Abstract
Mice infected with Plasmodium berghei, during the ten days of infection, showed significant pulmonary oedema, delayed activated partial thromboplastin time, augmented plasma fibrinolytic activity, oscillations in fibrinogen and unchanged plasminogen levels. These alterations can be expected to cause the release of inflammatory peptides, leading to increased vascular permeability and the generation and/or maintenance of the pronounced pulmonary oedema affecting these animals.