RESOLUTION OF CALVARIAL HYPEROSTOSIS IN AFRICAN LION CUBS (PANTHERA LEO LEO) AFTER VITAMIN A SUPPLEMENTATION.

Two female (FL 1, FL 2) and one male (ML) 11-wk-old, intact, captive African lion cubs (Panthera leo leo) were presented with a history of mild vestibular signs. Initial serum vitamin A concentrations were low (140 nmol/L) for ML. Calvarial hyperostosis was confirmed using computed tomography (CT) of the head and cervical vertebrae in each cub. CT measurements were adapted in relation to the skull width. ML showed the most pronounced thickening of the tentorium cerebelli and occipital bone, represented by a tentorium cerebelli to skull width ratio (TCR) of 0.08 (FL 1: 0.06, FL 2: 0.05) and a basisphenoid to skull width ratio (BBR) of 0.07 (FL 1: 0.06, FL 2: 0.04). Magnetic resonance imaging (MRI) revealed cerebellar herniation and cervical intramedullary T2-weighted hyperintensity from C1, extending caudally for at least two cervical vertebrae in all cubs. Treatment was initiated with subcutaneous vitamin A supplementation and feeding of whole carcasses. Improvement in ataxia was noticed 3 wk later. Follow-up CT and MRI examinations were performed in ML after 3 and 8 mon. The affected bones appeared slightly less thickened and TCR and BBR had decreased to 0.05 after 3 mon. The cerebellum remained mildly herniated, accompanied by amelioration of cervical T2w hyperintensities. After 8 mon, evaluation and diagnostic imaging revealed further improvement regarding the neurologic status and measurements (TCR 0.05, BBR 0.04) despite persistence of a subtle cerebellar herniation. In conclusion, bone remodeling and improvement in clinical signs may be achievable in young lion cubs presented with calvarial hyperostosis and may be attributable to high-dose vitamin A supplementation.

Vitamin A deficiency impairs intestinal physical barrier function of fish.

The present study was the first to investigate the effects of dietary vitamin A (VA) on the intestinal physical barrier function associated with oxidation, antioxidant system, apoptosis and cell-cellular tight junction (TJ) in the proximal (PI), mid (MI) and distal (DI) intestines of young grass carp (Ctenopharyngodon idella). Fish were fed graded levels of dietary VA for 10 weeks, and then a challenge test using an injection of Aeromonas hydrophila was conducted for 14 days. Results indicated that dietary VA deficiency caused oxidative damage to fish intestine partly by the reduced non-enzymatic antioxidant components glutathione (GSH) and VA contents as well as reduced antioxidant enzyme activities [not including manganese superoxide dismutase (MnSOD)]. Further results observed that the decreased antioxidant enzyme activities by VA deficiency were partly related to the down-regulation of their corresponding mRNA levels which were regulated by the down-regulation of NF-E2-related factor 2 (Nrf2) mRNA levels and up-regulation of kelch-like-ECH-associated protein (Keap1a) (rather than Keap1b) mRNA levels in three intestinal segments of fish. Meanwhile, VA deficiency up-regulated the mRNA levels of the apoptosis signalling [caspase-3, caspase-8, caspase-9 (rather than caspase-7)] associated with the inhibition of the target of rapamycin (TOR) signalling pathway in three intestinal segments of fish. Additionally, VA deficiency decreased the mRNA levels of TJ complexes [claudin-b, claudin-c, claudin-3, claudin-12, claudin-15a, occludin and zonula occludens-1 (ZO-1) in the PI, MI and DI, as well as claudin-7 and claudin-11a in the MI and DI] linked to the up-regulation of myosin light chain kinase (MLCK) signalling. These results suggested that VA deficiency impaired structural integrity in three intestinal segments of fish. Meanwhile, excessive VA also showed similar negative effects on these indexes. Taken together, the current study firstly demonstrated that VA deficiency impaired physical barrier functions associated with impaired antioxidant capacity, aggravated cell apoptosis and disrupted TJ complexes in the PI, MI and DI, but different segments performed different actions in fish. Based on protecting fish against protein oxidation, the optimal VA levels for grass carp were estimated to be 2622 IU/kg diet.

