FeLV infection can cause variable and multiple clinical signs. The most common disease consequences of persistent FeLV viraemia are: immune suppression, anaemia, and lymphoma [Hardy et al., 1976; Hardy et al., 1973].
The prognosis for persistently FeLV viraemic cats is poor and most will develop an FeLV related disease. 70-90 % of these cats will be dead within 18 months to three years [Hardy et al., 1976]. Some persistently viraemic cats may remain healthy for a prolonged period (many years) before FeLV related disease develops and occasional cases remain healthy indefinitely [Hofmann-Lehmann et al., 1995].
Age of the cat at the time of the infection is the most important factor determining the clinical outcome [Hoover et al., 1976]. Viral and host factors, including the virus subgroup and cellmediated immune response, influence the pathogenesis of infection within individual infected cats.
Immune suppression in FeLV is more complex and severe than the more selective one caused by FIV infection. Several abnormalities have been reported including thymic atrophy, lymphopenia, neutropenia, neutrophil function abnormalities, loss of CD4+, and more importantly loss of CD8+ [Ogilvie et al., 1988].
Irrespective of whether recognisable clinical signs are present or not, every FeLV-viraemic cat is immune suppressed [Orosz et al., 1985a; Orosz et al., 1985b; Perryman et al., 1972], with delayed and decreased primary and secondary antibody responses. The immune suppression can have many clinical consequences and may lead to infection with other primary infectious agents to which cats would be normally resistant, such as Salmonella spp. In addition, there may be exacerbation of disease caused by other pathogens, such as pox virus, Mycoplasma haemofelis and Cryptococcus, and infections normally not pathogenic in cats, e.g. due to Toxoplasma gondii. Concurrent FeLV infection may also predispose to chronic refractory disease such as stomatitis and chronic rhinitis [Knowles et al., 1989; Tenorio et al., 1991]. Some clinical problems such as chronic rhinitis and subcutaneous abscesses may take much longer to resolve in FeLV-infected cats and unexpected recurrences may arise.
FeLV-infected cats may develop many different types of anaemia, which are mainly nonregenerative and rarely regenerative. Regenerative anaemias, associated with haemolysis may be related to secondary opportunistic infections, for example by Mycoplasma haemofelis, or to immune-mediated destruction [Scott et al., 1973; Kociba, 1986]. FeLV-C can interfere with a haem transport protein [Cotter, 1979; Quigley et al., 2000], which directly results in a nonregenerative anaemia. Non-regenerative anaemias may be caused by chronic inflammatory mechanisms, myelodestruction, myelosuppression (either pancytopenia or pure erythrocyte aplasia) and myeloproliferative disease. Other cytopenias may be present, in particular thrombocytopenia and neutropenia, probably caused by virus-induced immune-mediated mechanisms and myelosuppression.
FeLV may cause different tumours in cats, mainly lymphoma and leukaemia, but also other non-haematopoietic malignancies. FeLV-induced lymphomas are among the most frequent tumour forms of the cat; myeloproliferative disorders are less common and not always associated with FeLV infection [Francis et al., 1979a; Louwerens et al., 2005].
Different forms of lymphoma have been classified according to its most frequent anatomic location:
Immune-mediated diseases associated to FeLV infection have been reported, including haemolytic anaemia, glomerulonephritis and polyarthritis. Antigen-antibody complex deposition and loss of T-suppressor activity may be the main factors contributing to immunemediated diseases.
Benign peripheral lymphadenopathy has been diagnosed in FeLV-infected cats [Moore et al., 1986]; a clinical picture with potential to be mistaken as peripheral lymphoma. Chronic enteritis associated with degeneration of intestinal epithelial cells and crypt necrosis has been associated with FeLV-infection in cats in which virus is present in intestinal crypt cells [Reinacher, 1987]. Inflammatory and degenerative liver disease has also been described associated with FeLV infection [Reinacher, 1989].
Reproductive disorders and fading kitten syndrome have been also reported. Foetal resorption, abortion and neonatal death are the main manifestations [Hardy et al., 1981]. Fading kittens and other reproductive disorders are rarely observed these days, largely as a result of the very low prevalence of infection in pedigree breeding cats, achieved by routine testing.
Neurological disease not associated to CNS lymphoma or opportunistic CNS infections has been described, mainly peripheral neuropathies presenting as anisocoria, mydriasis, Horner’s syndrome, urinary incontinence, abnormal vocalization, hyperesthesia, paresis and paralysis [Haffer et al., 1987]. Neuropathogenicity has been investigated as a possible direct effect of the virus [Dow & Hoover, 1992].