Laryngeal Neuropathy in Adult Goats With Copper Deficiency.

The aim of this study was to elucidate the cause of a neurological syndrome characterized by stridor in adult goats with clinical signs of copper deficiency. The main clinical signs consisted of apathy, emaciation, pale mucous membranes, mucous nasal discharge, dyspnea, severe achromotrichia, diffuse alopecia, torpor, ataxia, and stridor. When the goats were forced to move, the stridor increased. In a herd of 194 Toggenburg goats, 10 adult goats with clinical signs of copper deficiency were removed from the herd and divided into 2 groups: group 1, which consisted of 4 nannies and 1 buck with stridor, and group 2, which consisted of 4 nannies and 1 buck without stridor. Group 3, used as a control, consisted of 5 adult goats from another flock without any clinical signs of disease. The mean serum copper concentrations were 1.3 ± 0.3 µmol/L in group 1, 8.1 ± 1.1 µmol/L in group 2, and 11.3 ± 2.2 µmol/L in group 3. The mean serum iron concentrations were 42.3 ± 14.2 µmol/L in group 1, 39.1 ± 8.2 µmol/L in group 2, and 20.6 ± 6.1 µmol/L in group 3. The main histological lesions in goats from group 1 were axonal degeneration of the recurrent laryngeal nerves and atrophy of the muscles of vocal folds and of the dorsal cricoarytenoid and right and left cricothyroid muscles. Goats with ataxia had neuronal degeneration and necrosis of cerebellar Purkinje cells and of the cranial cervical ganglion. We concluded that the stridor was caused by axonal degeneration of the recurrent laryngeal nerves due to the severe copper deficiency.

Stringhalt in Brazilian horses caused by Hypochaeris radicata.

Two outbreaks of Hypochaeris radicata-induced Australian stringhalt involving two farms and seven horses from southern Brazil are reported here. Subsequently, the disease was experimentally reproduced in a feeding trial with one colt fed H. radicata from the suspect paddocks. Fresh H. radicata was fed to the experimental animal for 50 days at an average daily dosage of 9.8 kg. Initially, the plant was collected from the paddock where the clinical disease occurred and was fed for 19 consecutive days producing mild clinical signs. However, on days 20-23 fresh plant was collected from a neighboring farm where the disease had not been reported and fed to the colt at which time the colt appeared to recover. Therefore, plant collections from the original suspect paddock resumed and feeding trials continued with clinical signs reoccurring by day 36, and increasing in intensity from days 43-50 after which plant administration was stopped. Within 15 days after ending the feeding trial with H. radicata, the colt appeared to have recovered. This experimental reproduction of stringhalt in a single colt fed H. radicata demonstrated that the two outbreaks of the disease resulted from this plant. Interestingly, the change in location for collection of plant material 19 days into the treatment, and the subsequent recovery of the colt, would suggest that plant material may differ in toxicity depending on location.

Teratogenicity of Mimosa tenuiflora seeds to pregnant rats.

Bone and other malformations caused by the ingestion of Mimosa tenuiflora are common in ruminants in the Brazilian semiarid. The aim of this research was to study the teratogenic effects of M. tenuiflora in Wistar rats (Rattus novergicus). The experimental group had 15 females and was fed, from the 6th to the 21st day of pregnancy, with a ration containing 10% of M. tenuiflora seeds. The control group, with 10 females, was fed with the same ration without seeds. There were no differences in weight gains, and food and water consumption between treated and control rats. Ninety bone malformations were observed in 40 of the 101 fetuses born in the experimental group, and four malformations were observed in three of the 58 fetuses born in the control group (p<0.05). The weight and number of ossification centers of the fetuses from the experimental group were higher than those from the control group (p<0.05). It is concluded that the seeds of M. tenuiflora are teratogenic to rat fetuses.

Swainsonine-induced lysosomal storage disease in goats caused by the ingestion of Turbina cordata in Northeastern Brazil.