SUSPECTED HYPOVITAMINOSIS A-ASSOCIATED SALT GLAND ADENITIS IN NORTHERN ROCKHOPPER PENGUINS ( EUDYPTES MOSELEYI).

Supraorbital salt-excreting glands are present in at least 10 avian orders and are largest in marine species, including penguins. Diseases of the avian salt gland have been described infrequently. From September 2015, five captive northern rockhopper penguins ( Eudyptes moseleyi) were presented over a 6-wk period for unilateral or bilateral supraorbital swellings. In September 2016, two cases recurred and two additional cases were identified. Histopathology demonstrated salt gland adenitis with extensive squamous metaplasia. Blood plasma testing demonstrated marked vitamin A and E deficiencies within the colony. Prolonged frozen storage of feed-fish was implicated as a cause of vitamin depletion; reducing storage times and addition of dietary supplementation prevented recurrence.

Evaluation of ß-carotene assimilation in leopard geckos (Eublepharis macularius).

Although leopard geckos (Eublepharis macularius) are commonly kept under human care, their vitamin requirements are largely unknown. Many invertebrate preys display a low vitamin A concentration; thus, gut-loading insects with vitamin A or carotenoids is a common practice. The objective of this prospective experimental study was to investigate whether dietary supplementation with ß-carotene, including prey gut-loading, leads to sufficient vitamin A hepatic storage and prevents epithelial squamous metaplasia development in leopard geckos. Ten clinically healthy female leopard geckos were randomly divided in two groups with various supplementations: a group receiving vitamin A supplementation and a group receiving ß-carotene. Insects were gut-loaded continuously with a supplement containing vitamin A or ß-carotene, depending on the group. Oral supplementation with cod liver oil or carrot juice was administered weekly to each lizard from "vitamin A group" and "carotenoid group" respectively. After 10 weeks of supplementation, surgical hepatic biopsies were obtained in three geckos of each group while the two remaining geckos were euthanized to undergo complete necropsy. Hepatic vitamin A concentration was determined for each lizard (n = 10) by ultra-performance liquid chromatography. Histopathology revealed hepatocellular vacuolization and vitellogenic follicles in five females. Epithelial squamous metaplasia was not observed in any of the geckos. Hepatic vitamin A concentration was significantly higher in the carotenoid-supplemented group than in the vitamin A-supplemented group (p = 0.03). Our results suggest that in leopard geckos, dietary supplementation with ß-carotene allows sufficient vitamin A hepatic storage.

Vitamin A and marbling attributes: Intramuscular fat hyperplasia effects in cattle.

Twenty Angus steers were fed a diet low in ß-carotene and vitamin A for 10months. Ten steers were supplemented with vitamin A weekly, while the other ten steers did not receive any additional vitamin A. The results demonstrated that the restriction of vitamin A intake increased intramuscular fat (IMF) by 46%. This was a function of the total number of marbling flecks increasing by 22% and the average marbling fleck size increasing by 14%. Vitamin A restriction resulted in marbling flecks that were less branched (22%) and slightly more round (4%) with an increased minor axis length (7%). However, restricting vitamin A did not affect the size of the intramuscular or subcutaneous adipocyte cells or the subcutaneous fat depth. The results suggest that vitamin A affects the amount of marbling and other attributes of the marbling flecks due to hyperplasia rather than hypertrophy. This may explain why vitamin A restriction specifically affects IMF rather than subcutaneous fat deposition.

[Unusual case of struvite urolithiasis in a dog. A case report]. / Ungewöhnlicher Fall von Struvit-Urolithiasis bei einem Hund. Ein Fallbericht.

