Felis ISSN 2398-2950

Feline leukemia virus disease

Synonym(s): FeLV

Contributor(s): Stephen Barr, Severine Tasker

Introduction

  • Cause: feline leukemia virus (FeLV) Feline leukemia virus.
  • Signs: relate to specific malignancies, eg:
    • Weight loss.
    • Diarrhea.
    • Vomiting.
  • Immunosuppression, eg:
    • Chronic or repeated infections.
    • Anemia.
    • Reproductive disorders and glomerulonephritis.
  • Diagnosis: ELISA, RIM, immunofluorescence, PCR or virus isolation.
  • Treatment: cannot stop viral excretion; specific treatments for lymphomas and infections; supportive, eg transfusion.
  • Prognosis: good if transient viremia, poor if persistently viremic.
    Print off the Owner factsheet on FeLV Feline Leukaemia Virus (FeLV) to give to your client.

Pathogenesis

Etiology

Predisposing factors

General

  • Age (resistance develops with age).

Specific

  • Multi-cat households.
  • Outdoor access (contact with infected cats).
  • High local prevalence of infection.
  • Sick cats.

Pathophysiology

  • FeLV oronasal infection   →   replication in local lymphoid tissue   →    FeLV spreads via mononuclear cells = transient viremia and production of free p27 antigen   →    after ~3 weeks infection of bone marrow occurs   →    infected granulocytes and platelets occur which are positive for cell-associated p27 antigen   →    the longer the bone marrow is infected, the more likely persistent viremia is to occur.
  • The cat can mount an immune response to FeLV at different times following infection:
    • Abortive recovery occurs if the effective immune response occurs before a transient viremia develops.
    • Recovery is still possible after transient viremia, either before or shortly after bone marrow infection has occurred. Transient viremias typically last about 3 weeks but can be a maximum of 16 weeks.
    • If bone marrow infection occurs before recovery, cats can become latently infected after resolution of the transient viremia.
    • Not all, but the majority of cats that undergo bone marrow infection will become persistently viremic.
  • Latent infections can theoretically be reactivated by stress or corticosteroids (immunosuppression)   →   persistent viremia but this is believed to be rare.
  • Focal (localized) infections can result in a small percentage of infected cats. Here FeLV is sequestered in certain tissues (eg gastrointestinal tract, lymph nodes, spleen, bone marrow) where viral replication occurs.
  • Persistent viremia   →   various pathogenic variants of FeLV, eg immunosuppressive, anemogenic or tumorogenic.
  • There are three subgroups of FeLV:
    • FeLV-A - inter-host transmission; all infected cats.
    • FeLV-B - may be associated with increased risk of neoplastic disease; 50% infected cats.
    • FeLV-C - associated with the development of non-regenerative anemia via direct effect on erythroid precursors in bone marrow; <2% infected cats.
  • FeLV-B and FeLV-C are variants that are derived from FeLV-A which have differing vitro cell tropisms from the parent wild type (FeLV-A).

Timecourse

  • 85% persistently infected cats die within 3 years (cf 20% non-viremic controls).

Epidemiology

  • Free range, single cats: 50% exposed to FeLV, 1% develop active infection   →   low risk of disease.
  • Multi-cat household: 100% exposed to FeLV, 40% develop active infection   →   high risk of disease.
  • Latent/localized infection - virus can sometimes be transmitted in milk.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Cattori V, Tandon R, Riond B et al (2009) The kinetics of feline leukaemia virus shedding in experimentally infected cats are associated with infection outcome. Vet Microbiol 133 (3), 292-296 PubMed.
  • Lutz H, Addie D, Belák S et al (2009) Feline leukaemia. ABCD guidelines on prevention and management. J Fel Med Surg 11 (7), 565-574 PubMed.
  • Dunham S P & Graham E (2008) Retroviral infections of small animals. Vet Clinics North Am Sm Anim Pract 38 (4), 879-901 PubMed.
  • Goldkamp C E, Levy J K, Edinboro C H et al (2008) Seroprevalences of feline leukemia virus and feline immunodeficiency virus in cats with abscesses or bite wounds and rate of veterinarian compliance with current guidelines for retrovirus testing. JAVMA 232 (8), 1152-1158 PubMed.
  • Hofmann-Lehmann R, Cattori V, Tandon R et al (2008) How molecular methods change our views of FeLV infection and vaccination. Vet Immunol Immunopathol 123 (1-2), 119-123 PubMed.
  • Levy J, Crawford C, Hartmann K et al (2008) 2008 American Association of Feline Practitioners' feline retrovirus management guidelines. J Fel Med Surg 10 (3), 300-316 PubMed.
  • Hartmann K, Griessmayr P, Schulz B et al (2007) Quality of different in-clinic test systems for feline immunodeficiency virus and feline leukaemia virus infection. J Feline Med Surg (6), 439-445 PubMed.
  • Hofmann-Lehmann R, Cattori V, Tandon R et al (2007) Vaccination against the feline leukaemia virus: outcome and response categories and long-term follow-up. Vaccine 25 (30), 5531-5539 PubMed.
  • Pinches M D, Helps C R, Gruffydd-Jones T J et al (2007) Diagnosis of feline leukaemia virus infection by semi-quantitative real-time polymerase chain reaction. J Fel Med Surg (1), 8-13 PubMed.
  • de Mari K, Maynard L, Sanquer A et al (2004) Therapeutic effects of recombinant feline interferon-omega on feline leukemia virus (FeLV)-infected and FeLV/feline immunodeficiency virus (FIV)-coinfected symptomatic cats. JVIM 18 (4), 477-482 PubMed.
  • Lappin M R (2000) Feline infectious uveitis. J Feline Med Surg​ (3), 159-163 PubMed.
  • Malik R, Kendall K, Cridland J et al (1997) Prevalences of feline leukaemia virus and feline immunodeficiency virus infections in cats in Sydney. Aust Vet J 75 (5), 323-327 PubMed.

Other sources of information


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