CLINICAL AND PATHOLOGIC FINDINGS OF AN OUTBREAK OF VITAMIN D3-RESPONSIVE METABOLIC BONE DISEASE IN HERON AND EGRET (FAMILY ARDEIDAE) CHICKS FED CAPELIN (MALLOTUS VILLOSUS).

An increase in cases of metabolic bone disease (MBD) in chicks of six species of heron and egret (family Ardeidae) was identified at a wildlife rehabilitation center in the spring and summer of 2018. The outbreak affected 34.3% of birds in care for four or more days during the first 3 mo of the study and was the most common reason for euthanasia during that time. Cases were characterized by lameness, increased flexibility of multiple long bones, angular deformities, and bone fractures. Gross postmortem examinations were conducted on 145 nestlings and fledglings that died or were euthanatized either because of MBD or for unrelated conditions. Histology was performed in four cases and three controls. Histologic findings were characterized by multiple lesions in the appendicular long bones, including variable elongation of the physis, retention of cartilage cores in the metaphyseal primary spongiosa, poorly mineralized osteoid seams within the primary spongiosa, thinning or lack of diaphyseal cortical bone compaction, and folding fractures typically propagating through the physis-metaphyseal interface. Folding fractures were often associated with focal metaphyseal fibroplasia. The parathyroid gland diameter of birds diagnosed postmortem with MBD in care was significantly larger than that of unaffected birds. The authors hypothesized that a dietary deficiency of vitamin D3 because of low levels in the bird's captive diet of capelin (Mallotus villosus) was the cause of the MBD. Starting in mid-July every chick's diet was supplemented with 714 IU oral vitamin D3/kg body weight per day, after which the number of birds developing MBD declined to a rate of 4.3%. This study characterizes the clinical, gross, radiographic, and histologic features of vitamin D3-responsive MBD in young herons and egrets and provides evidence to support the recommendation that captive birds on a diet of capelin be supplemented with vitamin D3, especially during growth.

A review of vitamin D and its importance to the health of dairy cattle.

This Research Reflection short review will discuss vitamin D metabolism, its role in nutrition, disease prevention, and welfare of dairy cattle, as well as its toxicity. Vitamin D is an important fat-soluble vitamin. However, some researchers regard it as a hormone due to its function in the organism. Its role is not limited just to Ca homoeostasis and bone metabolism but is also associated with immunity. In dairy cattle it is known for preventing milk fever. Cows can acquire vitamin D in many ways for example through feed, parenteral injections or through UVB irradiation from the sun or artificial lighting. The vitamin D in feed can either be plant-/ fungi- based ergocalciferol or animal-based cholecalciferol. There is currently only one registered feed vitamin D supplement for cattle in the European Union and it is cholecalciferol. Animals can also synthesize their own vitamin D when 7-dihydrocholesterol in the skin is irradiated with UVB light resulting in cholecalciferol production. Despite its importance, many cattle are deficient in vitamin D due to inadequate supplementation or insufficient sun exposure. In a study performed at the Veterinary Faculty in Slovenia 12 high producing Holstein Friesian cows at a commercial dairy farm were blood tested for vitamin D status for three succeeding months and all but one were vitamin D insufficient in all testings. The cows were not exposed to direct sunlight and the content of vitamin D3 in feed was <400 IU/kg dry matter, which is less than half of the NRC (2001) recommendation. Deficiency can also occur due to diseases affecting the gastrointestinal tract, such as paratuberculosis, which lower the absorptive capacity of the gut. Vitamin D can be toxic if cows are over-supplemented or consume large quantities of plants like Trisetum flavescens, which contain an active form of vitamin D-calcitriol or its glycosides, that are activated by digestion in the rumen.

Determinants of vitamin D status in Kenyan calves.