A dog was referred for nutrition consultation after surgical removal of struvite uroliths from the bladder. Inspection of the dog's current ration revealed a pronounced vitamin-A deficiency together with a marked deficiency of protein, phosphorus and magnesium. Therefore, a supersaturation of the urine with ammonium, magnesium and phosphate, the three constituents of struvite, as a cause of struvite calculi formation appears rather unlikely. Vitamin-A deficiency can promote urinary infections and consequently struvite stone formation because of the lack of the protective effect of vitamin A on the epithelia of the urinary tract. Not only common causes for struvite urolith formation, including urinary supersaturation with stone-forming constituents and urinary tract infection, but also less common causes, including vitamin-A deficiency, which was the presumed trigger in the present case study, have to be taken into consideration. Dietetic measures appear to be a useful tool in such cases to prevent uroliths from reoccurring.

Serum selenium and liposoluble vitamins in Japanese Black cows that had stillborn calves.

Stillbirth and dystocia are major factors that negatively affect beef production. We sought to clarify serum selenium and liposoluble vitamin levels in Japanese Black cows that gave birth to stillborn calves (stillbirth cows). Blood samples were collected from 103 stillbirth cows and 95 cows that gave birth to healthy calves (control cows). Serum levels of selenium (45.8 ± 16.0 ng/ml) and vitamin A (73.0 ± 24.8 IU/dl) in stillbirth cows were lower (P<0.05) than those in control cows (52.2 ± 8.9 ng/ml and 93.3 ± 14.8 IU/dl, respectively). Our findings suggest that appropriate serum selenium and vitamin A levels are important for calving cows.

Serum and hepatic vitamin A levels in captive and wild marine toads (Bufo marinus).

The captive breeding program for the endangered Puerto Rican crested toad (Peltophryne [Bufo] lemur) has been hampered by an undiagnosed condition called "Brown Skin Disease" (BSD). Toads develop widespread skin darkening, skin thickening and abnormal shedding and eventually succumb to a chronic loss of viability. This project evaluated the marine toad (Bufo marinus) as a model for the PRCT, examining vitamin A deficiency as a potential cause of BSD. Wild caught marine toads had significantly higher liver vitamin A concentrations (61.89 ± 63.49 µg/g) than captive born marine toads (0.58 ± 0.59 µg/g); P<0.001). A significant difference in serum vitamin A concentration was found between the captive and wild caught toads (P=0.013) and between the low vitamin A-fed and wild caught toads (P=0.004), when controlling for liver vitamin A concentrations. After captive toads were treated with topical and/or oral vitamin A, their hepatic vitamin A concentrations were similar to those of the wild toads, averaging 48.41 ± 37.03 µg/g. However, plasma vitamin A concentrations pre- and post-vitamin A supplementation did not differ statistically. We concluded that plasma vitamin A concentrations do not provide a linear indication of liver/body vitamin A status, and that both topical and oral supplementation with an oil-based vitamin A formulation can increase liver stores in amphibians. No evidence of BSD or other signs of deficiency were noted in the marine toads, although this feeding trial was relatively short (127 days). To date, clinical, pathological and research findings do not support vitamin A deficiency as a primary factor underlying BSD.

Pneumonia bacteriana em jabuti-piranga (Chelonoidis carbonaria): aspectos clínicos, microbiológicos, radiológicos e terapêutica / Bacterial pneumonia in red-footed tortoise (Chelonoidis carbonaria): clinical aspects, microbiological, radiological and therapeutic

