caprine arthritis encephalitis
- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- caprine arthritis encephalitis
International Common Names
- English: CAEV infection; caprine arthritis encephalitis virus infection; caprine arthritis encephalomyelitis; caprine arthritis/encephalitis; caprine arthritis-encephalomyelitis, cae; hard udders in does; leukoencephalomyelitis
OverviewTop of page
Caprine arthritis-encephalitis virus (CAEV) is lentivirus within the group of small ruminant lentivirus (SRLV) in the family Retroviridae. The SRLV group also includes maedi-visna virus (MVV) [visna maedi virus] and ovine progressive pneumonia virus (OPPV). SRLV infections are life long in sheep and goats and are characterized by periods of latency, followed by recrudescence of virus replication. There are no known therapeutics and no commercially available vaccines. More than 70% of animals demonstrate sub-clinical (non-progressive, NP) disease and 30% of animals have moderate to severe, chronic recurrent (progressive, P) disease. Immunological control of SRLVs is associated with non-progressive status and is likely to be dependent on various factors including SRLV strain pathogenicity and tissue/cell tropisms, immunogenetics, and environmental conditions.
The original characterization of CAEV includes two primary disease manifestations: joint disease (arthritic form) and neurological disease (neurological form). The joint disease form manifests as chronic recurrent arthritis of primarily the carpi (Crawford et al., 1980). Clinically affected goats (progressors) are typically juvenile or adult animals that develop moderate to severe swelling of the bursa of the extensor carpal radialis tendon with variable involvement of the radiocarpal, middle carpal and carpometacarpal joints. Advanced lesions are characterized by marked synovial membrane hyperplasia with diffuse mononuclear cell infiltrates commonly accompanied by soft tissue mineralization and osteolysis. The neurological disease form of CAEV is characterized by leukoencephalomyelitis. It is primarily found in kids of 1-5 months of age and less commonly, adult goats (Cork et al., 1974; O'Sullivan et al., 1978; Norman and Smith, 1983). More recently, the reporting of neurological manifestation of CAEV, MVV and OPPV has declined, which may be a reflection of virus-host adaptation or control measures aimed to reduce neonatal transmission. Other clinical manifestations of CAEV in goats can occur alone or in combination with the primary disease manifestations and include cachexia, weight loss, chronic pneumonia with dyspnoea and mastitis (Phelps and Smith, 1993; Ellis et al., 1988; Cork et al., 1974).
CAEV infection is diagnosed by clinical signs and the detection of serum antibodies. The commonest used serological antibody detection systems include enzyme-linked immunosorbent assays (ELISA) or agar gel immunodiffusion assay (AGID). A recently developed and validated competitive inhibition ELISA for CAEV has shown higher sensitivity than the AGID test (Knowles et al., 1994; Özyörük et al., 2001; Herrmann et al., 2003). However, there is a potential for false negatives and positives using these diagnostic techniques. The number of false negatives depends upon the antigenic similarity of the infecting CAEV strain and the CAEV strain used in the diagnostic test. In addition, false positives may occur due to the presence of passively transferred maternal antibodies in kids less than 1 year of age. Moreover, delayed seroconversion has been reported in sheep and goats infected with SRLV. Given these issues with serological diagnostic tests, there is a need to develop and employ ancillary methods of confirming CAEV infection before death of the animal. Efforts to develop and validate some new tests such as the polymerase chain reaction (PCR) detection of integrated provirus and immunohistochemical detection of viral antigens will be discussed.
The primary mode of transmission of CAEV is through ingestion of colostrum/ milk following birth (Adams et al., 1983), however horizontal transmission between adult goats has been reported (Rowe et al., 1992a). The relative contribution of NP and P goats to transmission of CAEV is not known. However, it is generally believed that both groups of CAEV-infected goats serve as potential reservoirs of CAEV. Therefore, control measures include serological testing of adult goats and separation or elimination of seropositive animals, and heat inactivation of colostrum or milk (56ºC for 1 h) from CAEV-positive nannies.
CAEV and OPPV/MVV have similar modes of transmission. And since genetic information is indicating that CAEV can infect sheep and OPPV/MVV can infect goats under natural conditions, eradication of CAEV will need to include eradication efforts for OPPV/MVV as well.
This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Capra hircus (goats)||Domesticated host||Sheep & Goats: All Stages|
Hosts/Species AffectedTop of page
Caprine arthritis-encephalitis virus (CAEV) transmits between goats mainly through colostrum and milk secretions (Adams et al., 1983; Rowe et al., 1992b). In sheep, maedi-visna virus (MVV) transmits by colostrum/milk and/or respiratory secretions (Sigurdsson et al., 1953; Houwers et al., 1983). Studies focusing on genomic and phylogenetic analysis of small ruminant lentivirus (SRLV) suggested that CAEV can naturally infect sheep and MVV can naturally infect goats (Leroux et al., 1997; Zanoni 1998; Rolland et al., 2002; Shah et al., 2004). CAEV can infect sheep, and MVV can infect goats in an experimental setting (Banks et al., 1983), and lambs can be infected with milk from CAEV-infected does (Oliver et al., 1985). Given similar transmission sources and the results of experimental transmission, it is plausible that CAEV could infect sheep naturally. In naturally infected goats, persistent infections with both CAEV and MVV have been described, and viral chimeras generated by recombination between these variants have been detected (Pisoni et al., 2007; Cruz et al., 2013). In cases where sheep and goats are commonly housed together, a combination of CAEV and MVV/OPP prevention and control methods are advised.
