What Are the Symptoms of CAE in Goats?

Caprine arthritis encephalitis (CAE) is a viral infection in goats that can cause swollen, stiff joints, progressive pneumonia, neurological problems in young kids, and a hardened udder with reduced milk production. The tricky part is that many infected goats look perfectly healthy for months or even years before any signs appear, and some never show obvious symptoms at all. The virus quietly persists inside immune cells, which is why the disease often sneaks through a herd unnoticed until damage is already widespread.

What the Virus Does Inside the Goat

CAE is caused by a lentivirus, a type of slow-acting retrovirus in the same family as the virus that causes HIV in humans (though CAE poses no risk to people). The virus targets cells of the monocyte and macrophage lineage, which are white blood cells central to the immune system.¹ What makes CAE especially insidious is that the virus stays largely dormant inside monocytes circulating in the blood. It only becomes active when those monocytes mature into macrophages in the tissues.² This means the virus can hide from the immune system for a long time, replicating only in small bursts when conditions are right. The goat’s own immune response to infected macrophages in the joints, lungs, brain, and udder is what drives most of the tissue damage.

Because the virus integrates into the host cell’s DNA, infection is lifelong. There is no cure, and no vaccine is available. Once a goat tests positive, it remains positive and potentially infectious for the rest of its life.

Joint Disease: The Most Recognizable Sign

Arthritis is the hallmark of CAE in adult goats and the symptom most owners notice first. It typically shows up as gradual, progressive swelling of the carpal joints (the “knees” of the front legs), though hocks, stifles, and other joints can also be affected. Early on, you might see a goat that is slightly stiff getting up in the morning or reluctant to walk on rough ground. Over weeks to months, the joint capsules fill with inflammatory fluid and thicken, making the knees look obviously enlarged.

As the disease progresses, the cartilage and surrounding tissue break down. Affected goats may develop a characteristic stilted gait, shift their weight frequently, or spend more time lying down. In severe cases, the joints can become so damaged and painful that the goat has difficulty standing or moving to the feeder. Weight loss follows because the goat simply cannot compete for food or graze comfortably. Research has confirmed a genetic component to how severely arthritis develops. In Saanen goats, for instance, a specific DNA marker has been linked to greater susceptibility to CAE-induced arthritis, suggesting that some bloodlines within a breed are hit harder than others.³

One thing that confuses owners is the timeline. A goat can carry the virus for a year or two with no visible joint changes, then seemingly develop swollen knees “overnight.” In reality, the inflammation has been building at a microscopic level; it just crosses the threshold of what is visible all at once. This delay is why routine testing matters more than visual inspection for identifying infected animals.

Encephalitis in Kids

The “encephalitis” half of the disease name refers to brain and spinal cord inflammation, and it primarily strikes young kids between one and four months of age. Affected kids may develop a wobbly, uncoordinated gait that worsens over days. Rear-leg weakness is often the first thing an owner notices, sometimes mistaken for an injury or a nutritional deficiency. As the disease advances, kids may become unable to stand, develop head tilts, circle aimlessly, or show blindness in one or both eyes.

The underlying damage involves destruction of the myelin sheath that insulates nerve fibers in the brain and spinal cord. Microscopic examination of affected kids shows acute demyelinating inflammation as the most prominent change.⁴ The neurological form tends to progress rapidly and is usually fatal or severe enough to warrant euthanasia. Fortunately, the encephalitic form is less common than the arthritic form, but it is far more dramatic and distressing when it does appear.

A kid showing progressive rear-leg weakness that does not respond to selenium or vitamin E supplementation, and that worsens rather than improves, should raise suspicion of CAE encephalitis. Other causes of neurological signs in young goats, such as listeriosis, polioencephalomalacia, or spinal trauma, need to be ruled out by a veterinarian.

