Continued from page 4Non-infectious Neuromuscular Diseases
Key points: Head tremors and ataxia, fatal, possible genetic etiology, only reported in emus.
Lysosomal storage disease has been reported in a six month old female emu. The clinical signs that were noted were head tremors and ataxia. Gross necropsy showed no significant lesions at all, and histopathology of the brain revealed neuronal cytoplasm to be vacuolated and granular. Similar changes were noted in the spinal cord. Two possibilities were suggested regarding potential etiology: a genetic storage disease or plant toxicosis of the genus Astragalus (locoweed), with genetic etiology being most likely.
Toxicology
Numerous toxicologic problems have been documented in ratite species. These have manifested similarly, in general, to what is seen in other birds. Neuromuscular involvement and clinical signs may be seen compatable with the age, dose, and severity of the toxins and their active principles encountered.
Acute selenium toxicity was diagnosed in four ratite cases. These chicks had been given 3 mg doses of selenium as an injection to prevent or treat white muscle disease. These birds died acutely with pulmonary edema and conjestion. Liver selenium from those birds ranged from 6.97 ppm to 9.8 ppm. These types of cases suggest that empirical dosage with parenteral vitamin E/Se compounds may not always be the best management approach to consider.
Leg Deformities
Limb deformities are common in ratite chicks. "Leg abnormalities", "splay leg" or "leg problems" are popular all-inclusive terms used to describe conditions such as twisted or bowed bones and swollen hock joints with or without slipped tendons. The most common deformities encountered are usually characterized by progressive external rotation of the tibiotarsus and/or the tarsometatarsus, although numerous other deformities are also noted. Other deformities that are noted include tibial dyschondroplasia, perosis or chondrodystrophy, rickets, retained cartilage cores and osteochondrosis dissicans. The etiology of these problems are uncertain and most likely multifactorial. In the future study of these leg problems, it will be particularly important to characterize the type of leg problem being encountered, the environment the animalsare in (temperature, light, litter condition and type and air movement), genetics and heritige of the animals, health status of the breeder birds as well as the chicks and the nutrient content of the diet. Provision of adequate room for exercise tends to reduce the incidence of most of these deformities, lending support that many have primary roots in management and exercise. Derotational osteotomy may correct the deformity in select cases, particularly tibiotarsal rotation, but the prognosis is poor. Stack pinning with hemicerclage wires, K-E devices and plates have all been reported. Periosteal stripping is described for correction of tibiotarsal rotation in ratites, although the true success rate is questionable with this and most other techniques for correction of these problems of unknown cause.
Chondrodystrophy or Perosis
Chondrodystrophy or perosis is characterized in poultry species by shortened and thickened long bones, a gross enlargement and malformation of the tibiometatarsal joint with twisting and bending of the distal end of the gastrocnemius from its condyles. It is unlike rickets in that bone mineralization is not impaired. Even though chondrodystrophy has been shown to be heritable, it is precipitated by a wide variety of nutrient deficiencies, including manganeze, zinc, choline, niacin, biotin, folic acid and pyridoxine.
The complexity of the nutritional etiologies of some of these deformities can be enlightened by a review by Angell of the known poultry information on chondrodystrophy, or perosis:
A manganese deficiency will result in perosis in chicks. High intakes of calcium and phosphorus will aggrevate the manganese deficiency. A diet deficient in zinc but adequate in all other known nutrients will produce perotic signs. Choline deficiency causes histopathological changes in the epiphyseal cartilage similar to those found in manganese deficient chicks. Turkey poults deprived of dietary niacin exhibit lesions in the epiphyseal cartilage typical of perosis induced by manganese and choline deficiencies. Turkeys fed a diet deficient in biotin during the first four weeks of lifeexhibited reduced growth and an increased incidence of perosis. A folic acid deficiency has a detrimental effect on cartilage proliferation and maturation ahd has been found to induce perosis. Diets containing a high level of protein that was deficient in pyridoxine generated perotic chicks.
Tibial Dyschondroplasia
Tibial dyschondroplasia is characterized by an unmineralized, unvascularized plug of cartilage in the proximal metaphysis of the tibiotarsus and sometimes the tarsometatarsus. Severe bowing or fracture of the proximal end of the tibiotarsus occurs in some cases of tibial dyschondroplasia. Genetic and dietary influences have been described. Control in poultry is believed by some researchers to be genetically controlled, and possibly associated with a sex-linked recessive gene. Nutritional factors are still very likely in ratite species manifesting tibial dyschondroplasia.
Rickets
Rickets is generally accepted to be a pediatric disease precipitated by nutritional deficits. Specifically, vitamin D, calcium andn phosphorus nutritional imbalances are incriminated. The quantity of these nutrients as well as their ratios are important in evaluation of a diet for possible predisposing factors. Rickets is characterized by widening of the epiphyseal cartilage accompanied by decreased blood supply to the region, thus the osseus tissue is poorly calcified. The bones, beak and claws become soft and pliable and lameness may occur. Rickets associated with phosphorus imbalances differs from the classical form described above for calcium and vitamin D in that it does not usually involve the epiphyseal cartilage but all other signs are similar. Imbalances in the calcium to phosphorus ratio tend to occur when chicks are fed breeder diets, given free access to oyster shell or a high amount of alfalfa hay with no supplemental phosphorus. Ideally, chick diets are maintained with a calcium / phosphorus ratio no greater than 2.25/1.
Myopathies
Degenerative myopathies are common observations at the pathology floor in ostriches, emus and rheas submitted for necropsy. The majority of these birds are less than six months of age. Several etiologies have been reported, including capture myopathy, vitamin E/Selenium deficiency, furazolidone and iophore toxicity. Normal organ and tissue levels of vitamin E or Selenium are not yet determined in ratite species.
Slipped Tendons
Slipped tendons occur in both the ostrich and emu, and are more common in chicks than adults. Manganese nutritional deficiency has been suggested as a potential cause. The gastrocnemius tendon slips from the caudal aspect of the hock usually to the lateral side. The retinacular sheath that holds the tendon in place generally tears on the medial aspect of the hock. Early injuries in small chicks can be corrected by bandaging alone in many cases. Surgical repair of the retinacular sheath carries a good prognosis as long as the injury is acute, and the skin has not been broken open, contaminating the joint. Secondary bony growth abnormalities may occur following succesful repair of slipped tendon, and long term prognosis for these developing chicks remains guarded at best.
| Top | Back | Next |
 NetPets® Main Page |  The Bird Center |