Vitamin D plays a critical role in calcium homeostasis and in the maintenance and development of skeletal health. Vitamin D status has increasingly been linked to non-skeletal health outcomes such as all-cause mortality, infectious diseases and reproductive outcomes in both humans and veterinary species. We have previously demonstrated a relationship between vitamin D status, assessed by the measurement of serum concentrations of the major vitamin D metabolite 25 hydroxyvitamin D (25(OH)D), and a wide range of non-skeletal health outcomes in companion and wild animals. The aims of this study were to define the host and environmental factors associated with vitamin D status in a cohort of 527 calves from Western Kenya which were part of the Infectious Disease of East African Livestock (IDEAL) cohort. A secondary aim was to explore the relationship between serum 25(OH)D concentrations measured in 7-day old calves and subsequent health outcomes over the following 12 months. A genome wide association study demonstrated that both dietary and endogenously produced vitamin D metabolites were under polygenic control in African calves. In addition, we found that neonatal vitamin D status was not predictive of the subsequent development of an infectious disease event or mortality over the 12 month follow up period.

Rickets in white-eared opossums (Didelphis albiventris) / Raquitismo em gambás-de-orelha-branca (Didelphis albiventris)

Two young opossums were necropsied and diagnosed with rickets. This study aims to describe the clinical-pathological aspects of rickets in Didelphis albiventris. Macroscopically, the opossums presented kyphosis and scoliosis, lateral deviation of the limbs in varus, locomotion difficulty, and enlargement with softening of costochondral junctions (rickety rosary). Samples of bones and joints were processed for hematoxylin and eosin staining and Masson's trichrome. Microscopically, we observed thickening of the epiphyseal plate, characterized by irregular and multifocal proliferation of serialized and hypertrophic cartilage zones, which formed circular groups of large, dysplastic chondrocytes towards the spongy zone, often surrounded by non-mineralized osteoid tissue. In the cortical bone, there were pale eosinophilic zones around the Havers channels consistent with non-mineralized osteoid. The staining of Masson's trichrome evidenced the accumulation of osteoid tissue in cortical and trabecular bones. It is possible that a mixed cause of absorption deficiency of vitamin D3 associated with an unbalanced Ca:P diet based on lactose-free milk and fruits may have triggered the disease.(AU)

Dois gambás jovens foram necropsiados e diagnosticados com raquitismo. O objetivo do trabalho é descrever os aspectos clínico-patológicos de raquitismo em Didelphis albiventris. Macroscopicamente os gambás apresentaram cifose e escoliose, desvio lateral dos membros em varus, dificuldade de locomoção e alargamento com amolecimento das junções costocondrais (rosário raquítico). Amostras dos ossos e articulações foram processadas para coloração de hematoxilina e eosina e Tricrômico de Masson. Microscopicamente havia espessamento da placa epifisária, caracterizada pela proliferação irregular e multifocal das zonas de cartilagem seriada e hipertrófica, que formavam grupos circulares de condrócitos grandes, displásicos em direção a zona esponjosa frequentemente cercados por tecido osteoide não mineralizado. No osso cortical haviam zonas eosinofílicas pálidas ao redor dos canais de Havers consistentes com osteoide não mineralizado. A coloração de Tricrômico de Masson evidenciou o acúmulo de tecido osteoide no nosso cortical e trabecular. Acredita-se que uma causa mista de déficit de absorção de vitamina D3 associada a uma dieta desbalanceada em Ca:P a base de leite sem lactose e frutas tenha desencadeado a doença.(AU)

Serum vitamin D status in sick cats with and without cholestatic liver disease.

OBJECTIVES: Vitamin D deficiency accompanies chronic cholestatic liver disease (CLD) in humans. The vitamin D status of cats with CLD is unknown. The objectives of this study were to describe serum vitamin D concentrations in cats with CLD and to determine if they correlated with indices of liver disease severity. METHODS: Thirty-six cats with CLD, defined by increases in serum bilirubin and serum alanine aminotransferase, and 23 sick cats with non-hepatobiliary diseases were prospectively enrolled. Serum 25-hydroxyvitamin D (25[OH]D), parathyroid hormone (PTH) and ionized calcium were measured. Signalment, clinical signs, comorbidities, diet history, serum bilirubin, liver enzyme activity, albumin, phosphorus, white blood cell count, prothrombin time and final hepatic cytologic/histopathologic diagnosis, when available, were recorded. RESULTS: Median serum 25(OH)D levels were similar in cats with CLD (89.5 nmol/l; range 21-112 nmol/l) and sick cats (89.0 nmol/l; range 49-115 nmol/l). Overall 12/36 (33%) cats with CLD and 4/23 (17%) sick cats had 25(OH)D levels below the lower limit of the reference interval (<65 nmol/l). Median PTH concentrations in cats with CLD were significantly higher (0.95 pmol/l; range 0-11.3 pmol/l) than in sick cats (0.70 pmol/l; range 0.5-6 pmol/l). In cats with CLD, 6/36 (17%) had high PTH levels in contrast to only 1/23 (4%) sick cats. In cats with CLD, 25(OH)D concentrations did not correlate with serum bilirubin, albumin or serum liver enzymes but were moderately negatively correlated with white blood cell count (r = - 0.402, P = 0.013). Cats with hepatic lipidosis had the highest prevalence of 25(OH)D concentrations that fell below the reference interval. CONCLUSIONS AND RELEVANCE: Many cats with CLD have serum 25(OH)D concentrations below the lower limit of the reference interval. Further study is warranted to determine the clinical relevance and whether supplementation would provide benefits.