Respiratory Symptoms

CAE can cause a slowly progressing interstitial pneumonia that is easy to overlook until it becomes severe. Affected goats develop an increased breathing rate, exercise intolerance, and gradual weight loss. In a case series of Anglo-Nubian goats, animals ranging from five months to three and a half years old showed these signs, and post-mortem examination revealed extensive consolidation across all lung lobes with characteristic lymphocytic infiltration and thickened tissue between the air sacs.⁵

A larger study of goats with symptomatic CAE found that about seven in ten had some degree of pneumonia on tissue examination, with a chronic interstitial pattern present in roughly six out of ten. In most cases, the severity was mild.⁶ That finding is striking because it means a large share of clinically affected goats have lung involvement that may never produce obvious coughing or respiratory distress. The damage accumulates quietly, contributing to poor stamina and declining condition without a clear respiratory complaint that sends the owner looking for answers.

When respiratory signs do become noticeable, the goat may breathe with visible effort, show flared nostrils, or lag behind the herd during movement. Unlike bacterial pneumonia, there is usually no fever or nasal discharge in the early stages, and antibiotics do not help because the problem is viral and immune-mediated rather than bacterial.

Udder Changes and Milk Production

In dairy goats, one of the most economically important symptoms is a condition sometimes called “hard udder.” The virus triggers chronic inflammation in the mammary gland, causing the udder tissue to become firm and nodular. Does with this condition often freshen with a visibly abnormal udder after kidding, producing far less colostrum and milk than expected. Some does produce almost no usable colostrum at all, which is a serious problem for their kids’ nutrition and passive immunity.

Even in infected does whose udders still feel reasonably normal, milk yield can be reduced compared to uninfected herdmates. The chronic inflammatory process in the mammary tissue disrupts normal milk secretion. CAE-associated mastitis tends to be a subclinical, ongoing process rather than the sudden, hot, painful mastitis caused by bacterial infections. The reduction in production, combined with shortened useful life, contributes to significant economic losses in dairy herds.⁷

Why So Many Infected Goats Look Normal

One of the most frustrating aspects of CAE for goat owners is that a goat can test positive and never develop any visible symptoms during its productive life. Estimates vary, but a substantial proportion of seropositive goats remain subclinical carriers. This is partly because the virus replicates at a very low level inside resting monocytes and only activates in small numbers of cells at a time. The immune system keeps the virus in check enough to prevent widespread tissue damage in many animals, at least for years.

Age, stress, other illnesses, kidding, and nutritional status can all tip the balance. A goat that seemed fine for three years may develop swollen joints after a difficult pregnancy or a bout of internal parasites. The virus was there all along; the goat’s capacity to suppress it simply dropped. This is also why CAE tends to be more clinically apparent in intensively managed herds, where animals face more physiological stress from high production demands and close housing.

Seroprevalence studies have found significant differences in infection rates based on management system, breed, and age, reinforcing that how goats are kept matters as much as whether they are exposed.⁸ Older goats and those in confined, intensively managed settings generally show higher rates of both infection and clinical disease.

How CAE Spreads

The primary route of transmission is from doe to kid through infected colostrum and milk. The virus has been isolated directly from goat milk, and feeding studies confirm that milk and colostrum are the most efficient vehicles for passing the infection to newborns.⁹ A single feeding of heavily contaminated milk can be enough to infect a kid.¹⁰

Horizontal transmission between adult goats also occurs, though it is less efficient. Prolonged close contact in shared housing, exposure to respiratory secretions, and possibly shared milking equipment are all suspected routes.¹¹ This is why eradication programs focus heavily on preventing kids from nursing infected dams. A common protocol is to remove kids at birth before they nurse, feed them heat-treated colostrum or colostrum from tested-negative does, and raise them on pasteurized milk or milk replacer. This alone can drastically cut new infections in the next generation.

It is worth noting that the CAE virus and the maedi-visna virus of sheep are closely related lentiviruses, and genetic studies suggest they might be better understood as a spectrum of related viral strains rather than entirely separate species. Cross-species transmission between goats and sheep has been documented, and some viral sequences found in goats cluster more closely with sheep strains than with traditional goat strains.¹²¹³ For farms that keep both goats and sheep, this is relevant. Separating the two species may be advisable if CAE or maedi-visna is present in either flock.

