Burkholderia mallei

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A Microbial Biorealm page on the genus Burkholderia mallei

Contents

[edit] Classification

Immunogold electron micrograph of B. mallei Image courtesy of David DeShazer (10)
Immunogold electron micrograph of B. mallei Image courtesy of David DeShazer (10)

[edit] Higher order taxa

Kingdom: Bacteria Phylum: Proteobacteria; Class: Beta Proteobacteria; Order: Burkholderiales; Family: Burkholderiaceae

[edit] Species

Genus: Burkholderia; Species: B. mallei


NCBI: Taxonomy

[edit] Description and significance

'The genus Burkholderia was created by Yabuuchi et al. to accommodate the former rRNA group II Pseudomonads, excluding Pseudomonas pickettii and Pseudomonas solanacearum, which were transferred to the genus Ralstonia. Traditionally, the Burkholderia species are often known as plant pathogens and soil bacteria with two important exceptions, B. mallei and B. pseudomallei, which can cause glander and melioidosis respectively in humans and animals (Coenye and Vandamme, 2003). Once they enter the host, synthesis and release of certain toxin occur. Small amounts of toxin will not cause disease, but if a large quantity of the organism is incorporated, the amount of toxin is sufficient to cause specific symptoms(Thibault, 2004). Burkholderia mallei is a nonmotile, aerobic Gram-negative coccobacilus, which may or may not be oxidase positive or have growth potential on MacConkey agar. Burkholderia pseudomallei, on the other hand, is an oxidase positive, aerobic Gram-negative bacillus that is either straight or slightly curved(Newbauer,2005).

[edit] Genome structure

‘The genome of B. mallei consisits of two circular chromosomes. Chromosome 1 contains 3,510,148 bp, and chromosome 2 contains 2,325,379 bp. A total of 5,535 predicted protein-encoding ORFs are identified in the genome.’ (Nierman et al.,2004)The genome of this organism carries a large number of insertion sequences as compared to the related Burkholderia pseudomallei, with a large number of simple sequence repeats that may function in antigenic variation of cell surface proteins. (NCBI Genome Project)

[edit] Cell structure and metabolism

Burkholderia mallei is a genus of Gram-negative bacillus,width of the organism is 0.3 to 0.5 um and the length is 0.7 to 5.0 um, between rod and coccus shaped bacteria of the family Pseudomonadaceae, comprising animal and plant pathogens formerly classified in group II of the genus Pseudomonas. ( Nierman, 2004)

[edit] Ecology

Burkholderia mallei is not found in the United States and Western Europe due to a program of compulsory slaughter of infected horses or other animals. It is a highly adapted parasite of horses and cannot persist in nature outside of its host. However, it is still commonly seen among domestic animals in Africa, Asia, the Middle East, and Central and South America.(Godoy et al.,2003) Burkholderia mallei is quite sensitive to heat, UV light, desiccation and common disinfectants. In outbreaks, one must bury or burn all contaminated bedding and foodstuffs to prevent infection of accessible animals. Stalls and harness equipment should be thoroughly sterilized. Contact with infected animals, especially horses, should also be avoided. (Gilbert, 1992)

[edit] Pathology

Horse infected by B. mallei (12)
Horse infected by B. mallei (12)

Burkholderia mallei is the primary bacteria that causes glanders in horses and other animals and occasionally, in humans. Glanders is difficult to diagnose and often fatal. The types of infection include localized, pus forming cutaneous infections, pulmonary infections, bloodstream infections and chronic supportive infections of the skin. (CDC,2002) For localized infections, the ulceration will develop within 1 to 5 days at the site where the bacteria entered the body. Swollen lymph nodes may also appear. More mucus will be produced from the infected sites when bacteria enter into the eyes, nose or respiratory tract. Different infections may have different symptoms. In the case of a pulmonary infection, pneumonia, pulmonary abscess, and pleural effusion can occur. For bloodstream infections, it is fatal within 7 to 10 days. For chronic infections, multiple abscesses form within the muscles of the arms and legs, spleen, or liver.(Thibault et al 2004) There are no vaccines for glanders. However, the traditional veterinary treatment of streptomycin and sulfadiazine is somewhat effective.(Goody, 2003) B. mallei is less resistant to antibiotics comparing to many other Pseudomonas and it may be treated with sulfamethoxazole-trimethoprim, ceftazidime, and doxycycline.(CDC,2002)

[edit] Application to Biotechnology

Burkholderia mallei is considered as a recent concern about its past and potential future uses as a biological weapon in wars and terrorism. Glanders was believed to have been used during World War I to infect horses and mules that carried supplies, and during World War II on horse, civilians and prisoners of war and is currently being used in Afghanistan. It is considered to be a Category B bioterrist agent as listed on the Centers for Disease Control list and there are no vaccines are currently available for prevention of glanders in horses or humans. We are vulnerable to this biothreat agent because there is no rapid detection assay, no reliable antibiotics, or vaccine available, and we don't have much knowledge about this bacteria.(Goodoy et al., 2003) There is little known about the virulence factors of this microorganism because some experiments have shown‘…a highly pathogenic clinical isolate, has been expanded to generate whole genome shotgun sequences for 9 different phenotypically characterized strains in the natural host that differ greatly in virulence.’ (Nierman et al.,2004)

[edit] Current Research

1) Research from BMC Genomics, the August 2007 edition, used bioinformatic techniques to compile the ABC systems of Burkholderia mallei strain ATCC 23344 and Burkholderia pseudomallei strain K96243. The types and numbers of encoded ABC systems of these two microorganisms were identified. The ABC (ATP-binding cassette) systems involved using iron acquisition that was correlated with differences in genome size and lifestyles between the two related organisms. The result of comparing the encoded protein in this family shows that the ABC systems may play a key role in the different lifestyles and the pathogenic properties of these two bacteria. This finding may be useful in the development of new vaccines and therapeutics against diseases like melioidisis and glanders.(Harland DN)


