Myotonia Congenita

Myotonia congenita is a heritable disorder of goats in which the affected animal experiences tetanic muscle contraction when startled. Occasionally the contraction is severe enough that the goat collapses to the ground. Animals in which this phenomenon is observed have been referred to as “fainting goats.” The disorder is inherited as an autosomal dominant trait.¹ Some investigators speculate that the variability in clinical signs and intensity of muscle contractions may be related to homozygous versus heterozygous genotype, with homozygosity more likely than heterozygosity to be associated with clinical manifestations.¹ The condition closely resembles a form of myotonia congenita in humans, and the animal disease has therefore been used as a research model for the human disease.

The condition is caused by a mutation in the voltage-dependent chloride channel in skeletal muscle that leads to hyperexcitability of the sarcolemma and delayed relaxation of contracted muscle.³ Histochemical and ultrastructural abnormalities have been documented in goats with myotonia congenita.^1,2

Hereditary Chondrodysplasia (Spider Lamb Syndrome)

Hereditary chondrodysplasia, or spider lamb syndrome, is an inherited musculoskeletal condition that is seen primarily in the Suffolk and Hampshire breeds.⁴ Clinical signs may be present at birth, or affected lambs initially may appear normal, only to have the severe skeletal abnormalities develop by the age of 6 weeks.⁵ This later presentation may be associated with longer legs with angular deviations, shallower bodies, and narrower chests than normal lambs,⁵ and these animals display the expected radiographic abnormalities associated with this condition at birth. Skeletal abnormalities exhibited by affected lambs vary in severity and type. Chondrodysplasia is evident in the skull, sternum, appendicular skeleton, and vertebrae.

On radiographic evaluation, the dorsal silhouette of the skull may be rounded, the occipital condyles may be elongated (occasionally with cartilage erosion), and thickening of the occipital bone between the condyles and the poll may be evident. The sternebrae may be of abnormal size and shape. The sternum often is misaligned, dorsally deviated, and not fused across the midline. The scapula and olecranon usually have more cartilage and less bone distally than normal. Several islands of ossification near the anconeal process typically can be seen on flexed lateral radiographs of the elbow in animals with this syndrome. The distal physis of the radius is flared, and angular limb deformities are common. The forelimbs generally are more severely affected than the hindlimbs. Erosion of articular cartilage is common if the lamb survives for a few months. The vertebrae commonly have abnormal and excessive cartilage. Vertebral body abnormalities may contribute to scoliosis or, less commonly, kyphosis.⁵ On histopathologic examination, the typical osseous lesion is manifested as uneven growth cartilage. The pathologic changes are found by the end of the second trimester of gestation.⁵

Spider lamb syndrome is caused by a mutation in fibroblast growth factor receptor 3 (FGFR3) that leads to excessive skeletal growth.⁶ Although inheritance initially was considered to follow an autosomal recessive pattern with complete penetrance but variable expression, genetic testing has led to a suggestion of a codominant pattern. Heterozygotes occasionally are affected with spider lamb syndrome but more typically have a phenotype close to normal but with longer bones than in animals without the mutation.⁶ Carriers were difficult to identify until a DNA test became commercially available. The incidence of spider lamb syndrome has greatly decreased since the test became available.⁷

Arthrogryposis

Arthrogryposis, congenital fixation of multiple joints, has been reported to result from infectious, toxic, and genetic causes. Arthrogryposis and hydranencephaly may result from infection with Akabane virus, Cache Valley virus, Border disease virus, and possibly other organisms that affect the developing fetus. Affected animals have severely flexed forelimbs and overextended hind limbs. A spiral deviation of the spine also is evident. Neurologic conditions that may be seen with arthrogryposis and hydranencephaly include cerebellar hypoplasia, hydrocephalus, micromelia, and hydrocephaly.

Maternal ingestion of lupine (Lupinus spp.) and hemlock (Conium maculatum) has produced arthrogryposis in offspring. The type and severity of disorders will vary in accordance with stage of gestation, toxin dose, and duration of ingestion.

