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Burkholderia gladioli:Recurrent Abscesses in a Patient with Cystic Fibrosis
69
Case Reports doi:10.1053/jinf.2000.0770, available online at http://www.idealibrary.com on
Burkholderia gladioli: Recurrent Abscesses in a Patient with Cystic Fibrosis A. M. Jones1, T. N. Stanbridge2, B. J. Isalska2, M. E. Dodd1 and A. K. Webb*1 1
Manchester Adult Cystic Fibrosis Unit, 2Department of Microbiology, Wythenshawe Hospital, Southmoor Road, Manchester, M23 9LT, UK
We describe a case of an adult patient with cystic fibrosis who developed chronic pulmonary infection and multiple episodes of soft tissue abscesses with Burkholderia gladioli; this organism should be added to the list of potential pathogens for individuals with cystic fibrosis. © 2001 The British Infection Society
Introduction Burkholderia gladioli is a member of the genus Burkholderia, of which B. cepacia is the type species. Burkholderia cepacia is recognized as an opportunistic pathogen in cystic fibrosis (CF) individuals. Unlike some other organisms in the Burkholderia species, B. gladioli is not considered to be a virulent pathogen in CF patients.1 We report a case of an adult cystic fibrosis patient with chronic pulmonary infection with B. gladioli who suffered episodes of recurrent soft tissue abscess formation at multiple sites; each required surgical drainage and long courses of intravenous antibiotics. Burkholderia gladioli was isolated from the abscesses. The patient’s CF lung disease deteriorated and he developed hypertrophic pulmonary osteoarthropathy. This case demonstrates that B. gladioli should be regarded as a serious pathogen in CF individuals.
Case Report The patient was referred to the Manchester Adult Cystic Fibrosis (CF) Unit in 1986 aged 17 years. He worked in Italy as a professional ski instructor. He was diagnosed at 5 years old with a positive sweat test, and DNA typing (homozygous delta-F508) later confirmed the diagnosis. He required admission to hospital for intravenous therapy for his CF lung disease on average once every year through his teenage years, and was treated intermittently with oral steroids for episodes of allergic bronchopulmonary aspergillosis (ABPA). In 1993 a Burkholderia species was isolated from a sputum sample for the first time and he subsequently became chronically infected with this organism. Initial laboratory identification by API 20NE (API-bioMerieux, Marcyl’Etoile, France) was that of B. cepacia; however, subsequently the isolate was re-identified as B. gladioli by molecular analysis.
* Please address all correspondence to: Professor A. K. Webb, Adult Cystic Fibrosis Unit, Wythenshawe Hospital, Southmoor Road, Manchester M23 9LT, UK. Accepted for publication 26 October 2000.
In 1996, over the course of about 48 h, a tender fluctuant swelling developed in the right side of his neck in the mid-deep cervical region. Aspirate of the swelling yielded a Burkholderia species, confirmed by polymerase chain reaction (PCR) as B. gladioli. An operation was performed to explore and drain the abscess; this revealed a large right upper cervical abscess that was threatening the internal jugular vein and the contents of the carotid sheath on that side. Antibiotic treatment consisting of intravenous ceftazidime and tobramycin was commenced, and the wounds slowly healed. Two months later a second procedure was required to incise and drain an abscess that had reformed in the same area and B. gladioli was again isolated from the abscess. He was treated with intravenous meropenem and tobramycin for 3 weeks and the abscess healed. In 1998 his CF disease progressed, with deteriorating chest radiological signs, continuing chest pains, worsening spirometry, weight loss, intermittent fevers and the development of chronic wrist and ankle pain. X-rays demonstrated changes of hypertrophic pulmonary arthropathy (HPOA). In February 1998 a swelling developed over the right shoulder; this was incised and drained. A non-fermentative Gram-negative organism, later confirmed as B. gladioli, was isolated from culture of tissue taken from the abscess wall. He was treated with co-trimoxazole and the abscess healed over a period of 1 month. In June 1998 a swelling developed over the left forearm; this too was incised and drained. The abscess healed slowly over a period of 3 months. On this occasion the additional application of topical tetracycline to systemic antibiotic therapy did seem to produce a clinical improvement in the rate of healing of the forearm abscess. In September 1998 he developed pain over his chest wall and dense shadowing on his chest radiograph in an area adjacent to the site of discomfort. A computerized tomography (CT)-guided biopsy of the mass was performed. Culture of tissue taken from the inflammatory mass yielded B. gladioli. He was treated with intravenous Tazocin and tobramycin for a period of 2 months, and his chest pain and the dense chest radiograph shadowing both resolved. Towards the end of 1998 the patient developed cystic fibrosisrelated diabetes mellitus which was well controlled with insulin. In 1998 he was forced to give up his job as a professional ski instructor due to a combination of respiratory and lower limb symptoms. © 2001 The British Infection Society
70
Figure 1.