Seasonal and dietary effects on Vitamin D deficiencies detected in wild boar from mid-western Spain.

Vitamin D (VitD) is involved in important mammalian physiological mechanisms, such as Ca-P metabolism, bone development and immunological response. VitD deficiencies are frequently detected in domestic animals and related to various health problems (e.g., rickets, bone deformation). However, knowledge about the status of VitD in wildlife species, such as the wild boar, is scarce. The aims of this work were to explore VitD status in wild boar populations from mid-western Spain and to elucidate the influence of daylight exposure and food supplementation in levels of VitD. Serum concentration of VitD (measured as 25-hydroxivitaminD) was assessed in 276 wild boar from 27 game estates located in mid-western Spain using a commercial ELISA kit. In 19 out of 27 estates, the staff supplied a specific VitD-enriched food (2,000 UI/Kg) ad libitum throughout the year, while in the remaining estates (8), no food was supplied. Blood samples were extracted from hunted animals (198) between October and February of hunting seasons 2016/2017 and 2017/2018, and from live wild boar (78) that were captured, sampled and released (March-September of 2017). The percentage of animals with VitD deficiency (<20 ng/ml), VitD insufficiency (20-30 ng/ml) and VitD sufficiency (>30 ng/ml) was estimated, and the relationship of these levels to factors like sex, age and season was assessed using chi-square tests. Furthermore, associations between daylight exposure and supplemental food with VitD levels were explored using linear models. Of the studied wild boar population, 82.2% showed a VitD deficiency or insufficiency. VitD deficiencies were more frequent in animals sampled in winter and spring. Furthermore, levels of VitD positively correlated with daylight exposure and supplemental food intake. Ad libitum supplementation with VitD-enriched food was insufficient to prevent VitD deficiencies in wild boar from November to April, probably because food consumption is lower during this period.

Assessment of serum 25-hydroxyvitamin D concentrations of beef cows and calves across seasons and geographical locations.

Vitamin D is critical for the growth and development of calves and positively contributes to immune function of cattle. Serum 25-hydroxyvitamin D (25(OH)D) concentrations above 20 ng/mL have traditionally been considered adequate for growth and development of cattle, but recent evidence has indicated that concentrations below 30 ng/mL are insufficient for immunity. Because little information is available regarding vitamin D status of beef cattle, the objective of this study was to evaluate vitamin D status of beef cow-calf herds on pasture as affected by season and location. Serum samples were collected from 43 cow-calf pairs plus an additional 54 calves in herds located in Florida, Idaho, and Minnesota in the spring calving season. Samples were collected again over the summer months from animals in the Florida and Minnesota herds. Effects of subcutaneous injection of vitamins A, D, and E also were investigated in a subset of calves from the Idaho herd. All cows sampled had serum 25(OH)D concentrations above 30 ng/mL at the time of calving in the spring. The average serum 25(OH)D concentrations of cows rose from near 60 ng/mL in the spring to 75 ng/mL in the summer ( < 0.001). Most calves, on the other hand, had serum 25(OH)D concentrations below 20 ng/mL. The calves in the Florida and Minnesota herds similarly rose from averages of 10 to 15 ng/mL at birth to near 50 ng/mL by the end of summer. Serum 25(OH)D of severely deficient calves increased from 3 ng/mL in nonsupplemented calves to 11 ng/mL at 48 h after birth if given a bolus supplementation of 40,000 IU of vitamin D via subcutaneous injection of a vitamin A, D, and E supplement at birth ( < 0.001). Vitamin D supplementation of cows late in pregnancy has been shown to increase serum 25(OH)D of calves; however, beef cattle generally receive very little supplemental vitamin D, as was the case for the cows studied here. The lower serum 25(OH)D of cows in spring compared with summer and the prevalence of vitamin D deficiency of calves observed here indicate that increased vitamin D supplementation of cows over the winter months or vitamin D supplementation of newborn calves would be beneficial.