Inherited arthrogryposis has been reported in Suffolk⁸ and Corriedale⁹ sheep. It appears to follow an autosomal recessive pattern, and a site on chromosome 5 has been identified as the likely genetic locus.¹⁰

Polydactyly

By definition, polydactyly is a congenital anomaly in which extra digits are present. It is seldom seen in sheep and goats. The condition is certainly heritable in cattle and probably heritable in pigs, where cleft palate may concurrently be seen. Polydactyly is suggested to be heritable in horses. One report of polydactyly in goats describes an affected female that was sired by a male with polydactyly.¹¹ Polydactyly usually has only cosmetic consequences for affected animals but may be associated with serious gait abnormalities in some instances. The practitioner must thoroughly examine animals with gait abnormalities to determine whether the lameness is because of some other anomaly or clinically significant lesion. Radiographs are necessary to assess the anomaly fully and to determine any treatment to be rendered.

Patella Luxation

Animals with congenital patella luxation usually are brought for veterinary evaluation shortly after birth, because they tend to crouch on the rear legs when attempting to stand. The patella luxation functionally disrupts the quadriceps apparatus, rendering the animal unable to hold the stifle in extension. The primary consideration to be ruled out in the differential diagnosis with this presentation is femoral nerve injury, which also causes failure of the quadriceps apparatus because of lack of strength in the quadriceps muscle, producing the same abnormal stance. Femoral nerve injury is more commonly seen in calves after dystocia than it is in small ruminants.

A diagnosis of patella luxation is readily made by palpating the patella; a luxated patella easily dislocates either medially or laterally. In severely affected animals, the patella remains luxated and is difficult to reduce into its normal position. This manipulation is more easily accomplished with the stifle held in extension.

Standard radiographic views with the addition of a skyline image demonstrate the position of the patella, the depth of the trochlear groove, and other osseous abnormalities that may be present. The skyline view, which allows the best assessment of the trochlear groove, is taken with the stifle flexed and the x-ray beam directed proximally to distally, perpendicular to the tibia. However, the ease of luxation on palpation of the patella is much more important diagnostically than the location of the patella on a single craniocaudal radiograph. The affected patella often is in a normal position on a given radiograph if it is not purposely luxated by the examiner before the radiograph is obtained.

Surgery usually is indicated for young animals with congenital patella luxation. Most young animals respond well to imbrication of the fibrous joint capsule and overlying fascia on the side opposite the direction of patella luxation. However, the veterinarian must fully evaluate the limb preoperatively and assess the joint at surgery. Some severe cases may require trochleoplasty or tibial crest osteotomy and relocation. Detailed descriptions of the more complex stifle surgeries are available in small animal surgery texts.¹²

Affected animals should be thoroughly examined for other congenital abnormalities. Specifically, severely affected newborns may not be able to stand and suckle. Therefore failure of passive transfer and associated illness may become more significant to the health of these animals than even the primary patella luxation. In mild cases of luxation, especially if the condition is unilateral, small ruminants may compensate well enough biomechanically that the condition goes undiagnosed until they present in adulthood with lameness caused by luxation or degenerative joint disease caused by intermittent luxation. One report of development of patellar luxation as late as the age of 2 years in sheep with common bloodlines suggests some genetic predisposition to the condition.¹³ Adult animals also may exhibit acute lameness as a result of traumatic patella luxation. Surgical treatment of adults tends to be more involved in that orthopedic implants such as screws and wires may be required to secure the patella in the normal position. Older animals also may require wedge trochleoplasty or tibial tuberosity transposition in addition to imbrications and fascial release.¹³ The prognosis for a return to soundness is not good compared with that in neonates treated for congenital luxation.^14,15

