Difference between revisions of "Feline Immunodeficiency Virus"

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==Signalment==
 
==Signalment==
  
FIV infection increases in prevalence in older cats, and is more often found in male cats compared to females. It is the older male cat that is free to roam outdoors that is most likely to be infected with FIV.
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FIV infection increases in prevalence in older cats, and the average age at diagnosis is 5 years<sup>fmc</sup>. Male cats are more commonly infected than females as they roam more and exhibit a higher degree of territorial aggression. There are no breed predilections.
  
 
==Diagnosis==
 
==Diagnosis==

Revision as of 11:52, 27 August 2010



Also known as: FIV

Description

Feline immunodeficiency virus is a retrovirus that cuases immunodeficiency disease in the domestic cat.

Agent

FIV is prevalent in cat populations throughout the world and is an important cause of feline disease. FIV belongs to the lentivirus family of the retrovirus group.

Transmission and Epidemiology

The major route of transmission is via saliva, especially through biting, and those cats exhibiting territorial aggression are most at risk of infection. Vertical transmission can also occur but the importance of this is not known. Venereal transmission has not been reported. Within households horizontal transmission can occur but the level of infection can be very variable. In some households only a single cat in a group may be FIV positive, whereas in others nearly every cat may be infected. Overall it appears that if fighting among cats housed together is rare, the prevalence of FIV is likely to be low.

Seroepidemiological surverys of the prevalence of FIV in the UK have shown that 13-19% of sick cats may be infected with FIV compared to 2-3% of healthy cats.

Pathogenesis

The pathogenicity of FIV is strain dependent, and can vary widely. For all strains, feline lymphocytes and macrophages are the preferred cells for virus replication, and so FIV disrupts the function of the immune system. FIV gains entry to the cell via feline CD134, a surface molecule, and uses various chemokine receptors as secondary receptors,sup>fmc. In acute infection, the virus spreads from the site of entry to the lymphoid tissues and thymus, where it first infects T-lymphocytes and the macrophages. Although both CD4+ and CD8+ cells can be infected by FIV and lysed in culture, the virus appears to preferentially destroy CD4+ cells. This intially results in a change in the ratio of CD4+ to CD8+ cells, from roughly 2:1 to less than 1:1fmc. After several months of infection, an absolute reduction in CD4+ isa appreciable.

Hosts remain asymptomatic following FIV infection until cell-mediated immunity is disrupted by a decrease in the production of Th1 cytokines. In the advanced stages of infection, humoral immunity is also adversely affected. Although clinical signs are primarily due to changes related to T-cell populations, macrophages are the main reservoir of FIV in infected catsfmc. These cells are capable of transporting virus to the tissues of the body, and also suffer impairment of function, such as an increase in the production of TNF. Microglia and astrocytes in the brain, and megakaryocytes in the bone marrow, can become infected with FIV, and co-infection with feline leukaemia virus can increase the expression of FIV in many tissues, including the kidneys, liver and brain.

Signalment

FIV infection increases in prevalence in older cats, and the average age at diagnosis is 5 yearsfmc. Male cats are more commonly infected than females as they roam more and exhibit a higher degree of territorial aggression. There are no breed predilections.

Diagnosis

Clinical Signs

Laboratory Tests

  • ELISA for serum antibody
    • False positives occur, particularly in the presence of maternal Ab
  • Positives can be confirmed by lab work (Western blotting)

Pathology

On post-mortem examination, lymphadenopathy is seen. Intestinal lesions similar to those seen in feline panleukopenia virus infection may be apparentfmc.

In early disease, lymphadenopathy is seen histologically to be due to follicular hyperplasia and infiltration of plasmacytes to surround the cortex. Later in disese, a mixutre of follicular hyperplasia and follicular depletion may exist, and in the terminal stages of FIV infection, follicular involution is the key featurefmc. Lymphoplasmacytic infiltrates are seen in the gingiva, lymphoid tissues, spleen, kidney, liver and brain. Brain lesions also include perivascular cuffing, gliosis, neuronal loss, vacuolation of the white matter and, occasionally, the presence of giant cells.

Prognosis

The long-term prognosis for FIV-infected cats is guarded, but some cats will survive for many years following diagnosis. Around 20% of affected cats die within the first two years after diagnosis; this equates to a 20% mortality rate in the first 4.5-6 years after the estimated time of infectionfmc. In generally, the more chronic and severe the clinical signs, the worse the prognosis is.

Treatment

Control

  • No UK vaccine
  • Healthy positive cats should have diagnose confirmed by further testing
  • Isolate and castrate
  • Preventative neutering of males

Links

References

  1. Tilley, L P and Smith, F W K (2004) The 5-minute Veterinary Consult (Fourth Edition),Blackwell.
  2. Caney, S (2000) Feline immnunodeficiency virus: an update. In Practice, 22(5), 255-260.
  3. Johnson, C M (2005) Transmission of Feline Immunodeficiency Virus. Proceedings of the 56th Annual Meeting of the American College of Veterinary Pathologists and 40th Annual Meeting of the American Society for Veterinary Clinical Pathology.
  4. Merck & Co (2008) The Merck Veterinary Manual (Eight Edition), Merial.
  5. Morrision, W B (2002) Cancer in dogs and cats: medical and surgical management, Teton NewMedia.
  6. Rand, J (2006) Problem-based feline medicine, Elsevier Health Sciences.