Systems AffectedTop of page bone, foot diseases and lameness in small ruminants
digestive diseases of small ruminants
mammary gland diseases of small ruminants
nervous system diseases of small ruminants
reproductive diseases of small ruminants
respiratory diseases of small ruminants
urinary tract and renal diseases of small ruminants
DistributionTop of page
The global distribution of caprine arthritis-encephalitis virus (CAEV) is reported by OIE and is based upon serological and/or virological evidence of CAEV.
CAEV is typically found in countries that routinely serologically test for the virus. Countries that are not listed as having CAEV present do not routinely serologically test for CAEV. In 1984, a global CAEV survey was performed where serum samples came from 112 different locations around the world. At that time, 90% of the positive CAEV AGID tests came from Canada, France, Norway, Switzerland and the USA (Adams et al., 1984). In 2003, these same countries reported the presence but not the percentage of CAEV infection in their goatherds.
Regional seroprevalence studies of CAEV have been performed in the USA and Australia. In 1992, 3790 goats from 28 states in the USA were tested for CAEV using AGID, and 31% tested positive (Cutlip et al., 1992). In Australia in 1995, seroprevalence of CAEV in New South Wales was examined in 1484 goats in 14 dairy herds and 56.8% were CAEV-positive using an ELISA (Greenwood et al., 1995).
For current information on disease incidence, see OIE's WAHID Interface.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Afghanistan||No information available||OIE, 2009|
|Armenia||Disease not reported||OIE, 2009|
|Azerbaijan||Disease not reported||OIE, 2009|
|Bahrain||Disease never reported||OIE, 2009|
|Bangladesh||No information available||OIE, 2009|
|Bhutan||Disease never reported||OIE, 2009|
|Brunei Darussalam||Disease not reported||OIE Handistatus, 2005|
|Cambodia||No information available||OIE, 2009|
|China||No information available||OIE, 2009|
|-Hong Kong||Disease never reported||OIE, 2009|
|Georgia (Republic of)||Disease never reported||OIE Handistatus, 2005|
|India||Disease never reported||OIE, 2009|
|Indonesia||Disease never reported||OIE, 2009|
|Iran||No information available||OIE, 2009|
|Iraq||No information available||OIE, 2009|
|Japan||Disease not reported||OIE, 2009|
|Jordan||Disease never reported||OIE, 2009|
|Kazakhstan||Disease never reported||OIE, 2009|
|Korea, DPR||Disease not reported||OIE Handistatus, 2005|
|Korea, Republic of||Disease not reported||OIE, 2009|
|Kuwait||Disease not reported||OIE, 2009|
|Kyrgyzstan||Disease not reported||OIE, 2009|
|Laos||Disease never reported||OIE, 2009|
|Lebanon||Disease not reported||OIE, 2009|
|Malaysia||Disease never reported||OIE, 2009|
|-Peninsular Malaysia||Disease never reported||OIE Handistatus, 2005|
|-Sabah||Disease never reported||OIE Handistatus, 2005|
|-Sarawak||Disease never reported||OIE Handistatus, 2005|
|Mongolia||No information available||OIE, 2009|
|Myanmar||Disease never reported||OIE, 2009|
|Nepal||Disease never reported||OIE, 2009|
|Oman||Disease not reported||OIE, 2009|
|Pakistan||Disease not reported||OIE, 2009|
|Philippines||No information available||OIE, 2009|
|Qatar||No information available||OIE, 2009|
|Saudi Arabia||Disease not reported||OIE, 2009|
|Singapore||Disease not reported||OIE, 2009|
|Sri Lanka||Disease never reported||OIE, 2009|
|Syria||Disease not reported||OIE, 2009|
|Taiwan||Reported present or known to be present||OIE Handistatus, 2005|
|Tajikistan||Disease not reported||OIE, 2009|
|Turkey||No information available||OIE, 2009|
|Turkmenistan||Disease not reported||OIE Handistatus, 2005|
|United Arab Emirates||No information available||OIE, 2009|
|Uzbekistan||Disease never reported||OIE Handistatus, 2005|
|Vietnam||Disease never reported||OIE, 2009|
|Yemen||No information available||OIE, 2009|
|Algeria||Disease not reported||OIE, 2009|
|Angola||No information available||OIE, 2009|
|Benin||Disease not reported||OIE, 2009|
|Botswana||Disease not reported||OIE, 2009|
|Burkina Faso||No information available||OIE, 2009|
|Burundi||Disease never reported||OIE Handistatus, 2005|
|Cameroon||No information available||OIE Handistatus, 2005|
|Cape Verde||Disease never reported||OIE Handistatus, 2005|
|Central African Republic||Disease not reported||OIE Handistatus, 2005|
|Chad||No information available||OIE, 2009|
|Congo||No information available||OIE, 2009|
|Congo Democratic Republic||No information available||OIE Handistatus, 2005|
|Côte d'Ivoire||Disease never reported||OIE Handistatus, 2005|
|Djibouti||Disease not reported||OIE, 2009|
|Egypt||Disease never reported||OIE, 2009|
|Eritrea||No information available||OIE, 2009|
|Ethiopia||No information available||OIE, 2009|
|Gabon||No information available||OIE, 2009|
|Gambia||No information available||OIE, 2009|
|Ghana||No information available||OIE, 2009|
|Guinea||Disease never reported||OIE, 2009|
|Guinea-Bissau||No information available||OIE, 2009|
|Kenya||Disease not reported||OIE, 2009|