Spastic Paresis

Spastic paresis has been described in pygmy goats.¹⁶ Affected goats suffer constant contraction of the gastrocnemius muscles in the hind legs. The contraction produces extension of the tibiotarsal joint and arching of the back. Clinical signs are not significantly different from those described in several breeds of cattle.^17–19 This condition is suspected to be inherited, but the exact mode of transmission is unknown. No lesions have been noted in the spinal cord, tibial or peroneal nerve, or gastrocnemius muscle. The clinical signs appear to be caused by a defect in the myotactic reflex that results in an overstimulation or relative lack of inhibition of the efferent motor neurons.¹⁶

Carpal Contracture

Carpal contracture occasionally can manifest as a congenital condition in kids and lambs. Many will respond very quickly to treatment with splints and bandages. Radiographic examination of the limbs is recommended to identify any osseous lesion that may contribute to the flexural deformity. Careful palpation of the limb while attempting to straighten it will frequently identify the structures under tension. Tenotomy of the restrictive structure may relieve the flexural deformity (Figures 11-1 and 11-2). Flexural deformities may develop in older animals after an injury that leads to abnormal weight bearing. This secondary flexural deformity often will involve fibrosis of the joint capsule and seldom responds to tenotomy. Some cases will not resolve despite a release incision of the joint capsule and all flexural structures between the skin and joint capsule.

Figure 11-1 Congenital carpal contracture of the left leg in a 4-week-old Pygmy wether. The flexural deformity did not improve with 3 weeks of bandage-splint immobilization in extension (to the degree possible). The ulnaris lateralis was palpably tense on attempts to extend the carpus.

Figure 11-2 The same Pygmy wether as in Figure 11-1, 3 weeks after transection of the ulnaris lateralis and postoperative extension with a splint bandage. The animal could fully extend the carpus and exhibited normal flexion, with no residual lameness.

Predator Attack

Sheep and goats are of the stature and disposition to make them susceptible to predators. In the United States, predation accounts for about 37% of sheep and lamb losses, primarily involving attacks from coyotes and dogs.¹ Small ruminants seldom survive attacks by wild carnivores. However, veterinarians are sometimes called to treat survivors of attacks by domestic animals or interrupted attacks by wild animals. These survivors often ultimately die because of either lethal injury to internal organs or physical exhaustion from the chase and the attack. A veterinarian treating animals that survive the initial trauma may face a significant challenge. Although skin wounds are quite obvious after the animal is thoroughly examined and clipped, injuries to deeper structures and serious myopathy are more difficult to assess.

Attacking predators tend to “go for the jugular,” which leads to a concentration of wounds in the head and neck area. The associated injury to the great vessels usually is obvious and often fatal. Tracheal puncture can cause respiratory difficulties leading to subcutaneous emphysema. Subcutaneous emphysema also can result from the undermining skin wounds alone, making diagnosis of tracheal perforation difficult in some cases and adding to the difficulty of detecting a tracheal wound. Perforation of the esophagus is common. Esophageal injury may lead to abscess formation and tissue necrosis as a result of contamination of surrounding tissues by esophageal contents. An abscess may physically impinge on the airway, making swallowing difficult. Neurologic damage from the primary injury or damage caused by abscessation may inhibit normal function of the soft palate.

Tetanus antitoxin should be administered to these animals, as well as broad-spectrum antibiotics (e.g., florfenicol, 20 mg/kg every 48 hours) to combat wound infection and sepsis. Antibiotics with good efficacy against anaerobic bacteria (e.g., penicillin, 20,000 IU/kg twice daily) should be considered in cases in which massive trauma has resulted in some tissue devitalization. All skin wounds must be thoroughly cleaned of organic debris and foreign material. Establishing drainage in undermined skin wounds also is important. Some of these wounds lend themselves to débridement and delayed primary closure, whereas others are best managed by allowing healing by second intention. The veterinarian must be conscious of injury to muscle and joints deep beneath these skin wounds. Supportive care in the form of fluids and nonsteroidal antiinflammatory drugs (NSAIDs) (e.g., flunixin meglumine, 1 to 2 mg/kg given intravenously [IV]) is important in treating any myopathy.