A pneumonia é uma doença respiratória comum na clínica de répteis. Agentes infecciosos são capazes de causar pneumonia primária em répteis mantidos em cativeiro, porém na maioria dos casos, são secundárias a problemas de manejo, higiene e nutricionais. O objetivo desse trabalho foi relatar a ocorrência de pneumonia bacteriana em jabuti-piranga (Chelonoidis carbonaria), e descrever o diagnóstico clínico, microbiológico, radiográfico e a conduta terapêutica. O animal apresentava sinais de distúrbios respiratórios e foi descrito durante a anamnese que houve um diagnostico anterior de pneumonia. Os achados radiográficos foram sugestivos de pneumonia/edema pulmonar. Baseado nos exames radiográficos e sinais clínicos apresentados iniciou-se o tratamento com administração de Cloranfenicol (40mg/kg/SID/IM) por 10 dias. Foram isoladas Klebsiella spp. e Citrobacter spp. da cultura bacteriana realizada da coleta de lavado endotraqueal. Ambas com perfil de resistência múltipla aos antibióticos testados. Instituiu-se protocolo terapêutico utilizando Gentamicina (5mg/kg/IM), em sete aplicações com intervalos de 72h. Após o segundo protocolo terapêutico notou-se melhora dos sinais clínicos do animal, porém foi observada a persistência de secreção nasal. Foi realizado novo exame radiográfico, demonstrando discreta diminuição na opacidade do campo pulmonar direito e nenhuma alteração significativa no campo pulmonar esquerdo na projeção craniocaudal. Devido à permanência do sinal clínico apresentado, nova coleta de material endotraqueal foi realizada, e houve isolamento de Citrobacter spp. e Enterobacter spp. A partir dos resultados obtidos no antibiograma, instituiu-se novo protocolo com uso de amicacina (2,5mg/kg/IM), em sete aplicações com intervalos de 72h. Após antibioticoterapia, outro exame radiológico foi realizado, e demonstrou redução satisfatória do quadro pulmonar, e sinais clínicos...

Pneumonia is a common respiratory disease in clinical of reptiles. Infectious agents are capable of causing primary pneumonia in reptiles maintained in captivity, but in most cases are secondary to problems of management, hygiene and nutrition. The aim of this study was to report the occurrence of bacterial pneumonia in red-footed tortoise (Chelonoidis carbonaria), and describe the clinical, microbiologic, radiographic and therapeutic management. The animal showed signs of respiratory disorders and has been described in the clinical history before diagnosis of pneumonia. The radiographic findings were suggestive of pneumonia/pulmonary edema. Based on the displayed radiographic examination and clinical signs began treatment with administration of chloramphenicol (40mg/kg/SID/IM) for ten days. Were isolated Klebsiella spp. and Citrobacter spp. bacterial culture done collecting endotracheal lavage. Both with multiple antibiotic resistance profile tested. Treatment protocol was instituted using gentamicin (5mg/kg/IM) applications into seven intervals of 72h. There was improvement in clinical signs of the animal, but the presence of nasal secretion was still observed. New radiographic examination, demonstrating slight decrease in the opacity of the right lung field and no significant change in the left lung field in craniocaudal projection was performed. Because of the persistence of clinical signs presented new collection endotracheal material was performed, and there was isolation of Citrobacter spp. and Enterobacter spp. From the results obtained in the antibiogram, was instituted new protocol with the use of amikacin (2.5mg/kg/IM) applications into seven intervals of 72h. After antibiotic therapy, other radiological examination was performed, and showed satisfactory reduction in pulmonary function and clinical signs...

Dermatopathy in juvenile Angus cattle due to vitamin A deficiency.

In juvenile cattle, vitamin A deficiency is reported most commonly as a neurological condition; only rarely are there dermatologic manifestations. In the current study, alopecia, severe epidermal and follicular orthokeratosis, and acanthosis due to hypovitaminosis A are reported in 2 of 32 Angus calves, with a third animal suspected. Affected animals responded to vitamin A supplementation, and no additional calves displayed signs. Vitamin A acts on skin by regulating DNA transcription in keratinocytes, reducing the number of tonofilaments and desmosomes, both involved in cell-to-cell adhesion. Hence, adequate levels of dietary vitamin A are necessary for normal keratinocyte turnover, and deficiencies result in retention of keratinized cells (orthokeratosis). The present report reminds diagnosticians to consider vitamin A deficiency in cases of orthokeratotic dermatopathy in cattle.

