CAE in Goats (Caprine Arthritis and Encephalitis)

CAE (Caprine Arthritis and Encephalitis)

Caprine arthritis and encephalitis (CAE) virus infection is manifested clinically as polyarthritis in adult goats and less commonly as progressive paresis (leukoencephalomyelitis) in kids. Subclinical or clinical interstitial pneumonia, indurative mastitis (“hard udder”), and chronic wasting have also been attributed to infection with this virus. Most CAE virus infections, however, are subclinical. Infection with the CAE virus decreases the lifetime productivity of dairy goats and is a barrier to exportation of goats from North America.

CAE virus infection is widespread among dairy goats in most industrialized countries but rare among indigenous goat breeds of developing countries unless they have been in contact with imported goats. In countries such as Canada, Norway, Switzerland, France, and the USA, seroprevalence of CAE virus is >65%.

Etiology, Epidemiology, and Pathogenesis:

The CAE virus is an enveloped, single-stranded RNA lentivirus in the family Retroviridae. There are several genetically distinct isolates of the virus that differ in virulence. Under natural conditions, CAE virus appears to be host-specific, but experimental infection of sheep with this virus is possible. Prolonged commingling of naive sheep with infected goats usually does not result in infection or seroconversion, but lambs allowed to suckle infected goats seroconvert and develop persistent CAE virus infections. Experimental inoculation of CAE virus into the joints of lambs produces arthritis, seroconversion, and virus-positive joints. CAE virus infection is widespread in dairy goat breeds but uncommon in meat- and fiber-producing goats. This has been attributed to genetics, management practices such as feeding colostrum and milk from a single dam to multiple kids, and industrialized farming practices (eg, frequent introductions of new animals into a herd). Prevalence of infection increases with age but is not influenced by sex. Most goats are infected at an early age, remain virus positive for life, and develop disease months to years later. The chief mode of spread of CAE is through ingestion of virus-infected goat 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 may 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 experimental studies, include in utero transmission to the fetus, infection of the kid during parturition, and infection through breeding or embryo transfer. The pathogenesis of CAE is not fully understood. Virus-infected macrophages in colostrum and milk are absorbed intact through the gut mucosa. Infection is subsequently spread throughout the body via infected mononuclear cells. Periodic virus replication and macrophage maturation induces the characteristic lymphoproliferative lesions in target tissues such as the lungs, synovium, choroid plexus, and udder. Persistence of the CAE virus in the host is facilitated by its ability to become sequestered as provirus in host cells. Infection induces a strong humoral and cell-mediated immune response, but neither is protective.

Clinical Findings:

Arthritis is the syndrome exhibited by adult goats infected with CAE virus. Clinical signs include joint capsule distention and varying degrees of lameness. The carpal joints are most frequently involved. The onset of arthritis may be sudden or insidious, but the clinical course is always progressive. Affected goats lose condition and usually have poor hair coats. Encephalomyelitis is generally seen in kids 2-4 mo old but has been described in older kids and adult goats. Affected kids initially exhibit lameness, ataxia, and hindlimb placing deficits. Hypertonia and hyperreflexia are also common. Over time, signs progress to paraparesis or tetraparesis and paralysis. Depression, head tilt, circling, opisthotonos, torticollis, and paddling have also been described. The interstitial pneumonia component of CAE virus infection rarely produces clinical signs in kids. However, in adult goats with serologic evidence of CAE virus infection, chronic interstitial pneumonia that leads to progressive dyspnea has been documented. The “hard udder” syndrome attributed to CAE virus 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 normal amounts of milk, production remains low in many goats suffering from indurative mastitis.