Fractures

The hallmark of long bone fracture in small ruminants is acute non–weight-bearing lameness. A thorough physical examination must be performed to rule out other causes of severe lameness, including septic arthritis, joint luxation, and severe footrot. Clinical assessment should readily detect instability and crepitance on palpation of the fracture site. The exception is an incomplete or greenstick fracture that manifests itself as less severe acute lameness that resolves with time. The clinician should not overlook the possibility that an incomplete fracture may suffer a catastrophic breakdown and become unstable, rather than healing. Because of economic constraints, radiographic examination may be impractical. However, whenever possible, radiographic evaluations before and after repair will enhance the success of the procedure.

The most commonly treated fractures occur in the metacarpal and metatarsal bones.²² These fractures usually are treated successfully with casting. Fractures of the distal half of the metacarpal and metatarsal bones often respond well to use of lower limb casts that incorporate the foot and extend proximally to a point just distal to the carpus or tarsus respectively. Proximal or comminuted metacarpal and metatarsal fractures may require full-limb casting with or without transfixation pins to stabilize the fracture properly and prevent collapse.

Many fractures of the carpus or tarsus also respond to treatment with a full-limb cast.²³ However, these injuries are often associated with contamination of the joint, and the incidence of septic arthritis is high. Septic arthritis requires more intensive antibiotic therapy, as well as local treatment provided through a window in the cast. One frequent complication with using treatment windows in casts is “window edema.” The cast window should be cut out as one piece. Edema can be minimized by securing this piece in the window with tape between treatments. The management of carpal or tarsal fractures with concomitant septic arthritis is difficult. Ankylosis of the joint often results even if successful fracture healing occurs.²³

Radius fractures must be evaluated individually to determine the best mode of treatment. Fractures of the distal radius may respond to a full-limb cast. Proximal radius fractures may heal better with the use of an external fixator, a transfixation cast, or possibly a modified Thomas splint. Use of splints may be very applicable for neonates, and the splint need stay in place for only 2 to 4 weeks in most instances.²⁴ Some radius fractures may be best treated with internal fixation using plates and screws. Internal fixation is seldom required, however, and often is not economically feasible in small ruminants. If a splint is used for a radius fracture, it should extend from the ground or fetlock to the elbow and preferably above it.²⁴

Treatment decisions for tibia fractures are very similar to those for radius fractures. Distal fractures heal well with full-limb casting.²⁵ The fractured tibia responds well to an external fixator or in larger goats (over 60 pounds) a transfixation full-limb cast (Figure 11-3). Fractures of the humerus and femur occur less frequently in small ruminants.²² Humerus fractures often heal with stall rest alone. However, the distal limb frequently suffers carpal contracture, rendering the animal unsound regardless of fracture healing. Femoral fractures may heal if the limb is taped to the abdomen in a modified Ehmer sling (made of tape placed in figure-eights around the limb). This method is less costly but is still effective in young or lightweight animals.²⁴ Fractures of the humerus and femur frequently heal better with internal fixation using plates and screws or intramedullary pins. The mode of internal fixation depends on the complexity of the fracture and the experience of the veterinarian. Financial considerations may dictate the use of intramedullary pins rather than plates and screws when possible.

Figure 11-3 Lateral and dorsoplantar radiographs of a midshaft oblique fracture of the tibia in a mixed-breed goat. This is the type of fracture that usually responds well to use of an external fixator or transfixation cast, depending on the weight of the animal.

Fractures in other areas such as the scapula and pelvis can be treated much as they are in the dog. Small ruminants usually are good orthopedic patients because of their relatively small size and ability to maneuver well on three limbs. Often pelvic or scapula fractures heal if the animal is confined for 3 to 6 weeks.²⁴ The veterinarian can form a plan for treating unusual orthopedic injuries in small ruminants by applying principles of small animal orthopedics and considering cost-benefit decision-making processes for food animal medicine.

