Hypertrophic Osteopathy
■ Clinical Signs Horses of any age or breed and either gender can be affected with HO. Some evidence suggests that HO may be more common in male horses and large-breed horses.6 Ponies and donkeys can also be affected.11,14
Common clinical signs of HO include lameness, stiff gait, and reluctance to move or trot.1,6,7 Firm bony enlargements are present on the distal extremities.
In some cases, there may be soft tissue swelling or edema adjacent to the bony enlargements. In some horses the limb swelling is warm and painful to palpation, whereas in others the swelling is cold and painless.6 Pain can frequently be elicited by forced flexion of the major joints. Bony enlargements are usually bilateral and symmetric and often affect the cranial, lateral, and medial aspects of the affected bones.1,6,7 All four limbs are often affected, although the forelimbs are sometimes more severely affected.6 The metacarpal and metatarsal bones are most often affected; other sites that can be affected include the phalanges, carpus, tarsus, radius, and tibia, as well as the maxilla, facial crest mandible, and nasal bones.2,6Affected horses may or may not show signs related to the primary underlying disorder, such as cough, fever, weight loss, ventral edema, tachypnea, or colic.6 Clinicopathologic features are highly variable and depend on the underlying primary disease process. Generally, there is increased serum activity of alkaline phosphatase, associated with increased osteoblastic activity at the sites of periosteal proliferation.6
Radiographically, the bony enlargements are characterized by periosteal proliferative new bone formation of the diaphysis and metaphysis of affected bones.1-3,6,7 The periosteal reaction often exhibits an irregular palisade pattern of osteophyte forma- tion.1,6,7 The bony reaction may extend to the chondrosynovial junctions; the articular surfaces are usually not affected.7 Nuclear scintigraphy may reveal focal areas of intense uptake of radiopharmaceuticals at the sites of bony enlargement.1,4
■ Treatment and Prognosis The prognosis for horses with HO is guarded and depends on the underlying disorder.
In one study, 71% of horses with HO were euthanized.6 Gradually progressive limb swelling and pain are the typical clinical course in most affected horses for which an underlying cause is either not identified or effectively managed.7 Thus management of HO should be directed at identification and treatment of the underlying primary disorder if possible. Common methods to help identify the underlying disease include hematologic studies, serum chemistries, fibrinogen, thoracic radiography, thoracic and abdominal ultrasonography, abdominocentesis, thoracocentesis, gastroscopy, rectal examination, laparoscopy, and in some cases computed tomography.2,6,7 Successful management of the primary underlying disorder has resulted in partial or complete regression of the skeletal disease in a limited number of equine cases.1,3-6,19 Regression of HO is characterized by a decrease in limb swelling and lameness, and a return to athletic performance is possible if bony lesions are not advanced.1,6 In a few idiopathic cases in which an underlying disorder was not identified, lameness and bony reactions decreased with rest, phenylbutazone, or corticosteroid therapy.2,6Fescue Foot
Meredyth L. Jones
■ Definition and Etiology Tall fescue (Festuca arundinacea) is a cool-season grass native to Western Europe and introduced into the United States perhaps as a contaminant of other seeds in the late 1800s. It is well adapted to the transitional areas between the northern and southeastern regions of the United States but can be found in areas across the country. Fescue is associated with several toxic syndromes in livestock when infected by endophyte Neotyphodium (Acremonium) coenophialum, a Clavicipitaceae fungus. Ergot alkaloids, most importantly ergovaline, are produced by the fungus and have vasoconstrictive effects on the feet and other extremities, leading to tissue slough. Fescue foot is considered a disease of cattle, but sheep may also be affected.1
■ Clinical Signs, Diagnosis, and Differential Diagnoses Clinical symptoms of fescue foot occur within 42 days of exposure to endophyte-infected fescue.1 Affected cattle may arch their back and have a rough hair coat in addition to limb signs.
