Objectives To create awareness of single RHDV2 infections and cases of death despite immunisation with RHDV2‐specific vaccine. Materials and Methods Retrospective case series of four companion rabbits. Patient signalment, vaccination history, pathology and molecular examinations were obtained from the medical records. Results The animals died peracutely or with nonspecific symptoms like apathy and inappetence. Pathological examination indicated and molecular biological findings confirmed RHDV2 infection in four animals. Several partner animals died at the same time under the same circumstances. Clinical Significance This is the first report of fatalities in RHDV2‐vaccinated companion rabbits due to rabbit haemorrhagic disease virus 2 infection with documented case and vaccination history. Veterinarians should be aware of possible single fatal RHDV2 infections despite vaccination, should initiate the clarification of suspected cases and inform vaccine manufacturers and competent authorities.

A six-month-old foal was initially presented with recurrent, progressive respiratory symptoms over a period of three months. During fixation for medical treatment of a suspected bacterial infection of the respiratory tract, the horse developed acute circulatory failure and was referred to an equine clinic. Cardiac auscultation revealed holosystolic murmur centered around the mitral valve, whilst thoracic auscultation and radiography revealed pulmonary edema and a highly enlarged cardiac silhouette. The foal collapsed during echocardiographic examination and was humanely euthanized. At necropsy, the heart was enlarged with severe dilation of all four chambers and the endocardium was markedly thickened and diffusely opacified. Histopathologically, the endocardium was also severely thickened to up to 601 µm by a significantly increased amount of collagen fibers and discontinuous and irregularly arranged elastic fibers, consistent with severe endocardial fibroelastosis (EFE). In contrast, five control horses with a median age of six months lacking cardiac alterations had a mean left ventricular endocardial thickness of 29.8 ±17.3 µm with few, regularly arranged collagen and elastic fibers. Further pathological findings included pulmonary edema and fibrosis, detection of hemosiderin-laden macrophages in the alveoli, vascular and perivascular fibrosis, as well as ascites and were consistent with biventricular heart failure. Idiopathic EFE has very rarely been described in young horses and other animals and its intravital diagnosis is very difficult. However, EFE should be considered as a differential diagnosis in foals with acute or chronic congestive heart failure. As in the present case, therapeutic approaches have to date always been unrewarding in animals and therefore, prognosis is generally considered poor.

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A 15-year-old donkey gelding was referred to the Equine Clinic of the Freie Universität Berlin because of acute onset of anorexia, bradycardia and multiple syncopes. The clinical examination revealed an irregular heartbeat (11-18 bpm) and syncopes. A continuous ECG revealed absence of P-waves and an irregular ventricular escape rhythm. An echocardiography revealed a pericardial effusion with reduction of left and right ventricular function. Laboratory abnormalities revealed increased troponin I, alpha hydroxybutyrate dehydrogenase and symmetric as well as asymmetric dimethylarginine. Increased concentrations of the cardiac glycoside digitoxin was evident in serum. Clinical findings were consistent with myocarditis with pericardial effusion and atrial standstill. Because of increasing severity of symptoms and grave prognosis the donkey was humanely euthanized. Histopathological examination of the cardiac atria including the sinoatrial node revealed severe, subacute, diffuse, suppurative myocarditis.