Molossinema wimsatti infection in the brain of Pallas's mastiff bats (Molossus molossus).

The present report describes two cases of infection by Molossinema wimsatti in the brain of Pallas's mastiff bats (Molossus molossus). The first bat was captured and killed by a domestic cat in a suburban area of the municipality of Patos, Paraiba, northeastern Brazil. The second bat was found crawling on the ground in the same area before dying. No gross lesions were found at necropsy. Histology of the central nervous system revealed filarioid nematodes in the brain ventricles and cerebellum. There were adults, subadults and eggs, the latter sometimes containing microfilariae. No inflammatory response was observed in bat 1, while bat 2 presented a mild lymphoplasmacytic meningoencephalitis. Three nematodes were recovered and submitted for parasitological examination. The diagnosis of M. wimsatti infection was based on the histomorphological and parasitological characteristics of the agent and its location in the brain ventricular system of insectivorous bats. The infection likely occurs in other insectivorous bats from South American and Caribbean countries but may be overlooked.

Neurotoxicosis in horses associated with consumption of Trema micrantha.

BACKGROUND: Trema micrantha is a tree widely distributed throughout the Americas. The tree produces highly palatable leaves that have been associated with natural poisoning in goats, sheep and horses, in which hepatic necrosis and hepatic encephalopathy have been observed. OBJECTIVES: This study describes malacia and haemorrhage in the central nervous system (CNS) due to T. micrantha consumption, with minimal to absent hepatic lesions. STUDY DESIGN: Retrospective case series. METHODS: A total of 14 horses with a history of neurological signs and spontaneous consumption of T. micrantha leaves were submitted to necropsy and multiple samples were collected for histopathology. Details of clinical history and signs of the horses were obtained through inquiries to the owners and attending veterinarians. RESULTS: All the 14 horses had neurological signs of ataxia, severe sialorrhoea, involuntary running movements, sternal and lateral recumbency, and death after a clinical course that lasted from 24 h to 9 days. For a few days prior to onset of clinical signs, all horses had spontaneously consumed, potentially toxic doses of T. micrantha leaves. All 14 brains had diffuse yellowish discoloration affecting the rhombencephalon, mesencephalon, diencephalon, telencephalon and corpus striatum. In all cases, the most severe lesions were observed in the pons. Spinal cord lesions were observed affecting the lumbar intumescence, which was swollen with darken and depressed areas at the dorsal and ventral horns, and at the sacral level, which on cut surface displayed a friable and yellowish grey matter. The lesions observed grossly in brain and spinal cord consisted microscopically of severe vasculitis and liquefactive necrosis of white and grey matter of the brainstem, cerebellum and spinal cord. MAIN LIMITATIONS: This is a small retrospective series relying on clinical observations reported by owners and attending veterinarians. The mechanism of action of the plant toxin in the CNS is still unidentified. CONCLUSION: T. micrantha poisoning in horses causes predominantly a neurological disease, with minimal to absent hepatic lesions.

Field observations of Ateleia glazioviana poisoning in cattle in Southern Brazil.

Ateleia glazioviana is an important poisonous plant from southern Brazil. Heavy losses in cattle from this region occur each year due to ingestion of the plant. The epidemiological, clinical, gross and histopathological features of A. glazioviana poisoning in cattle are described here from a 5-year field survey in southern Brazil. A. glazioviana poisoning in cattle induces 3 clinical presentations: abortions, disease characterized by lethargy, and cardiac failure. The latter is associated with marked necrosis and fibrosis of the myocardium and can cause sudden death or congestive heart failure.

Monensin poisoning in Brazilian horses.

Three outbreaks of monensin poisoning caused 12 deaths in 16 horses. The illnesses were associated with the ingestion of the same batch of a commercial ration labeled for feeder calves which contained 180 +/- 20 ppm sodium monensin. The morbidity rate was 100% and lethality was 60%, 75%, and 100%. Clinical signs were tachycardia and cardiac arrythmia, groaning, incoordination, sudoresis, recumbency, and paddling movements with the limbs before death. Two horses had dark discolored urine (myoglobinuria). Serum levels of creatine phosphokinase activity were increased. Main necropsy findings were in the skeletal muscles and myocardium.

