Chromobacterium violaceum | |
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Blood agar plate culture of C. violaceum. Image from the CDC. | |
Scientific classification | |
Domain: | Bacteria |
Phylum: | Pseudomonadota |
Class: | Betaproteobacteria |
Order: | Neisseriales |
Family: | Neisseriaceae |
Genus: | Chromobacterium |
Species: | C. violaceum |
Binomial name | |
Chromobacterium violaceum (Bergonzini 1880) | |
Chromobacterium violaceum is a Gram-negative, facultative anaerobic, non-sporing coccobacillus. It is motile with the help of a single flagellum 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 called violacein , 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 down tarballs. [5]
C. violaceum ferments glucose, trehalose, N-acetylglucosamine and gluconate but not L-arabinose, D-galactose, or D-maltose. It is positive for catalase and oxidase reactions. [1] Bacterial isolates in many cases can show high level resistance to a range of antibiotics. [6]
C. violaceum rarely infects humans, but when it does it causes skin lesions, sepsis, and liver abscesses that may be fatal. [7] The first reported case of Chromobacterium 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 because Burkholderia pseudomallei is commonly misidentified as C. violaceum by many common identification methods. [15] [16] The two are readily distinguished because B. pseudomallei produces large wrinkled colonies, whereas C. 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]
Infection caused by C. violaceum is rare, therefore there are no clinical trials evaluating different treatments. Antibiotics that have been used to successfully treat C. violaceum include pefloxacin, [4] ciprofloxacin, amikacin, [1] and co-trimoxazole. [18] Other antibiotics that appear to be effective in vitro include chloramphenicol and tetracycline. [19] For theoretical reasons, infection would not be expected to respond to penicillins, cephalosporins, or aztreonam, although carbapenems like meropenem or imipenem may possibly work. [20] Though the bacteria is reported to be resistant to first generation cephalosporins, susceptibility to the newer cephalosporins is variable. [21]
The complete genome was sequenced and the results were published in 2003. C. violaceum type strain ATCC 12472 was found to have 4,751,080 base pairs with a G + C content of 64.83% and 4,431 ORFs. [3]
Streptococcal pharyngitis, also known as streptococcal sore throat, is pharyngitis caused by Streptococcus pyogenes, a gram-positive, group A streptococcus. Common symptoms include fever, sore throat, red tonsils, and enlarged lymph nodes in the front of the neck. A headache and nausea or vomiting may also occur. Some develop a sandpaper-like rash which is known as scarlet fever. Symptoms typically begin one to three days after exposure and last seven to ten days.
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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. B. cepacia is an opportunistic human pathogen that most often causes pneumonia in immunocompromised individuals with underlying lung disease. 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 is also found in marine environments and some strains of Burkholderia cepacia can tolerate high salinity. S.I. Paul et al. (2021) isolated and biochemically characterized salt tolerant strains of Burkholderia cepacia from marine sponges of Saint Martin's Island of the Bay of Bengal, Bangladesh.
Burkholderia pseudomallei is a Gram-negative, bipolar, aerobic, motile rod-shaped bacterium. It is a soil-dwelling bacterium endemic in tropical and subtropical regions worldwide, particularly in Thailand and northern Australia. It was reported in 2008 that there had been an expansion of the affected regions due to significant natural disasters, and it could be found in Southern China, Hong Kong, and countries in America. B. pseudomallei, amongst other pathogens, has been found in monkeys imported into the United States from Asia for laboratory use, posing a risk that the pathogen could be introduced into the country.
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Escherichia coli is a gram-negative, rod-shaped bacterium that is commonly found in the lower intestine of warm-blooded organisms (endotherms). Most E. coli strains are harmless, but pathogenic varieties cause serious food poisoning, septic shock, meningitis, or urinary tract infections in humans. Unlike normal flora E. coli, the pathogenic varieties produce toxins and other virulence factors that enable them to reside in parts of the body normally not inhabited by E. coli, and to damage host cells. These pathogenic traits are encoded by virulence genes carried only by the pathogens.
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