Case Reports
Chest wall abscess caused by Burkholderia gladioli.
In January 1999 he developed a lump on his right thigh. An ultrasound scan revealed an echogenic mass within the muscle of the leg. A large amount of pus was surgically drained from an abscess communicating between the inguinal ligament and fascia around the knee; B. gladioli was isolated from the pus. The wound was slow to heal and required frequent debridement and dressings under general anaesthesia. Two months later an 85 cm chest wall abscess developed, affecting the right pectoralis major (photograph). Burkholderia gladioli was isolated on several occasions from this abscess. Repeated blood cultures were negative. Tissue histology demonstrated foreign body type multinucleated giant cells; stains for acid-fast bacilli and fungi were negative. During this period he received broad-spectrum antibiotic treatment with a variety of combinations of intravenous piperacillin, Tazocin, co-trimoxazole, meropenem, imipenem, tobramycin and ceftazidime. The B. gladioli was resistant to all antibiotics on disc diffusion testing, except Tazocin and piperacillin. The patient lost weight and overnight gastrostomy feeding was commenced to try to improve his nutritional status. Opiate injections were required for pain control. Pentaglobulin infusions were given for a trial period but without any clinical benefit, and therefore were discontinued. Both abscess cavities took over 4 months to heal. Detailed immunological tests failed to show any evidence of a primary or acquired immunodeficiency disorder. HIV serology was negative. Neutrophil function tests demonstrated normal neutrophil phagocytosis and killing. Serum immunoglobulin levels were typical for a patient with CF, with an elevated IgG level of 18.9 gms/l and normal levels of IgA and IgM. His lung disease continued to progress, and he suffered frequent episodes of haemoptyses. In July 1999 he required an elective bronchial artery embolisation procedure. HPOA caused increasing discomfort and mobility problems. Six months later, the patient underwent a heart-lung transplant operation but this was unsuccessful and he died.
Discussion Pseudomonas cepacia (Burkholderia cepacia) became recognized as a significant opportunist pulmonary pathogen in cystic fibrosis patients in the 1980s.2 Chronic B. cepacia pulmonary infection is generally associated with increased morbidity and mortality; in
about 20% of CF patients it causes a rapidly fatal necrotizing pneumonic illness (the ‘cepacia syndrome’). In 1992 it was proposed that Pseudomonas RNA group II be transferred to a new genus, Burkholderia, and this should include B. cepacia, B. gladioli, B. mallei, B. pseudomallei, B. caryophylli (Ralstonia pickettii and Ralstonia solanacearum were also initially included but have since been transferred to the genus Ralstonia, whilst others have been added to the Burkholderia species).3 Burkholderia gladioli (Pseudomonas gladioli) is closely related to B. cepacia;4 both originally were isolated as phytopathogens. Although B. gladioli is recognized as an organism which may lead to chronic pulmonary colonization in individuals with CF, it is less frequently isolated than B. cepacia.5 Furthermore, its role as a potential pathogen in CF has been questioned.1 Indeed, it has been suggested that B. gladioli is more of a hindrance to the identification of B. cepacia than a pathogen in its own right.1 Both B. cepacia and B. gladioli have intrinsic resistance to many antibiotics4 and this complicates the clinical management of patients infected by these organisms. Burkholderia gladioli can be extremely difficult to distinguish phenotypically from B. cepacia, even with the use of selective media and biochemical tests, such as the API 20NE system.4 Newer techniques using the polymerase chain reaction (PCR) allow rapid, sensitive and species-specific discrimination for B. gladioli.6–8 In the present case it was initially thought that the patient had become infected with a unique non-epidemic strain of B. cepacia. PCR, however, identified the isolate as B. gladioli. As PCR methodology is used more frequently by reference laboratories to identify and differentiate Burkholderia species, some isolates previously thought to be