|Lesotho||Disease not reported||OIE, 2009|
|Libya||No information available||OIE Handistatus, 2005|
|Madagascar||Disease never reported||OIE, 2009|
|Malawi||Disease never reported||OIE, 2009|
|Mali||No information available||OIE, 2009|
|Mauritius||Disease never reported||OIE, 2009|
|Morocco||No information available||OIE, 2009|
|Mozambique||Disease not reported||OIE, 2009|
|Namibia||Disease never reported||OIE, 2009|
|Nigeria||Disease never reported||OIE, 2009|
|Réunion||Disease never reported||OIE Handistatus, 2005|
|Rwanda||No information available||OIE, 2009|
|Sao Tome and Principe||No information available||OIE Handistatus, 2005|
|Senegal||No information available||OIE, 2009|
|Seychelles||No information available||OIE Handistatus, 2005|
|Somalia||No information available||OIE Handistatus, 2005|
|South Africa||Disease never reported||OIE, 2009|
|Sudan||Disease never reported||OIE, 2009|
|Swaziland||Disease never reported||OIE, 2009|
|Tanzania||No information available||OIE, 2009|
|Togo||No information available||OIE, 2009|
|Tunisia||Disease not reported||OIE, 2009|
|Uganda||No information available||OIE, 2009|
|Zambia||No information available||OIE, 2009|
|Zimbabwe||Disease not reported||OIE, 2009|
|Bermuda||Disease not reported||OIE Handistatus, 2005|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Disease not reported||OIE, 2009|
Central America and Caribbean
|Barbados||Disease not reported||OIE Handistatus, 2005|
|Belize||Disease never reported||OIE, 2009|
|British Virgin Islands||Disease not reported||OIE Handistatus, 2005|
|Cayman Islands||Disease not reported||OIE Handistatus, 2005|
|Costa Rica||Absent, reported but not confirmed||OIE, 2009|
|Cuba||Disease never reported||OIE, 2009|
|Curaçao||Disease not reported||OIE Handistatus, 2005|
|Dominica||Disease not reported||OIE Handistatus, 2005|
|Dominican Republic||Disease not reported||OIE, 2009|
|El Salvador||Disease not reported||OIE, 2009|
|Guadeloupe||No information available||OIE, 2009|
|Haiti||Absent, reported but not confirmed||OIE, 2009|
|Honduras||No information available||OIE, 2009|
|Jamaica||Disease not reported||OIE, 2009|
|Martinique||Disease not reported||OIE, 2009|
|Nicaragua||Disease never reported||OIE, 2009|
|Saint Kitts and Nevis||Reported present or known to be present||OIE Handistatus, 2005|
|Saint Vincent and the Grenadines||Disease not reported||OIE Handistatus, 2005|
|Trinidad and Tobago||Last reported||1996||OIE Handistatus, 2005|
|Bolivia||Disease never reported||OIE, 2009|
|Colombia||Disease not reported||OIE, 2009|
|Ecuador||Disease never reported||OIE, 2009|
|Falkland Islands||Disease never reported||OIE Handistatus, 2005|
|French Guiana||Disease not reported||OIE, 2009|
|Guyana||Disease never reported||OIE Handistatus, 2005|
|Paraguay||No information available||OIE Handistatus, 2005|
|Peru||No information available||OIE, 2009|
|Uruguay||Disease never reported||OIE, 2009|
|Venezuela||Disease not reported||OIE, 2009|
|Albania||No information available||OIE, 2009|
|Andorra||No information available||OIE Handistatus, 2005|
|Austria||No information available||OIE, 2009|
|Belarus||Disease never reported||OIE, 2009|
|Belgium||Disease not reported||OIE, 2009|
|Bosnia-Hercegovina||Disease not reported||OIE Handistatus, 2005|
|Bulgaria||Disease not reported||OIE, 2009|
|Croatia||Disease not reported||OIE, 2009|
|Czech Republic||Disease not reported||OIE, 2009|
|Denmark||Absent, reported but not confirmed||OIE, 2009|
|Estonia||Disease never reported||OIE, 2009|
|Finland||Disease never reported||OIE, 2009|
|France||No information available||OIE, 2009|
|Germany||Disease not reported||OIE, 2009|
|Greece||Disease not reported||OIE, 2009|
|Hungary||Disease not reported||OIE, 2009|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease not reported||OIE, 2009|
|Isle of Man (UK)||Disease never reported||OIE Handistatus, 2005|
|Italy||No information available||OIE, 2009|
|Jersey||Disease never reported||OIE Handistatus, 2005|
|Latvia||Disease not reported||OIE, 2009|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Disease never reported||OIE, 2009|
|Luxembourg||Disease never reported||OIE, 2009|
|Macedonia||Absent, reported but not confirmed||OIE, 2009|
|Moldova||Disease never reported||OIE Handistatus, 2005|
|Montenegro||Disease not reported||OIE, 2009|
|Norway||Disease not reported||OIE, 2009|
|Poland||Disease never reported||OIE, 2009|
|Russian Federation||Disease never reported||OIE, 2009|
|Serbia||Disease not reported||OIE, 2009|
|Slovakia||Disease not reported||OIE, 2009|
|Slovenia||Disease not reported||OIE, 2009|
|Spain||Restricted distribution||OIE, 2009|
|UK||Disease not reported||OIE, 2009|
|-Northern Ireland||Disease never reported||OIE Handistatus, 2005|
|Ukraine||Disease not reported||OIE, 2009|
|Yugoslavia (former)||No information available||OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||Disease not reported||OIE Handistatus, 2005|
|French Polynesia||Disease not reported||OIE, 2009|
|New Caledonia||Disease never reported||OIE, 2009|