Mandible fractures may occur in small ruminants that have been kicked by a large animal such as a horse or cow and those that have caught the rostral mandible in a fence or some other object. A kick injury may result in any number of fracture configurations; the veterinarian must refer to information on small animal fundamentals to determine whether plates, wires, or pins are the most appropriate surgical stabilizers. Frequently external fixators can be used to treat mandibular fractures. In our own practice, we use cortical bone screws placed in the mandible through stab incisions, leaving the screw to protrude about 2 to 4 cm out of the skin. Then acrylic is made to fit over the screw heads and act as connecting bars of an external fixator. The screws provide better stability in the mandible than that afforded by transcortical pins, and the acrylic allows more liberty in screw placement than that permitted by traditional connecting bars. Rostral fractures may involve mostly teeth and soft tissues but very little bone. They often cause loss of teeth but minimal instability. Therefore the veterinarian may wish to debride the area, institute antibiotic therapy, and recommend appropriate modifications to the animal’s diet. If the mandibular fracture occurs between the incisors and the cheek teeth, it may be stabilized by securing wires from the rostral mandible to the cheek teeth.^26,27 Animals with these types of fractures require nutritional support, provided either orally or parenterally (see Chapters 2). Many of these animals can be fed a moistened pelleted diet.

Occasionally digit or leg amputation is required to treat septic conditions, fractures, or luxations. Amputation can be done with the animal under general anesthesia or with use of sedation and local anesthesia (see Chapter 18). For digit amputation, a tourniquet should be applied proximal to the fetlock after the surgical site is prepared in an aseptic manner. A circumferential skin incision is made just proximal to the coronary band. The surgeon may then make two incisions perpendicular to the circumferential incision (one dorsal and another palmar or plantar) to create a skin flap that is elevated to allow amputation with Gigli wire. We prefer to make one incision over the abaxial aspect of the affected digit perpendicular to the coronary band to create an inverted T incision. The two flaps of the inverted T can be undermined to allow the passage and crossing of the Gigli wire. The amputation should be completed on an angle at the distal aspect of the proximal phalanx (Figure 11-4), with removal of all of the articular cartilage and synovial membrane of the proximal interphalangeal joint; the interdigital ligaments are left intact to provide stability to the fetlock. The corners of the flaps of the inverted T can be trimmed to minimize dead space when the surgical site is closed. The site can be closed completely if the amputation is performed as a treatment for fracture or luxation. However, if infection is present in the form of septic arthritis or osteomyelitis, the clinician should consider the advantages of drainage facilitated by partial closure. With either closure, a bandage should be placed on the foot to aid in hemostasis before the tourniquet is removed. The bandage should be changed as needed until the incision site has healed. The use of broad-spectrum antibiotics (oxytetracycline 10 mg/kg given IV or intramuscularly [IM] twice daily, or 20 mg/kg once a day every 48 hours) and antiinflammatory drugs should be considered.

Figure 11-4 Intraoperative photograph of claw amputation in a goat. The amputated claw is to the left and the angled cut end of P1 is in the center of the photograph. The skin edges will be trimmed and partially closed to allow drainage.

If a limb is to be amputated, the practitioner should first determine postoperative use, living environment, and management of the animal in detailed interviews with the owner. The impact of age and weight on these considerations can then be assessed. Limbs usually are amputated as high as possible (midhumerus, midfemur) to prevent trauma to the remaining “stump” of the limb. In our experience, violation of this principle in amputations of the hindlimb of camelids can nonetheless lead to good results. The amputation done just below the hock allows a partial limb to aid in rising. This approach does present additional management concerns in that the hock must be protected from trauma by bandages or a protective boot. However, the practitioner should consider this technique when amputating the distal hind limb in small ruminants. Once the location of the amputation has been determined, techniques similar to those used in other small animals can be applied to limb removal in sheep and goats.

