Portal de Periódicos da CAPES

EMPYEMA AND BLOODSTREAM INFECTION CAUSED BY BURKHOLDERIA GLADIOLI IN A PATIENT WITH CYSTIC FIBROSIS AFTER LUNG TRANSPLANTATION

1996; Lippincott Williams & Wilkins; Volume: 15; Issue: 7 Linguagem: Inglês

10.1097/00006454-199607000-00020

1532-0987

Saeed Uz Zaman Khan, Steven M. Gordon, Paul C. Stillwell, Thomas J. Kirby, Alejandro C. Arroliga,

Plant Pathogenic Bacteria Studies

Burkholderia (formerly Pseudomonas) gladioli is a Gramnegative bacterium primarily known as a plant pathogen. Although isolation of B. gladioli from sputum cultures in patients with cystic fibrosis has been reported, it was considered a colonizer of the respiratory tract and did not appear to cause disease in any of the patients.1,2 Recent reports suggest that B. gladioli can be a pathogen in immunocompromised patients.3 In this report we describe a patient with empyema and bacteremia caused by B. gladioli following lung transplantation for cystic fibrosis. The respiratory tract was colonized by B. gladioli before the transplant surgery. We conclude that B. gladioli can be more than just a colonizing organism of the respiratory tract of patients with cystic fibrosis and should be considered a potential pathogen in these patients, especially with immunosuppression after lung transplantation. Case report. A 22-year-old-white man with cystic fibrosis was referred to Cleveland Clinic Foundation for lung transplant evaluation. The diagnosis of cystic fibrosis had been made at the age of 9 weeks, and aside from few minor pulmonary exacerbations, his pulmonary status had remained stable until the age of 18 years. During the subsequent 4 years his pulmonary function gradually deteriorated, requiring home oxygen supplementation at the age of 20 years. In the year before transplantation, he was hospitalized three times with pneumonia and respiratory failure and required mechanical ventilation on one occasion. At the time of lung transplantation forced respiratory volume in first second (FEV1) was 0.70 L/m (16% of predicted), his forced vital capacity (FVC) was 1.12 l/min (22% of predicted) and the FEV1:FVC ratio was 0.62. Sputum cultures performed 6 and 3 months before his lung transplant grew B. gladioli(Table 1). On August 12, 1995, he underwent a successful bilateral orthotopic sequential lung transplantation through a "clamp shell" incision. Cultures from the explanted lung grew Streptococcus viridans and B. gladioli. His early postoperative course was complicated by an episode of mild acute allograft rejection (Grade A2) which was treated with high dose methylprednisolone (1 g/day) for 3 days and he was discharged to home on the 19th posttransplant day. Immunosuppression included cyclosporin A, azathioprine and prednisone along with oral trimethoprim-sulfamethoxazole (for Pneumocystis carinii infection prophylaxis). Because of the mismatch between patient (cytomegalovirus (CMV)-seronegative) and the donor (CMV-seropositive), he also received preemptive treatment with intravenous gancyclovir (4 weeks) and CMV-human immunoglobulin (100 mg/kg every 2 weeks for 8 weeks). On the 40th postoperative day he was seen in the outpatient clinic with a 3-day history of low grade fever and a 2- by 1-cm abscess in the left chest wall incision site. There was mild surrounding erythema but no pain and tenderness. A chest radiograph showed small bilateral pleural effusions, unchanged from previous films. The white blood cell count was 13 660/μl with 73% neutrophils and 14% lymphocytes. The abscess was aspirated and therapy was started with dicloxacillin for presumed staphylococcal infection. Two days later he developed another abscess close to the first one, and he was admitted to the hospital for surgical incision and drainage of this abscess. A Gram-stained smear of the pus from the abscesses showed Gram-negative bacilli and cultures grew B. gladioli(Table 1). This unusual Gram-negative aerobic motile organism was initially identified by the GNI card system (Biomerieux Vitek, Inc., Hazelwood, MO). Biochemical characterization, as outlined by the Special Bacterial Reference Laboratory of the Centers for Disease Control, were used to identify the organism.4 Antimicrobial susceptibilities were determined by microtiter dilution according to published guidelines and breakpoints.5 The patient was treated with intravenous imipenem (10 mg/kg twice a day) for 3 weeks through a peripheral venous central catheter. One week later purulent drainage recurred at the incisional site on the left chest wall, and a chest radiograph an showed increased right pleural effusion. Computerized tomography of the chest showed