|New Zealand||Present||OIE, 2009|
|Samoa||Disease never reported||OIE Handistatus, 2005|
|Vanuatu||Disease never reported||OIE Handistatus, 2005|
|Wallis and Futuna Islands||No information available||OIE Handistatus, 2005|
PathologyTop of page
Caprine arthritis-encephalitis virus (CAEV) infection results in an immunopathological disease affecting primarily the bursa of the extensor carpal radialis tendon and the radiocarpal, middle carpal and carpometacarpal joints (Cheevers and McGuire, 1988), although involvement of tarsal, stifle, fetlock and atlanto-occipital joints and associated tendon bursa are less commonly affected. Infection with CAEV results in systemic lymphocyte activation and proliferation in lymphoid tissue (lymphoid hyperplasia). CD45R+ CD5- B lymphocytes and IgG-positive plasma cells are the principal mononuclear cell types found in perivascular infiltrates of the radiocarpel joint synovium of progressor goats (Wilkerson et al., 1995a). The titre of antibody to CAEV surface envelope glycoprotein (SU) in the serum and synovial fluid correlates and predicts with the severity of lesions in the radiocarpel joint of CAEV-infected goats (Johnson et al., 1983; Knowles et al., 1990). Moreover, the dominant serum antibody isotype response to SU at the time of seroconversion predicts which goats will become symptomatic progressor goats where a predominance of IgG1 is found early in CAEV infection in eventual progressor goats and increased anti-SU IgG2 is found in eventual nonprogressors (Trujillo et al., 2004a). Results suggest that isotype-specific immunoglobulin production to SU may contribute to the pathogenesis of CAEV-induced arthritis.
CAEV replicates in cells of the monocytes/macrophage lineage (Anderson et al., 1983). Using in situ hybridization, CAEV RNA has been identified in cells consistent with macrophage morphology in the brain, spinal cord, lung, joints and mammary gland of naturally CAEV-infected goats (Zink et al., 1990). Others have later shown that proviral DNA is found in cells consistent with macrophages, microglia, astrocytes, oligodendrocytes, ependymal epithelium and choroid plexus (Sanna et al., 1999). Using rabbit antiserum to recombinant capsid and matrix proteins, some have had some success in identifying CAEV-infected cell types consistent with macrophage morphology in brain, spinal cord, lung, mammary gland, and lymph nodes (Storset et al., 1997). Identification of CAEV capsid-positive cells in the synovial fluid of CAEV-infected goats has been shown (Cheevers et al., 1994). Other specific cell-types that propagate CAEV infection in vitro include the following: synovial membrane cells, peripheral blood monocytes/macrophages, microglia, endothelial cells, mammary epithelial cells, granulosa cells and fibroblasts (Adams et al., 1980; Klevjer-Anderson and Cheevers, 1981; Klevjer-Anderson and Anderson, 1982; Anderson et al., 1983; Baszler et al., 1994; Adeyemo et al., 1996; Chebloune et al., 1996; Silva Teixeira et al., 1997; Lerondelle et al., 1999; Mselli-Lakhal et al., 2001; Lamara et al., 2001; Lechat et al., 2005).
DiagnosisTop of page
Clinical signs and the detection of antibodies to caprine arthritis-encephalitis virus (CAEV) in serum are the main techniques for CAEV diagnosis. Differential diagnosis exists for clinical signs caused by CAEV infection.
Clinical characterization of CAEV progressor status (chronic arthritis goats) and non-progressor status (asymptomatic goats) is subjective and depends primarily on the severity of arthritis. Adult CAEV progressor goats may exhibit debilitating lameness or severe arthritis and may show swelling of the carpel bursa, middle carpel and distal carpal joints or ‘water knee’. Other clinical signs associated with arthritis include lameness, reluctance to move and general recumbency. Radiographs can be very useful for identifying soft tissue mineralization osteoarthritis accompanied by osteolysis. There is a good correlation between radiographic abnormalities and the severity of the joint lesions (Woodard et al., 1982). A ratio of the circumference of the carpel and metacarpal (C/MC) regions is greater than 2.0 is a good clinical indicator of inflammatory radiocarpel lesions caused by CAEV infection and has been used to define progressor goats. However, in studies involving experimental infection C/MC ratios of greater than 2.0 typically occur 1-2 years after inoculation (Cheevers et al., 1988; Wilkerson et al., 1995b; Trujillo et al., 2004a).
Other clinical disease syndromes caused by CAEV infection in adult goats can occur singularly or in conjunction with CAEV-induced arthritis. These include mastitis or ‘hard-bag’ and chronic pneumonia characterized by dyspnoea. Kids experiencing encephalomyelitis typically display progressive hind-limb ataxia, paresis and paralysis; however, numerous non-specific clinical signs associated with white matter destruction and motor dysfunction are reported. Pneumonia presented as dyspnoea has been reported to occur with the neurological form of CAEV.