Vitamin A deficiency and hepatic retinol levels in sea otters, Enhydra lutris.

Vitamin A deficiency has rarely been reported in captive or free-ranging wildlife species. Necropsy findings in two captively housed southern sea otters (Enhydra lutris nereis) included irregular thickening of the calvaria characterized by diffuse hyperostoses on the internal surface. One animal also had moderate squamous metaplasia of the seromucinous glands of the nose. There was no measurable retinol in the liver of either sea otter. For comparison, hepatic retinol concentration was determined for 23 deceased free-ranging southern and northern (Enhydra lutris kenyoni) sea otters from California and Alaska. Free-ranging otters were found to have similar hepatic retinol concentrations (316 +/- 245 mg/kg wet weight) regardless of their location and subspecies. All of these values were significantly higher than the levels in the affected animals. Consumption of a diet with very low vitamin A concentrations and noncompliance in daily supplementation are hypothesized as the causes of vitamin A deficiency in these two sea otters.

A comparison of oral and topical vitamin A supplementation in African foam-nesting frogs (Chiromantis xerampelina).

Vitamin A is essential for a variety of functions, including cellular differentiation, morphogenesis, growth, vision, immune response, and reproduction. A captive population of African foam-nesting frogs (Chiromantis xerampelina) with a known history of vitamin A deficiency had higher than expected incidence of sudden death, bacterial osteomyelitis, and stunted growth. Due to the high prevalence and untreatable nature of the diseases in the population, euthanasia of the population was recommended. Before euthanasia, the population was entered into a study to compare oral dietary supplementation of vitamin A to topical treatment with water-miscible vitamin A palmitate (AQUASOL A Parenteral, Mayne Pharma Inc., Paramus, New Jersey 07652, U.S.A.). Eighty-four frogs, weighing 2-7 g, were divided into a control and three treatment groups of 21 frogs per group, with normalized weight distribution. The control group received standard daily nutrition of crickets dusted with a supplement containing 342,000 international units (IU) vitamin A/kg. The treatment groups consisted of oral supplementation with crickets dusted with a fortified supplement containing 822,510 IU vitamin A/kg; topical vitamin A palmitate 50 IU every other day; and topical vitamin A palmitate 50 IU once a week. After 30 days, all frogs were euthanized, and 12 frogs from each group were analyzed for whole-body vitamin A levels. The control and treatment groups 1, 2, and 3 had average whole-body vitamin A levels of 1371.4 IU/kg (SE 284.4), 908.7 IU/kg (SE 186.5), 6385.9 IU/kg (SE 675.9), and 3521.8 IU/kg (SE 575.1), respectively. These results suggest that oral supplementation using a product high in vitamin A may be ineffective at raising whole-body vitamin A levels above those achieved with standard nutrition. Topical administration of vitamin A on an every other day and once a week dosing schedule achieved levels 4.5- and 2.5-fold higher than standard nutrition, respectively.

Diagnosis and surgical treatment of a Chiari I-like malformation in an African lion (Panthera leo).

A 13-mo-old intact male African lion (Panthera leo) presented with a 3-mo history of lethargy, ventral flexion of the neck, abnormal vocalization, and ataxia. Hemogram and serum biochemistries were within normal limits except for the presence of hypokalemia (2.7 mEq/L) and hypochloridemia (108 mEq/L). When no improvement was noted with oral potassium gluconate supplementation, a computed tomography scan of the brain and skull was performed, and no abnormalities were noted. However, magnetic resonance imaging detected occipital bone thickening, crowding of the caudal cranial fossa with cerebellar compression and herniation, and cervical syringohydromyelia, which was consistent with a Chiari I-like malformation. Foramen magnum decompression was performed to relieve the compression of the cerebellum. The animal recovered well with subsequent resolution of clinical signs. Hypovitaminosis A has been proposed previously as the underlying etiology for this malformation in lions with similar clinical presentations. This lion's serum and liver vitamin A concentrations were low (100 ng/ml and 25.31 microg/g, respectively) compared to concentrations reported for domestic carnivores and support hypovitaminosis A as the underlying cause of this animal's Chiari I-like malformation.