Medical Management of Hypovitaminosis D With Cholecalciferol and Elastic Therapeutic Taping in Red-legged Seriema (Cariama cristata) Chicks.

Three hand-reared, 50-53 day-old, red-legged seriema (Cariama cristata) chicks were evaluated for acute lameness and reluctance to ambulate. Two of the 3 chicks presented with angular limb deformities of the proximal tarsometatarsi and external rotation of the legs. Radiographs demonstrated decreased opacity of the long bone of the legs, with poorly delineated cortices and deviation of the proximal tarsometarsi. Serum concentrations of 25-hydroxycholecalciferol revealed all 3 chicks were deficient in vitamin D(3) at presentation. The chicks were administered injectable vitamin D(3) (cholecalciferol), oral vitamin D(3), and an ultraviolet B (UV-B) light was placed in their enclosure. Elastic, therapeutic taping was used to correct angular limb deformities present in 2 of the 3 chicks. Taping was continued until the angular limb deformities were corrected and lameness resolved. Hypovitaminosis D is a common cause of metabolic bone disease in captive avian species. Cholecalciferol administration, UV-B light supplementation, and elastic, therapeutic taping were effective treatments for osteodystrophy and secondary angular limb deformities due to hypovitaminosis D. This multifaceted treatment may be useful in other long-legged juvenile birds with similar clinical signs.

Seasonal variation in vitamin D status of beef cattle reared in the central United States.

The objective was to retrospectively measure seasonal sunlight-associated variation in serum concentrations of 25-hydroxyvitamin D (25OHD) in beef cattle. The concentration of 25OHD was measured in crossbred animals born from March to May in 2011 and 2012. Vitamin D status 2 to 3 mo after birth (period 1) was only available for 2012 calves and was measured in June 2012. Period 1 animals had serum 25OHD concentrations of 26.3 ± 1.5 ng/mL. The 25OHD concentrations for late summer (period 2) were 46.6 ± 1.4 and 51.0 ± 1.5 ng/mL for 2011 and 2012, respectively. Serum concentration of 25OHD in early fall (period 3) were 63.8 ± 1.4 and 55.2 ± 1.5 ng/mL for calves in 2011 and 2012, respectively. Values observed for both late summer and early fall indicated vitamin D sufficiency (P < 0.001) compared with period 1. With diminishing exposure to ultraviolet B and consuming ∼800 IU or 1800 IU (2011 and 2012, respectively) of supplemental vitamin D, the calves' midwinter (period 4) 25OHD concentrations fell to 15.2 ± 1.6 and 16.7 ± 1.5 ng/mL for 2011 and 2012, respectively, after 4 to 5 mo on a finishing diet (P < 0.0001). This is considered vitamin D insufficiency in most species. Results indicate that calves are marginally sufficient to insufficient for vitamin D based on serum 25OHD concentrations soon after birth and during winter. Some individual animals would be classified vitamin D deficient. In the absence of sufficient UVB exposure, the dietary vitamin D requirements for rapidly growing beef cattle may need to be increased.

Acute phase response elicited by experimental bovine diarrhea virus (BVDV) infection is associated with decreased vitamin D and E status of vitamin-replete preruminant calves.