If only postmortem investigation is available for diagnosis, gross and histological evaluation of target tissues (synovial lining of the carpal joints and bursa of the extensor carpal radialis tendon, central nervous system, mammary gland, lung, and lymph nodes) can be used to support the diagnosis of CAEV. Arthritis is characterized by mononuclear inflammation within the synovial lining and surrounding supportive tissue, proliferation of the synovium accompanied by oedema and necrosis in severe lesions. A semi-quantitative grading system for lesion severity in the radiocarpel joint has been developed for research studies (Cheevers et al., 2003). CNS lesions occur in the brain and spinal cord and include mild to moderate mononuclear meningoencephalitis including involvement of the choroid plexus, white matter gliosis, demyelination, oedema and hyperemia. Mammary gland lesions consist of minimal to severe infiltrates of mononuclear inflammatory cells in the periductal and periacinar stroma where severe lesions consist of coalescing infiltrates of inflammatory cells, lymphoid follicle formation, stroma oedema and fibrosis and inspissation or mineralization of duct contents (Cheevers et al., 1988). Lung lesions are generally mild to moderate and include interstitial infiltrates of mononuclear inflammatory cells predominately around airways and the pulmonary vasculature accompanied by variable hyperplasia of the respiratory epithelium. Typically in progressor goats there is marked hyperplasia of the lymphoid cells in the axillary and prescapular lymph nodes, which in severe cases can efface the normal nodal architecture.
Differential diagnoses for CAEV-induced disease were reported by East (2002). Differential diagnoses for the neurological form of CAEV in goat kids include, but are not limited to, copper deficiency, lumbar cord abscesses, selenium and vitamin E deficiency, bacterial septicemia, septic arthritis or spinal cord injury. Differential diagnoses of the arthritic form of CAEV include septic arthritis, Chlamydia- and Mycoplasma-induced arthritis, and trauma. On occasion, the respiratory and cachexia forms of CAEV will manifest without clinical arthritis or encephalitis. The chronic form of pneumonia needs to be differentiated from lungworm infection, chronic bacterial pneumonia and pulmonary abscesses. The mastitis form of CAEV is often observed with the arthritic form of CAEV. The two primary differentials for mastitis in goats include bacterial infections and CAEV.
Serological tests, PCR tests, immunohistochemical detection of CAEV antigens, and virus isolation are the four laboratory diagnostic tests used to confirm CAEV.
The presence of antibodies to CAEV in the serum of infected adult goats confirms infection and is the most reliable laboratory test. Serological diagnosis can be made using a variety of tests including Western blot analysis, immunoprecipitation (IP) of [35S] methionine/cysteine-labeled CAEV, agar gel immunodiffusion assay, and ELISA. Western blot analysis and IP are typically used as confirmatory serological tests and are performed in a research laboratory setting. The CAEV AGID tests for the presence of antibody to the CAEV capsid protein, p28, and surface envelope glycoprotein, gp135; however, if the ovine progressive pneumonia virus (OPPV) AGID is used instead of the CAEV AGID with goat sera, approximately 40% of CAEV-positive goats will show negative (Knowles et al., 1994). ELISA tests are most commonly used for serological diagnosis, but some have better sensitivities and specificities than others do. Many ELISAs have been produced using whole CAEV and recombinant CAEV proteins (Simard et al., 2001; Clavijo and Thorsen, 1995; Rimstad et al., 1994; Celer et al., 1993; Heckert et al., 1992; Zanoni et al., 1991; Archambault et al., 1988). Indirect ELISAs are more problematic due to the dilutions required to lower background effects, which also increases the number of false negatives. The CAEV competitive inhibition ELISA (cELISA) does not require dilution of the sera before testing and since it depends on the presence of serological antibodies to bind to CAEV envelope glycoprotein (SU) and inhibit the binding of a monoclonal antibody to SU, the CAEV cELISA has a sensitivity of 100% and specificity of 96.4% when compared with IP (Herrmann et al., 2003). The CAEV cELISA offers a higher sensitivity than CAEV AGID when compared to IP (Knowles et al., 1994; Herrmann et al., 2003). However, the CAEV cELISA (96.4%) has a slightly lower specificity than CAEV AGID (100%), but this may be due to the increased sensitivity of the CAEV cELISA. Overall, results of CAEV serological tests are dependent on the infecting strain of CAEV; goats infected with a similar strain as the strain used in the serological test will test positive while goats infected with a markedly different strain of CAEV will test negative. If the animal has clinical signs of CAEV but tests negative in initial serological testing, different serological tests and other ancillary tests are advised. Moreover, a CAEV-seropositive kid goat, less than 1 year in age may be affected by passive transfer of material antibody, but may not necessarily be infected. Therefore, seropositive kid goats not displaying neurological disease or pneumonia should be tested by other means such as the PCR method described below.
