The patient with severe symptoms had acute lung injury according to the definition of the American-European Consensus Conference on ARDS [18] , with acute onset, bilateral changes in chest radiography, a PaO2/FiO2 ratio of ≤ 300, and absence of clinical left ventricular failure. Importantly, these respiratory complications appeared before initiation of anti-malarial drug treatment, an observation also reported in two other severe clinical cases of lung injury due to P. vivax [19, 20] . Two main hypotheses have been proposed to explain lung damage in P. vivax malaria infections. The first suggests that there is no sequestration of P. vivax-infected reticulocytes in the deep capillaries of internal organs, postulating instead an inflammatory process due to an increase in capillary permeability associated with cytokine-induced damage in the pulmonary epithelium [21] . The second suggests cytoadherence of P. vivax-infected reticulocytes in lung capillaries, causing obstruction of blood flow and reduction of respiratory function before treatment and alveolar capillary damage and inflammation 24 to 48 hours after initiation of anti-malarial drug treatment [22] . The possibility that antibiotics given 24 hours before respiratory failure might have destroyed P. vivax-infected reticulocytes, inducing lung damage and favouring the second hypothesis, cannot formally rule out. Yet, it is clear that the lack of sequestration in P. vivax needs to be re-evaluated, as cytoadherence has been hypothesized to occur in both the spleen [23, 24] and the lungs [22] .