Limb lesions occur most often in the hindlimbs, starting as a red line at the coronary band with edema,2 and the hair is easily epilated. A gangrenous process leads to purple-black discoloration and eventual sloughing of the skin. The tips of the ears and tail may be similarly affected. Lameness becomes severe as lesions progress, and animals may knuckle and prefer not to stand. There appears to be individual variation in susceptibility to fescue toxicity and severity of lesions.Diagnosis is based on characteristic clinical signs and documentation of high endophyte infection of fescue to which animals were exposed. A sharp line of demarcation will be present between perfused and nonperfused tissues. Histopathology reveals vascular thrombosis and necrosis of compromised tissues.
Fields can be screened for percent infection by endophytes by submitting tillers (grass shafts at ground level), seed stems, and seeds. The target laboratory for this analysis should be contacted regarding the best sample for current growth phase of the plant and sample handling instructions. Ergovaline testing via high-performance liquid chromatography (HPLC) is available through some reference laboratories, and samples should be shipped on ice or kept frozen until shipment.3
Differential diagnoses for the lesions of fescue foot include ergotism of Clavicepspurpurea, selenium toxicity, salmonellosis, and frostbite. Sarcocystosis in cattle has been associated with hair loss at the tip of the tail.4 In the very early phases of the disease when only redness and edema are present, traumatic injury, laminitis, and foot rot may be suspected.
■ Pathophysiology The toxicity of fescue is likely multifactorial and may include compounds produced by the grass itself (loline, pergoline, others); however, fungal endophytes are widely accepted as the primary mechanisms of toxicity.5-10
N. coenophialum production of ergovaline, ergonine, ergosine, and lysergamide results in vasoconstriction and is noted to be the primary etiologic agent5,6,10; however, several other fungal types from infected fescue have produced dermal edema and necrosis when experimentally evaluated in rabbits.11 Threshold dietary levels of ergovaline of 400 to 750 ppb in cattle and 500 to 500 ppb in sheep have been established for the production of fescue foot lesions.1
Studies of blood flow in sheep and cattle fed highly endophyte-infected fescue indicated that blood flow was reduced in the adrenal glands and limb skin of sheep and in the truncal skin, cerebellum, duodenum, and colon of steers.12 Although the visible clinical lesions indicate peripheral vasoconstriction, core visceral vasoconstriction clearly occurs as well.
Lesions occur most often in cooler weather,1 which is the season favored by the grass, especially when there is snow and ice, which likely worsen vasoconstriction.■ Treatment and Prognosis As soon as the disease is suspected, all animals should be removed from the pasture if possible. Once necrosis is occurring, treatment is unrewarding and euthanasia is recommended for animals whose pain cannot be controlled. Early cases may respond to supportive therapy on soft ground and local or systemic antimicrobial therapy for protection of deep digital tissues from bacterial invasion through compromised skin. The use of NSAIDs should be considered carefully. Inhibition of the COX-2 pathway may result in vasoconstriction and platelet aggregation, making a theoretical case for avoiding NSAIDs in cases of fescue foot.
■ Control and Prevention In a USDA study of fescue pastures, 61.6% were infected with endophyte nationwide, with more than 75% of pastures in the Southern United States infected.13 In such conditions, providing legume supplementation or overseeding with clover or lespedeza, along with sufficient protein and adequate trace minerals, has shown the most consistent benefit in reducing the impact of the toxin. Feeding fescue as hay before the seed heads are out may reduce the impact, but toxic pasture grass will remain toxic even as hay. However, one study in Missouri indicated that, with stockpiling and storage of hay, endophyte levels in infected fescue were reduced, while nutritive value was retained.14
When starting fescue, certain strains, such as Ky-31, should be avoided for livestock, as they have high toxic potential.15 High soil nitrogen exacerbates toxicity, and fertilization of infected cultivars should be limited. Endophyte-free cultivars of fescue do exist, and some states require the packaging of fescue seed to declare the level of endophyte infection, with target levels of 0% to 5%. Unfortunately, endophyte-free fescues are less hardy and easily overtaken by infected fescue contaminating the pasture.