Hepatogenic photosensitization in lambs supplemented with different levels of extruded urea in Brachiaria spp. pastures in the Brazilian Cerrado: Case report.

The aim was to report cases and risk factors for hepatogenous photosensitization in lambs kept on Brachiaria spp. pastures and supplemented with levels of extruded urea (EU). The herd consisted of 69 Texel crossbred lambs with known parentage (fathers and mothers adapted to the consumption of forage of the genus Brachiaria), randomly divided into 5 groups and distributed in individual paddocks for each group. The animals were supplemented with increasing levels of EU (Amireia® 200S): 0, 6, 12, 18, and 24 g of EU per 100 kg-1 of body weight (BW). The concentration of protodioscin was estimated in the mixed pastures of Brachiaria spp. (cv. Marandu and cv. Basilisk), structural components (leaf, stem, and dead material), samples of each cultivar, and in the months of December (2018), February, and April (2019). The animals were examined daily, and when behavioral changes were identified, they underwent clinical examinations and anamnesis. Weighing was performed every 14 days, followed by necropsy and serum biochemical analysis, including gamma-glutamyltransferase (GGT). The highest concentrations of protodioscin (p < 0.0001) were found in the pastures used by animals supplemented without extruded urea (7.07 ± 0.56), in the Basilisk cultivar (11.35 ± 0.06), in the leaf blade components (2.08 ± 0.05), and thatch (2.20 ± 0.00), and in the month of April (7.34 ± 0.29) (the month with the lowest rainfall), respectively. Fourteen (20.29%) cases of photosensitization were observed in lambs, of which six recovered, and eight died. Serum GGT levels ranged from 42.2 to 225 IU/L; however, in animals that died, values ranged from 209.4 to 225 IU/L. The use of levels 12 g and 18 g per 100 kg-1 of body weight of extruded urea may contribute to the lower occurrence of photosensitization, as the animals selected pastures with lower protodioscin content, presenting a smaller number of cases.

Toxicity testing of saponin-containing Yucca schidigera Roetzl. juice in relation to hepato- and nephrotoxicity of Narthecium ossifragum (L.) Huds.

Yucca schidigera juice in doses of 1.5 g (63 mg sapogenin) and 3.0 g (126 mg sapogenin) per kg live weight was administered intraruminally to 30 lambs for 21 days to investigate whether the saponins in Y. schidigera were toxic to lambs and whether they could cause hepatogenous photosensitisation. Twelve lambs died or had to be euthanised. The main pathological findings in the diseased lambs were acute tubular necrosis in the kidneys, dehydration and watery content in the gastrointestinal tract. Fifteen lambs were euthanised at the end of the study, and the main pathological findings in dosed animals were accumulation of homogeneous pale PAS-positive material in the hepatocytes. There was a rise in serum creatinine and urea concentrations in the lambs with renal lesions the day before they died. Major Y. schidigera-related saponins were found in the liver and kidney samples from all lambs that were dosed with Y. schidigera juice. The results of the present study demonstrate that un-hydrolysed saponins can be absorbed from the gastrointestinal tract. The possible role of saponins in causing nephrotoxicity is discussed.

Experimentally induced cholangiohepatopathy by dosing sheep with fractionated extracts from Brachiaria decumbens.

Cholangiohepatopathy was induced in 5 lambs by oral administration of extracts from signal grass (Brachiaria decumbens) in Brazil. Grossly there were pale foci multifocally distributed throughout the hepatic parenchyma in 4 lambs. The microscopic changes, which were similar to those produced by other steroidal sapogenins-containing plants such as Tribulus terrestris and Panicum spp., included multifocal cholangitis, bile duct proliferation, and the presence of crystals in the biliary system.

Ergotism and photosensitization in swine produced by the combined ingestion of Claviceps purpurea sclerotia and Ammi majus seeds.

Poisoning of domestic animals happens frequently in the southeast of Buenos Aires Province (Argentina). Intoxications are produced mainly by the ingestion of plants and mycotoxins, but animals are rarely affected simultaneously by both types of agents. One herd of pigs suffered simultaneous intoxications by ergot alkaloids from Claviceps purpurea sclerotia and furocoumarins from Ammi majus seeds. Pigs were fed a diet composed of wheat (poor quality) or corn and protein and vitamin supplements. This diet was completed with forage sorghum. Nervous signs were first observed 5-7 days after the initiation of feeding the suspect ration. These signs were followed by cutaneous irritation. Snout ulcers, eyelid edema, and conjunctivitis were observed in several piglets. Ten days after the start of feeding the incriminated ration, 8 abortions were observed. Many of the sows that were nursing piglets developed udder edema and teat cracking. Dermal lesions were observed in most of the animals with unpigmented areas in the skin but not in a Duroc-Jersey boar. Removal of the incriminated diet and feeding of another diet prepared with good-quality wheat allowed all the animals to recover in 15 days. The herd experienced normal pregnancies and parturitions, litter sizes, and piglet weights when fed a cleaned portion of the poor-quality wheat. No photosensitization lesions were observed. Examination of impurities in the suspected wheat indicated the presence of 2.2% of A. majus seeds and 0.14% of C. purpurea sclerotia. The quantitative analysis indicated the presence of 3.2 g xanthotoxin and 0.65 g bergaptene/100 g A. majus seeds and 0.73 g ergot alkaloids (expressed as ergonovine) per 100 g of C. purpurea sclerotia. Qualitative analysis demonstrated the presence of ergotamine, ergocristine, and ergonovine. These results indicate that clinical signs and lesions were caused by the ingestion of large quantities of these biologically active compounds.

