Experimental poisoning by Enterolobium contortisiliquum in sheep / Intoxicação experimental por Enterolobium contortisiliquum em ovinos

Ingestion of Enterolobium contortisiliquum pods causes digestive disturbances, secondary hepatogenous photosensitization and abortions in ruminants. Pods were administered to sheep via a ruminal cannula to characterize acute poisoning. In Experiment 1, a single dose of 12g/kg of body weight (BW) was administered to three sheep in one experiment. One sheep died, and the other two recovered after presenting clinical signs. In Experiment 2, 10g/kg BW were administered daily to 15 sheep until the onset of clinical signs or for three consecutive days. Fourteen sheep showed mild to severe signs after the ingestion of 1-3 doses. Two sheep died, and the others recovered. Clinical signs in both experiments were diarrhea, anorexia, rumen atony, apathy, dehydration and tachypnea. The main macroscopic findings were an orange, frothy ruminal content witch contained pods fragments. The intestinal content was liquid. Detachment of the mucosa from the submucosa and ballooning degeneration of mucosal cells were observed histologically in the forestomachs. Evaluation of ruminal contents revealed acute lactic ruminal acidosis (ALRA). Bromatological analysis of E. contortisiliquum pods revealed 537.8g/kg DM (dry matter) of non-fibrous carbohydrates, which is sufficient to cause ALRA. Only one sheep in Experiment 2 had liver failure, characterized by jaundice, elevated serum activity of liver enzymes and histological lesions in liver biopsies. It is concluded that the administration of E. contortisiliquum pods in forage-fed sheep at doses of 10g/kg BW or higher may cause ALRA. The induction of liver failure in one sheep suggests that liver damage may occur in those sheep that do not develop acidosis.(AU)

A ingestão das favas de Enterolobium contortisiliquum causa distúrbios digestivos, fotossensibilização hepatógena e abortos em ruminantes. Para caracterizar a intoxicação aguda, favas de E. contortisiliquum foram administradas a ovinos por meio de cânula ruminal. No Experimento 1, uma dose única de 12g/kg de peso corporal (pc) foi administrada a três ovinos. Um dos ovinos morreu e os outros dois se recuperaram após mostrar sinais clínicos. No experimento 2, 10g/kg/pc foram administradas diariamente a 15 ovinos, por três dias consecutivos ou até o parecimento dos sinais clínicos. Catorze ovinos mostraram sinais clínicos leves a acentuados após ingestão de 1-3 doses. Dois ovinos morreram e os outros se recuperaram. Observou-se nos ovinos dos experimentos 1 e 2, diarreia, anorexia, atonia ruminal, apatia, desidratação e taquipneia. Os principais achados macroscópicos incluíram conteúdo ruminal espumoso e alaranjado em meio ao qual se observavam fragmentos das favas de E. contortisiliquum, e conteúdo intestinal líquido. Histologicamente, havia degeneração balonosa e desprendimento do epitélio de revestimento dos pré-estomagos. A avaliação do conteúdo ruminal revelou acidose ruminal láctica aguda (ARLA). Análise bromatológica das favas de E. contortisiliquum revelou 537.8g/kg de matéria seca de carboidratos não fibrosos, quantidade suficiente para causar ARLA. Um ovino do Experimento 2 teve insuficiência hepática aguda, caracterizada por icterícia, elevação da atividade sérica das enzimas hepáticas e alterações histológicas observadas em biópsia hepática. Concluiu-se que a administração de favas de E. contortisiliquum na alimentação de ovinos, nas doses de 10g/kg pc ou maiores, pode causar ARLA. A ocorrência de insuficiência hepática num dos ovinos deste experimento sugere que a lesão hepática pode se desenvolver em ovinos que não apresentam ARLA.(AU)

Relationship between indocyanine green clearance test and feed intake and impaired hepatic function in dairy cows.

