Caprine arthritis and encephalitis (CAE) is a persistent infection of goats caused by Lentivirus capartenc. There are multiple clinical presentations, including leukoencephalomyelitis, which affects 2- to 6-month-old kids; chronic, hyperplastic polysynovitis; indurative mastitis; interstitial pneumonia, and progressive weight loss. Presence of L capartenc can be confirmed in a goat herd by means of serological testing; however, a positive result does not guarantee an individual animal will develop clinical signs of disease. A presumptive diagnosis is based on clinical signs. There is no vaccine or specific treatment for CAE; supportive care is indicated, especially in cases presenting with polysynovitis, with euthanasia necessary in severe cases.
Caprine arthritis and encephalitis is caused by Lentivirus capartencvirus infection and manifests clinically as polysynovitis-arthritis in adult goats and less commonly as leukoencephalomyelitis in kids. Subclinical or clinical interstitial pneumonia, indurative mastitis ("hard udder”), and chronic wasting have also been attributed to infection with this virus. However, most L capartenc infections are subclinical. Infection with L capartenc decreases the lifetime productivity of dairy goats and is a barrier to exportation of goats from North America.
L capartenc infection is widespread among dairy goats in most high-income economies, including Canada, Norway, France, and the US, whereas it is comparatively rare among indigenous goat breeds raised in more resource-limited countries, except where there is a history of contact with imported goats.
Etiology, Epidemiology, and Pathogenesis of Caprine Arthritis and Encephalitis
L capartenc is an enveloped, single-stranded RNA lentivirus in the family Retroviridae. There are several genetically distinct isolates of the virus that differ in virulence.
This virus is closely related to the ovine lentiviruses that cause ovine progressive pneumonia and maedi-visna in North America and Europe, respectively. Cross-species transmission is possible via feeding of infected milk and colostrum. Therefore, the ovine and caprine lentiviruses are commonly referred to as small ruminant lentiviruses.
L capartenc infection is widespread in dairy goat breeds but uncommon in meat- and fiber-producing goats. This distinction has been attributed to genetic factors; management practices, such as feeding colostrum and milk from a single dam to multiple kids; and farming practices in highly resourced countries (eg, frequent introductions of new animals into a herd). Prevalence of infection increases with age but is apparently not influenced by sex. Most goats are infected at an early age, remain seropositive for life, and can develop clinical signs of disease months to years after infection.
The chief mode of transmission of L capartenc is via ingestion of virus-infected colostrum or milk by kids. The feeding of pooled colostrum or milk to kids is a particularly risky practice, because a few infected does will spread the virus to a large number of kids. Horizontal transmission also contributes to disease spread within herds and can occur through direct contact, exposure to fomites at feed bunks and waterers, ingestion of contaminated milk in milking parlors, or serial use of needles or equipment contaminated with blood.
Unlikely methods of transmission, as indicated by results of experimental studies, include in utero transmission to the fetus, infection of the kid during parturition, and infection via natural breeding or embryo transfer (1).
The pathogenesis of CAE is not fully understood. Virus-infected macrophages in colostrum and milk are absorbed intact through the GI mucosa. Infection is subsequently spread throughout the body via infected mononuclear cells. Periodic viral replication and macrophage maturation induce characteristic lymphoproliferative lesions in target tissues and organs such as the lungs, synovium, choroid plexus, and udder. Persistence of L capartenc in the host is facilitated by its ability to become sequestered as provirus in host cells. Infection induces strong humoral and cell-mediated immune responses; however, neither response is protective.
Clinical Findings for Caprine Arthritis and Encephalitis
Clinical signs of caprine arthritis and encephalitis are observed in approximately 20% of L capartenc–infected goats during their lifetime (2). The most common manifestation of infection is polysynovitis-arthritis, which occurs primarily in adult goats but can occur in kids as young as 6 months old. Clinical signs of polysynovitis-arthritis include joint swelling and lameness of varying severity. The carpal joints are most frequently involved. Onset of arthritis can be acute or chronic, but the clinical course is always progressive. Affected goats also lose weight and usually have poor coats.
