Continued from page 1Nutrition
Numerous pelletized diets are currently available for ratite species. Most of these products are quite variable in price, content and quality, and very few fomulated diets are actually supported by scientific trials and clinical evaluation methods. Range raised ostriches in Africa are fed on alfalfa pastures and supplemented with maize. General targets of 16-20% protein, 10% fat, 10% fiber are believed to be good starting points for most captive ratite species. Diets of 18% protein produced the best weight gains in one study of ostrich chicks that compared only the effects of varying the dietary levels of protein.
In adult bird nutrition, the adequacy of the breeder diet is believed to be reflected in the eggs produced. Generally speaking, hens deficient in carbohydrates, proteins and fats produce fewer and smaller eggs. Vitamin and mineral deficient breeder diets can result in similar nutrient deficient eggs.
The feeding of higher protein diets to young birds is expected to induced accelerated rates of growth and potentially predispose to some leg deformities. Hypovitaminosis A was described in rhea chicks with clinical epiphora, oral abscesses and decreased growth rates. A goose stepping gait was believed to have been corrected with supplemental vitamin B6. Thiamine deficiencies are thought to produce "star gazing" in ostriches. Riboflavin is possibly incriminated in the curled toe deformities of ostriches. Pantothenic acid and biotin are associated with curling of the feathers and hyperkeratosis of the skin around the mouth, beak, feet and neck. Hypovitaminosis E was suspected in a group of ostrich chicks fed a diet of crushed corn. Clinical signs were characterized by paresis, poor weight gains, high AST and CPK levels.
Metabolizable energy values (ME) for 3,6,10 and 17 week old and 30 month old ostriches was determined, and fat and neutral detergent fiber (NDF) digestibilities were also determined. The determined levels of ME were: 3 weeks, 1731; 6 weeks, 2337; 10 weeks, 2684; 17 weeks, 2739, and 30 months, 2801 kcal/kg. Fat digestibility was 44.1% at 3 weeks and 91.1% by 17 weeks of age. NDF digestibility was 6.5% at 3 weeks, 51% at 10 weeks and 61.6% at 30 months. Also, vitamin and mineral levels were determined in the eggs of ostriches and emus and compared to poultry values. Deficiencies or excesses of vitamins and/or minerals in the laying hen, and thus in the egg can lead to infertility, poor hatchability and early chick health problems.
The emu was found to have digested 35-45% of the neutral deterget fiber (NDF) in their diet when fed a high fiber diet (26-36%) and that the energy from the digestion of NDF contributed up to 50% of the maintenance requirements. When compared to similar data of the ostrich above, the emu is clearly less efficient at NDF digestion than the emu.
Infectious Diseases With Neuromuscular Manifestations
Viral Diseases
Newcastles Disease (PMV-1)
Key points: Seen in all ratites; extremely variable signs - including neuromuscular signs of limb paralysis, torticollis, tremors and opisthotonus. Limp neck, twitching of neck muscles, inability to get up and ataxia may be seen in ratites. Infected and vaccinated birds rapidly mount HI titers. Gross lesions lesions include enlarged livers and epicardial hemorrhage, but histopathological lesions may not be found.
The causative agent of newcastles disease is an enveloped 100-200 NM virus from the paramyxoviridae family, and is classically attributed to serotype 1 (PMV-1). there are five pathotypes known: viscerotropic velogenic, neurotropic velogenic, mesogenic. lentogenic and an asymptomatic pathotype. There are nine recognized serotypes of newcastles virus.
Clinical signs of newcastles virus infection are extremely variable, ranging from sudden death to no signs at all. In general, viscerotropic velogenic pathotype infection is associated with intestinal signs, neurotropic velogenic and mesogenic are associated with respiratory and neurologic signs, and lentogenic is associated with respiratory signs. Depression, diarrhea, anorexia, coryza, conjunctivitis, rhinitis, sneezing, coughing, dyspnea, limb paralysis, torticollis, tremors and opisthotonus have all been noted. Perhaps most significantly, however, a break in egg production, or "egg pause syndrome" is commonly seen with no other outward clinical signs.
Transmission of virus is primarily by the fecal-oral routes and respiratory aerosols. Humans seem to play a central role in the spread of NDV, usually by the movement of live birds, fomites, personnel and bird products including feces to susceptible birds. Artificially created conditions such as ventilation exhaust has had particular importance in the spread of this disease in poultry houses. Non-VVND newcastles virus is endemic in the wild bird population of some areas of the United States, and VVND is recognized as endemic in many other countries.
Newcastle Disease has been reported in ostriches, emus, rheas and cassowaries. A 1988 outbreak of Newcastle Disease in an ostrich flock 5 to 8 months in age had13 out of 46 chicks die in a three week period. Clinical signs included a limp neck while the head was bent in a torticolis posture. Rhythmic tics of the cervical muscles were observed. Loss of balance, inability to stand up and total paralysis developed in a few days, followed by edema of the head and neck. Gross necropsies revealed enlarged livers and epicardial hemorrhage. Of significant interest from a diagnostic point of view, no histologic lesions were detected, although virus was isolated from the brain of one chick. Surviving chicks had hemagglutination inhibition titers for Newcastle Disease on convalescent samples. Three of five ostrich chicks died following experimental infection with a chicken isolate of Newcastle Disease virus by intramuscular injection and by aerosol. Neurologic signs developed at 5-10 days post- and virus was recovered from various organs. HI antibodies increased rapidly. No histologic lesions specific for Newcastles Disease were seen in these experimentally infected chicks either. Infected chicken flocks are believed to be most common sources of infection. Fomite transmission via visitors or wild birds is suspected. Vaccination with a modified live eye drop product (LaSota) has been shown to produce antibody in ostrich and emus.
PMV-1 (non-VVND) and PMV-2 have been isolated from ostrich chicks in the United States, but not necessarily correlated with disease. Of interest, newcastles virus (PMV-1), non VVND strains, is viewed as endemic in some regions of California, particularly in the sierra foothills. Numerous wild bird populations including pigeons, sparrows and finches are known to carry lentogenic and mesogenic strains of this virus asymptomatically. Concurrently, a popular means of routine vaccination for the turkey and chicken flocks in the same area is via nebulization of live lentogenic PMV-1 strains. This results in the release to the outside environment of large amounts of live virus - some of these locations are fairly close to ratite collections and farms. There are no known adverse effects of this practice, but the potential pathogenicity of some of these PMV-1 strains on neonatal ostrich chicks is truely unknown.
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