We appreciate Drs. Byrd and Roy's interest in our paper. Our patient's diffuse pulmonary infiltrates (these were predominantly interstitial, but later some had an alveolar component) may have been multifactorial, as they commonly are in critically ill patients. Swan-Ganz catheter measurements suggested that the patient had volume overload, which was addressed with periodic hemodialysis. In addition, the patient was treated for pneumonia; Enterobacter cloacae was cultured from bronchial brushings and washings (no transbronchial lung biopsy specimen was obtained, and blood cultures were negative). We cannot rule out the possibility that the patient also had increased capillary permeability in association with the adult respiratory distress syndrome; this syndrome has been reported to be a complication of infection with various Babesia species, other infections, and many other conditions.

Clearly, we need a better understanding of the pathogenesis of babesiosis, which can directly or indirectly affect multiple organ systems, including the lungs. Possible mechanisms of the noncardiogenic pulmonary edema that has been associated with babesiosis and that can develop despite a decrease in the parasitemia level have been discussed in the references cited by Drs. Byrd and Roy.