Encephalomyelitis generally occurs in kids 2–6 months old but has been reported in older kids and adult goats. Affected kids initially exhibit weakness, ataxia, and hind limb proprioceptive deficits. Hypertonia and hyperreflexia are also common. Over time, clinical signs progress to paraparesis or tetraparesis and paralysis. Depression, head tilt, circling, opisthotonos, torticollis, and paddling of the limbs have also been reported.
Interstitial pneumonia due to L capartenc infection rarely produces clinical signs in kids. However, in adult goats with serological evidence of L capartenc infection, chronic interstitial pneumonia can lead to progressive dyspnea. Indurative mastitis, the hard udder syndrome attributed to L capartenc infection, is characterized by a firm, swollen mammary gland and agalactia at the time of parturition. Milk quality is usually unaffected. Although the mammary gland may soften and produce close to a normal volume of milk, production remains low in many goats with indurative mastitis. Some affected adults develop progressive weight loss, despite a good appetite, without any of the more common musculoskeletal, neurological, respiratory, or mammary signs.
Lesions
Histopathological lesions due to L capartenc infection are generally described as lymphoproliferative, with degenerative mononuclear cell infiltration. Lesions in joints are characterized by thickening of the joint capsule and marked proliferation of synovial villi. In chronic cases, soft tissue calcification involving joint capsules, tendon sheaths, and bursae is not uncommon. Severe cartilage destruction, rupture of ligaments and tendons, and periarticular osteophyte formation have also been described in advanced cases.
Gross lesions associated with the neurological form of CAE include asymmetric, brownish-pink, swollen areas, most commonly located in the cervical and lumbosacral spinal cord segments. Histopathologically, these lesions are characterized by multifocal, mononuclear cell inflammatory infiltrates and a varying extent of demyelination. During gross examination, lungs of affected goats appear firm and gray-pink, with multiple small white foci, and do not collapse. The bronchial lymph nodes are invariably enlarged.
Microscopic features of articular lesions include synovial cell hyperplasia, subsynovial mononuclear cell infiltration, villous hypertrophy, synovial edema, and synovial necrosis. Histopathological findings include chronic interstitial pneumonia with mononuclear cell infiltration in alveolar septae and in perivascular and peribronchial regions. In does with udder induration, mononuclear infiltration of periductular stroma obliterates healthy mammary tissue.
Diagnosis of Caprine Arthritis and Encephalitis
Clinical signs and history
Serological testing to determine herd L capartenc status
A presumptive diagnosis of caprine arthritis and encephalitis can be based on clinical signs and patient history. Infectious arthritis caused by Mycoplasma spp and traumatic arthritis are differential diagnoses for arthritis due to L capartenc infection. Differential diagnoses for the progressive paresis and paralysis exhibited by young kids should include enzootic ataxia, spinal cord abscess, cerebrospinal nematodiasis, spinal cord trauma, and congenital anomalies of the spinal cord and vertebral column. If a neurological examination indicates brain involvement, polioencephalomalacia, listeriosis, and rabies should be considered. The pulmonary form of caseous lymphadenitis can have a similar clinical presentation to the pulmonary form of CAE in adult goats.
Both an agar gel immunodiffusion (AGID) test and ELISA for L capartenc are considered sufficiently reliable for use in herd control programs; most diagnostic laboratories offer ELISA for testing individual or pooled samples. The AGID is reported to be more specific but less sensitive than the ELISA.
A positive test result in an adult goat implies infection but does not confirm that the clinical signs are caused by L capartenc. Kids infected at birth develop a measurable antibody response 4–10 weeks after infection. However, positive test results in kids < 90 days old usually reflect colostral antibody transfer. Negative test results do not reliably exclude L capartenc infection, because the time for postinfection seroconversion is variable, and some goats have a very low antibody titer that might not be detectable. Low antibody titers are common in late pregnancy.
Because of the limitations of serological testing, definitive diagnosis of clinical CAE requires demonstration of characteristic lesions in biopsy specimens or post mortem. Virus isolation or PCR assay to demonstrate presence of viral antigen in tissues may be used to further confirm the diagnosis.