Coffee Senna (Senna occidentalis) poisoning in cattle in Brazil.

Four 4-5-y-old cows out of a group of 20 developed a toxic myopathy approximately 10 d after being started on a ration contaminated with 21.5% Senna occidentalis beans. Clinical signs included progressive muscle weakness, incoordination of hindlimbs, reluctance to move, dragging of the tip of the hooves of the hindlimbs, and sternal and lateral recumbency. Gross lesions included white to whitish-yellow discolored areas of several groups of skeletal muscle in various regions of the body, but more markedly in the hindlimbs. Significant histopathological changes were restricted to skeletal muscles with variable degrees of segmental degenerative myopathy associated with reparative events. The earliest change seen at electron microscopy of affected skeletal muscles was mitochondrial swelling. More advanced changes ranged from disruption of sarcoplasm and myofibrils to complete lysis of a myofiber segment and early regeneration. Myocardial fibers had swollen mitochondria, disruption of cristae and dense matrical globules. The epidemiology, clinical data and gross, histopathological, and ultrastructural features of S occidentalis poisoning in cattle are presented.

Ionophore antibiotic (narasin) poisoning in rabbits.

Outbreaks of narasin poisoning in rabbits from several commercial rabbit-raising farms in the state of Parana, Brazil, are reported. Approximately 5,000/35,000 rabbits died after having consumed a pelleted ration to which poultry ration premix had been added. Clinical signs included apathy, anorexia, muscle weakness, impaired walking, diarrhea, respiratory distress, and opistothonus. Gross findings were not remarkable, but varying degrees of degeneration, necrosis and regeneration of skeletal muscles were consistent histopathological features in affected rabbits. Myocardial changes were mild or absent. Thirty ppm of narasin were detected in the ration fed the rabbits. The disease was experimentally reproduced by feeding the suspected ration and by administering narasin po to rabbits.

Senecio spp poisoning in cattle in southern Brazil.

Epidemiological, clinical, necropsy and histopathological data were accumulated during the study of 15 outbreaks of Senecio spp poisoning in cattle occurring during the last 3 y in the State of Rio Grande do Sul, Brazil. Morbidity averaged 17% and mortality was virtually 100%. The peak mortality occurred during spring and early summer. The most constant clinical signs included anorexia, depression, tenesmus often followed by rectal prolapse, and rough hair coat. Affected animals remained apart from the rest of the herd, lost weight, presented ascites, and had signs of digestive and neurological disturbances. Icterus, photodermatitis, polydipsia, and dependent subcutaneous edema were occasionally noticed. Two main clinical courses could be distinguished. In the protracted form, progressive weight loss terminated with death within many weeks or months. Alternatively, an acute or subacute course led to death in a few days. In both forms, necropsy and histopathological findings included diffuse fibrosis of the liver, hepatomegalocytosis, and biliary hyperplasia. Extrahepatic lesions included gastrointestinal and mesenteric edema, distension, edema and adenomatoid hyperplasia of the gallbladder, and spongy degeneration of the cerebral white matter. S brasiliensis and S oxyphyllus were the species involved in the field outbreaks.

Acute effects of Solanum malacoxylon on bone formation rates in growing rats.

The plant Solanum malacoxylon is responsible for a syndrome of hypercalcemia, soft tissue mineralization, and progressive wasting in South American cattle known as enteque seco or espichamento. There is evidence that a glycoside of 1,25-dihydroxycholecalciferol is the active principle in the plant. The basis for the hyperostosis seen in the disease is unclear. To study the acute effects on bone formation rates, 8-week-old rats were given an aqueous extract equivalent to 250 or 1000 mg of Solanum daily per os for 7 days. Bones were labeled by injection of fluochrome 2 days before the start of treatment and 2 days prior to sacrifice. Morphometric evaluation of undecalcified sections of caudal vertebrae revealed an increased amount of trabecular bone in both Solanum treated groups with no difference due to dose level. This was associated with an increase in the bone apposition rate on trabecular surfaces. No differences were found in the amount of osteoid seam width. Periosteal apposition rate and endochondral bone formation were also measured and no significant differences found. The findings indicate that acute stimulation of cell level bone formation on trabecular surfaces may play a role in the hyperostosis seen in the naturally occurring condition.