non-epidemic strains of B. cepacia may be confirmed as B. gladioli. As discussed later, this raises the question as to whether CF patients with different Burkholderia species should be further segregated from each other. This case report identifies B. gladioli as an opportunistic pathogen in CF patients. Following the development of B. gladioli infection, the patient suffered severe debility from his progression of CF lung disease, development of HPOA and repeated episodes of pyomyositis. Each B. gladioli abscess was difficult to treat and slow to heal. Although the organism was never isolated from blood cultures, transient bacteraemia is the most likely mode of spread. The repeated episodes of abscess formation at different sites suggest that transient bacteraemia was occurring at frequent intervals. Burkholderia gladioli bacteraemia has been described in an immunocompromised CF post-transplant patient, who eventually died from widespread infection.9 Indeed, it has since been questioned whether B. gladioli-infected patients should be selected for transplantation,10 although others dispute this view.11 Previously, significant disease caused by B. gladioli has only been described in severely immunocompromised patients.9,12,13 Detailed investigations in the present case revealed no evidence of a primary or acquired immunodeficiency disorder. Diabetes mellitus and prolonged oral steroid therapy may have been factors predisposing to the pyomyositis in this patient, although his diabetic control had been good. A late possible exacerbating factor may have been malnutrition associated with poor appetite, malabsorption and chronic sepsis. Despite surgical intervention and prolonged courses of intravenous antibiotics, the abscesses were slow to heal. The patient’s clinical condition deteriorated with each abscess and he required prolonged periods of in-patient care. Burkholderia cepacia is transmissible – the degree is straindependent.14 Segregation of colonised from non-colonised
Case Reports patients is now standard practice in most CF centres. Although one paper described cross-infection by B. gladioli among six CF patients,15 the organism was mis-identified and later, using species-specific PCR, was shown to be B. cepacia epidemic strain ET12.16 Whether B. gladioli may cross-infect between CF patients is unknown. No true reports of cross-infection by this organism have been published. The strain of B. gladioli in the present case had not previously been identified from any other patients in our CF unit. The question as to whether B. gladioli patients should be segregated from B. cepacia patients remains unanswered. Strict segregation policies would have resource implications for large CF centres with big patient numbers. This case report highlights the potential of B. gladioli to cause disease in CF individuals. Patients with chronic granulomatous disease (CGD)12 and immunocompromised organ transplant recipients also appear to be at risk from this organism.9 The potential use of Burkholderia species as biocontrol agents remains controversial. Burkholderia species, including B. gladioli, have biocidal activity in plant pathogenic species.17 Pseudomonas antimicrobica, a potent antifungal agent, has now been identified as B. gladioli. This further adds to the concern among the CF community of the possible widespread use of these organisms by the agricultural and petrochemical industries.
References 01 Christenson J, Welch D, Mukwaya G, Muszynski MJ, Weaver RE, Brenner DJ. Recovery of Pseudomonas gladioli from respiratory tract specimens of patients with cystic fibrosis. J Clin Microbiol 1989; 27: 270–273. 02 Isles P, MacLusky I, Corey M, Gold R, Prober C, Fleming P, Levinson H. Pseudomonas cepacia infection in cystic fibrosis: an emerging problem. J Pediatr 1984; 104: 206–210. 03 Yabuuchi E, Kosako Y, Oyaizu H et al. Proposal of Burkholderia gen. Nov. an transfer of seven species of the genus Pseudomonas homology group II to the new genus with the type species Burkholderia cepacia. Microbiol Immunol 1992; 36: 897–904. 04 Baxter IA, Lambert PA, Simpson IN. Isolation form clinical sources of Burkholderia cepacia possessing characteristics of Burkholderia gladioli. J Antimicrob Chemother 1997; 39: 169–175.