Sub-occipital craniectomy in a lion (Panthera leo) with occipital bone malformation and hypovitaminosis A.

Neurologic dysfunction accompanied by malformation of both the skull and the cervical vertebrae has been previously described in lions kept in captivity worldwide, and this dysfunction and malformation were most often related to vitamin A deficiency. Diagnosis of the bone malformation and its effects on the neural tissue was until recently limited to postmortem examination, with characteristic thickening of the bones of the cranial vault, cerebellar herniation, compression of the foramen magnum, and enlargement of the lateral ventricles. For some mildly affected lion cubs with neurologic signs, improvement was reported with excessive vitamin A supplementation. However, definitive diagnosis was only available for those that eventually died or were euthanized. This case documents the antemortem diagnosis of the disease using computed tomographic imaging and liver biopsy. While conservative treatment failed, suboccipital craniectomy removed the thickened occipital bone and was demonstrated to be a successful surgical intervention that can be used to treat more severely affected lions.

Effect of dietary vitamin A restriction on marbling and conjugated linoleic acid content in Holstein steers.

To determine the effect of duration of dietary vitamin A restriction on site of fat deposition in growing cattle, 60 Holstein steers (BW = 218.4 +/- 6.55 kg) were fed a diet based on high-moisture corn, with 2,200 IU of supplemental vitamin A/kg of DM (control) or no supplemental vitamin A for a long (243 d; LR) or short (131 d; SR) restriction before slaughter at 243 d. The SR steers were fed the control diet for the first 112 d. Steers were penned individually and fed for ad libitum intake. Jugular vein blood samples for serum retinol analysis were collected on d 1, 112, and 243. Carcass samples were collected for composition analysis. Subcutaneous fat samples were collected for fatty acid composition. Fat samples from the i.m. and s.c. depots were collected to measure adipocyte size and density. Feedlot performance (ADG, DMI, and G:F) was not affected (P > 0.05) by vitamin A restriction. On d 243, the i.m. fat content of the LM was 33% greater (P < 0.05) for LR than for SR and control steers (5.6 vs. 3.9 and 4.2% ether extract, respectively). Depth of back-fat and KPH percentage were not affected (P = 0.44 and 0.80, respectively) by vitamin A restriction. Carcass weight, composition of edible carcass, and yield grade were similar among treatments (P > 0.10). Liver retinol (LR = 6.1, SR = 6.5, and control = 44.7 microg/g; P < 0.01) was reduced in LR and SR vs. control steers. On d 243, LR and SR steers had similar serum retinol concentrations, and these were lower (P < 0.01) than those of control steers (LR = 21.2, SR = 25.2, and control = 36.9 microg/dL). Intramuscular adipose cellularity (adipocytes/mm2 and mean adipocyte diameter) on d 112 and 243 was not affected (P > 0.10) by vitamin A restriction. Restricting vitamin A intake for 243 d increased i.m. fat percentage without affecting s.c. or visceral fat deposition, feedlot performance, or carcass weight. Restricting vitamin A intake for 131 d at the end of the finishing period appears to be insufficient to affect the site of fat deposition in Holstein steers.

Effect of low vitamin A status on fat deposition and fatty acid desaturation in beef cattle.

