in another third. Autoimmune hemolytic anemia, while usually occurring spontaneously, may also develop secondary to FeL.V infection. An autoimmune thrombocytopenia has also been reported to be associated with FeLV infection.
Primary immunodeficiencies are rarely recorded in the cat. Thymic hypoplasia and lymphopenia have been reported in a Siberian tiger, while 'nude' cats -thymic aplasia and hypotrichosis - have been recorded in a litter of kittens. These kittens had no thymus, and showed lymphocyte depletion in T cell areas of the lymph nodes, spleen and Peyers patches. Their most common congenital defect in immune function is the Chediak-Higashi syndrome. This is classically seen in some Persian cats. Affected animals show defects in pigmentation with a characteristic pale coat color and red tapetal light reflection. Their leukocytes contain enlarged lysosomal granules but increased susceptibility to infections has not been observed. Of considerably greater importance as a cause of feline disease is failure of passive transfer of colostral immunoglobulins. This results in the development of severe and intractable bacterial infections in newborn kittens. The most important cause of secondary immunodeficiency in the cat is FeLV infection. Despite its name, this virus usually causes severe immunodeficiency in infected animals. Kittens born to FeLV-infected queens may show thymic atrophy and depressed allograft responses, while infected adult cats may develop a panleukopenia. As a result, they die due to fulminating bacterial infections. Many cats with chronic bacterial or fungal infections such as pneumonias, abscesses and stomatitis are found to be FeLV infected. Feline panleukopenia, due to a parvovirus, also causes an acquired immunodeficiency syndrome with severe leukopenia and lethal secondary infections.
Feline immunodeficiency virus (FIV) is a widespread lentivirus that infects domestic and wild cats. Infection with this virus results in progressive depletion of CD4+ T lymphocytes. The resulting disease in many respects resembles human acquired immune deficiency syndrome (AIDS) and is an important model of the human disease. FIV replicates preferentially in feline T lymphoblastoid cells and causes a characteristic cytopathic effect in vitro. The virus receptor is probably not mediated through fCD4 (which is expressed on only a subset of T cells) but through fCD9. Infection is also associated with a marked, polyclonal expansion of B cells and of a subset of fCD8" cells. As a result the CD4:CD8 ratio can be reduced to as low as 1.6, compared with a normal ratio of 3.3. Kittens artificially infected with
FIV initially exhibit few clinical signs, most notably anemia, lymphopenia, neutropenia and lymphadeno-pathy. Eventually a terminal AIDS-like illness develops. Natural FIV infections result in death as a result of secondary infections of the oral cavity, upper respiratory tract, gastrointestinal tract, skin or urinary system. Neurologic signs have also been described. Epidemiologic analysis suggests that FIV is mainly transmitted between cats by biting.
Plasmacytomas, although uncommon, are well recognized in the cat. The great majority of these tumors secrete immunoglobulins of the IgG isorvpe, but IgA- and IgM-secreting myelomas have also been described. In some cases these plasmacytomas maybe associated with the deposition of immuno-globulin-associated amyloidosis.
See also: CD antigens; Cytokines; Leukemia viruses. Further reading
Agar NS and Board NG (cds) (1983) Red Blood Cells of
Domestic Mammals. Amsterdam: Elsevier. Bauer RM and Olsen RG (1988) Parameters of production and partial characterization of feline interleukin 2.
Veterinary Immunology and Immunopathology 19: 73-183.
Casal ML et al (1994) Congenital hypotrichosis with thymic aplasia in nine Birman kittens. Journal of the American Hospital Association 30: 600-602. F.lyar JS, Tellier MC, Soos JM et al (1997) Perspectives on
FIV vaccine development. Vaccine 15: 1437-1444. Foster AP, Duffus WP, Shaw SF. et al (1995) Studies on the isolation and characterization of a reaginic antibody in a cat. Research in Veterinary Science 58: 70-74. Matsumura S, Ishida T, Washizu T et al (1993) Pathologic-features of acquired immunodeficiency-like syndrome in cars experimentally infected with feline immunodeficiency virus. Journal of Veterinary Medical Science 55: 387-394.
Pecoraro MR, Kawaguchi Y, Miyazawa T et al (1994) Isolation, sequence and expression of a cDNA encoding the a-chain of the feline CDS. Immunology 81: ! 27— 131.
Willett BJ, Hosie MJ, Jarrett O and Neil JC ( .1994) Identification of a putative cellular receptor for feline immunodeficiency virus as the feline homologue of CD9. Immunology 81: 228-233. Yuhki H, Heidecker GF and O'Brien S.f (1989) Characterization of MHC cDNA clones in the domestic car: diversity and evolution of class 1 genes. Journal of Immunology 142: 3676-3682.
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