Very commonly febrile patients with bacteraemia develop a variety of acid-base and electrolyte disturbances which play a significant role in the morbidity and mortality of these patients. This study was undertaken to describe the pathogenetic mechanisms of these abnormalities in febrile patients with bacteraemia. Fifteen febrile patients with bacteraemia, aged 24-62 years, were studied. In all patients blood cultures revealed Gram-negative rods. None of them had septic shock, diabetes mellitus, renal or liver failure and none was receiving drugs influencing acid-base balance and electrolyte levels or was a heavy alcohol consumer. Nine patients had respiratory alkalosis, which was possibly due to bacterial toxins, while the remaining 6 had a wide-gap metabolic (lactic) acidosis coexisting with respiratory alkalosis. Hypokalaemia was found in four patients and was mainly due to respiratory alkalosis. However, kaliuria due to hypomagnesaemia contributed to hypokalaemia in 2 patients. Hypomagnesaemia was detected in 3 patients and was attributed to respiratory alkalosis as well as to magnesiuria induced by metabolic acidosis or phosphate depletion. Hypophosphataemia was found in 5 patients who also had respiratory alkalosis and/or phosphaturia due to metabolic acidosis or hypomagnesaemia. Finally, one patient had multifactorial origin hypocalcaemia. Febrile patients with bacteraemia develop a number of acid-base and electrolyte disturbances attributed to various pathogenetic mechanisms.