A group of Angus beef cattle was removed from temperate pastures and fed a very low beta-carotene cereal-based ration in a feedlot for over 300 d. Half the group was supplemented weekly with retinyl palmitate (at the rate of 60,000 IU vitamin A/100 live weight (LW)/day), sufficient to offset clinical vitamin A deficiency; the other half received no supplement. Blood was sampled from all animals at biweekly intervals to assess beta-carotene and vitamin A status. Adipose tissue was sampled by biopsy on three occasions throughout the experimental period and at slaughter to assess FA composition. Muscle was sampled at slaughter to determine the intramuscular fat content. The mean plasma concentration of beta-carotene of all animals fell from an initial value of 20.1 to 5.2 microg/mL at 14 d, to 1.4 microg/mL at 35 d, and to zero at 105 d. Mean vitamin A in plasma was not significantly different between the treatment groups initially. The values then rose to almost twice their initial values by 35 d, but subsequently fell to below initial values by day 119. Thereafter, plasma vitamin A of the supplemented group was significantly greater than that of the unsupplemented group (P < 0.05). Muscle samples at slaughter from supplemented animals contained significantly (P < 0.01) more intramuscular lipid (13.0 vs. 9.6%). Major changes occurred over time in FA composition in both groups. Saturated FA decreased as monounsaturated FA increased over the first 60 d. An index of desaturation of FA was significantly lower (P < 0.001) in the vitamin A-supplemented group than in the nonsupplemented group. M.P. of the adipose tissue of nonsupplemented animals was 32.3 degrees C, significantly less (P< 0.05) than that of supplemented animals (34.1 degrees C). Feeding vitamin A was associated with less intramuscular fat but with a less desirable (less unsaturated, more solid) FA profile.

Suspected hypovitaminosis A in a colony of captive green anoles (Anolis carolinensis).

In a colony of 18 green anoles (Anolis carolinensis), 3 animals experienced focally thickened lips, ulcerative cheilitis, lethargy, depression, and weight loss over a 5-month period. In addition to crickets fed fresh fruit and leafy green vegetables, the diet of the green anoles consisted of a supply of mealworms that had been dusted with a commercial liquid vitamin supplement. The history, clinical findings, and histopathologic lesions were suggestive of hypovitaminosis A, which is known to cause squamous metaplasia of the mucus secreting glands and epithelial surfaces in many species.

[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.

Serum vitamin A and vitamin E in Japanese black fattening cattle in Miyazaki prefecture as determined by automatic column-switching high performance liquid chromatography.

Japanese Black fattening cattle in Miyazaki prefecture, Japan were examined for serum vitamin A (V. A) and vitamin E (V. E) by automatic column-switching high performance liquid chromatography with automated deproteinization. Results indicated that most Japanese Black fattening cattle in Miyazaki prefecture may be provided with V. A supplement and diets including little V. E, moderate beta-carotene and V. A during the early fattening stage, and diets including little beta-carotene, V. A and V. E during the middle and later fattening stages. Therefore, monitoring serum V. A and V. E in Japanese Black fattening cattle throughout the fattening period seems necessary for farmers in Miyazaki prefecture to avoid economic loss attributable to these deficiencies.

Effects of vitamin A deficiency on the reproductive system of mature White Leghorn hens.

Two groups of 100 white leghorn hens were fed rations either supplemented or deficient in vitamin A for 32 weeks. At the conclusion of the study, vitamin A-supplemented hens laying normally were also compared with a group of vitamin A-supplemented hens in a state of low egg production. Mean egg retinol equivalents (microgram retinol/g egg yolk), egg production, and hatchability in the vitamin A-deficient group were decreased significantly by 4, 20, and 28 weeks, respectively, after beginning treatment. The ovaries of vitamin A-deficient chickens had increased numbers of atretic follicles compared with the ovaries of vitamin A-supplemented hens (20, 24, 28, and 32 weeks), and these atretic follicles contained moderate to severe hemorrhage. Hemorrhage was located either uniformly throughout the follicle or more commonly between the detached granulosa cell layer and the theca interna. Hemorrhagic follicles were uncommon in both vitamin A-supplemented hens and low-production vitamin A-supplemented hens.