71
05 Butler SL, Doherty CJ, Hughes JE, Nelson JW, Govan JRW. Burkholderia cepacia and cystic fibrosis: do natural environments present a potential hazard? J Clin Microbiol 1995; 33: 1001–1004. 06 Bauernfeind A, Scheider I, Jungwirth R, Roller C. Discrimination of Burkholderia gladioli from other Burkholderia species detectable in cystic fibrosis patients by PCR. J Clin Microbiol 1998; 36: 2748–2751. 07 Clode FE, Kaufmann ME, Malnoick H, Pitt TL. Evaluation of three oligonucleotide primer sets in PCR for the identification of Burkholderia cepacia and their differentiation form Burkholderia gladioli. J Clin Pathol 1999; 52: 173–176. 08 Whitby PW, Pope LC, Carter KB, LiPuma JJ, Stull TL. Species-specific PCR as a tool for the identification of Burkholderia gladioli. J Clin Microbiol 2000; 38: 282–285. 09 Khan SU, Gordon SM, Stillwell PC, Kirby TJ, Arroliga AC. Empyema and bloodstream infection caused by Burkholderia gladioli in a patient with cystic fibrosis after lung transplantation. Ped Infect Dis J 1996; 15: 637–639. 10 Khan SU, Arroliga AC, Gordon SM. Significance of airway colonization by Burkholderia gladioli in lung transplant candidates. Chest 1998; 114: 658. 11 Kanj SS, Tapson V, Davis RD, Madden J, Browning I. Infections in patients with cystic fibrosis following lung transplantation. Chest 1997; 112: 924–930. 12 Ross JP, Holland SM, Gill VJ, DeCarlos ES, Gallin JI. Severe Burkholderia (Pseudomonas) gladioli infection in chronic granulomatous disease: report of two successfully treated cases. Clin Infect Dis 1995; 21: 1291–1293. 13 Graves M, Robin T, Chipman AM, Wong J, Khashe S, Janda JM. Four additional cases of Burkholderia gladioli infection with microbiological correlates and review. Clin Infect Dis 1997; 25: 838–842. 14 Govan JRW, Brown PH, Maddison J, Doherty CJ, Nelson JW, Dodd M, Greening A, Webb A. Evidence for transmission of Pseudomonas cepacia by social contact in cystic fibrosis. Lancet 1993; 342: 15–19. 15 Wilsher ML, Kolbe J, Morris AJ, Welch DF. Nosocomial acquisition of Burkholderia gladioli in patients with cystic fibrosis. Am J Respir Crit Care Med 1997; 155: 1436–1440. 16 Clode FE, Metherell LA, Pitt TL. Nosocomial acquisition of Burkholderia gladioli in patients with cystic fibrosis [letter]. Am J Respir Crit Care Med 1999; 60: 374–375. 17 Hu FP, Young JM. Biocidal activity in plant pathogenic Acidorax, Burkholderia, Herbaspirallum, Ralstonia and Xanthomonas species. J Appl Microbiol 1998; 84: 263–271.
Case Reports doi:10.1053/jinf.2000.0770, available online at http://www.idealibrary.com on
Burkholderia gladioli: Recurrent Abscesses in a Patient with Cystic Fibrosis A. M. Jones1, T. N. Stanbridge2, B. J. Isalska2, M. E. Dodd1 and A. K. Webb*1 1
Manchester Adult Cystic Fibrosis Unit, 2Department of Microbiology, Wythenshawe Hospital, Southmoor Road, Manchester, M23 9LT, UK
We describe a case of an adult patient with cystic fibrosis who developed chronic pulmonary infection and multiple episodes of soft tissue abscesses with Burkholderia gladioli; this organism should be added to the list of potential pathogens for individuals with cystic fibrosis. © 2001 The British Infection Society
Introduction Burkholderia gladioli is a member of the genus Burkholderia, of which B. cepacia is the type species. Burkholderia cepacia is recognized as an opportunistic pathogen in cystic fibrosis (CF) individuals. Unlike some other organisms in the Burkholderia species, B. gladioli is not considered to be a virulent pathogen in CF patients.1 We report a case of an adult cystic fibrosis patient with chronic pulmonary infection with B. gladioli who suffered episodes of recurrent soft tissue abscess formation at multiple sites; each required surgical drainage and long courses of intravenous antibiotics. Burkholderia gladioli was isolated from the abscesses. The patient’s CF lung disease deteriorated and he developed hypertrophic pulmonary osteoarthropathy. This case demonstrates that B. gladioli should be regarded as a serious pathogen in CF individuals.
Case Report The patient was referred to the Manchester Adult Cystic Fibrosis (CF) Unit in 1986 aged 17 years. He worked in Italy as a professional ski instructor. He was diagnosed at 5 years old with a positive sweat test, and DNA typing (homozygous delta-F508) later confirmed the diagnosis. He required admission to hospital for intravenous therapy for his CF lung disease on average once every year through his teenage years, and was treated intermittently with oral steroids for episodes of allergic bronchopulmonary aspergillosis (ABPA). In 1993 a Burkholderia species was isolated from a sputum sample for the first time and he subsequently became chronically infected with this organism. Initial laboratory identification by API 20NE (API-bioMerieux, Marcyl’Etoile, France) was that of B. cepacia; however, subsequently the isolate was re-identified as B. gladioli by molecular analysis.
