Burkholderia cepacia complex
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| Burkholderia cepacia complex | ||||||||||||||
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| Burkholderia cepacia complex (Palleroni and Holmes 1981) Yabuuchi et al. 1993 |
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| ATCC 25416 CCUG 12691 and 13226 |
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Pseudomonas cepacia Burkholder 1950 |
Burkholderia cepacia complex (BCC), or simply Burkholderia cepacia is a group of catalase-producing, non-lactose-fermenting Gram-negative bacteria composed of at least nine different species, including B. cepacia, B. multivorans, B. cenocepacia, B. vietnamiensis, B. stabilis, B. ambifaria, B. dolosa, B. anthina, and B. pyrrocinia.[1] B. cepacia is an important human pathogen which most often causes pneumonia in immunocompromised individuals with underlying lung disease (such as cystic fibrosis or chronic granulomatous disease).[2]
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[edit] Pathogenesis
BCC organisms are typically found in water and soil and can survive for prolonged periods in moist environments. Person-to-person spread has been documented; as a result, many hospitals, clinics, and camps for patients with cystic fibrosis have enacted strict isolation precautions for those infected with BCC. Infected individuals are often treated in a separate area than noninfected patients to limit spread, since BCC infection can lead to a rapid decline in lung function and result in death.
Diagnosis of BCC involves isolation of bacteria from sputum cultures. BCC organisms are naturally resistant to many common antibiotics including aminoglycosides and polymyxin B.[3] The bacteria is so hardy that it has been found to persist in betadine (a common topical antiseptic).[4] Treatment typically includes multiple antibiotics and may include ceftazidime, doxycycline, piperacillin, chloramphenicol, and co-trimoxazole.[3] In April 2007 Researchers from the Schulich School of Medicine & Dentistry at The University of Western Ontario, working with a group from Edinburgh, announced they had discovered a way to kill the organism.[5][6]
[edit] History
B.cepacia was discovered by Walter Burkholder in 1949 as the culprit of onion skin rot, and first described as a human pathogen in the 1950s.[7] In the 1980s, it was first recognized in individuals with cystic fibrosis, and outbreaks were associated with a 35% death rate. Burkholderia cepacia has a large genome, containing twice the amount of genetic material as E. coli.
[edit] See also
[edit] References
- ^ Lipuma J (2005). "Update on the Burkholderia cepacia complex". Curr Opin Pulm Med 11 (6): 528–33. doi:. PMID 16217180.
- ^ Mahenthiralingam E, Urban T, Goldberg J (2005). "The multifarious, multireplicon Burkholderia cepacia complex". Nat Rev Microbiol 3 (2): 144–56. doi:. PMID 15643431.
- ^ a b McGowan J (2006). "Resistance in nonfermenting gram-negative bacteria: multidrug resistance to the maximum". Am J Infect Control 34 (5 Suppl 1): S29–37; discussion S64–73. doi:. PMID 16813979.
- ^ Anderson R, Vess R, Panlilio A, Favero M (1990). "Prolonged survival of Pseudomonas cepacia in commercially manufactured povidone-iodine". Appl Environ Microbiol 56 (11): 3598–600. PMID 2268166.
- ^ "Key Found to Kill Cystic Fibrosis Superbug", Innovations Report, April 25 2007. Retrieved on 2007-04-26.
- ^ Ortega XP (May 2007). "A putative gene cluster for aminoarabinose biosynthesis is essential for Burkholderia cenocepacia viability": 3639–3644. American Society for Microbiology. doi:. PMID 17337576.
- ^ Burkholder WH (1950). "Sour skin, a bacterial rot of onion bulbs". Phytopathology 40: 115–7.
