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Chromobacterium violaceum

From Wikipedia, the free encyclopedia
Species of bacterium
For bacteria previously classified as Chromobacterium violaceum(Ford 1927) or Chromobacterium violaceum(Leifson 1956), seeJanthinobacterium lividum.

Chromobacterium violaceum
Blood agar plate culture ofC. violaceum. Image from theCDC.
Scientific classificationEdit this classification
Domain:Bacteria
Kingdom:Pseudomonadati
Phylum:Pseudomonadota
Class:Betaproteobacteria
Order:Neisseriales
Family:Neisseriaceae
Genus:Chromobacterium
Species:
C. violaceum
Binomial name
Chromobacterium violaceum
(Bergonzini 1880)

Chromobacterium violaceum is aGram-negative,facultativeanaerobic, non-sporingcoccobacillus. It is motile with the help of a singleflagellum which is located at the pole of the coccobacillus. Usually, there are one or two more lateral flagella as well.[1] It is part of the normal flora of water and soil of tropical and sub-tropical regions of the world. It produces a natural antibiotic calledviolacein, which may be useful for the treatment of colon and other cancers.[2] It grows readily on nutrient agar, producing distinctive smooth low convex colonies with a characteristic striking dark violet metallic sheen (due to violacein production).[3] Some strains of the bacteria which do not produce this pigment have also been reported.[4] It has the ability to break downtarballs.[5]

Biochemistry

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C. violaceum fermentsglucose,trehalose,N-acetylglucosamine andgluconate but not L-arabinose, D-galactose, or D-maltose. It is positive for catalase and oxidase reactions.[1] Bacterialisolates in many cases can show high level resistance to a range of antibiotics.[6]

Medical significance

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C. violaceum rarely infects humans, but when it does it causes skin lesions,sepsis, andliver abscesses that may be fatal.[7] The first reported case ofChromobacterium violaceum infection in humans in literature is from Malaysia in 1927.[1] Only 150 cases have been reported in literature since then.[8] To date, cases have been reported from Argentina, Australia, Brazil, Canada, Cuba, India, Japan, Nigeria, Singapore, Sri Lanka, Taiwan, United States and Vietnam. The most common mode of entry of the bacteria into the body is through the injured skin coming in contact with soil or water containing the bacteria.[1][9] The disease usually starts as a limited infection of the skin at the point of entry of the bacteria, which progresses to necrotizing metastatic lesions, then multiple abscesses of the liver, lung, spleen, skin, lymph nodes or brain, leading to severe septicaemia, culminating in multiorgan failure which may be fatal.[10] Other reported pathologies include chronic granulomatosis, osteomyelitis, cellulitis, diarrhoea, septic spondylitis, conjunctivitis, periorbital and ocular infection.[1][11][12][13][14] Care must be taken becauseBurkholderia pseudomallei is commonly misidentified asC. violaceum by many common identification methods.[15][16] The two are readily distinguished becauseB. pseudomallei produces large wrinkled colonies, whereasC. violaceum produces a distinctive violet pigment.

C. violaceum produces a number of natural antibiotics:

It has been described as a cause of infection in gibbons.[17]

Treatment

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Infection caused byC. violaceum is rare, therefore there are no clinical trials evaluating different treatments. Antibiotics that have been used to successfully treatC. violaceum includepefloxacin,[4]ciprofloxacin,amikacin,[1] andco-trimoxazole.[18] Other antibiotics that appear to be effectivein vitro includechloramphenicol andtetracycline.[19] For theoretical reasons, infection would not be expected to respond topenicillins,cephalosporins, oraztreonam, althoughcarbapenems likemeropenem orimipenem may possibly work.[20] Though the bacteria is reported to be resistant to first generation cephalosporins, susceptibility to the newer cephalosporins is variable.[21]

Genome

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The complete genome was sequenced and the results were published in 2003.C. violaceum type strain ATCC 12472 was found to have 4,751,080base pairs with a G + C content of 64.83% and 4,431ORFs.[3]

