01/12/2017 · Hemorrhagic Diathesi..
[Hemorrhagic diathesis in calves as a result of …
A hemorrhagic diathesis is the cause of pulmonary lesions: hemorrhages occur in the lungs, pleura, or pericardium, and in severe infections there may be acute hemorrhagic lobar pneumonia.
of hemorrhagic diathesis in cattle …
The neurologic clinical signs presented by cattle of this report affected by SLP are typical of hepatic encephalopathy. Cattle poisoned by the larvae (8) and sheep fed (21) also show signs of hepatic encephalopathy, and the fatally poisoned calves presented increased plasma ammonia sufficient to account for the clinical signs.(8) Hepatic encephalopathy is common in ruminants and horses with hepatic failure.(3) Undetermined as yet are the specific metabolites that cause the neurologic dysfunction in hepatic encephalopathy, but increased concentrations of plasma ammonia derived from amines absorbed from the gastrointestinal tract may be responsible.(3) Normally, amines are absorbed from the intestines into the portal blood and metabolized by the liver. The toxic products may not be fully eliminated by severely damaged liver. However, abnormal ammonia concentrations are not the only possible cause of hepatic encephalopathy. An imbalance between inhibitory and excitatory amino acid neurotransmitters, -aminobutyric acid, and L-glutamate, respectively, and increased brain concentrations of endogenous benzodiazepines are other possible explanations.(3) Alternatively a low blood sugar can account for the neurological signs and a fall in glucose was noticed in and the fatally poisoned calves by .(8)
Widespread hemorrhages are prominent in some field cases of SLP, but they were not invariably present and their severity varied. Lengthened thrombin, activated thromboplastin times and reduced fibrinogen concentration have been reported in calves experimentally poisoned with the larvae of.(8) Hemorrhagic diathesis occurs terminally in animals with severe liver necrosis.(3) In these cases bleeding tendencies associated with hepatic failure may be due to impaired synthesis of clotting factors, reduced clearance of the products of the clotting process, and metabolic abnormalities affecting platelet function that affect normal clotting, individually or in combination. In acute liver failure (as is the case of liver failure in SLP) diminished synthesis of clotting factors with a short half-life, such as factors V; VII, IX, and X, impairs the ability of blood to coagulate. Diminished clearance of fibrin degradation products activated coagulation factors, and plasminogen factors by the damaged liver also perturbs clotting. Metabolic disturbances resulting from liver failure can affect platelet function and lead to synthesis of abnormal fibrinogen, a condition termed dysfibrinogenemia.(3)
Due to the short course of the disease, jaundice and photosensitization were not common findings, although both were not were seen in some field cases. An increased concentration of serum bilirubin has been seen in experimental sawfly larval poisoning of cattle and sheep.(8,21)
Tubular and degeneration of the renal epithelium tubular as described in cattle,(2,19) sheep,(14) and pigs(18) were not observed in our cases.