* Please address all correspondence to: Professor A. K. Webb, Adult Cystic Fibrosis Unit, Wythenshawe Hospital, Southmoor Road, Manchester M23 9LT, UK. Accepted for publication 26 October 2000.
In 1996, over the course of about 48 h, a tender fluctuant swelling developed in the right side of his neck in the mid-deep cervical region. Aspirate of the swelling yielded a Burkholderia species, confirmed by polymerase chain reaction (PCR) as B. gladioli. An operation was performed to explore and drain the abscess; this revealed a large right upper cervical abscess that was threatening the internal jugular vein and the contents of the carotid sheath on that side. Antibiotic treatment consisting of intravenous ceftazidime and tobramycin was commenced, and the wounds slowly healed. Two months later a second procedure was required to incise and drain an abscess that had reformed in the same area and B. gladioli was again isolated from the abscess. He was treated with intravenous meropenem and tobramycin for 3 weeks and the abscess healed. In 1998 his CF disease progressed, with deteriorating chest radiological signs, continuing chest pains, worsening spirometry, weight loss, intermittent fevers and the development of chronic wrist and ankle pain. X-rays demonstrated changes of hypertrophic pulmonary arthropathy (HPOA). In February 1998 a swelling developed over the right shoulder; this was incised and drained. A non-fermentative Gram-negative organism, later confirmed as B. gladioli, was isolated from culture of tissue taken from the abscess wall. He was treated with co-trimoxazole and the abscess healed over a period of 1 month. In June 1998 a swelling developed over the left forearm; this too was incised and drained. The abscess healed slowly over a period of 3 months. On this occasion the additional application of topical tetracycline to systemic antibiotic therapy did seem to produce a clinical improvement in the rate of healing of the forearm abscess. In September 1998 he developed pain over his chest wall and dense shadowing on his chest radiograph in an area adjacent to the site of discomfort. A computerized tomography (CT)-guided biopsy of the mass was performed. Culture of tissue taken from the inflammatory mass yielded B. gladioli. He was treated with intravenous Tazocin and tobramycin for a period of 2 months, and his chest pain and the dense chest radiograph shadowing both resolved. Towards the end of 1998 the patient developed cystic fibrosisrelated diabetes mellitus which was well controlled with insulin. In 1998 he was forced to give up his job as a professional ski instructor due to a combination of respiratory and lower limb symptoms. © 2001 The British Infection Society
70
Figure 1.
Case Reports
Chest wall abscess caused by Burkholderia gladioli.
In January 1999 he developed a lump on his right thigh. An ultrasound scan revealed an echogenic mass within the muscle of the leg. A large amount of pus was surgically drained from an abscess communicating between the inguinal ligament and fascia around the knee; B. gladioli was isolated from the pus. The wound was slow to heal and required frequent debridement and dressings under general anaesthesia. Two months later an 85 cm chest wall abscess developed, affecting the right pectoralis major (photograph). Burkholderia gladioli was isolated on several occasions from this abscess. Repeated blood cultures were negative. Tissue histology demonstrated foreign body type multinucleated giant cells; stains for acid-fast bacilli and fungi were negative. During this period he received broad-spectrum antibiotic treatment with a variety of combinations of intravenous piperacillin, Tazocin, co-trimoxazole, meropenem, imipenem, tobramycin and ceftazidime. The B. gladioli was resistant to all antibiotics on disc diffusion testing, except Tazocin and piperacillin. The patient lost weight and overnight gastrostomy feeding was commenced to try to improve his nutritional status. Opiate injections were required for pain control. Pentaglobulin infusions were given for a trial period but without any clinical benefit, and therefore were discontinued. Both abscess cavities took over 4 months to heal. Detailed immunological tests failed to show any evidence of a primary or acquired immunodeficiency disorder. HIV serology was negative. Neutrophil function tests demonstrated normal neutrophil phagocytosis and killing. Serum immunoglobulin levels were typical for a patient with CF, with an elevated IgG level of 18.9 gms/l and normal levels of IgA and IgM. His lung disease continued to progress, and he suffered frequent episodes of haemoptyses. In July 1999 he required an elective bronchial artery embolisation procedure. HPOA caused increasing discomfort and mobility problems. Six months later, the patient underwent a heart-lung transplant operation but this was unsuccessful and he died.
