No abstract

During the period, 47 (3.48%) out of 1.347 ascensions were reported as malformations. Based in the type of malformation and in the origin of the animals, malformations were divided in: 1) caused by the ingestion of M. tenuiflora, and 2) sporadic malformations of unknown causes. In sheep, 21 out of 418 ascensions were malformations, being 18 (4.3%) of malformations caused by M. tenuiflora and 3 (0.71%) of sporadic malformations. In cattle, 14 out of 434 ascensions were malformations, from these 8 (1.84%) were caused by M. tenuiflora and 6 (1.38%) were sporadic malformations. In goats, 12 out of 495 ascensions were malformations, being 9 (1.81%) malformations related with the ingestion of M. tenuiflora and 3 (0.6%) sporadic malformations. More frequent malformations caused by M. tenuiflora were arthrogryposis, micrognatia, palatoschisis, microphtalmia and unilateral or bilateral hypoplasia or aplasia of the incisive bones. Sporadic malformations were acephaly and hermaphrodite, dicephaly and malformations of mesenteric vessel in sheep; atresia ani in three goats; and hydranencephaly, atresia ani, ribs malformation with eventracion, cerebellar hypoplasia with hydrocephalus, pulmonary choristoma and meningocele, and siamese twins in cattle. A case of cerebellar hypoplasia with hydrocephalus was negative on immunohistochemistry to bovine viral diarrhea virus. Malformations caused by M. tenuiflora occurred during the whole year. The highest frequency in sheep seems to be associated with the consumption of the plant by ewes after first rains, in the first two months of gestation, when they are supplemented with concentrates, and M. tenuiflora is the main green forage available. Malformations occur mainly in degraded areas of native forest (caatinga) invaded by M. tenuiflora, with lesser variety of other species.INDEX TERMS: Congenital defects, teratogenic plants, poisonous plants, Mimosa tenuiflora, plant poisoning.

Seeds of Crotalaria retusa containing 6.84% (dry weight) of monocrotaline (MCT) were administered experimentally to sheep. Three sheep that received 136.8mg MCT/kg bw daily for 70 days had no clinical signs. Five out of six sheep ingesting single doses of 205.2 and 273.6mg MCT/kg bw died with acute (three sheep) or chronic intoxication (two sheep). Acute intoxicated sheep had periacinar liver necrosis and chronic intoxicated sheep liver fibrosis and megalocytosis. Another three sheep had no clinical signs after the ingestion of 20 daily doses of 136.8mg MCT/kg, followed by seven doses of 273.6mg MCT/kg, and one single dose of 342mg MCT/kg. These experiments demonstrated that sheep are susceptible to acute intoxication by MCT being intoxicated by a single oral dose of approximately 205.2mg/kg. In contrast, they develop strong resistance to MCT after the daily ingestion of non lethal doses (136.8mg/kg). It is suggested that chronic poisoning does not occur by the repeated ingestion of non acutely toxic doses, but probably by the ingestion of single toxic doses. It is also suggested that sheep do not become intoxicated with the ingestion of C. retusa in the vegetative non-seeding stage.

RESUMO A infecção em cães por Dioctophyma renale, relatada em diversas partes do mundo, é considerada incomum, na maioria das vezes. No entanto, em algumas regiões são descritos números crescentes da infecção e muitos dados da epidemiologia e do ciclo biológico do parasito ainda são obscuros. Dessa forma, o trabalho tem como objetivo descrever os aspectos epidemiológicos, clinicopatológicos e ultrassonográficos de casos de infecção por Dioctophyma renale em cães na região da Fronteira Oeste do Rio Grande do Sul. Foram estudados 28 casos de dioctofimose em cães necropsiados ou clinicamente avaliados, submetidos à ultrassonografia e cirurgia para retirada dos parasitos. Os cães errantes foram os mais acometidos e todos com possível acesso às margens do Rio Uruguai. As lesões renais e extrarrenais foram caracterizadas predominantemente por atrofia do parênquima renal com glomerulonefrite esclerosante e peritonite granulomatosa associada a parasitos adultos livres na cavidade abdominal e ovos, bem como migrações erráticas para o tecido subcutâneo. Por fim, os achados ultrassonográficos corresponderam, especialmente, a imagens transversais circulares de até 0,6 cm de diâmetro, com margem hiperecoica e centro hipoecoico. Esses achados foram patognomônicos para infecção por Dioctophyma renale, e o exame ultrassonográfico se mostrou indispensável para o diagnóstico definitivo durante a avaliação clínica. Os achados observados nesse estudo demonstram a importância dessa parasitose na região. Além disso, alertam para a importância do diagnóstico, que vem sendo subestimado, além de apontar a necessidade de mais dados acerca da epidemiologia da doença para que se chegue a métodos efetivos de controle.

AimTo determine the dose of monosodium iodoacetate (MIA) required to induce oxidative stress, as well as pain and edema; to confirm the induction of knee osteoarthritis (OA) symptoms in rats by the presence of reactive oxygen species (ROS) and reduction of antioxidant agents; and to verify the presence of histopathological injury in these affected joints.MethodBiological markers of oxidative stress, pain, knee edema, and cartilage degeneration provided by different doses of MIA (0.5; 1.0 or 1.5 mg) in rat knee joints were analyzed. The animal evaluations were conducted during 15 days for mechanical and cold hypersensitivity, spontaneous pain and edema. After that, blood serum, intra‐articular lavage and structures of knee, spinal cord and brainstem were collected for biochemical analysis; moreover, the knees were removed for histological evaluation.ResultsThis study demonstrates that the highest dose of MIA (1.5 mg) increased the oxidative stress markers and reduced the antioxidant reactions, both in the focus of the lesion and in distant sites. MIA also induced the inflammatory process, characterized by pain, edema, increase in neutrophil count and articular damage.ConclusionThis model provides a basis for the exploration of underlying mechanisms in OA and the identification of mechanisms that may guide therapy and the discovery of OA signals and symptoms.