PCR-based laboratory diagnostic tests for the detection of provirus in peripheral blood leukocytes (PBL) or peripheral blood mononuclear cells (PBMC) are becoming more common (Reddy et al., 1993; Rimstad et al., 1993; Barlough et al., 1994; Leroux et al., 1997; Wagter et al., 1998; Konishi et al., 2004). In addition, tissues and fluids such as brain, bone marrow, mammary gland, uterus, oviduct, seminal fluid, synovial membranes, lung, spinal cord, and lymph nodes have been found PCR-positive for CAEV in CAEV-infected goats (Barlough et al., 1994; Leroux et al., 1995; Travassos et al., 1998; Sanna et al., 1999; Fieni et al., 2003). At this time, PCR tests are considered secondary tests to serology. Some have found that PCR detection of CAEV provirus in peripheral blood mononuclear cells may precede seroconversion or antibody responses (Rimstad et al., 1993; Reddy et al., 1993); however, since false PCR positives are common, precautions are needed to reduce contamination and positives should be sequenced until the assay is optimized and validated (Zanoni et al., 1996). PCR diagnostic tests for CAEV have yet to be validated and, like serologic diagnostic tests, the sensitivity and specificity of PCR detection of CAEV depends upon sequence similarity of the infective provirus and the sequence used to develop primers. Therefore, primers for PCR amplification of CAEV provirus needs to be designed to amplify regions of the provirus with high similarity or regions conserved within all known small ruminant lentivirus (SRLV) provirus sequences. Although once optimized and validated, PCR tests for provirus in PBL or PBMC show promise in becoming an early indicator of CAEV-infection and may prove useful as a live-animal, confirmatory laboratory test.
Few studies have been published regarding immunohistochemical (IHC) detection of CAEV-infection in goats. CAEV-infected synovial cells in synovial fluid of CAEV-infected goats have been identified by immunohistochemical detection using monoclonal antibody 10A1, which binds to a capsid protein (p28) of CAEV (McGuire et al., 1987; Cheevers et al., 1994). Results of this study suggest that IHC could be used as a confirmatory test for CAEV-induced arthritis in live animals. Storset et al. (1997) identified CAEV-infected cells in brain, spinal cord, lung, mammary gland and lymph node tissues embedded in paraffin wax, followed by immunohistochemical detection using rabbit antiserum to recombinant capsid and matrix proteins. Results of this study suggest that IHC could be used as a postmortem test for CAEV-induced encephalitis, pneumonia, and mastitis. At present, there have been no dual immunohistochemical or immunofluorescence studies performed in situ identifying specific cell types in the joint, mammary gland, lung, lymph nodes, brain, or spinal cord that accumulate CAEV. This is presumably due to the low levels of replicating virus within macrophages, or the lack of adequate sampling in tissues.
Virus isolation is often performed in a research setting due to the high degree of technical difficulty and lack of sensitivity. Free viremia rarely or never occurs in CAEV-infected goats and isolation of virus from synovial fluid is sporadic. Therefore, suspected CAEV-infected cells or tissues are co-cultured with newborn goat synovial membrane cells for up to 6 weeks (Crawford et al., 1980). Synovial tissue from CAEV-infected goats can be cultured directly for up to 6 weeks. Mammary and peripheral blood mononuclear cells can be successfully co-cultured with goat synovial membrane cells (Cork and Narayan, 1980; Klevjer-Anderson et al., 1984; Kennedy-Stoskopf et al., 1985).
List of Symptoms/SignsTop of page
|Cardiovascular Signs / Arrhythmia, irregular heart rate, pulse||Sheep & Goats:All Stages||Sign|
|Cardiovascular Signs / Bradycardia, slow heart beat or pulse||Sheep & Goats:All Stages||Sign|
|Cardiovascular Signs / Ventricular tachycardia, multifocal or unifocal||Sheep & Goats:All Stages||Sign|
|Digestive Signs / Abdominal distention||Sheep & Goats:All Stages||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Decreased borborygmi, gut sounds, ileus||Sheep & Goats:All Stages||Sign|
|Digestive Signs / Difficulty in prehending or chewing food||Sheep & Goats:All Stages||Sign|
|Digestive Signs / Dysphagia, difficulty swallowing||Sign|
|General Signs / Abnormal proprioceptive positioning, knuckling||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Exercise intolerance, tires easily||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Sign|
|General Signs / Forelimb atrophy, wasting||Sign|
|General Signs / Forelimb lameness, stiffness, limping fore leg||Sign|
|General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area||Sign|
|General Signs / Forelimb weakness, paresis, paralysis front leg||Sign|
|General Signs / Generalized lameness or stiffness, limping||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Sign|
|General Signs / Head, face, ears, jaw weakness, droop, paresis, paralysis||Sign|
|General Signs / Hemiparesis||Sheep & Goats:All Stages||Diagnosis|
|General Signs / Hindlimb atrophy, wasting||Sign|
|General Signs / Hindlimb lameness, stiffness, limping hind leg||Sign|
|General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Sheep & Goats:All Stages||Sign|
|General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia||Sign|
|General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia||Sign|
|General Signs / Neck weakness, paresis, paralysis, limp, ventroflexion||Sheep & Goats:All Stages||Diagnosis|
|General Signs / Opisthotonus||Sign|
|General Signs / Paraparesis, weakness, paralysis both hind limbs||Sign|
