Caprine arthritis-encephalitis

Preferred citation: Anipedia, JAW Coetzer and P Oberem (Directors) In: Infectious Diseases of Livestock, JAW Coetzer, GR Thomson,
NJ Maclachlan and M-L Penrith (Editors). B G Murphy, D P Knowles and M A Highland, Caprine arthritis-encephalitis, 2018.
Caprine arthritis-encephalitis

Caprine arthritis-encephalitis

Previous authors: D WERLING AND W LANGHANS

Current authors:
B MURPHY - Associate Professor, DVM, PhD, Dip ACVP, VetMed PMI, 4206 VetMed, 3A One Shields Ave, Davis, California, USA
D P KNOWLES - Research Leader, DVM, PhD, DACVP, 405 Bustad Hall, Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington, WA 99164-7040, USA
M A HIGHLAND - Veterinary medical officer - Researcher/scientist, DVM, PhD, Diplomate ACVP, USDA-ARS-ADRU, ADBF 3033, Washington State University, Pullman, Washington, WA 99164-7040, USA


Caprine arthritis-encephalitis (CAE) is a persistent, progressive and multisystemic disease of goats caused by the lentivirus caprine arthritis-encephalitis virus (CAEV).  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 Genomically, CAEV is  very similar to the visna-maedi virus (VMV) of sheep , which had originally been described in Iceland as the aetiologic agent of chronic interstitial pneumonia (maedi, "breathlessness") and demyelinating leukoencephalomyelitis (visna, "wasting") (see Visna-maedi).42, 43

Compelling evidence gathered over the past ten years indicates that CAEV and VMV are able to cross species barriers and coinfect both sheep and goats. As a result of their phylogenetic proximity, similarities in disease pathogenesis, and natural interspecies transmission, these viruses are now collectively referred to as small ruminant lentiviruses (SRLV).32 In addition to domestic goats (Capra aegagrus hircus) and domestic sheep (Ovis aries), CAEV is capable of infecting wild small ruminants, such as ibex (Capra ibex) and mouflon (Ovis aries orientalis).14, 16, 24 The ability of SRLV to cross species barriers is unusual, as most lentiviruses have a limited ability to grow in cells from non-host species.5

Small ruminant lentiviruses have a tropism for four different tissue types - central nervous system (CNS) tissue (brain and spinal cord), joint synovium, lung, and mammary gland.   Viral tissue tropism, and resultant clinical signs, are relatively predictable for goats (CNS and synovial joints) and sheep (lung and CNS).  As a result of the cellular tropism for histiocytic cells, infection with this group of viruses  results in inflammatory syndromes, rather than immunodeficiency diseases, as typically seen with some other lentiviruses. The main clinical signs in young kids are ataxia, lameness, and paralysis caused by leukoencephalomyelitis. In older goats, the disease usually presents as a slowly progressive polyarthritis referred to as caprine arthritis, and occasionally as progressive interstitial pneumonia or chronic mastitis.


Caprine arthritis-encephalitis virus is a lentivirus within the Retroviridae family. Lentiviruses are slowly progressive, non-oncogenic viruses that cause chronic degenerative diseases with long incubation periods and life-long viral persistence.  Other lentiviruses include the human immunodeficiency virus (HIV), simian immunodeficiency virus (SIV), feline immunodeficiency virus (FIV), equine infectious anaemia virus (EIAV), and bovine immunodeficiency virus (BIV). Caprine arthritis-encephalitis virus isolation was initially reported in 1980 by two different research groups using explanted tissue obtained from virus-infected goats.10, 34

 Small ruminant lentiviruses are 80-100 nm in diameter and have a host cell-derived lipid bilayer surrounding core proteins encasing the viral genome.  The genomes of lentiviruses are composed of two single-stranded, 8.4-9.2 kb-long polyadenylated RNA molecules. In the early phase of infection, the viral RNA is converted into a double-stranded DNA form, known as the provirus, through the process of reverse transcription. 18 All lentiviruses share a similar genomic organization with gag, pol and env genes, and a varying number of regulatory and/or accessory 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, protease and integrase enzymes. 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.  In addition to gag, pol and rev, SRLV also have three accessory genes, vif, rev and a vpr-like gene (formerly known as tat).


The clinical signs of caprine arthritis were first reported in Switzerland in 1969.45, 52 Similar reports came from studies performed in Germany44 and Japan,33 and the encephalitic form was subsequently recognized in Germany44 and also recorded in the USA8 before the retroviral aetiology was discovered.10, 34 Caprine arthritis-encephalitis occurs almost worldwide.2 In some African countries, infection is limited to imported animals and their progeny.2 International movement of goats has been implicated as the major mechanism of virus dissemination.

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