MAIN RETROVIRUSES OF WILD MAMMALS

FELINE LEUKAEMIA

Feline leukaemia virus (FeLV) is a gammaretrovirus causing neoplastic and degenerative diseases of the lymphoreticular system, including lymphosarcoma, leukaemia and anaemia syndromes, and feline acquired immunodeficiency syn­drome (AIDS).

FeLV is enzootic in domestic and feral cat (Felis silvestris catus) populations worldwide, but overall prevalence of FeLV infection is typically low (less than 5%), whereas prevalences of FeLV infection in free- ranging European wildcats (Felis silvestris silvestris) and Iberian lynxes (Lynx pardinus) reach up to 77% and 18%, respectively. FeLV or FeLV nucleic acids have been identified in both species. Domestic and feral cats are reservoir hosts. To what extent FeLV is transmitted between wild and domestic popula­tions is unclear, and wild felids may also be natural hosts. In domestic and feral cats, FeLV is horizontally transmit­ted oronasally via secretions and excretions, through bites and intimate contact, and may be vertically transmitted from mother to fetus. Transmission in free- ranging wild felids is probably similar. FeLV is present in high titres in the saliva of viraemic cats. It is secreted in semen, vaginal fluids, faeces and urine, but venereal and faecal-oral routes are not important. FeLV is poorly preserved in the envi­ronment. Risk factors for free-ranging wild felids are prob­ably similar to those in domestic and feral cats (high density populations, male aggression and free-roaming).

Infectious Diseases of Wild Mammals and Birds in Europe, First Edition. Edited by Dolores Gavier-Widen, J. Paul Duff, and Anna Meredith. © 2012 Blackwell Publishing Ltd. Published 2012 by Blackwell Publishing Ltd.

FeLV infection has been studied in naturally and experi­mentally infected domestic cats. FeLV first replicates in oropharyngeal lymphoid tissues. Cell-associated viraemia spreads the virus to lymphoreticular tissues, bone marrow and intestinal epithelium.

Initially the infection is largely subclinical in most cats, although it may lead to illness or death within 4 to 8 weeks, as a result of leucopenia and acute immunosuppression. Latent infection does not lead to clinical signs or disease, but immunosuppression (e.g. by concurrent Feline immu­nodeficiency virus infection) can cause reactivation of FeLV infection and persistent viraemia. Viraemic cats may develop disease, including progressive immunosuppres­sion, lymphoid and myeloid cell depletion, and finally cell transformation. Eventually these cats develop a plethora of neoplastic and degenerative diseases. Development of per­sistent viraemia or latent infection of the bone marrow depends on the ability to mount an effective immune response. Persistent viraemia is usually not accompanied by virus neutralizing antibodies, whereas latent infection is, at least in part, kept under control by these antibodies.

Clinical signs in non-domestic felids include lethargy, anorexia, emaciation, dehydration, anaemia and lymphad­enopathy. Poor body condition in European wild cats(¹) and severe acute anaemia and mortality in Iberian lynxes(²) correlated with FeLV infection.

Gross and microscopic pathology of FeLV- related dis­eases is described in cats with persistent viraemia. No lesions have been reported in association with FeLV infec­tion in European free- ranging wild felids. Dead Iberian lynxes infected with FeLV had succumbed to bacterial infection in the wild and to a severe acute anaemic disease in captivity(²). A free-ranging FeLV-infected cougar (Felis concolor) presented with generalized benign lymphoprolif­erative disease and bacterial septicaemia⁽³⁾.

The infection is traditionally diagnosed by detecting FeLV antigen with immunofluorescent assays (IFA) on blood smears or enzyme-linked immunosorbent assays (ELISA) on plasma or serum. Positive serum antibody tests may indicate latent infection. In addition, polymerase chain reaction (PCR) assays and immunohistochemistry can be performed on a range of organs taken from necropsy, e.g. lymph nodes, spleen, digestive and respiratory tract, kidneys, urinary bladder, salivary glands and pancreas.

There are no regulation, management or control plans for FeLV infection in European free- ranging wild felids. FeLV is not considered zoonotic. The suspected associa­tion between severe conditions in European wild cats and Iberian lynxes and FeLV infection indicates that it may pose a threat to these endangered wild felids(⁴). Monitoring the prevalence and the impact of FeLV infection in free- ranging wild felids in Europe is indicated.

