Since its discovery in the 1960s, the incidence of this disease has been decreasing worldwide, due primarily to rigorous vaccination and elimination strategies of affected cats. In North America, the prevalence of FeLV-infected cats is about 2.3% of the general population.
FeLV is transmitted horizontally (from cat to cat) primarily through saliva, which contains high concentrations of the virus. While biting, licking and grooming are the most common routes of infection, kittens may be infected transplacentally or by nursing from infected mothers. However, virus contact does not ensure persistent viremia or disease.
There are three antigenic types of feline leukaemia virus - A, B and C - based on differences in envelope antigens. Cells transformed by either FeLV or feline sarcoma virus express a novel viral antigen (FOCMA) in their plasma membrane, antibodies to which protect the cat against the disease. The serum of persistently infected cats lacks both neutralizing and FOCMA antibodies. Strains of virus from immunosuppressed cats infect CD4+ and CD8+ T-lymphocytes, B-lymphocytes and myeloid cells. Bone marrow-infected cats are usually persistently viraemic and antigenaemic, and often succumb to FeLV-associated diseases within a few years. The FeLV-945 surface glycoprotein (SU), a member of the FeLV-A subgroup is asociated with an unusual multicentric lymphoma of non-T-cell origin, observed in natural and experimental infections in cats.
The stages of FeLV infection include:
- replication in local lymphoid tissue (tonsillar and pharyngeal lymph nodes); 2 - 12 days
- dissemination in circulating lymphocytes and monocytes; 2 - 12 days
- replication in spleen, distant lymph nodes and gut-associated lymphoid tissue; 2 - 12 days
- replication in bone marrow cells and intestinal epithelial crypts; 2 - 6 weeks
- peripheral viremia, dissemination via infected bone marrow derived neutrophils and platelets; 4 - 6 weeks
- disseminated epithelial cell infection with virus secretion in saliva and tears; 4 - 6 weeks
In some cases, the cat mounts an immune response, making the cat resistant to infections for an undetermined period. In other cats, there is a persistent viraemia. In others cases, the cat fails to produce immunity but does not become viraemic and becomes a carrier: the virus is sequestered in epithelial tissues and is replicating, but it does not leave the cells because of antibody production.
Some cats are asymptomatic in early infection with FeLV, especially younger cats. Ocular disease can occur such as anisocoria and anterior uveitis. The incidence of ocular disease among clinically affected cats FeLV-positive cats is reported to be low (2% or less); however, FeLV has been shown to be a common cause of anterior uveitis of affected eyes.
Over months and years, more serious clinical signs appear, including anorexia, weight loss, enlarged lymph nodes, persistent fever, anaemia, gingivitis, infections of the skin, cystitis, splenomegaly and upper respiratory tract, persistent diarrhoea, seizures, and abortion in queens. Secondary infections are common such as Toxoplasma gondii and systemic fungal infections. The development of anaemia is associated with the emergence of a novel viral subgroup, FeLV-C.
Systemic diseases which occur secondary to FeLV infection include leukemia, lymphoma, immunosuppression, FeLV enteropathy, myelodysplasia (bone marrow disorders), plasmacytoma and reproductive disorders.
Cutaneous disorders have been associated with FeLV infection, including cutaneous lymphosarcoma, giant cell dermatosis, epidermal horns, epidermal vasculitis, plasma cell stomatitis, plasma cell pododermatitis, plasma cell chondritis
ELISA testing for the presence of antibodies to the p27 antigen in blood, plasma, serum, saliva, or tears. Serum is the fluid of choice for ELISA testing because saliva and tears may not contain sufficient p27 for viral detection. Antibody titers to FeLV envelope antigens and FOCMA antibodies may be used for diagnostic purposes, but are of little clinical relevance.
Immunoflourescent antibody testing (IFA) detects FeLV antibodies after bone marrow infection and therefore are more sensitivie predictors of staging of illness. Viral isolation or PCR amplification of FeLV sequences from cells of the bone marrow can also be utilised.
Gross pathological findings depend on the type of disease that occurs. Bone marrow hypercellularity often accompanies leukemias. Lymphoplasmacytic infiltrates of the gingiva, lymph nodes, spleen, kidney, and liver may be seen. Intestinal lesions similar to those seen in feline panleukopenia may occur with enteric FeLV infection. These gross changes include an edematous, turgid small intestine with petechial to ecchymotic hemorrhages on the serosal and/or mucosal surfaces of the jejunum and ileum.
Treatment of FeLV-infected cats is symptomatic and supportive. The majority of cases with clinical signs referable to FeLV-viraemia and antigenaemia usually succumb to a variety of diseases. Use of antibiotics such as doxycycline and amoxicillin/clavulanate are indicated in most cases.
Treatment of anaemia associated with bone marrow erythrocyte suppression may require blood transfusion. Cats with leukemia or myeloproliferative diseases generally do not respond well to available therapy and have a poor prognosis.
The use of Interferon-Ω has resulted in perceived improvements. Chemotherapy is the principle therapy for addressing secondary lymphoma. In a cattery situation or multi-cat household, identification of affected cats and isolation is required to minimise further spread of the virus.
Vaccination should be considered in FeLV-negative at-risk cats such as stray, outdoor or feral cats. Immunisation affords >80% protection for 2 years against exposure to live virus challenge under experimental conditions.
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