A 67-yr-old man was admitted to the hospital on February 13, 1996 with an exacerbation of chronic obstructive pulmonary disease. He was treated with ceftazidime (1 g intravenously every 8 h) and ciprofloxacin (500 mg orally twice a day) for P. aeruginosa bronchitis with initial improvement. He was transferred to a rehabilitation facility on March 11, 1996. His hospital course at the second facility was remarkable for methicillin-resistant S. aureus bronchitis treated with vancomycin. On May 2, 1996 he developed increased respiratory distress and a cough productive of purulent sputum; pulse oximetry revealed decreased oxygen saturation. Sputum culture yielded pure growth of P. aeruginosa that was susceptible only to colistin (Table 1). The patient was initially treated with clarithromycin (500 mg orally twice a day) and ciprofloxacin (750 mg orally twice a day) but his respiratory status continued to worsen with increased sputum production and the development of a new right upper lobe infiltrate on his chest X-ray. A repeat sputum culture yielded two different isolates of P. aeruginosa; one isolate was resistant to all antibiotics except colistin and a second isolate was sensitive to colistin, amikacin, ceftazidime, and aztreonam. Treatment with ceftazidime (1 g intravenously every 8 h), amikacin (500 mg intravenously every 12 h), and aerosolized colistin (150 mg in 2 ml of water diluted in 2 ml of normal saline twice a day) administered with a Respirgard II nebulizer (Marquest Medical Products Inc., Englewood, CO) led to improvement in the patient's respiratory status and clearing of both strains of P. aeruginosa from the patient's sputum.

Peak and trough serum levels of amikacin were monitored every 3 d and were consistently in the therapeutic range. Complete blood counts, serum creatinine, and electrolytes were tested every 3 d and transaminases, total bilirubin, and alkaline phosphatase were evaluated weekly during colistin administration. Based on these tests, there was no evidence of any biochemical or hematological toxicity resulting from the treatment. The patient had no additional respiratory tract infections until the time of his discharge from the hospital, 1 mo after the completion of colistin therapy.

A 45-yr-old-man was originally admitted to the hospital on December 22, 1996 with group A streptococcal toxic shock syndrome complicated by adult respiratory distress syndrome, acute renal failure requiring hemodialysis, disseminated intravascular coagulation, and liver failure. His hospital course was notable for the development of P. aeruginosa pneumonia with bacteremia, prolonged respiratory failure with a tracheostomy, and a severe cutaneous allergic reaction to ceftazidime. His condition slowly improved and he was transferred to a rehabilitation facility on February 25, 1997. His chest X-ray on admission revealed multilobar infiltrates and a sputum culture grew P. aeruginosa that was susceptible to amikacin, gentamicin, tobramycin, and colistin (Table 1).

Because of the presence of fever, cough, and copious purulent sputum production, therapy with gentamicin (90 mg intravenously every 12 h) for probable P. aeruginosa pneumonia was initiated on February 28, 1997. On March 3, 1997 the patient still was producing copious purulent secretions and had not progressed in being weaned from the ventilator so therapy with twice daily aerosolized colistin (100 mg in 2 ml of water diluted in 2 ml of normal saline administered with a Respirgard II nebulizer via the tracheostomy tube) was initiated. Gentamicin levels were therapeutic. During the following 2 wk, the patient's pulmonary secretions became progressively less purulent and his overall respiratory status improved to such an extent that he could be weaned off the ventilator and have his tracheostomy removed. Renal function and hematological indices (monitored two to three times per week) remained stable throughout the course of colistin therapy.

A 59-yr-old man with chronic renal insufficiency, hypertension, and coronary artery disease was admitted to the hospital with a cerebrovascular accident on November 5, 1996. His hospital course was notable for the development of pneumonia with respiratory failure requiring intubation and eventual tracheostomy placement. He was transferred to a rehabilitation facility on February 27, 1997. Initial evaluation revealed evidence of P. aeruginosa tracheobronchitis. Sputum culture grew P. aeruginosa that was susceptible to ceftazidime, piperacillin, gentamicin, and tobramycin. The patient was treated with ceftazidime (500 mg intravenously every 12 h) with gradual resolution of his fever and purulent sputum production.

On March 24, 1997 the patient developed recurrent fever, dyspnea, and cough productive of purulent sputum. There was no radiographic evidence of pneumonia. Sputum culture again yielded P. aeruginosa that was susceptible to ceftazidime, piperacillin, gentamicin, and tobramycin. The isolate was also found to be susceptible to colistin (Table 1). The patient was treated with ceftazidime (500 mg intravenously every 12 h) and gentamicin (50 mg intravenously every 12 h) but the latter agent had to be discontinued after 4 d because of deteriorating renal function and high trough levels of gentamicin. Due to the presence of persistent fever and purulent sputum production, treatment with aerosolized colistin (150 mg twice a day via a Respirgard II nebulizer through the patient's tracheostomy) was initiated on March 31, 1997. During an 11-d course of therapy with colistin (in conjunction with ceftazidime), the patient's respiratory distress, fever, and purulent sputum production all resolved. Twice weekly monitoring of complete blood counts, serum creatinine, electrolytes, and transaminases revealed no evidence of renal or hematological toxicity during treatment with colistin. The patient had no further episodes of respiratory tract infections during the subsequent 3 wk of his hospitalization.