LAUSR

Cardiorespiratory syndrome (also called lung-heart syndrome) among common foxes was described for the first time in mid 1980s in Poland and Canada and has been reported as a cause of significant losses in fox farms (3, 9). However, despite extensive research, the etiology of the disease still remains elusive. Usually, the disease affects young, 2to 6-month-old, animals. The most characteristic clinical symptom of the cardiorespiratory syndrome in foxes is severe dyspnea; furthermore, the animals present with increased heart rate and complete loss of appetite. Elevating the fox and holding it by the tail with head down causes massive foamy bloody nasal discharge, exacerbation of dyspnea and even death. The symptoms are present suddenly and persist for several hours to several days. Eventually, the animal dies with the symptoms of exacerbating dyspnea, and sometimes also progressive cachexia. Postmortem examination usually reveals variable volume of fluid in pleural and pericardial cavities and an enlargement of the heart. Also pulmonary edema can be observed, sometimes with signs of pneumonia. Moreover, some authors documented pathological changes corresponding to dilated cardiomyopathy (6). Motz et al. (7) observed typical signs of hypoxia on histopathological examination of the myocardial specimens; only few specimens showed discrete infiltration with mononuclear cells. Based on the results of many studies, the involvement of infectious factors in etiopathogenesis of the cardiorespiratory syndrome can be virtually excluded (2, 11, 14, 15). Also the role of taurine deficiency was studied extensively, as involvement of this amino acid in the etiopathogenesis of cardiorespiratory syndrome was suspected, similarly as in the case of feline cardiomyopathy. However, this hypothesis was not confirmed experimentally; moreover, administration of taurine did not influence the therapeutic outcomes of the Pathological findings in common foxes suffering from cardiorespiratory syndrome