Splints

Splints can be useful in treating some musculoskeletal conditions in small ruminants. However, the veterinarian should be selective in using them. Many practitioners are more comfortable using casts and external fixators than applying and monitoring splints. Many of the small ruminants presented to referral centers for malunion or delayed union of fractures have previously been treated with splints. For this reason alone, the initial use if other techniques that achieve more stable fracture fixation should be considered. However, splints can be useful in selected cases if the practitioner is skilled at splint management. In emergency situations, a splint can be made of cut polyvinyl chloride (PVC) pipe or other such material.²⁷

A spoon splint, either commercially manufactured or fashioned from cast material, probably is best used to support greenstick fractures of the distal limb. When used in this way, the spoon splint helps prevent catastrophic breakdown of the fracture. However, a more important role may be in preventing the limb contracture that can occur if the carpus is allowed to remain flexed for a prolonged period in a non–weight-bearing animal. With this technique, a padded bandage is placed on the limb and the splint is conformed to the bandage and secured with adhesive tape.

Another type of splint occasionally used in small ruminants is the traction splint, commonly referred to as the Schroeder-Thomas splint (Figure 11-5). This splint usually is made of aluminum rods and consists of a ring that fits in the axillary or inguinal region of the animal with bars on the dorsal and palmar or plantar aspect of the limb joined distally. The shape of the splint varies, as does the way particular parts of the limb are secured to the splint depending on the specific reason the splint is applied. Traction is applied by securing the foot to the distal splint with adhesive tape or by placing wires through the hoof wall. A soft bandage should be placed on the limb, after which the limb is secured strategically to the splint. Usually tape is placed over the entire limb and distal splint.¹¹

Figure 11-5 Application of a Schroeder-Thomas splint to the front limb of a yearling mixed-breed goat. Notice the bandage on the limb as well as the padding and initial tape to secure the limb to the splint before it is covered with more tape.

Septic Arthritis

Bacterial infections of the joints (septic arthritis) occur most commonly in neonates. However, older sheep and goats sporadically suffer from joint infection as a result of a penetrating injury or spread from adjacent infected tissues, as in the case of footrot. In neonates, septic arthritis is most often a sequela of septicemia and often is a consequence of failure of passive transfer.¹ Bacteria isolated from lambs include Streptococcus, Escherichia coli, Arcanobacterium pyogenes (formerly Actinomyces pyogenes), Erysipelothrix insidiosa (rhusiopathiae), Pasteurella haemolytica, Corynebacterium pseudotuberculosis, and Fusobacterium necrophorum. Staphylococcus aureus arthritis is associated with tick pyemia, a disease seen in lambs 2 to 6 weeks old in areas infested with Ixodes ricinus ticks. Streptococcus dysgalactiae has been reported as a cause of arthritis in dairy goats and was the most common pathogen isolated from arthritic lambs in England and Wales. Other isolates included E. coli, coagulase-positive Staphylococcus, E. rhusiopathiae, and A. pyogenes.² Coexisting omphalitis was found in 16% of arthritic lambs.

Erysipelothrix polyarthritis is a nonsuppurative condition usually seen in 2- to 6-month-old lambs, but it also may be seen in neonates. Outbreaks may affect as many as 40% of the lambs in a flock. Hallmarks of this infection are fever and lameness, with minimal swelling of joints. This nonsuppurative polyarthritis will progress to chronic arthritis if not treated appropriately.¹

Chlamydial Polyarthritis

Chlamydial polyarthritis is a common contagious disease of feedlot lambs in the United States. The disease is suspected to occur in goats as well.⁵ The causative agent formerly was considered to be a strain (immunotype 2) of Chlamydia psittaci but has been reclassified as Chlamydophila pecorum.^6,7 Economic losses associated with chlamydial arthritis result from weight loss and treatment costs. Disease occurs in 1- to 8-month-old lambs, with 3- to 5-month-old lambs most commonly affected.⁸ Outbreaks in feedlots often occur a few weeks after lambs are introduced.⁸ Morbidity can be as high as 80%, with less than 1% mortality.⁷