References

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  1. ^abcdefRay, P; Sharma, J; Marak, SK; Singhi, S; Taneja, N; Garg, RK (2004). "Chromobacterium violaceum septicaemia from North India".Indian J Med Res.120 (6):523–6.PMID 15654137.
  2. ^Kodach LL, Bos CL, Durán N, Peppelenbosch MP, Ferreira CV, Hardwick JC (2006)."Violacein synergistically increases 5-fluorouracil cytotoxicity, induces apoptosis and inhibits Akt-mediated signal transduction in human colorectal cancer cells".Carcinogenesis.27 (3):508–16.doi:10.1093/carcin/bgi307.PMID 16344270.
  3. ^abBrazilian National Genome Project Consortium (2003)."The complete genome sequence ofChromobacterium violaceum reveals remarkable and exploitable bacterial adaptability".Proc Natl Acad Sci USA.100 (20):11660–5.Bibcode:2003PNAS..10011660..doi:10.1073/pnas.1832124100.PMC 208814.PMID 14500782.
  4. ^abLee, J; Kim, JS; Nahm, CH; Choi, JW; Kim, J; Pai, SH; Moon, KH; Lee, K; Chong, Y (1999)."Two Cases ofChromobacterium violaceum Infection after Injury in a Subtropical Region".J Clin Microbiol.37 (6):2068–2070.doi:10.1128/JCM.37.6.2068-2070.1999.PMC 85035.PMID 10325383.
  5. ^Itah AY, Essien JP (2005). "Growth Profile and Hydrocarbonoclastic Potential of Microorganisms Isolated from Tarballs in the Bight of Bonny, Nigeria".World Journal of Microbiology and Biotechnology.21 (6–7):1317–22.doi:10.1007/s11274-004-6694-z.S2CID 84888286.
  6. ^de Siqueira IC, Dias J, Ruf H, Ramos EA, Maciel EA, Rolim A, Labur L, Vasconcelos L, Silvany C (2005)."Chromobacterium violaceum in siblings, Brazil".Emerging Infect. Dis.11 (9):1443–5.doi:10.3201/eid1109.050278.PMC 3310629.PMID 16229777.
  7. ^Sneath, PH; Whelan, JP; Bhagwan Singh, R; Edwards, D (1953). "Fatal infection byChromobacterium violaceum".Lancet.265 (6780):276–7.doi:10.1016/S0140-6736(53)91132-5.PMID 13085740.
  8. ^M Ravish Kumar. (2012)."Chromobacterium violaceum: A rare bacterium isolated from a wound over the scalp".Int J Appl Basic Med Res.2 (1):70–2.doi:10.4103/2229-516X.96814.PMC 3657989.PMID 23776815.
  9. ^Duran, N; Menck, FM (2001). "Chromobacterium violaceum: A review of pharmacological and industrial perspectives".Crit Rev Microbiol.27 (3):201–22.doi:10.1080/20014091096747.PMID 11596879.S2CID 39515820.
  10. ^Slesak, G; Douangdala, P; Inthalad, S; Silisouk, J; Voungsouath, M; Sengduangphachanh, A; et al. (2009)."Fatal Chromobacterium violaceum septicaemia in northern Laos, a modified oxidase test and post-mortem forensic family G6PD analysis".Ann Clin Microbiol Antimicrob.8: 24.doi:10.1186/1476-0711-8-24.PMC 2725030.PMID 19640274.
  11. ^Dutta, S; Dutta, SK (2003)."Multidrug resistant chromobacterium violaceum: An unusual bacterium causing long standing wound abscess".Indian J Med Microbiol.21 (3):217–8.doi:10.1016/S0255-0857(21)03082-6.PMID 17643028. Retrieved6 March 2015.
  12. ^Chou, YL; Yang ., PY; Huang, CC; Leu, HS; Tsao, TC (2000). "Fatal and non-fatal chromobacterial septicemia: report of two cases".Chang Gung Med J.23 (8):492–7.PMID 11039252.
  13. ^Shao, PL; Hsueh, PR; Chang, YC; Lu, CY; Lee, PY; Lee, CY; Huang, LM (2002)."Chromobacterium violaceum infection in children: a case of fatal septicemia with nasopharyngeal abscess and literature review".Pediatr Infect Dis J.21 (7):707–9.doi:10.1097/00006454-200207000-00022.PMID 12237610.
  14. ^Chen, CH; Lin, LC; Liu, CE; Young, TG (2003). "Chromobacterium violaceum bacteremia: a case report".J Microbiol Immunol Infect.36 (2):141–4.PMID 12886967.
  15. ^Inglis, TJ; Chiang, D; Lee, GS; Chor-Kiang, L (1998). "Potential misidentification ofBurkholderia pseudomallei by API 20NE".Pathology.30 (1):62–64.doi:10.1080/00313029800169685.PMID 9534210.S2CID 31987728.
  16. ^Lowe, P; Engler, C; Norton, R (2002)."Comparison of Automated and Nonautomated Systems for Identification of Burkholderia pseudomallei".J Clin Microbiol.40 (12):4625–7.doi:10.1128/JCM.40.12.4625-4627.2002.PMC 154629.PMID 12454163.
  17. ^Groves, MG; Strauss, JM; Abbas, J; Davis, CE (1969). "Natural infections of gibbons with a bacterium producing violet pigment (Chromobacterium violaceum)".J Infect Dis.120 (5):605–610.doi:10.1093/infdis/120.5.605.PMID 5388196.
  18. ^Moore, C; Lane, J; Stephens, J (2001)."Successful treatment of an infant withChromobacterium violaceum sepsis".Clin Infect Dis.32 (6): E107–10.doi:10.1086/319356.PMID 11247733.
  19. ^Martinez, R; Velludo, MA; Santos, VR; Dinamarco, PV (2000)."Chromobacterium violaceum infection in Brazil. A case report".Rev Inst Med Trop Sao Paulo.42 (2):111–3.doi:10.1590/s0036-46652000000200008.PMID 10810326.
  20. ^Midani, S; Rathore, M (1998). "Chromobacterium violaceum infection".South Med J.91 (5):464–466.doi:10.1097/00007611-199805000-00011.PMID 9598856.S2CID 37485951.
  21. ^Howard, AJ; Ison, CA (1996). "Haemophilus, Gardnerella and other bacilli". In Collee, JG; Fraser, AG; Marmion, BP; Simmons, A (eds.).Mackie and McCartney Practical Medical Microbiology (14th ed.). New York: Churchill Livingstone. pp. 329–41.

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