Baccharis vulneraria Backer is a sub-shrub frequently found in southern Brazil, which leads to gastrointestinal tract intoxication. The objective of this study is to describe epidemiological, clinical and anatomopathological aspects of two cases of B. vulneraria poisoning in cattle. Two bovines from two different municipalities in the Itajaí Valley, Santa Catarina, Brazil were necropsied and performed the histopathological evaluation and botanical classification of the plant found in the pasture. Bovine 1 had dehydration, ruminal atony, diarrhea, congested mucous membranes and hypothermia for 20 hours, and died during clinical care. At necropsy, there was moderate multifocal detachment and reddening of the forestomachs mucosa. Bovine 2 presented anorexia, dry feces, ruminal atony, vocalization and muscle tremors for ten days, unresponsive to treatments, evolving to death. At necropsy were seen loosening of the mucosa with marked diffuse reddening and transmural edema. The microscopic exam revealed degeneration, necrosis, vesiculation, and detachment of the forestomachs’ mucosa, associated with moderate multifocal neutrophilic infiltrate (Bovine 1); marked diffuse transmural necrosis, edema, hemorrhage, and marked fibrinous exudation (Bovine 2). A large amount of B. vulneraria was found in the pastures, with signs of consumption. In this report, a case of subacute evolution of B. vulneraria poisoning was observed, since the poisoning by this plant is usually acute. More knowledge about poisoning by this plant is necessary for the prevention and control, avoiding new mortality cases.
Polioencephalomalacia (PEM) is the morphological characterization for softening of brain gray matter, and excess sulfur intake is one of its main causes. This study describes an outbreak of this disease in 1-to-3-month-old calves in a farm located in Santa Catarina state, Brazil. The herd consisted of 27 Jersey male calves whose diet was composed of initial feed, ground whole corn, and mineral salt. From this herd, 10 animals became ill, showing signs of apathy, anorexia and blindness, evolving to generalized weakness and death. Necropsy was performed in three of these animals, which showed flattening of the cerebral convolutions in addition to softened, yellowish areas in the cerebral cortex. Histopathological examination revealed deep laminar necrosis associated with perineuronal and perivascular edema, as well as neurons with wrinkled, eosinophilic, or vacuolated cytoplasm. The following sulfur doses were observed: 8,010mg/kg in corn, 6,385mg/kg in initial feed, 1,060mg/kg in mineral salt and 2.3mg/L in water, reaching dose values far above the accepted, totaling a daily intake of approximately 6,533.5mg sulfur/animal/day. As differential diagnosis, lead was dosed in the kidneys and liver of the three calves, with negative results. Also, the calf that sickened last was treated with 20mg/kg thiamin and 0.2mg/kg dexamethasone (IM; QID) for three days and eventually recovered. According to anatomopathological findings, excess sulfur intake and therapeutic diagnosis, sulfur poisoning was suggested as the cause of PEM in these 1-to-3-month-old calves. Occurrence of PEM is rare in calves at such a young age.
Polysaccharide storage myopathy (PSSM) is a genetic disorder or by undetermined cause characterized by the abnormal accumulation of glycogen and polysaccharides in skeletal muscle fibers. The present report describes two Percheron horses, from different properties in the municipality of Pouso Redondo - SC, with locomotor clinical signs that started after work. The clinical signs observed were rigid gait, mainly of the pelvic limbs, muscle weakness, and recumbency. In the first case, the animal was diagnosed with severe multifocal rhabdomyonecrosis, moderate multifocal myoglobin nephrosis and severe diffuse transmural fibrinonecrotic gastritis. PSSM was confirmed by the presence of polysaccharide inclusions in myofiber sarcolemma visualized by periodic acid-Schiff (PAS) staining. In the second case, the horse presented two episodes of muscle disorder after work. The therapeutic protocol was based on penicillin, flunixin meglumine and fluid therapy with ringer lactate. An increase in creatine kinase (669.0 UI/L) and aspartate aminotransferase (669.0 UI/L) was observed in the serum biochemical evaluation. Research for mutation in the GYS1 gene was performed, with a positive heterozygote result. After rest and gradual recovery, the horse was only submitted to light work, with no return of the clinical condition since then. Thus, this report describes two cases of PSSM with distinct clinical evolution and diagnostic methods.
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