Studies in young animals have shown an association between vitamin deficiencies and increased risk of infectious disease; however, there is a paucity of information regarding the effect of acute infection on the vitamin status of the vitamin-replete neonate. To characterize the effects of acute infection on vitamin D and E status of the neonate, 6 vitamin-replete preruminant Holstein bull calves were experimentally infected with bovine viral diarrhea virus (BVDV; strain BVDV2-1373). Six mock-inoculated calves served as controls. Sustained pyrexia, leukopenia, and asynchronous increases in serum haptoglobin and serum amyloid A characterized the response of calves to infection with BVDV. Infection was also associated with increased serum IFN-γ, IL-2, and IL-6 concentrations. During the last 8 d of the 14-d postinoculation period, serum 25-hydroxyvitamin D and α-tocopherol concentrations in infected calves decreased by 51 and 82%, respectively. The observed inverse association between vitamin D and E status and serum amyloid A in infected calves suggests that the infection-induced acute phase response contributed to the reduced vitamin status of these animals. Additional studies are necessary to determine if the negative effect of infection on status are unique to this specific infection model or is representative of preruminant calf's response to acute infection. Studies are also needed to characterize mechanisms underlying infection-related changes in vitamin D and E status and to determine whether additional vitamin D or E supplementation during an acute infection diminishes disease severity and duration in the young animal.

Vitamin D status in cattle with malignant catarrhal fever.

The aim of the present study was to determine the vitamin D status in cattle with malignant catarrhal fever (MCF). Twelve cattle diagnosed as MCF and 6 healthy cattle (controls) were used in the study. Serum 1,25-dihydroxyvitamin D(3) (1,25-D), 25-hydroxyvitamin D(3) (25-D), calcium, phosphorus and parathyroid hormone (PTH) levels were determined as 96.83 pg/ml, 30.0 ng/ml, 2.19 mmol/l, 1.57 mmol/l and 15.21 pg/ml in MCF group and 42.33 pg/ml, 37.0 ng/ml, 2.43 mmol/l, 1.96 mmol/l and 36.08 pg/ml in controls, respectively. Although serum 1,25-D level in the MCF group was increased (P<0.01), serum calcium (P<0.01) and PTH (P<0.05) levels were decreased compared to the controls. The results suggest that there might be an interaction between vitamin D status and MCF.

A survey of the husbandry of captive tuatara (Sphenodon spp.) in relation to factors implicated in nutritional secondary hyperparathyroidism.

AIM: To examine selected aspects of the diet and husbandry of captive tuatara (Sphenodon spp.) in New Zealand, in order to develop recommendations on provision of ultraviolet B light and diet, to reduce the incidence of nutritional secondary hyperparathyroidism (NSHP). METHODS: Information was collected from 18/20 institutions holding tuatara in New Zealand, on the numbers kept, dimensions and type of enclosures, and type of light sources used. Historical information on breeding activity and problems known to be associated with NSHP, and standardised measurements of levels of ultraviolet B light in enclosures were also recorded. Diet samples were collected (n=17) and analysed for Ca, P and vitamin D content. RESULTS: The intensity of ultraviolet B light was lower where there was a history of previous high, compared with medium or low, risk of NSHP for tuatara kept indoors (p>0.001). Light sources varied significantly in both output of ultraviolet B light (spectral irradiance) at the source, and fractional reduction in electromagnetic fluence with increasing distance from the source. The average exposure to ultraviolet B light of captive tuatara kept indoors was 26.44 (SE 4.29) microW/cm2, and there was significant variation between enclosures, with 4/14 (29%) institutes having no measurable ultraviolet B light present. For tuatara kept outdoors ultraviolet B light at ground level was influenced by weather conditions (p< or =0.007), roofing material (p=0.004), and substrate shading (p=0.003). The Ca:P ratio of dietary samples was 2.3 (SE 1.9), but this included one extreme outlier (32.7). When the outlier was excluded, it was 0.53 (SE 0.16). The levels of vitamin D in the feed samples were below the minimum detectable level of the assay (<20 IU/100 g) for all but one sample (72 IU/100 g) that had been dusted with vitamin/mineral supplement prior to freezing. CONCLUSIONS AND CLINICAL RELEVANCE: The current diet and husbandry of captive tuatara in New Zealand predisposes the animals to NSHP. The ultraviolet B light emitted from commercial light sources dissipates rapidly with increasing distance from the source. Regular direct measurement of ultraviolet B light at substrate level is recommended for indoor enclosures, whereas tuatara kept outdoors should have access to an unshaded basking area through a wire-meshed roof. The Ca:P ratio and concentration of vitamin D of most common food items fed to tuatara is deficient, and reptile vitamin and mineral supplements should be provided by dusting or gut-loading insect food items.