A disease of the central nervous system in goats was observed in the municipalities of Juazeiro, Casa Nova and Curaça, state of Bahia, and Petrolina, state of Pernambuco, Northeastern Brazil. The disease was produced experimentally in two goats by the administration of dry Turbina cordata mixed with grain. Clinical signs were observed after the ingestion of 62 and 106 g/kg body weight in 28 and 54 days, respectively. The concentration of swainsonine in the plant varied from less than 0.001% to 0.14% (dry weight). Clinical signs of natural and experimental cases included difficulties in standing, ataxia, hypermetria, wide-based stance, intention tremors, spastic paresis mainly in the hind legs, nystagmus, abnormal postural reactions, head tilting, and falling. Diffuse vacuolation of neurons, epithelial cells of pancreas, thyroids, and renal tubules were observed on the histology. From the electron microscopy of Purkinje cells the vacuoles represented dilated lysosomes. These findings demonstrated that T. cordata causes an acquired glycoprotein lysosomal storage disease. The intoxication occurs at least in an area of 27,000 km2 causing severe losses in goats, and some farmers report the disease also in cattle.

Intoxication by Ipomoea sericophylla and Ipomoea riedelii in goats in the state of Paraíba, Northeastern Brazil.

A disease of the nervous system was observed in goats from two farms of the semiarid of the state of Paraíba, northeastern Brazil. Ipomoea sericophylla was found in one farm and I. riedelii in the other. Both plants were administered experimentally to five goats each. Both plants induced clinical signs similar to those observed in spontaneous cases. Two goats died spontaneously and five were euthanatized. Three goats recovered after the withdrawal of the plants. Histological examination showed that all goats that died spontaneously or were euthanized had diffuse vacuolation of neurons, macrophages of lymphatic tissues, and epithelial cells of pancreas, thyroid, renal tubules and liver. On electron microscopy of Purkinje cells, numerous dilated membrane bordered vacuoles were identified as lysosomes. On lectin-histochemical analysis, cerebellar cells gave positive reactions to Concanavalia ensiformis, Triticum vulgaris, and succinylated-T. vulgaris, which indicate the storage of alpha-D-mannose, alpha-D-glucose, beta-D-N-acetyl-glucosamine, and acetyl-neuraminic acid. The chemical analysis of I. sericophylla and I. riedelii showed 0.11 and 0.14% of swainsonine, respectively. The latter also contained calystegines B1, B2 and C1. It is concluded that I. sericophylla and I. riedelli cause a lysosomal storage disease.

Tremorgenic syndrome in goats caused by Ipomoea asarifolia in Northeastern Brazil.

Green leaves of Ipomoea asarifolia were dosed to 10 goats. Nine goats ingesting 5-37 g/kg bw daily had clinical signs in 4-38 days. One goat ingesting 2.5 g/kg bw daily during 125 days and two control goats had no clinical signs. Clinical signs were characteristic for a tremorgenic syndrome. Five goats recovered in 4-9 days after the withdrawal of the plant. Two goats died spontaneously and three were euthanased for histologic and ultrastructural studies. No significant lesions were observed at necropsies or on the histologic and ultrastructural studies. Samples of the plant analyzed for enzymatic inhibitors were negative for calystegines and contained an almost undetectable amount of swainsonine (less than 0.001%). It is concluded that I. asarifolia causes a tremorgenic syndrome due to an unknown tremorgenic phytotoxins or mycotoxins.

Periacinar liver fibrosis caused by Tephrosia cinerea in sheep.

Tephrosia cinerea has been associated with ascites and liver fibrosis in sheep in Brazil. The dried plant was fed ad libitum to three sheep for 55-80 days. Three additional sheep were used as controls. All the treated sheep presented with hypoalbuminemia and increased γ-glutamyltransferase and aspartate aminotransferase activities. Anorexia, apathy, rough coat, ascites, and emaciation were observed after 45-60 days of feeding with T. cinerea. At necropsy 55-80 days after feeding of the plant commenced, the treated sheep had ascites, hydrothorax and hydropericardium, and their livers were firm and whitish, with a nodular surface. Histologically, the main hepatic lesions were periacinar fibrosis associated with hemorrhages and necrosis. On electron microscopy, a severe swelling of sinusoidal endothelial cells, frequently obstructing the lumen of the sinusoid was observed. The space of Disse was compressed by the swollen endothelial cells and microvilli usually present on the surface of hepatocytes adjacent to the space of Disse were not apparent. Dense bundles of collagen fibers were present in the spaces of Disse and within the sinusoids between profiles of swollen endothelial cells. It is concluded that T. cinerea causes periacinar fibrosis, similar to poisoning by Galenia africana in sheep and goats and veno-occlusive disease in different species.