The purposes of this study were 1) to examine changes in the indocyanine green (ICG) clearance by feeding and 4-day fasting in dry cows, and (2) to investigate the relationship between ICG clearance and blood chemistry profile in postpartum cows. In 3 dry cows, post-feeding ICG half-life (T(1/2)) was shorter than the pre-feeding value, and post-fasting T(1/2) was longer than pre-feeding and post-feeding values. In 16 lactating cows, T(1/2) value at 2 weeks postpartum showed positive correlations with AST, T-Bil and γ-GTP. These results suggested that ICG clearance correlated with T-Bil and liver enzymes can be sensitive and accurate diagnostic marker for impaired liver function in dairy cows. In addition, ICG clearance is greatly affected by feeding and fasting.

Encefalopatía hepática en perros y gatos / Hepatic encephalopathy in dogs and cats

La encefalopatía hepática (EH) en perros y gatos es un disturbio metabólico complejo del sistema nerviosocentral que puede deberse a insufi ciencia hepática, defi ciencias enzimáticas en el ciclo de la urea o a desvíosportosistémicos. Como resultado, las funciones hepáticas de desintoxicación se alteran y/o son eludidas, y losconstituyentes inalterados de la sangre portal penetran directamente a la circulación sistémica. La patogénesisde la encefalopatía asociada a la insufi ciencia hepática es compleja. Probablemente, la EH es un síndrome enel que intervienen múltiples factores que adquieren distinta importancia de acuerdo a la situación clínica. Lospuntos clave a considerar en la patogenia de la EH son: a) las neurotoxinas; b) las alteraciones de los sistemasde neurotransmisión; y c) las alteraciones astrocitarias. Los signos clínicos de EH incluyen obnubilación delestado mental, trastornos del comportamiento, deambulación, apoyo de la cabeza contra superfi cies diversas,defi ciencias visuales y actividad convulsiva. A menudo se presentan también otros signos asociados a la insufi -ciencia hepática como pérdida de peso, anorexia, vómitos, diarreas y poliuria-polidipsia. El diagnóstico de EHse basa en la identifi cación de la alteración hepática en un paciente con trastornos neurológicos típicos de unaencefalopatía metabólica. Aunque hay una gran variedad de métodos, el de elección es la centellografía portaltranscolónica. El tratamiento de la EH está orientado a reducir los niveles de las toxinas provenientes de la absorciónintestinal y a controlar las convulsiones, si se presentan; pero lo fundamental para controlar los signosneurológicos es el tratamiento de la causa del trastorno hepático subyacente. En este artículo se describen losprincipales avances descritos hasta el momento en relación a la fi siopatología de la encefalopatía hepática, asícomo las estrategias terapéuticas(AU)

Hepatic encephalopathy (HE) in dogs and cats is a complex metabolic disturbance of the central nervoussystem that may result from hepatic failure, urea cycle enzyme defi ciency, or portosysistemic shunting. As aresult, the metabolic and detoxifi cation functions of the liver are impaired and/or bypassed and the unalteredconstituents of the portal blood go directly into the systemic circulation. The pathogenesis of hepatic failure-associatedencephalopathy is complex. Probably, the HE is a syndrome in which take part multiple factors that canhave different importance according the clinical situation. The key points to consider in the pathogeny of HEare: a) neurotoxins; b) alterations of neurotransmission systems; and c) astrocytes alterations. Clinical signs ofHE include obtunded mental status, abnormal behavior, compulsive pacing, head-pressing, visual defi cits andseizure activity. Other clinical signs consistent with hepatic failure, as weight loss, anorexia, vomiting, diarrheaand polyuria-polydipsia, are often present. Diagnosis of HE is based upon documenting hepatic dysfunction ina patient with neurologic defi cits typical of a metabolic encephalopathy. Although there are multiple methods,the preferred is per-rectal scintigraphy. Treatment for HE is directed at reducing the level of gut-derived toxinsand controlling seizures, if present; but treatment of the underlying hepatic disorder is the key to controllingsigns of neurologic dysfunction. This article describes the major developments described so far regarding thepathophysiology of hepatic encephalopathy and therapeutic strategies(AU)