Llama dermatology.

The purpose of this article is to add information to the many dermatologic topics initially discussed in the 1989 issue on llama medicine (normal anatomy; bacterial, fungal, ectoparasitic, immune-mediated, and zinc-responsive disease) and make mention of newly recognized diseases. Since 1989, it appears that one of the most common and perplexing groups of dermatoses seen at Colorado State University are hyperkeratotic/inflammatory dermatoses. These remain poorly understood. Idiopathic hyperkeratosis (zinc-responsive dermatosis) may be a true zinc deficiency or a keratinizing disorder responsive to supraphysiologic dosages of zinc supplementation. Idiopathic nasal/perioral hyperkeratotic/ inflammatory dermatosis (munge) and idiopathic necrolytic/neutrophilic/hyperkeratotic dermatosis bear clinical, histologic, and therapeutic similarities, and may be subsets of the same disease. Further studies (e.g., looking for metabolic derangements) are necessary to better answer these questions.

Failure to induce toxicity in lambs by administering saponins from Narthecium ossifragum.

It has been suggested that saponins produced by Narthecium ossifragum (Bog asphodel) may be the direct cause of the toxicity leading to the hepatogenous photosensitivity disease alveld seen in Norwegian lambs. Lambs fed large quantities of freeze-dried N. ossifragum did not develop alveld. Chemical investigations on the freeze-dried material and fresh N. ossifragum showed no difference in their saponin content. These results indicate that alveld is not caused solely by the saponins produced by N. ossifragum.

Photosensitivity in South Africa. II. The experimental production of the ovine hepatogenous photosensitivity disease geeldikkop (Tribulosis ovis) by the simultaneous ingestion of Tribulus terrestris plants and cultures of Pithomyces chartarum containing the mycotoxin sporidesmin.

The mycoflora of toxic pastures were surveyed during a number of outbreaks of ovine hepatogenous photosensitivity in South Africa. Pure cultures of several isolates were dosed to sheep, but only those of Pithomyces chartarum and Myrothecium verrucaria proved to be toxic. Photosensitization was induced in sheep by dosing them with cultures of a P. chartarum isolate (GA10) obtained from Tribulus terrestris plants collected during an outbreak of geeldikkop in the Karoo. Thus for the first time a mechanism whereby T. terrestris plants can contribute to the causation of ovine hepatogenous photosensitivity was demonstrated. When cultures of GA10 equivalent to approximately 0,75--4,0 mg/kg sporidesmin were dosed at Onderstepoort Veterinary Research Institute to Highveld and Karoo sheep on a diet of lucerne, facial eczema was produced. Dosing the same cultures at levels equivalent to c. 1,0 mg/kg of sporidesmin in the Karoo resulted in lesions characteristic of both facial eczema and geeldikkop. Typical hepatic lesions of geeldikkop could be elicited by dosing GA10 at levels equivalent to c. 0,25--0,7 mg/kg of sporidesmin to Karoo sheep grazing on predominantly T. terrestris pastures in the Karoo. In the latter experiment geeldikkop was induced in the sheep on T. terrestris pastures, while those receiving identical doses on veld with little T. terrestris developed facial eczema. Geeldikkop, therefore, can be brought about by the ingestion of T. terrestris plants together with toxic cultures of P. chartarum. The plant appears not only to act as a vehicle for ingestion of spores, but also to interact with sporidesmin to induce lesions typical of geeldikkop, whereas sporidesmin alone results in facial eczema. Indications are that it can enhance the ability of sporidesmin to cause photosensitivity or, possibly, vice versa. The histopathological findings of these experiments are described in detail.

Photosensitization in sheep fed Ammi majus (Bishop's weed) seed.

Ammi majus (bishop's weed) grows on the coastal region of southern United States and in other parts of the world. This plant causes severe photosensitization in livestock and probably contributes to the severe photosensitization outbreaks seen in Texas. Sheep were fed finely ground seed of A majus via stomach tube at dose rates of 1, 2, 4, and 8 g/kg of body weight and exposed to sunlight. The single dose of 8 g/kg produced severe clinical signs (in 24 to 48 hours): cloudy cornea, conjunctivokeratitis, photophobia, and edema of the muzzle, ears, and vulva. Daily dosing at 2 and 4 g/kg produced (in 72 to 96 hours) similar signs, whereas the smallest dose (1 g/kg) produced mild irritation of the muzzle. Pathologic changes included (1) corneal edema and marked neutrophilic infiltration of the cornea and corneal/ciliary process, (2) subacute ulcerative and exudative dermatitis of the skin of ears, muzzle, and vulva, and (3) mild focal tubular degeneration (vacuolar type) of the kidney.

Photosensitization in cattle and sheep caused by feeding Ammi majus (greater Ammi; Bishop's-Weed).

Feeding Ammi majus to cattle and sheep caused photosensitization in both species. It also caused photosensitization in human beings who had dermal contact with the plant and subsequent exposure to sunlight.