Mycoplasmal Polyarthritis

Mycoplasmal arthritis is a highly fatal disease of goats marked by polyarthritis, septicemia, and mastitis. This disease usually is caused by Mycoplasma mycoides subsp. mycoides Large Colony (MmmLC), recently reclassified as a serovar of Mycoplasma mycoides subsp. capri.¹² Other mycoplasmal species (Mycoplasma agalactiae, Mycoplasma capricolum, Mycoplasma putrefaciens) cause similar syndromes.¹³ This is distinct from the small colony (SC) or bovine biotype of Mmm that causes contagious bovine pleuropneumonia (CBPP), a disease eradicated from the United States in 1892. Sheep may be experimentally infected, and natural infection in sheep is suspected to occur.¹⁴

Mycoplasmal arthritis occurs as an epizootic condition in many countries throughout the world. In the United States, most outbreaks are in large goat dairies. Morbidity and mortality rates as high as 90% have been reported in kids.¹⁵ M. putrefaciens was responsible for the loss of 700 goats in one California dairy.¹⁶

Mmm usually is introduced to a farm by an asymptomatic shedder. The bacteria are shed in the colostrum and milk of infected does, and ingestion is thought to be the primary source of infection of kids.^14–16 In one outbreak, approximately half of the does were noted to shed Mmm organisms in milk. Some were intermittent asymptomatic shedders, but clinical mastitis ultimately developed in most animals.¹⁷ Horizontal transmission was documented among kids housed together and is likely to occur among adults, especially in the milking parlor.¹⁸ Illness often follows stress such as from castration, dehorning, concurrent disease, bad weather, and overcrowding.^16,17,19

Osteomyelitis

Bone infections usually result from hematogenous spread of organisms or from direct inoculation associated with trauma to soft tissues covering the bone. The soft tissue damage may be from either an acute injury (trauma or surgical incision) or that associated with development of decubitus ulcers in a recumbent animal. Occasionally the tissue damage is incurred during normal recumbency when animals are housed on hard, rough surfaces and is not a sequela of debilitation. The infectious agents include Corynebacterium, A. pyogenes, Rhodococcus equi,²² and E. coli.

Caprine Arthritis-Encephalitis

Caprine arthritis-encephalitis (CAE) is a chronic multisystemic disease of goats caused by a nononcogenic retrovirus. Infection with caprine arthritis-encephalitis virus (CAEV) is widespread, and chronic polyarthritis is the most common clinical manifestation.²³ CAEV is closely related to the viruses that cause ovine progressive pneumonia (OPP) and maedi-visna,²⁴ and together these are referred to as small ruminant lentiviruses (SRLVs). Phylogenetic analysis has determined four sequence groups, designated A to D, and several subtypes for SRLVs. Some subtypes of these viruses occur in both sheep and goats, and there is evidence of transmission of SRLVs between the species.²⁵

Seroprevalence rates for CAEV in goats in the United States, Canada, and Europe range from 38% to 81%.^23,26,27 Seroprevalence in England, Australia, and developing countries usually is less than 10%.²⁸ Clinical arthritis is estimated to occur in less than 25% of seropositive animals but it may be more prevalent in some herds.^23,27 The prevalence of other clinical syndromes is not known. Infection occurs by transmission of fluids that contain infected macrophages from an infected animal to an uninfected animal. The most efficient manner of transmission is from dam to kid by ingestion of colostrum or milk from infected does.²⁹ The presence of antiviral antibodies in colostrum is not protective. Feeding nonpasteurized milk increases the risk of infection.^26,27

Horizontal transmission of CAEV also is important.^29,30,31 When uninfected goats are housed with infected goats for long periods, a significant number seroconvert.²⁹ Uninfected does readily seroconvert when milked with infected does, presumably as a result of transfer of the virus during the milking process.²⁹ Venereal transmission is possible, especially if one of the animals exhibits clinical disease.³² Transmission from doe to kid before or during parturition has been documented.³⁰ No evidence supports transmission by an insect vector. Iatrogenic transmission (on dehorning equipment or needles) also is possible. The likelihood of transmission from a contaminated environment is very low.^31,32