Pulmonary and hepatic lesions caused by the dehydropyrrolizidine alkaloid-producing plants Crotalaria juncea and Crotalaria retusa in donkeys.

The effects and susceptibility of donkeys to Crotalaria juncea and Crotalaria retusa poisoning were determined at high and low doses. Seeds of C. juncea containing 0.074% of dehydropyrrolizidine alkaloids (DHPAs) (isohemijunceines 0.05%, trichodesmine 0.016%, and junceine 0.008%) were administered to three donkeys at 0.3, 0.6 and 1 g/kg body weight (g/kg) daily for 365 days. No clinical signs were observed and, on liver and lung biopsies, the only lesion was a mild liver megalocytosis in the donkeys ingesting 0.6 and 1 g/kg/day. Two other donkeys that received daily doses of 3 and 5 g seed/kg showed initial respiratory signs 70 and 40 days after the start of the administration, respectively. The donkeys were euthanized following severe respiratory signs and the main lung lesions were proliferation of Clara cells and interstitial fibrosis. Three donkeys ingested seeds of C. retusa containing 5.99% of monocrotaline at daily doses of 0.025, 0.05 and 0.1 g/kg for 365 days. No clinical signs were observed and, on liver and lung biopsies, the only lesion was moderate liver megalocytosis in each of the three donkeys. One donkey that received a single dose of 5 g/kg of C. retusa seeds and another that received 1 g/kg daily for 7 days both showed severe clinical signs and died with diffuse centrilobular liver necrosis. No lung lesions were observed. Another donkey that received a single dose of 2.5 g/kg of C. retusa seeds showed no clinical signs. The hepatic and pneumotoxic effects observed are consistent with an etiology involving DHPAs. Furthermore, the occurrence of lung or liver lesions correlates with the type of DHPAs contained in the seeds. Similarly as has been reported for horses, the data herein suggest that in donkeys some DHPAs are metabolized in the liver causing liver disease, whereas others are metabolized in the lung by Clara cells causing lung disease.

Spontaneous acute poisoning by Crotalaria retusa in sheep and biological control of this plant with sheep.

After the diagnosis of acute Crotalaria retusa poisoning, 21 healthy sheep from the affected flock were returned to the paddock and continued to consume the sprouting plants. Two years after returning these sheep to the paddock, very few plants were still alive, and after 3 years, no C. retusa plants were observed. The sheep had neither clinical signs nor biochemical alterations and delivered healthy lambs. It is concluded that resistant sheep can be used for the biological control of C. retusa.

Experimental poisoning of guinea pig (Cavia porcellus) with Indigofera suffruticosa.

Indigofera suffruticosa causes hemolytic anemia and hemoglobinuria in cattle. The plant was administered to six groups of two guinea pigs each, at the daily dose of 10 g/kg body weight, for periods of 2, 4, 6, 8, 10 and 15 days. The guinea pigs progressively developed reduced hematocrits and hemoglobin concentrations, and finally presented anemia, without hemoglobinuria. Urine passed by guinea pigs that had ingested the plant for more than 24 h acquired a turquoise blue pigmentation 8-10 h after urination. It is suggested that the anemia is caused by the aniline contained in I. suffruticosa.

Mimosa tenuiflora as a cause of malformations in ruminants in the northeastern Brazilian semiarid rangelands.