FELINE IMMUNODEFICIENCY

Feline immunodeficiency virus (FIV) is a lentivirus that replicates in feline T lymphoblastoid cells, inducing immu- nosuppression(⁵). Lentivirus infections are characterized by long incubation periods. Although typically species­specific, lentiviruses may cross species barriers between related species, as has been thought to occur with the primate lentiviruses HIV and SIV.

The prevalence of FIV infection in domestic and feral cats in Europe ranges from less than 1% to 30%. Clinical FIV has not been identified in free-ranging wild felids in Europe and the infection appears rare, although little information is available. Most serological studies did not find evidence of FIV circulation in the European wildcat. In one study in eastern and central France however, 3 out of 38 wildcats had antibodies against FIV(¹). FIV antibod­ies have not been detected in the European lynx (Lynx lynx) or Iberian lynx in Europe, although one study reports Iberian lynxes with cross-r eactive antibodies against species-specific strains of FIV(⁶).

The pathogenesis of FIV infection has been studied in naturally and experimentally infected domestic cats. Infection typically follows a bite via infected saliva. FIV replicates primarily in lymphocytes, macrophages and other non-T cells, including renal cells and cells of the central nervous system. Virtually all lymphoid tissues and the salivary glands are infected within 1 week and by 3 weeks FIV is present in all non-lymphoid tissues, includ­ing the brain. It persists for life in the infected host.

The course of the disease in domestic cats is variable and can be divided into five successive stages.

1. The acute stage develops between 4 and 6 weeks, and lasts several weeks with mild fever, neutropenia and generalized lymphadenopathy.

2. The subclinical phase can last several years, during which FIV is present in saliva, peripheral blood mono­nuclear cells and plasma.

3. Persistent lymphadenopathy follows with progressive depletion of CD4+ T lymphocytes lasting several months with non-specific signs of disease, such as fever, anorexia and weight loss.

4. The AIDS-related complex (ARC) phase may last several months to years and is associated with chronic secondary infections by non-opportunistic pathogens.

5. The terminal feline AIDS phase can last several months and is characterized by severe secondary infections, often with opportunistic pathogens, as well as neoplas­tic and neurological disorders.

Serum antibodies against FIV appear 2 to 6 weeks post­infection and tend to persist throughout life.

In domestic cats, multiple haematologic abnormalities are observed, including frequent cytopenia (leucopenia, anaemia or both), especially during the later stages of disease.

Histological lesions in the lymph nodes and spleen of domestic cats include follicular hyperplasia and polymor­phism during the initial stages of infection. Both follicular hyperplasia and involution are observed during the ARC stage of the disease. Marked follicular involution and depletion characterize the final feline AIDS stage. Histo­logical lesions in non- lymphoid tissues appear later and include lesions of gliosis, perivascular cuffing, white-matter vacuolation, and choroid plexus fibrosis predominantly in the cerebral cortex, glomerulosclerosis and tubular degen­erative changes in the kidney and lesions associated with secondary infection.

The presence of FIV-specific antibodies in wild felids, demonstrating ongoing infection, can be detected by sero­logical assays, most commonly ELISA. ELISA results should be confirmed by western immunoblotting. Viral isolation, molecular methods (e.g. PCR), and immunohis­tochemical tests for FIV antigen can indicate ongoing infection.

No regulations, management or control plans are in place for FIV infection in free-ranging wild mammals in Europe. There are no indications that FIV has zoonotic potential.

FIV may represent a threat to endangered European wildcats and Iberian lynxes, with domestic and feral cats representing a source of FIV infection⁽⁴⁾. Monitoring of European wildcat and Iberian lynx populations for the prevalence and the impact of FIV infection would be indicated.

ALCES Leucotropic oncovirus infection

Since the mid-1980s, large numbers of moose (Alces alces) have been found in poor condition or dead in south­western regions of Sweden. Among the numerous names used for the disease, moose wasting syndrome (MWS) was probably the most appropriate. Among its possible causes, diet-related factors (mineral deficiencies) and infection with Alces Ieucotropic oncovirus (ALOV) have been consid- ered⁽⁷’⁸⁾.