Calf hemorrhagic diathesis. - CAB Direct

Weil syndrome, the severe form of leptospirosis, primarily manifests as profound jaundice, renal dysfunction, hepatic necrosis, pulmonary dysfunction, and hemorrhagic diathesis. Pulmonary manifestations include cough, dyspnea, chest pain, bloodstained sputum, hemoptysis, and respiratory failure.

01/12/2017 · Hemorrhagic Diathesi..

T1 - Hemorrhagic diathesis associated with a hereditary platelet disorder in Simmental cattle.

[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.

Hemorrhagic diathesis associated with a hereditary platelet disorder in Simmental cattle
" Hemorrhagic diathesis associated with a hereditary platelet disorder in Simmental cattle "

Bovine Neonatal Pancytopenia causes hemorrhagic diathesis in calves

AB - A severe bleeding disorder in Simmental cattle has been described in widespread locations in the USA and Canada. The clinical findings are consistent with a hemophilia-like disease or, more precisely, a hereditary hemorrhagic diathesis and include spontaneous epistaxis, hematuria, and excessive bleeding associated with trauma or standard management procedures such as tattooing, ear tagging, and castration. A preliminary investigation of this defect showed that blood-platelet numbers and coagulation profiles of affected cattle were normal. Affected animals have a marked dysfunction of platelets (thrombopathy), termed Simmental hereditary thrombopathy. The defect is very similar or identical to that described in the same breed by 2 other laboratories.

Hemorrhagic diathesis associated with a hereditary platelet disorder in Simmental cattle.

Hemorrhagic diathesis in neonatal calves

Outbreaks of idiopathic haemorrhagic diathesis syndrome in young calves. outbreaks of idiopathic haemorrhagic diathesis syndrome diagnosed in springborn suckled calves. Neonatal calves affected by haemorrhages unrelated to BNP. May 11, 2012. Bovine neonatal pancytopenia BNP; previously known as idiopathic haemorrhagic diathesis and commonly known as bleeding calf syndrome.

diathesis. It is used as a supportive therapy in various infectious diseases and during

Cattle Diseases/chemically induced*

N2 - A severe hereditary hemorrhagic diathesis in Simmental cattle has been identified in North America. Platelet numbers and coagulation profiles of affected cattle are normal. We have further characterized the severe dysfunction of platelet aggregation. All agonists tested elicited normal shape change. Aggregations in response to ADP, A23187, and collagen were absent. Aggregations were decreased or required more time for completion in response to PAF and thrombin. No ultrastructural abnormalities were observed in transmission electron micrographs. Dense granule release of ATP in response to PAF was normal. Thrombin-induced aggregation was dependent upon external calcium concentration in normal but not affected animals. Clot retraction in the blood from affected animals was abnormal. The data implicate a defect of Ca++ mobilization or utilization.