Caprine arthritis-encephalitis

Caprine arthritis-encephalitis

D WERLING AND W LANGHANS

Introduction

Caprine arthritis-encephalitis (CAE) is a persistent, progressive and multisystemic disease of goats caused by a lentivirus. The main clinical signs in young kids are ataxia, lameness and paralysis caused by leukoencephalomyelitis. In older animals, the disease usually presents as a slowly progressive arthritis and, occasionally, as progressive interstitial pneumonia or chronic mastitis.

Caprine arthritis-encephalitis is present in goat populations in many parts of the world and the prevalence of infection may reach over 80 per cent in some countries.2 The disease has been diagnosed in some East African countries such as Uganda and Kenya,56 but it has not yet been clinically diagnosed in South Africa. Antibodies to CAE virus (CAEV ) were not detected in a survey of a population consisting mainly of indigenous South African goats,2 but more recently a low prevalence has been found in milk goats of European origin.63

Aetiology

Caprine arthritis-encephalitis virus is a lentivirus within the Retroviridae family. It was first isolated from a synovial membrane explant of an adult goat suffering from arthritis. 15 A similar agent was isolated from a thymic explant of a goat experimentally inoculated with a brain suspension from a natural case of CAE.45

Lentiviruses cause chronic degenerative diseases with long incubation periods and life-long viral persistence, accompanied by strong humoral and cellular immune responses. The best-known lentivirus is human immunodeficiency virus (HIV), the causative agent of human acquired immunodeficiency syndrome (AIDS). Other animal lentiviruses include equine infectious anaemia virus (EIAV), feline immunodeficiency virus (FIV), bovine immunodeficiency virus (BIV) and maedi-visna virus (MVV).

Caprine arthritis-encephalitis virus is very similar to the sheep MVV which was originally described in Iceland as the aetiologic agent of chronic interstitial pneumonia (maedi) and demyelinating leukoencephalomyelitis (visna) in sheep (see Maedi-visna).58, 59 It may also cause clinical arthritis in sheep, although less frequently than CAEV does in goats.

Antibodies induced by CAEV cross-react with the p30 antigen of MVV, but not with other proteins of MVV.49 Significant genetic differences between CAEV and MVV have been shown using molecular techniques.49, 52 It is therefore clear that the CAEV is genetically distinct from the ovine lentiviruses, although it is morphologically and physically indistinguishable from MVV.

The genomes of lentiviruses are composed of two singlestranded, polyadenylated RNA molecules of approximately 9 kb. In the early phase of infection, the viral RNA is converted into double-stranded DNA by reverse transcription. 28 All lentiviruses share a similar genomic organization with gag, pol and env structural genes, and a varying number of regulatory genes. The gag (group-specific antigen) gene encodes for the matrix, capsid and nucleic acid-binding proteins. The pol (polymerase) gene encodes for the reverse transcriptase and the integrase needed for reverse transcription and integration of viral DNA into cell DNA. The env (envelope) gene encodes for the two envelope glycoproteins, which are cleaved from a larger precursor protein. The transmembrane (TM) protein anchors the surface protein (SU)-TM complex in the virion envelope, and contains a domain responsible for the fusion of viral and cellular membranes with the SU protein that recognizes cell surface receptors. Because of their presence on the viral surface, a strong humoral response against these two glycoproteins is induced during infection.

Epidemiology

The clinical signs of chronic arthritis in goats were first reported in Switzerland in 1969.61, 72 Similar reports came from studies performed in Germany60 and Japan,44 and the encephalitic form was subsequently recognized in Germany60 and also recorded in the USA10 before the retroviral aetiology was discovered.14, 45 Caprine arthritis-encephalitis occurs almost worldwide,2 the only possible exceptions being Somalia and Sudan. In some African countries infection is limited to imported animals and their progeny.2 All the evidence therefore suggests a European origin for the disease. International movement of goats has been implicated as the major mechanism of its dissemination.

Transmission occurs mainly via colostrum and milk, but infections via the respiratory tract and other routes cannot be excluded. As for certain other retroviruses, field observations suggest that in utero transmission may occasionally occur, but further studies are necessary to prove it. Young goats infected by ingestion of virus-containing milk may develop leukoencephalomyelitis with hind limb paralysis and occasional quadriplegia.11 More often, however, disease signs manifest themselves months or years later.

Pathogenesis

As for other lentiviruses, viral replication in tissue macrophages is the primary factor in the induction of encephalitis, pneumonia, arthritis and mastitis.

Following infection, CAEV persists in the host for life by integration of the viral DNA into the target cell’s genome and subsequent replication occurs at a low level in infected cells. As is common with other lentiviruses, infected animals may not develop clinical signs for months or years after infection. Although many cell types may be infected...

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