a "split pleura sign" of the right pleura suggestive of empyema (Fig. 1). A diagnostic thoracentesis proved the collection to be an empyema, which was thoracoscopically drained. Cultures of the abscess, the pleural fluid and two sets of blood cultures grew B. gladioli. The antibiotic susceptibility pattern showed the B. gladioli isolates to be susceptible to imipenem (Table 1). Despite treatment with intravenous imipenem (15 mg/kg three times a day) for 6 weeks, the pleural cutaneous fistula did not completely resolve. Unfortunately during this time he also developed another episode of acute lung rejection with subsequent cytomegalovirus pneumonia, invasive Aspergillus fumigatus lung infection and bronchiolitis obliterans. He died 6 months after lung transplantation. Significant findings at autopsy included bronchiolitis obliterans, several bilateral necrotizing bronchopneumonias (special stains negative for bacteria, fungal organisms and P. carinii) and a pleural cutaneous fistula with a small (2- by 2-cm) abscess. Discussion.B. gladioli, also called Bacterium marginatum, is a nonfermenting Gram-negative bacillus in pseudomonad group. Other species in this group and the disease they cause in humans are Burkholderia pseudomallei (melioidosis6), Pseudomonas mallei (glanders7), Pseudomonas pickettii (nosocomially acquired bacteremia and urinary tract infections8) and Burkholderia cepacia (respiratory infections and sepsis in cystic fibrosis patients9 and pneumonia and adenitis in patients with chronic granulomatous disease10). B. gladioli is primarily a plant pathogen and can be isolated from decaying onions, gladiolus and iris species.11 Phenotypically it resembles B. cepacia and was initially recognized as growing in sputum cultures from cystic fibrosis patients. Although various biochemical tests such as oxidase reaction,10 lactose and maltose fermentation1, 12, 13 and lysine decarboxylase reaction have been suggested as differentiating B. gladioli from B. cepacia, separation of these two species may be difficult. Simpson et al.14 used fatty acid analysis and reported multiresistant strains possessing biochemical characteristics of both B. cepacia and B. gladioli. Christenson et al.1 and Mortensen et al.2 reported isolating B. gladioli from cystic fibrosis patients; the organisms behaved as colonizers and did not cause disease in these patients. Despite these reports suggesting a benign nature of B. gladioli, Simpson et al.14 argued that isolation of B. gladioli and B. cepacia from patients with cystic fibrosis should be considered equally significant. Our patient did have B. gladioli in the sputum before lung transplantation, indicating colonization of the airways. We believe that the right pleural cavity and the incisional site were seeded during the transplant surgery resulting in subsequent empyema and the recurrent abscesses. The clinical course of our patient including empyema, chest wall abscesses and presistence of the organism despite prolonged antibiotic therapy is similar to the pleuropulmonary infectious complications caused by B. cepacia in lung transplant patients. B. gladioli has only recently been reported as a pathogen in humans. Ross et al.3 reported two patients with chronic granulomatous disease who developed B. gladioli pneumonia; one patient responded to treatment with intravenous ciprofloxacin and gentamicin, and the other patient responded to ampicillin-sulbactam and oral trimethoprim-sulfamethoxazole. Immunosuppression after lung transplantation predisposes patients to various infections. Patients with cystic fibrosis harbor many pathogenic bacteria in their respiratory tract and these organisms persist in the native trachea and sinuses after lung transplantation. Although B. gladioli has been reported as a colonizer in patients with cystic fibrosis, it has not been shown to cause disease in them. We conclude that B. gladioli caused invasive disease in a patient with cystic fibrosis after lung transplantation and that this organism should be considered a pathogen for patients with cystic fibrosis who undergo lung transplantation. Acknowledgments. We are indebted to Kathy Pratt-Rippin, M.T. (ASCP) and our other colleagues in the clinical microbiology laboratory. Saeed U. Khan, M.D.; Steven M. Gordon, M.D.; Paul C. Stillwell, M.D.; Thomas J. Kirby, M.D.; Alejandro C. Arroliga, M.D. Departments of Pulmonary and Critical Care Medicine (SUK, PCS, ACA), Infectious Diseases (SMG), and Thoracic and Cardiovascular Surgery (TJK) Cleveland Clinic Foundation Cleveland, OHFIG. 1: Computerized tomography scan of the chest showing split pleura sign (arrow) suggesting empyema.