2) BMC microbial, the July 2007 edition, released a study on Burkholderia Hep_Hep autotransporter (BuHA) proteins inducing an antibody response during experimental glanders but not human melioidosis. Epidemiological and genomic studies have shown that B. amllei is a recently emerged, host restricted clone of B. pseudomallei. Scientists have identified genes expressed in vivo during experimental galnders infection using bacteriophage-mediated immunoscreening. A total of 53% positive clones of a B. mallei expression library screened with sera from two infected horses belonged to this family was contrasted with 3% of a B. pseudomallei expression library screened with serum from 21 patients with culture-proven melioidosis. The genomes of both B.mallei and B. pseudomallei contain a relative abundance of BuHA proteins. The domain structures of these proteins function as multimeric surface proteins that modulate interactions of the cell with the host and environment.(Tiyawisutsri R)


3) A research article in Infect Immn of the July 2004 issue talked about Burkholderia pseudomallei as the bacteria that causes melioidosis. It also stated that Burkholderia thailandensis is a closely related species that can readily use 1-arabinose as the only carbon source while B. pseudomallei cannot. Scientists cloned the B. thailandernsis E264 arabinose assimilation operon and introduced the entire operon into the chromosome of B. pseudomallei SZ5028, which was then able to use 1-arabinose as a sole carbon source. These findings suggest that the ability to metabolize 1-arabinose reduces the virulence of B.pseudomallei and that the genes encoding arabinose assimilaton proteins may be considered anti-virulence genes. The increase in virulence and the loss of these genes suggested a selective advantage for B.pseudomallei as they adapted to survival in mammalian hosts.(Moore RA)

[edit] References

1.Harland DN, Dassa E, Titball RW, Brown KA, Atkins HS.ATP-binding cassette systems in Burkholderia pseudomallei and Burkholderia mallei. BMC Genomics. 2007; 8: 83.

2.Tiyawisutsri R, Holden MT, Tumapa S, Rengpipat S, Clarke SR,Foster SJ, Nierman WC, Day NP, Peacock SJ. Burkholderia Hep_Hap autotransporter (BuHA) proteins elicit a strong antibody response during experimental glanders but not human melioidosis. BMC Microbiol. 2007; 7: 19.

3.Nierman WC, DeShazer D, Kim HS, Tettelin H, Nelson KE, Feldblyum T, Ulrich RL, Ronning CM, Brinkac LM, Daugherty SC, Davidsen TD, Deboy RT, Dimitrov G, Dodson RJ, Durkin AS, Gwinn ML, Haft DH, Khouri H, Kolonay JF, Madupu R, Mohammoud Y, Nelson WC, Radune D, Romero CM, Sarria S, Selengut J, Shamblin C, Sullivan SA, White O, Yu Y, Zafar N, Zhou L, Fraser CM. Structural flexibility in the Burkholderia mallei genome.Proc Natl Acad Sci U S A. 2004 Sep 28; 101(39): 14246-14251.

4.Neubauer et al., 2005: Neubauer H, Sprague LD, Zacharia R, Tomaso H, Al Dahouk S, Wernery R, Wernery U, Scholz HC. Serodiagnosis of Burkholderia mallei infections in horses: state-of-the-art and perspectives. J Vet Med B Infect Dis Vet Public Health. 2005; 52(5): 201 - 205.

5.Godoy D, Randle G, Simpson AJ, Aanensen DM, Pitt TL, Kinoshita R, Spratt BG. Multilocus sequence typing and evolutionary relationships among the causative agents of melioidosis and glanders, Burkholderia pseudomallei and Burkholderia mallei. J Clin Microbiol. 2003; 41(5): 2068 - 2079.

6.Thibault FM, Hernandez E, Vidal DR, Girardet M, Cavallo JD. Antibiotic susceptibility of 65 isolates of Burkholderia pseudomallei and Burkholderia mallei to 35 antimicrobial agents. The Journal of Antimicrobial Chemotherapy. 2004; 54(6): 1134 - 1138.

7.[http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=427422 Moore RA, Reckseidler-Zenteno S, Kim H, Nierman W, Yu Y, Tuanyok A, Warawa J, DeShazer D, Woods DE. Contribution of Gene Loss to the Pathogenic Evolution of Burkholderia pseudomallei and Burkholderia mallei.Infect Immun.2004 Jul; 72(7): 4172- 4187.]

8.Coenye and Vandamme, 2003: Coenye T, Vandamme P. Diversity and significance of Burkholderia species occupying diverse ecological niches. Environ Microbiol. 2003; 5(9): 719 - 729.

9.Timoney et al., 1988: Timoney JF, Gillespie JH, Scott FW, Barough JE Pseudomonas mallei. 40 - 44. In: Timoney JF, Gillespie JH, Scott FW, Barough JE Hagan and Bruner's microbiology and infectious diseases of domestic animals : with reference to etiology, epizootiology, pathogenesis, immunity, diagnosis, and antimicrobial susceptibility.1988. Cornell University Press, Ithaca, New York, USA.

10.DeShazer David

11.2000: Centers for Disease Control (CDC). Laboratory-acquired human glanders--Maryland, May 2000. MMWR Morb Mortal Wkly Rep. 2000; 49(24): 532 - 535.

12.http://www.marchaweb.blogger.com.br/2004_01_11_archive.html

13.Gilbert, 1992: Gilbert RO Glanders. 210 - 217. In: Foreign Animal Diseases1992. Cummings Corporation, Richmond, Va.


Edited by student of Rachel Larsen and Kit Pogliano kmg

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