Burkholderia cepacia complex

Burkholderia cepacia complex (BCC), or simply Burkholderia cepacia, is a group of catalase-producing, lactose-nonfermenting, Gram-negative bacteria composed of at least 20 different species, including B. cepacia, B. multivorans, B. cenocepacia, B. vietnamiensis, B. stabilis, B. ambifaria, B. dolosa, B. anthina, B. pyrrocinia and B. ubonensis.[1] B. cepacia is an opportunistic human pathogen that most often causes pneumonia in immunocompromised individuals with underlying lung disease (such as cystic fibrosis or chronic granulomatous disease).[2] Patients with sickle-cell haemoglobinopathies are also at risk. The species complex also attacks young onion and tobacco plants, and displays a remarkable ability to digest oil.

Burkholderia cepacia complex
Scientific classification
Kingdom:
Bacteria
Phylum:
Proteobacteria
Class:
Betaproteobacteria
Order:
Burkholderiales
Family:
Burkholderiaceae
Genus:
Burkholderia
Species:
B. cepacia complex
Binomial name
Burkholderia cepacia complex
(Palleroni and Holmes 1981)
Yabuuchi et al. 1993
Type species
ATCC 25416
CCUG 12691 and 13226
CFBP 2227
CIP 80.24
DSM 7288
HAMBI 1976
ICMP 5796
JCM 5964
LMG 1222
NBRC 14074
NCCB 76047
NCPPB 2993
NCTC 10743
NRRL B-14810
Synonyms
  • Pseudomonas cepacia Burkholder 1950
  • Pseudomonas multivorans Stanier et al. 1966
  • Pseudomonas cepacia (ex Burkholder 1950) Palleroni and Holmes 1981
  • Pseudomonas kingii Jonsson 1970

Pathogenesis

BCC organisms are typically found in water and soil and can survive for prolonged periods in moist environments. They show a relatively poor virulence. Virulence factors include adherence to plastic surfaces (including those of medical devices) and production of several enzymes such as elastase and gelatinase. Also relevant might be their ability to survive attacks from neutrophils.[3]

Person-to-person spread has been documented; as a result, many hospitals, clinics, and camps have enacted strict isolation precautions for those infected with BCC. Infected individuals are often treated in a separate area from uninfected patients to limit spread, since BCC infection can lead to a rapid decline in lung function and result in death.

Diagnosis

Diagnosis of BCC involves culturing the bacteria from clinical specimens, such as sputum or blood. BCC organisms are naturally resistant to many common antibiotics, including aminoglycosides and polymyxin B.[4] and this fact is exploited in the identification of the organism. The organism is usually cultured in Burkholderia cepacia agar (BC agar), which contains crystal violet and bile salts to inhibit the growth of Gram-positive cocci, and ticarcillin and polymyxin B to inhibit the growth of other Gram-negative bacilli. It also contains phenol red pH indicator which turns pink when it reacts with alkaline byproducts generated by the bacteria when it grows.

Alternatively, oxidation-fermentation polymyxin-bacitracin-lactose (OFPBL) agar can be used. OFPBL contains polymyxin (which kills most Gram-negative bacteria, including Pseudomonas aeruginosa) and bacitracin (which kills most Gram-positive bacteria and Neisseria species).[5][6] It also contains lactose, and organisms such as BCC that do not ferment lactose turn the pH indicator yellow, which helps to distinguish it from other organisms that may grow on OFPBL agar, such as Candida species, Pseudomonas fluorescens, and Stenotrophomonas species.

Treatment

Treatment typically includes multiple antibiotics and may include ceftazidime, doxycycline, piperacillin, meropenem, chloramphenicol, and trimethoprim/sulfamethoxazole(co-trimoxazole).[4] Although co-trimoxazole has been generally considered the drug of choice for B. cepacia infections, ceftazidime, doxycycline, piperacillin, and meropenem are considered to be viable alternative options in cases where co-trimoxazole cannot be administered because of hypersensitivity reactions, intolerance, or resistance.[7] In April 2007, researchers from the University of Western Ontario School of Medicine, working with a group from Edinburgh, announced that they had discovered a potential method to kill the organism, involving disruption in the biosynthesis of an essential cell membrane sugar.[8][9]

In people with cystic fibrosis, evidence is insufficient about the effectiveness of long-term antibiotic treatment with continuous inhaled aztreonam lysine (AZLI) in terms of lung function or chest infections.[10]

History

B. cepacia was discovered by Walter Burkholder in 1949 as the cause of onion skin rot, and first described as a human pathogen in the 1950s.[11] It was first isolated in patients with cystic fibrosis (CF) in 1977, when it was known as Pseudomonas cepacia.[12] In the 1980s, outbreaks of B. cepacia in individuals with CF were associated with a 35% death rate. B. cepacia has a large genome, containing twice the amount of genetic material as E. coli.

See also

References
  1. Lipuma J (2005). "Update on the Burkholderia cepacia complex". Curr Opin Pulm Med. 11 (6): 528–33. doi:10.1097/01.mcp.0000181475.85187.ed. PMID 16217180. S2CID 19117513.
  2. Mahenthiralingam E, Urban T, Goldberg J (2005). "The multifarious, multireplicon Burkholderia cepacia complex". Nat Rev Microbiol. 3 (2): 144–56. doi:10.1038/nrmicro1085. PMID 15643431. S2CID 21736359.
  3. Torok, E.; Moran, E.; Cooke, F (2009). Oxford Handbook of Infectious Diseases and Microbiology. Oxford University Press. ISBN 978-0-19-856925-1.
  4. 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:10.1016/j.ajic.2006.05.226. PMID 16813979.
  5. Becton, Dickinson and Company (2003). BD Difco and BD BBL Manual: Manual of Microbiological Culture Media. Franklin Lakes, New Jersey: Becton Dickinson. pp. 422–423.
  6. "OFPBL agar". Remel Technical Manual. Lenexa, Kan: Remel. 1997.
  7. Avgeri SG; Matthaiou DK; Dimopoulos G; Grammatikos AP; Falagas ME (May 2009). "Therapeutic options for Burkholderia cepacia infections beyond co-trimoxazole: a systematic review of the clinical evidence". Int. J. Antimicrob. Agents. 33 (5): 394–404. doi:10.1016/j.ijantimicag.2008.09.010. PMID 19097867.
  8. "Key Found to Kill Cystic Fibrosis Superbug". Innovations Report. April 25, 2007. Retrieved April 26, 2007.
  9. Ortega XP; Cardona ST; Brown AR; et al. (May 2007). "A Putative Gene Cluster for Aminoarabinose Biosynthesis Is Essential for Burkholderia cenocepacia Viability". J. Bacteriol. 189 (9): 3639–44. doi:10.1128/JB.00153-07. PMC 1855895. PMID 17337576.
  10. Frost, F; Shaw, M; Nazareth, D (June 13, 2019). "Antibiotic therapy for chronic infection with Burkholderia cepacia complex in people with cystic fibrosis". The Cochrane Database of Systematic Reviews. 6: CD013079. doi:10.1002/14651858.CD013079.pub2. PMC 6564086. PMID 31194880.
  11. Burkholder WH (1950). "Sour skin, a bacterial rot of onion bulbs". Phytopathology. 40 (1): 115–7.
  12. Lararya-Cuasay LR, Lipstein M, Huang NN (1977). "Pseudomonas cepacia in the respiratory flora of patients with cystic fibrosis". Pediatr Res. 11 (4): 502. doi:10.1203/00006450-197704000-00792.

Further reading
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