Discussion Pseudomonas cepacia (Burkholderia cepacia) became recognized as a significant opportunist pulmonary pathogen in cystic fibrosis patients in the 1980s.2 Chronic B. cepacia pulmonary infection is generally associated with increased morbidity and mortality; in
about 20% of CF patients it causes a rapidly fatal necrotizing pneumonic illness (the ‘cepacia syndrome’). In 1992 it was proposed that Pseudomonas RNA group II be transferred to a new genus, Burkholderia, and this should include B. cepacia, B. gladioli, B. mallei, B. pseudomallei, B. caryophylli (Ralstonia pickettii and Ralstonia solanacearum were also initially included but have since been transferred to the genus Ralstonia, whilst others have been added to the Burkholderia species).3 Burkholderia gladioli (Pseudomonas gladioli) is closely related to B. cepacia;4 both originally were isolated as phytopathogens. Although B. gladioli is recognized as an organism which may lead to chronic pulmonary colonization in individuals with CF, it is less frequently isolated than B. cepacia.5 Furthermore, its role as a potential pathogen in CF has been questioned.1 Indeed, it has been suggested that B. gladioli is more of a hindrance to the identification of B. cepacia than a pathogen in its own right.1 Both B. cepacia and B. gladioli have intrinsic resistance to many antibiotics4 and this complicates the clinical management of patients infected by these organisms. Burkholderia gladioli can be extremely difficult to distinguish phenotypically from B. cepacia, even with the use of selective media and biochemical tests, such as the API 20NE system.4 Newer techniques using the polymerase chain reaction (PCR) allow rapid, sensitive and species-specific discrimination for B. gladioli.6–8 In the present case it was initially thought that the patient had become infected with a unique non-epidemic strain of B. cepacia. PCR, however, identified the isolate as B. gladioli. As PCR methodology is used more frequently by reference laboratories to identify and differentiate Burkholderia species, some isolates previously thought to be non-epidemic strains of B. cepacia may be confirmed as B. gladioli. As discussed later, this raises the question as to whether CF patients with different Burkholderia species should be further segregated from each other. This case report identifies B. gladioli as an opportunistic pathogen in CF patients. Following the development of B. gladioli infection, the patient suffered severe debility from his progression of CF lung disease, development of HPOA and repeated episodes of pyomyositis. Each B. gladioli abscess was difficult to treat and slow to heal. Although the organism was never isolated from blood cultures, transient bacteraemia is the most likely mode of spread. The repeated episodes of abscess formation at different sites suggest that transient bacteraemia was occurring at frequent intervals. Burkholderia gladioli bacteraemia has been described in an immunocompromised CF post-transplant patient, who eventually died from widespread infection.9 Indeed, it has since been questioned whether B. gladioli-infected patients should be selected for transplantation,10 although others dispute this view.11 Previously, significant disease caused by B. gladioli has only been described in severely immunocompromised patients.9,12,13 Detailed investigations in the present case revealed no evidence of a primary or acquired immunodeficiency disorder. Diabetes mellitus and prolonged oral steroid therapy may have been factors predisposing to the pyomyositis in this patient, although his diabetic control had been good. A late possible exacerbating factor may have been malnutrition associated with poor appetite, malabsorption and chronic sepsis. Despite surgical intervention and prolonged courses of intravenous antibiotics, the abscesses were slow to heal. The patient’s clinical condition deteriorated with each abscess and he required prolonged periods of in-patient care. Burkholderia cepacia is transmissible – the degree is straindependent.14 Segregation of colonised from non-colonised
Case Reports patients is now standard practice in most CF centres. Although one paper described cross-infection by B. gladioli among six CF patients,15 the organism was mis-identified and later, using species-specific PCR, was shown to be B. cepacia epidemic strain ET12.16 Whether B. gladioli may cross-infect between CF patients is unknown. No true reports of cross-infection by this organism have been published. The strain of B. gladioli in the present case had not previously been identified from any other patients in our CF unit. The question as to whether B. gladioli patients should be segregated from B. cepacia patients remains unanswered. Strict segregation policies would have resource implications for large CF centres with big patient numbers. This case report highlights the potential of B. gladioli to cause disease in CF individuals. Patients with chronic granulomatous disease (CGD)12 and immunocompromised organ transplant recipients also appear to be at risk from this organism.9 The potential use of Burkholderia species as biocontrol agents remains controversial. Burkholderia species, including B. gladioli, have biocidal activity in plant pathogenic species.17 Pseudomonas antimicrobica, a potent antifungal agent, has now been identified as B. gladioli. This further adds to the concern among the CF community of the possible widespread use of these organisms by the agricultural and petrochemical industries.