The effect of breeder age and egg storage time on phosphorus utilization by broiler progeny fed a phosphorus deficiency diet with 1alpha-OH vitamin D3.

Two experiments were conducted to determine that variation in broiler P utilization is due to breeder age and egg storage time. Experiment 1 was conducted with chicks hatched from eggs laid by Ross x Ross 308 breeders (27 vs. 61 wk old) and stored for 0 or 10 d. The age of breeders had significant effects (P < 0.05) on 0 to 16 d chick growth (379 +/- 18 vs. 308 +/- 19 for 27- and 61-wk-old breeders, respectively). The longer egg storage time of chicks from older breeders resulted in higher P rickets scores and incidence, but longer egg storage time of chicks from younger breeders resulted in lower P rickets score and incidence (significant interaction, P = 0.0455). The longer egg storage time of chicks from older breeders resulted in lower bone ash (%), and the longer egg storage time of chicks from younger breeders resulted in higher bone ash (%). Experiment 2 was conducted with chicks hatched from eggs laid by Ross x Ross 308 breeders (26 vs. 60 wk old) and stored for 0 or 10 d. The diets were P deficient and with or without 5 microg/g of 1alpha-OH cholecalciferol (1alpha-OH vitamin D(3)). Breeder age had significant effects (P = 0.0003) on 0 to 16 d chick growth (272 +/- 7 vs. 339 +/- 8 for 26- and 60-wk-old breeders, respectively) and chick mortality (P = 0.0134). The P rickets score increased with breeder age (P = 0.0186) and egg storage time (P = 0.1057). The factors influencing the incidence of P rickets in broilers should include breeder age and egg storage time as well as genetics and dietary levels of Ca, P, and vitamin D activity of the P-deficient diets.

Vitamin D3 metabolism in dogs.

Plasma concentrations of the main vitamin D(3) metabolites (i.e., 25(OH)D(3), 1,25(OH)(2)D(3), and 24,25(OH)(2)D(3)) were measured in 14 weeks old large- and small-breed dogs (adult body weight 60 kg vs. 6 kg), raised under the same conditions. Levels of 25(OH)D(3) (approx. 22 microg/l) and 1,25(OH)(2)D(3) (approx. 40 ng/l) were similar in both groups, whereas plasma 24,25(OH)(2)D(3) concentrations were lower in large-breed dogs (7 microg/l vs. 70 microg/l, large- vs. small-breed dogs, respectively). The lower plasma 24,25(OH)(2)D(3) concentrations could be explained by the higher plasma GH and IGF-I concentrations in the large- vs. small-breed dogs, and these hormones are known to suppress 24-hydroxylation. Plasma 24,25(OH)(2)D(3) concentrations increased during Ca supplementation in small-breed but not in large-breed dogs (100 microg/l vs. 7 microg/l, respectively). Hypophosphatemia induced by a high dietary Ca content was only seen together with increased plasma 1,25(OH)(2)D(3) concentrations in euparathyroid dogs and not in hypoparathyroid dogs. Hyperparathyroidism due to Ca deficiency was accompanied by increased plasma 1,25(OH)(2)D(3) concentrations and decreased plasma 24,25(OH)(2)D(3) concentrations in both large- and small-breed dogs, together with generalized osteoporosis. Large-breed pups fed on a standard diet supplemented with Ca and P had decreased plasma concentrations of both 25(OH)D(3) and 1,25(OH)(2)D(3), which may indicate an increased clearance of these metabolites; the low plasma concentrations of the di-hydroxylated vitamin D metabolites were considered responsible for the disturbance in cartilage maturation (i.e., osteochondrosis) in these dogs. Even lower concentrations of all vitamin D(3) metabolites were seen in young dogs raised on a vitamin D(3)-deficient diet, and led to disturbed osteoid and cartilage mineralization (i.e., rickets). These studies indicate that there is a hierarchy of factors regulating vitamin D(3) metabolism in dogs, i.e., GH and IGF-I suppress 24-hydroxylase more than hypercalcemia or hypophosphatemia does; 1,25(OH)(2)D(3) and 24,25(OH)(2)D(3) are only reciprocally related in hyperparathyroidism; excessive Ca and P intake increases the turnover of vitamin D(3) metabolites; and the synergism between parathyroid hormone and 1,25(OH)D(3) seems to play a role in skeletal mineralization. The low plasma 24,25(OH)(2)D(3) concentrations in large-breed dogs raised on standard dog food may play a role in the etiology of disturbances in endochondral ossification during the rapid growth phase.