|General Signs / Reluctant to move, refusal to move||Sheep & Goats:All Stages||Sign|
|General Signs / Tetraparesis, weakness, paralysis all four limbs||Sign|
|General Signs / Torticollis, twisted neck||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weakness of one hindlimb, paresis paralysis rear leg||Sign|
|General Signs / Weight loss||Sign|
|Musculoskeletal Signs / Back spasms, myoclonus||Sheep & Goats:All Stages||Sign|
|Musculoskeletal Signs / Decreased mobility of forelimb joint, arthrogryposis front leg||Sign|
|Musculoskeletal Signs / Decreased mobility of hindlimb joint, arthrogryposis rear leg||Sign|
|Musculoskeletal Signs / Decreased, absent mobility, back region or joints||Sheep & Goats:All Stages||Diagnosis|
|Nervous Signs / Abnormal behavior, aggression, changing habits||Sign|
|Nervous Signs / Abnormal forelimb reflexes, increased or decreased||Sign|
|Nervous Signs / Abnormal hindlimb reflexes, increased or decreased||Sign|
|Nervous Signs / Circling||Sign|
|Nervous Signs / Coma, stupor||Sheep & Goats:All Stages||Diagnosis|
|Nervous Signs / Disoriented, memory loss||Sheep & Goats:All Stages||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Excessive or decreased sleeping||Sheep & Goats:All Stages||Sign|
|Nervous Signs / Excitement, delirium, mania||Sheep & Goats:All Stages||Sign|
|Nervous Signs / Forelimb hypoesthesia, anesthesia front leg||Sign|
|Nervous Signs / Head pressing||Sheep & Goats:All Stages||Diagnosis|
|Nervous Signs / Head tilt||Sign|
|Nervous Signs / Head, face, neck, tongue hypoesthesia, anesthesia||Sign|
|Nervous Signs / Hindlimb hypoesthesia, anesthesia rear leg||Sign|
|Nervous Signs / Hyperesthesia, irritable, hyperactive||Sign|
|Nervous Signs / Hypertonia of muscles, myotonia||Sheep & Goats:All Stages||Diagnosis|
|Nervous Signs / Muscle hypotonia||Sheep & Goats:All Stages||Diagnosis|
|Nervous Signs / Seizures or syncope, convulsions, fits, collapse||Sheep & Goats:All Stages||Sign|
|Nervous Signs / Tremor||Sign|
|Ophthalmology Signs / Abnormal pupillary response to light||Sign|
|Ophthalmology Signs / Blindness||Sign|
|Ophthalmology Signs / Decreased or absent menace response but not blind||Sheep & Goats:All Stages||Sign|
|Ophthalmology Signs / Miosis, meiosis, constricted pupil||Sheep & Goats:All Stages||Sign|
|Ophthalmology Signs / Mydriasis, dilated pupil||Sheep & Goats:All Stages||Sign|
|Ophthalmology Signs / Nystagmus||Sign|
|Ophthalmology Signs / Strabismus||Sign|
|Pain / Discomfort Signs / Forelimb pain, front leg||Sheep & Goats:Hogget,Sheep & Goats:Gimmer,Sheep & Goats:Mature female,Sheep & Goats:Breeding male||Diagnosis|
|Pain / Discomfort Signs / Hindlimb pain, hind leg||Sheep & Goats:Hogget,Sheep & Goats:Gimmer,Sheep & Goats:Mature female,Sheep & Goats:Breeding male||Sign|
|Pain / Discomfort Signs / Pain mammary gland, udder||Sheep & Goats:Mature female||Sign|
|Pain / Discomfort Signs / Pain, neck, cervical, throat||Sheep & Goats:All Stages||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Sign|
|Reproductive Signs / Anestrus, absence of reproductive cycle, no visible estrus||Sign|
|Reproductive Signs / Edema of mammary gland, udder||Sheep & Goats:Mature female||Sign|
|Reproductive Signs / Firm mammary gland, hard udder||Sign|
|Reproductive Signs / Firm mammary gland, hard udder||Sign|
|Reproductive Signs / Galactorrhea, inappropriate milk production||Sheep & Goats:Mature female||Sign|
|Reproductive Signs / Mastitis, abnormal milk||Sheep & Goats:Mature female||Diagnosis|
|Reproductive Signs / Slough of mammary gland, udder||Sheep & Goats:Mature female||Sign|
|Reproductive Signs / Warm mammary gland, hot, heat, udder||Sheep & Goats:All Stages||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Sheep & Goats:All Stages||Diagnosis|
|Respiratory Signs / Coughing, coughs||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Sign|
|Urinary Signs / Dysuria, difficult urination, stranguria||Sheep & Goats:All Stages||Sign|
|Urinary Signs / Oliguria or anuria, retention of urine||Sheep & Goats:All Stages||Sign|
|Urinary Signs / Urinary incontinence, dribbling urine||Sheep & Goats:All Stages||Sign|
Disease CourseTop of page
Adult goats naturally infected with caprine arthritis-encephalitis virus (CAEV) typically segregate into 2 groups: non-progressor (NP) (70%) and progressor goats (P) (30%) (Woodard et al., 1982). NP goats generally remain asymptomatic and develop humoral and cellular responses to CAEV antigens; however, NP goats can experience mild mastitis and loss of body condition. However, progressor goats become severely arthritic and may incur some lameness by sexual maturity (Woodard et al., 1982; Phelps and Smith, 1993). Typical signs of CAEV infection such as chronic arthritis, mastitis, cachexia, dyspnoea and chronic pneumonia are considered progressive, although intermittent disease can occur (Mdurvwa et al., 1994; Phelps and Smith, 1993; Ellis et al., 1988; Kennedy-Stoskopf et al., 1985). The course of disease is variable in progressors, with some animals showing mild to moderate lameness for years and others showing acute rapid progression leading to marked restriction of movement (Cheevers et al., 1988).
The neurological form of CAEV typically occurs in kids of 1-5 months of age where the primary clinical signs include depression, head tilt, torticollis and circling; however, CAEV infection in adult and juvenile goats can manifest as neurological disease (Norman and Smith, 1983; Phelps and Smith, 1993). Encephalomyelitis can be accompanied by chronic pneumonia manifested as dyspnoea and weight loss. The neurological form of CAEV is less frequently reported in CAEV-infected goats.