Treatment and Control of Caprine Arthritis and Encephalitis
No vaccine or specific treatments
Supportive care
Appropriate management practices, particularly of kids
No specific treatments exist for any of the clinical manifestations of Lentivirus capartenc infection. However, supportive treatments can benefit some patients. The condition of goats with polysynovitis-arthritis may be improved with regular hoof trimming, use of additional bedding, and administration of NSAIDs, such as meloxicam, flunixin meglumine, or phenylbutazone (3). No NSAIDS are labeled for use in goats in the US; however, meloxicam (2 mg/kg loading dose, IV, SC, or PO; followed by 0.5 mg/kg, IV or SC, or 1 mg/kg, PO, every 24 hours) (4, 5) and flunixin meglumine (2.2 mg/kg, IV, every 24 hours) (6, 7) have been effective in regions where these medications are labeled for use in goats.
Goats with encephalomyelitis can be managed for weeks with good nursing care. Antimicrobial treatment is indicated to treat secondary bacterial infections that might complicate interstitial pneumonia or indurative mastitis components in cases of L capartenc infection; the choice of antimicrobial is ideally based on culture results, but the only antimicrobial labeled for use in goats in the US is ceftiofur sodium (which is labeled only for pneumonia).
Pearls & Pitfalls
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Providing high-quality, readily digestible feed to goats with a positive L capartenc test result may delay the onset of wasting. Eventually, euthanasia might be necessary for animals with advanced disease.
In commercial herds, several measures have been recommended for control of CAE:
permanent isolation of kids, beginning at birth
feeding of heat-treated colostrum (45°C [113°F] for 60 minutes) and pasteurized milk
semiannual serological testing of the herd, with identification and segregation of seronegative and seropositive goats
eventual culling of seropositive goats
If the control program includes segregation of herds into seropositive and seronegative groups, groups should be separated by a minimum of 1.8 m (6 feet), and shared equipment should be disinfected using phenolic or quaternary ammonium compounds.
Key Points
Caprine arthritis and encephalitis typically manifests as neurological disease in kids and as arthritis, pneumonia, or mammary disease in adult goats.
No vaccine or specific treatment exists; therefore, supportive care is indicated for affected animals.
Disease control may be achieved by appropriate kid and colostrum management and by using test-and-segregate/cull practices with adult goats.
For More Information
Spickler AR. Small ruminant lentiviruses: maedi-visna & caprine arthritis and encephalitis. Center for Food Security & Public Health. 2015.
Caprine arthritis/encephalitis. World Organisation for Animal Health. Terrestrial Animal Health Code. 2024.
Caprine arthritis encephalitis (CAE). Australian Vet Association.
CAEV. British Goat Society.
References
Peterhans E, Greenland T, Badiola J, et al. Routes of transmission and consequences of small ruminant lentiviruses (SRLVs) infection and eradication schemes. Vet Res. 2004;35(3):257-274. doi:10.1051/vetres:2004014
Smith BP, Van Metre DC, Pusterla N, eds. Diseases of the bones, joints, and connective tissues. Large Animal Internal Medicine. 6th ed. Mosby; 2024.
Matthews JG. Diseases of the Goat. 4th ed. Wiley-Blackwell. 2016.
Smith JS, Schleining J, Plummer P. Pain management in small ruminants and camelids: analgesic agents. Vet Clin N Am Food Anim. 2021;37(1):1-16. doi:10.1016/j.cvfa.2020.12.001
Mercer MA, Zhang Z, Clapham MO, et al. Plasma pharmacokinetics, milk residue depletion profile, and milk withdrawal interval estimation following multiple-dose oral administration of meloxicam to lactating dairy goats. Front Vet Sci. 2025;12:1620476. doi:10.3389/fvets.2025.1620476
Reppert EJ, Kleinhenz MD, Montgomery SR, et al. Pharmacokinetics and pharmacodynamics of intravenous and transdermal flunixin meglumine in meat goats. J Vet Pharmacol Ther. 2019;42(3):309-317. doi:10.1111/jvp.12756
Giles CB, Ferdous F, Halleran JL, Yeatts JL, Baynes RE, Mzyk DA. Flunixin meglumine tissue residues after intravenous administration in goats. Front Vet Sci. 2024;10:1341779. doi:10.3389/fvets.2023.1341779