References 01 Christenson J, Welch D, Mukwaya G, Muszynski MJ, Weaver RE, Brenner DJ. Recovery of Pseudomonas gladioli from respiratory tract specimens of patients with cystic fibrosis. J Clin Microbiol 1989; 27: 270–273. 02 Isles P, MacLusky I, Corey M, Gold R, Prober C, Fleming P, Levinson H. Pseudomonas cepacia infection in cystic fibrosis: an emerging problem. J Pediatr 1984; 104: 206–210. 03 Yabuuchi E, Kosako Y, Oyaizu H et al. Proposal of Burkholderia gen. Nov. an transfer of seven species of the genus Pseudomonas homology group II to the new genus with the type species Burkholderia cepacia. Microbiol Immunol 1992; 36: 897–904. 04 Baxter IA, Lambert PA, Simpson IN. Isolation form clinical sources of Burkholderia cepacia possessing characteristics of Burkholderia gladioli. J Antimicrob Chemother 1997; 39: 169–175.
71
05 Butler SL, Doherty CJ, Hughes JE, Nelson JW, Govan JRW. Burkholderia cepacia and cystic fibrosis: do natural environments present a potential hazard? J Clin Microbiol 1995; 33: 1001–1004. 06 Bauernfeind A, Scheider I, Jungwirth R, Roller C. Discrimination of Burkholderia gladioli from other Burkholderia species detectable in cystic fibrosis patients by PCR. J Clin Microbiol 1998; 36: 2748–2751. 07 Clode FE, Kaufmann ME, Malnoick H, Pitt TL. Evaluation of three oligonucleotide primer sets in PCR for the identification of Burkholderia cepacia and their differentiation form Burkholderia gladioli. J Clin Pathol 1999; 52: 173–176. 08 Whitby PW, Pope LC, Carter KB, LiPuma JJ, Stull TL. Species-specific PCR as a tool for the identification of Burkholderia gladioli. J Clin Microbiol 2000; 38: 282–285. 09 Khan SU, Gordon SM, Stillwell PC, Kirby TJ, Arroliga AC. Empyema and bloodstream infection caused by Burkholderia gladioli in a patient with cystic fibrosis after lung transplantation. Ped Infect Dis J 1996; 15: 637–639. 10 Khan SU, Arroliga AC, Gordon SM. Significance of airway colonization by Burkholderia gladioli in lung transplant candidates. Chest 1998; 114: 658. 11 Kanj SS, Tapson V, Davis RD, Madden J, Browning I. Infections in patients with cystic fibrosis following lung transplantation. Chest 1997; 112: 924–930. 12 Ross JP, Holland SM, Gill VJ, DeCarlos ES, Gallin JI. Severe Burkholderia (Pseudomonas) gladioli infection in chronic granulomatous disease: report of two successfully treated cases. Clin Infect Dis 1995; 21: 1291–1293. 13 Graves M, Robin T, Chipman AM, Wong J, Khashe S, Janda JM. Four additional cases of Burkholderia gladioli infection with microbiological correlates and review. Clin Infect Dis 1997; 25: 838–842. 14 Govan JRW, Brown PH, Maddison J, Doherty CJ, Nelson JW, Dodd M, Greening A, Webb A. Evidence for transmission of Pseudomonas cepacia by social contact in cystic fibrosis. Lancet 1993; 342: 15–19. 15 Wilsher ML, Kolbe J, Morris AJ, Welch DF. Nosocomial acquisition of Burkholderia gladioli in patients with cystic fibrosis. Am J Respir Crit Care Med 1997; 155: 1436–1440. 16 Clode FE, Metherell LA, Pitt TL. Nosocomial acquisition of Burkholderia gladioli in patients with cystic fibrosis [letter]. Am J Respir Crit Care Med 1999; 60: 374–375. 17 Hu FP, Young JM. Biocidal activity in plant pathogenic Acidorax, Burkholderia, Herbaspirallum, Ralstonia and Xanthomonas species. J Appl Microbiol 1998; 84: 263–271.