Getting a Diagnosis

Clinical signs alone are not enough to diagnose CAE, both because the symptoms overlap with other conditions and because so many infected goats show no signs. Blood testing is the standard approach. ELISA (enzyme-linked immunosorbent assay) tests detect antibodies against the virus in serum and are the most widely used screening tool. They are highly sensitive, meaning they catch most truly infected animals, but they can occasionally flag a goat that is not actually infected.¹⁴

PCR testing, which looks for the viral DNA itself rather than antibodies, is more specific but less sensitive. It will rarely give a false positive, but it can miss some infected goats because the viral load in blood can be very low at any given time. Combining both tests improves overall accuracy. Running them in parallel (calling a goat positive if either test is positive) boosts sensitivity to nearly 99%, which is useful for screening herds where you want to catch every possible carrier.¹⁵

One advantage of PCR is that it can detect infection earlier. In experimentally infected animals, viral DNA was detectable about two weeks after infection, while antibody-based tests did not turn positive until 40 to 60 days later.¹⁶ This window matters if you are testing a newly purchased goat that may have been recently exposed. A negative ELISA within the first month or two of exposure does not guarantee the goat is free of the virus.

Milk-based ELISA testing has also been validated for dairy herds. Commercial kits using individual milk samples can achieve high accuracy, making bulk-tank or individual-milk screening a practical option for dairies that want to avoid repeated blood draws.¹⁷ Not all milk-based kits perform equally well, though, so asking your veterinarian which test the lab uses and its known sensitivity is a reasonable step.

Pain, Welfare, and What Owners Miss

Goats are prey animals, and like most prey species, they tend to mask pain. A goat with chronically inflamed joints may not vocalize or act dramatically distressed, even when the damage is considerable. Signs of pain in goats can include teeth grinding, frequent posture changes, reluctance to move, and subtle increases in breathing rate.¹⁸ These signals are easy to miss, especially in a herd setting where you may not watch each animal closely.

This stoicism means CAE-related arthritis often progresses further than it should before an owner intervenes. By the time a goat is visibly lame, the joint damage may be advanced. Regularly handling your goats’ front legs and checking for warmth, swelling, or thickening around the carpal joints can catch changes earlier than waiting for obvious lameness. Any goat that seems to be “aging fast,” losing condition, or falling behind the herd in movement should be evaluated, particularly if the herd has not been tested or has a known history of CAE.

Breed Differences and Herd-Level Risk

CAE has been identified in virtually every dairy goat breed, and no breed is immune. However, the disease has historically been most prevalent in Swiss-origin dairy breeds like Saanens, Toggenburgs, and Alpines, largely because these breeds were widely traded internationally during the twentieth century, spreading the virus across continents in the process. Meat and fiber breeds kept in more extensive, pasture-based systems have generally had lower prevalence, though this likely reflects management differences (less close contact, less milk sharing) as much as any inherent resistance.

That said, genetic susceptibility does vary. Studies have found that seroprevalence and the severity of clinical disease differ significantly across breeds and even among family lines within a breed.¹⁹ The identification of a specific genetic marker associated with arthritis susceptibility in Saanen goats suggests that selective breeding could theoretically reduce clinical disease, though this has not been pursued as a practical strategy in most countries.²⁰ For most producers, testing and removing positive animals remains far more practical than trying to breed for resistance.

Living with CAE in a Herd

Because there is no treatment that eliminates the virus, management decisions after a positive test revolve around containment and quality of life. Some owners choose to cull positive animals immediately. Others keep positives in a separate group, away from negative goats and kids, milking them last to reduce cross-contamination risk through equipment. The right choice depends on herd size, goals, and how many animals are affected. In a herd where prevalence is already very high, immediate culling of every positive goat may not be realistic.

For individual animals with arthritis, supportive care can slow the decline. Soft, deep bedding reduces joint stress. Anti-inflammatory drugs prescribed by a veterinarian can ease pain during flare-ups. Keeping affected goats at a healthy weight, rather than pushing for high milk production, reduces the load on damaged joints. None of this reverses the disease, but it can keep a goat comfortable and productive for longer than doing nothing.

Prevention in the next generation is where the real progress happens. Pulling kids at birth, feeding heat-treated colostrum, testing the herd at least annually, and isolating or culling positive animals can clean up a herd over several kidding seasons. New additions should always be tested before they join the herd, ideally twice, with the second test at least 60 days after the first to account for the antibody detection window. Buying from tested-negative herds and asking for documentation is the simplest way to avoid introducing CAE in the first place.