Naturally occurring acute parvoviral myocarditis in puppies 3 to 8 weeks of age was characterised clinically by sudden death or death following a brief period of dyspnoea. Mortality within litters varied from 20% to 100%. The principal lesion was in the myocardium, which in most cases was mottled by pale patches and bands. Moderate to severe pulmonary oedema with marked peribronchial and perivascular oedema was present. In some cases, the wall of the gall bladder was oedematous. Microscopically the ventricular myocardium had myofibre loss, multifocal myofibre necrosis, a mononuclear cell infiltrate of variable intensity and reactive stromal elements. In every case there were Feulgen-positive, amphophilic, intranuclear inclusion bodies in myocardial nuclei. Ultrastructurally the inclusions were composed of dense granular material and particles resembling parvovirions. Pulmonary alveolar septae were thickened by fibroblasts. Peribronchial and perivascular lymphatics were distended with oedema fluid and occasionally erythrocytes. The pulmonary lesions were considered secondary to the myocardial dysfunction. Some of the puppies that survived the acute disease developed ventricular myocardial fibrosis and died in congestive heart failure.
Positive in vitro wound healing effects of functional inclusion bodies of a lipoxygenase from the Mexican axolotl