Craniofacial anomalies, eye malformations, and permanent flexures of the forelimbs are common malformations seen in ruminants grazing semiarid rangelands of Northeastern Brazil. To investigate the cause of these malformations, we fed 2 suspected plants, Mimosa tenuiflora or Prosopis juliflora, to groups of 4 pregnant goats each. Fresh green M. tenuiflora was collected daily and fed ad libitum to 4 goats in group 1 throughout pregnancy. This treatment group also received a supplemental feed concentrate equivalent to 1% body weight. Four goats in group 2 received a ration with 70% of P. juliflora pods and 30% hay throughout pregnancy. Four control goats were fed supplemental feed concentrate (1% body weight) and hay ad libitum throughout pregnancy. Goats treated with P. juliflora pods and the control goats delivered 9 normal kids. The four goats that were fed M. tenuiflora during pregnancy delivered 4 kids, 3 of which had abnormalities similar to those observed in field cases, including cleft lip, unilateral corneal opacity, ocular bilateral dermoids, buphthalmos with a cloudy brownish appearance of the anterior chamber due to an iridal cyst, and segmental stenosis of the colon. Malformations induced experimentally by M. tenuiflora were similar to those observed in field cases, suggesting that M. tenuiflora is a cause of the field cases observed in the Brazilian semiarid rangelands.

Neurohistologic and ultrastructural lesions in cattle experimentally intoxicated with the plant Prosopis juliflora.

Intoxication by pods of Prosopis juliflora (mesquite beans) causes an impairment of cranial nerve function in cattle and goats. In goats, vacuolation of neurons in the trigeminal motor nuclei has been reported. To study the lesions in cattle caused by consumption of P. juliflora pods and dry ground pods, eight 6- to 12-month-old male cattle were divided into 4 groups: group 1 was fed a ration containing 50% of pods; groups 2 and 3 received a ration containing 50 and 75% of dry ground pods, respectively; group 4 was the control. After 200 days, all cattle were killed and sampled for histologic evaluation. Samples of the trigeminal motor nucleus were examined by electron microscopy. All cattle from groups 1, 2, and 3 showed clinical signs resulting from impaired function of cranial nerves V, IX, X, and XII, starting 45-75 days after consumption of the plant. The main histologic lesions were vacuolation and loss of neurons in trigeminal motor nuclei and other motor cranial nerve nuclei with Wallerian-like degeneration in the cranial nerves. Mild denervation atrophy was observed in the masseter and other masticatory muscles. On electron microscopy, neurons of the trigeminal nuclei had markedly swollen mitochondria, with the mitochondrial cristae displaced peripherally, disoriented and disintegrating. Intoxication by P. juliflora seems to have a novel pathogenesis, characterized by a selective, primary, chronic, and progressive injury to mitochondria of neurons of the trigeminal and other cranial nerve nuclei. Cranial nerve degeneration and denervation atrophy of the muscles occurs as a consequence of the neuronal lesion.

Outbreaks of pythiosis in two flocks of sheep in northeastern Brazil.

Two outbreaks of cutaneous pythiosis caused by Pythium insidiosum were diagnosed in two herds of crossbred hair wool sheep of different ages in the semiarid region of Northeastern Brazil. In one herd of 120 sheep, 40 were affected. The other outbreak affected six sheep out of 80. Local swellings with ulcerative lesions were observed in the limbs and abdominal and prescapular regions. Three sheep were necropsied. Two of them had lung metastasis characterized by multifocal nodules measuring 0.5-2 cm. In one animal, the prescapular lymph node was also affected. In another, the cutaneous lesion extended to the sesamoid bone. Microscopically, there were multifocal granulomas with intralesional P. insidiosum hyphae and Splendore-Hoeppli material surrounding the hyphae. The diagnosis was based on the histologic lesions, immunohistochemical identification, and culture of the etiologic agent. One sheep treated with potassium iodide recovered. Standing in swampy water for long periods in a warm aquatic environment seems to be the reason for the high prevalence of the disease.

Effects of milk from goat fed Crotalaria spectabilis seeds on growing rats

Seeds of Crotalaria spectabilis, containing the pyrrolizidine alkaloid (PA) monocrotaline (MCT), were fed to a lactating dairy goat. Milk from this goat was fed to rats for 8 weeks to determine whether MCT or its toxic metabolites are transferred into the goat's milk. Rats from the experimental group showed significantly higher (p<0.05) serum levels of ALT, AST, GGT and LDH and less weight gains (p<0.05) than control rats. The most significant lesions in rats consuming the experimental ration were mild to moderate interstitial pneumonia and a vacuolar degeneration and occasionally necrosis of periportal hepatocytes. The results of this study indicate that the PA and/or its metabolites are eliminated in milk