Seneciose crônica em ovinos no sul do Rio Grande do Sul / Chronic seneciosis in sheep in southern Rio Grande do Sul, Brazil

Descrevem-se dois surtos de intoxicação por Senecio spp. em ovinos a campo no sul do Rio Grande do Sul. A enfermidade ocorreu no ano 2006 em duas propriedades que estavam severamente invadidas pela planta e com acentuada escassez de forragem. A morbidade nos dois surtos variou de 10 por cento a 9,5 por cento nas duas propriedades, respectivamente. Na primeira propriedade os animais eram nascidos e criados na área e na outra os ovinos haviam sido adquiridos alguns meses antes do surto. Os sinais clínicos caracterizaram-se por emagrecimento progressivo, apatia, fraqueza, icterícia e fotossensibilização. Macroscopicamente, o fígado dos ovinos necropsiados estava aumentado de tamanho, amarelado, com superfície capsular irregular e vesícula biliar aumentada de tamanho e com edema da parede. Ao corte no fígado havia nódulos bem delimitados, esbranquiçados com 1-3mm de diâmetro. Havia, ainda, ascite e discreto edema de mesentério. Microscopicamente, as lesões hepáticas eram semelhantes em todos os fígados e caracterizadas por megalocitose, fibrose periportal, presença de hepatócitos tumefeitos, vacuolizados e de hepatócitos necróticos distribuídos aleatoriamente pelo parênquima hepático, hiperplasia das células dos ductos biliares e presença de pseudo-inclusões nos núcleos de hepatócitos. Encefalopatia hepática (status spongiosus) foi observada em todos os ovinos necropsiados. O diagnóstico foi baseado na epidemiologia, sinais clínicos, lesões macroscópicas e histológicas observadas. Concluiu-se que, apesar de a intoxicação por Senecio spp. ser pouco frequente em ovinos e essa espécie animal controlar eficientemente a planta, isso, aparentemente, depende da lotação utilizada e surtos da intoxicação podem ocorrer quando esta lotação é menor que 0,2 ovinos por hectare e há carência de forragem acentuada.

Two outbreaks of Senecio spp. poisoning in grazing sheep in southern Rio Grande do Sul are described. The disease occurred in 2006 on two farms that were heavily infested with Senecio spp. and had shortage of forage. The morbidity in both outbreaks was 10 percent and 9.5 percent, respectively. In one case the sheep were born and had grown up on the farm. On the other, the sheep flock was introduced into the farm some months before the outbreak. Clinical signs included progressive emaciation, apathy, weakness, jaundice and photodermatitis. At necropsy, the sheep had an augmented yellowish and firm liver with irregular capsular surface, and an extended and edematous gallbladder. There was distension and edema of the gallbladder. The cut surface the liver showed well-circumscribed whitish nodules measuring 1-3mm in diameter, which were randomly scattered throughout the hepatic parenchyma. There was also edema of mesentery and ascitis. Histopathological findings of the liver included hepatomegalocytosis, bile duct hyperplasia and periportal fibrosis. There were also swollen hepatocytes, randomly scattered necrotic hepatocytes and nuclear pseudo inclusions. Hepatic encephalopathy (status spongiosus) was observed in the brain in all necropsied sheep. The diagnosis of Senecio poisoning was based on epidemiological data, clinical signs, necropsy findings and histological lesions. It was concluded that despite infrequent, Senecio spp. poisoning in sheep may occur when animals are placed in areas heavily invaded by the plants. Although sheep can efficiently control Senecio spp. in paddocks, this apparently depends on the stocking rate, and outbreaks may occur when stocking rate is less than 0.2 sheep per hectare and when there is severe shortage of forage.

iceA genotypes of Helicobacter pylori strains isolated from Brazilian children and adults.

Data concerning the geographic distribution of iceA alleles are scarce, and information on the association of the gene with the disease is rare and still controversial. Furthermore, no such study has been developed in Brazil, where duodenal ulcer and gastric adenocarcinoma are very common. We investigated, by PCR, the frequency of iceA alleles and cagA status in Helicobacter pylori strains isolated from 142 patients (62 children and 80 adults; 66 female; mean age, 30.0 years; age range, 3 to 78 years) with gastritis, duodenal ulcer, or gastric adenocarcinoma. iceA was identified in bacterium samples obtained from all patients. Eleven (7.7%) of them were infected with multiple strains. Among the patients with nonmixed infection, iceA2 allele was detected in 118 (90.1%). iceA2 allele was associated with ulcer (P = 0.02) and with carcinoma (P = 0.001). iceA2 amplicons of 229, 334, or 549 bp were detected, but none of them was associated with the patient's disorder. iceA2 strains were more frequent in patients older than 7 years (P = 0.001). The gene was also more frequent in strains obtained from males (P = 0.02). cagA was more common in strains obtained from carcinoma (P = 0.0008) and ulcer patients (P < 0.006). cagA-positive strains were more frequent in children older than 7 years (P < 0.003). No association between cagA status and sex was found (P = 0.28). In conclusion, we think iceA should not be used as a reliable marker for predicting the clinical outcome of H. pylori infection.