EpidemiologyTop of page
Routes of transmission of CAEV are reviewed by Peterhans et al. (2004). Colostrum and milk are considered to be of prime importance in the transmission of CAEV from mother to offspring (Adams et al., 1983; East et al., 1993). Aerosol transmission between animals of all ages in close contact and over distances of up to several metres appears to be a significant route of spread both within and between flocks and herds, particularly under intensive housing or grazing conditions (East et al., 1993). The significance of intrauterine viral transmission is unclear. Semen has been shown to contain CAEV (Travassos et al., 1998) and Souza et al. (2013) demonstrated that the virus can be transmitted through artificial insemination with infected semen. Transmission by contaminated milking machines or buckets is considered to be a risk factor (Adams et al., 1983; Lerondelle et al., 1995). Humans may also contribute to the spread of infection by not changing clothing, boots and equipment when dealing with infected and unifected flocks (Greenwood et al., 1995). Live animal trading is considered a major risk factor in the spread of CAEV infection between herds (Contreras et al., 1998).
Impact: EconomicTop of page
Disease caused by caprine arthritis-encephalitis virus (CAEV) is on the List of Diseases Notifiable to the World Organisation for Animal Health (OIE). These diseases are considered to be of socioeconomic and/or public health importance within countries and are significant in the international trade of animals and animal products. CAEV causes economic losses to the goat producer primarily due to the lack of goat exports in territories or countries that have high seroprevalence of CAEV. In addition, there have been significant associations made between positive CAEV serology and overall goat production and butterfat production in goatherds in the USA (Smith and Cutlip, 1988). A Spanish study of milk production losses associated with CAEV infection found that test-day milk yield was 10% less in seropositive compared to seronegative does (Martínez-Navalón et al., 2013).
Zoonoses and Food SafetyTop of page
Caprine arthritis-encephalitis virus (CAEV) is not considered a zoonotic disease, and there are no regulations regarding human food safety and CAEV.
Disease TreatmentTop of page
Currently, antiretroviral therapy is impractical in a field setting, and treatment is directed at the signs it causes rather than the virus itself. No cures are available for any known lentiviral infection.
Prevention and ControlTop of page
Immunization and vaccines
There are no commercially available vaccines for caprine arthritis-encephalitis virus (CAEV) infection. In research settings, various vaccination strategies have been tested using niaive goats as an animal model for HIV vaccine development. These studies used inactivated CAEV, vaccinia-based CAEV genes with and without vaccinia-based cytokine genes, and plasmid-based CAEV genes with and without plasmid-based cytokine genes followed by challenge using CAEV molecular clones or CAEV field isolates (McGuire et al., 1986; Russo et al., 1993; Vitu et al., 1993; Cheevers et al., 1994; Cheevers et al., 2003). Most of these vaccination strategies have failed to protect against challenge. However, plasmid DNA vaccinations encoding CAEV SU followed by a boost with viral SU in Freund's incomplete adjuvant (SU-FIA) provided protection in 4 of 4 goats based upon the absence of severe radiocarpel joint lesions and lower provirus loads in the radiocarpel joint (Cheevers et al., 2003). More recently, a protein-based vaccination strategy using an engineered SU mutated at two sites E542N and R539S (SU-M) and administered subcutaneously with saponin adjuvant produced high titres of type-specific and cross-reactive neutralizing antibodies (Trujillo et al., 2004b). The production of long-lived cross-reactive neutralizing antibodies is a major goal of lentivirus vaccine strategies. Reina et al. (2013) review immunization strategies against small ruminant lentiviruses and progress that has been made towards the development of an effective vaccine.
Husbandry methods and good practice
Control and prevention methods for CAEV in goat herds have focused primarily on serological testing and isolating or culling infected goats, and heat inactivation of colostrum (56ºC for 1 h) and supplementation with bovine colostrum for kids born to CAEV-infected nannies (Adams et al., 1983; Rowe and East, 1997). Separating CAEV seropositive goats from seronegative goats has significantly helped the goat dairy industry by reducing the risk of transmission (Rowe et al., 1992b). These prevention and control strategies have not completely eradicated CAEV; however, utilizing a more sensitive serological diagnostic test such as cELISA to identify and eliminate seropositive goats annually can virtually eliminate the herd presence of CAEV over the course of 6 years in a commercial dairy goatherd (Herrmann et al., 2003). There are two reasons for incomplete eradication of CAEV. One is that there is delayed seroconversion where essentially seronegative goats are transmitting virus, and second, the serological test lacks sensitivity to detect all infected goats. Seropositive progressor goats transmit virus to niaive goats in a natural herd situation (Woodard et al., 1982); however, the transmission contribution of seropositive non-progressor goats remains to be determined. Furthermore, since lentiviruses and other infectious diseases can be transmitted through blood, re-use of needles should be discouraged.
There is evidence that host genetics play a role in determining susceptibility/resistance to SRLV infection and disease progression, but little work has been performed in small ruminants (Herrmann-Hoesing et al., 2008; Larruskain and Jugo, 2013). A number of genes implicated in SRLV infection and disease have been identified, but more research is necessary to understand the host-SRLV interaction. A better understanding of loci involved in SRLV infection and pathology and their polymorphism could lead to the identification and selective breeding of naturally resistant animals (Heaton et al., 2012; White and Knowles, 2013).
ReferencesTop of page
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