Hypophosphatemia associated with hypovitaminosis-D in Speke's gazelles (Gazella spekei).

Two juvenile male Speke's gazelles (Gazella spekei) at the St. Louis Zoo showed poor body condition, slowed growth, hunched stance, rough hair coat, and profound hypophosphatemia. The first gazelle was treated with parenteral phosphorous supplements but continued to deteriorate clinically and was euthanatized. The second gazelle had serum 25-hydroxyvitamin D levels of 0 nmol/L and was treated with i.m. injections of vitamin D. It died shortly after starting therapy. The only significant necropsy finding was multiple rib fractures in various stages of healing. Hypovitaminosis D has been confirmed in multiple Speke's gazelles in this collection, indicating possible deficiencies in the diet or in the amount of ultraviolet light available to the gazelles.

Vitamin D doses for alpacas (Lama pacos).

OBJECTIVE: To assess the effectiveness of cholecalciferol (D3) doses for maintaining adequate vitamin D status in crias and adult female alpacas at pasture. DESIGN: A field experiment during winter and early spring in a herd on a farm in South Australia. ANIMALS AND PROCEDURE: Crias, usually less than 6 months of age and female alpacas, aged 2 to 6 years, were given a single subcutaneous dose of 0, 1000 or 2000 IU D3/kg body weight. Plasma concentrations of 25-hydroxycholecalciferol (25-OH D3), phosphorus, calcium and vitamins A and E and alkaline phosphatase activity were measured at intervals over a period of 16 weeks after treatment. RESULTS: Crias not given a vitamin D supplement had reduced growth rate during winter and one animal showed clinical signs of rickets. Vitamin D treatment had no effect on the body weight of mature females. Vitamin D supplements increased the 25-OH D3 and phosphorus concentrations in plasma of both crias and adult females; alkaline phosphatase activity was not affected by treatment. CONCLUSION: It is suggested that for alpacas in southern Australia a subcutaneous dose of 1000 IU D3/kg body weight to crias in late autumn and again in mid winter and to adult females in mid winter should prevent vitamin D inadequacy.

[Nutrition-related problems in pet birds]. / Voedingsgerelateerde problemen bij gezelschapsvogels.

The detection and correction of dietary errors plays an important role in avian medicine. Examples of diseases caused in part by a deficiency or abundance of a nutrient include hypovitaminosis A in birds of the parrot (Psittacidae) family, hypocalcemia in the African grey parrot, goitre in budgerigars, and iron storage diseases in the minah and toucan. Hypovitaminosis A can lead to metaplasia of mucous membranes, which in turn can lead to chronic rhinitis and respiratory fungal infections. Vitamin A deficiency is caused by feeding a seed based diet. Seed mixtures are often deficient in calcium, and nutritional secondary hyperparathyroidism can develop if an additional source of calcium, in the form of ground shells, is not provided. Tetanic symptoms as a result of hypocalcemia are only seen in the African grey parrot and the timneh parrot. Over supplementation of vitamin D gives rise to poisoning with polyuria and polydipsia as common initial symptoms. The exact cause of iron storage diseases in toucans and minahs is not known. A diet low in iron and vitamin C is advised as therapy. Goitre can develop in budgerigars as a result of iodine-deficient drinking water and provision of a seed mixture based on millet. An unbalanced or multideficient diet can give rise to reproductive disorders, abnormal feathers, or infections as a result of diminished resistance. It is usually not possible to relate the cause of these diseases in a simple way to the composition of the diet. Obesity, which occurs in the galah, Amazon parrot, and budgerigars, can lead to fatty liver and lipoma. A gradual reduction in weight, by means of calorie restriction, is recommended. Commercially available nutritionally balanced bird food is often effective.