Granulibacter bethesdensis

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A Microbial Biorealm page on the genus Granulibacter bethesdensis

Classification

Higher order taxa

Bacteria; Proteobacteria; Alphaproteobacteria; Rhodospirillales; Acetobacteracease; Granulibacter

Species

Granulibacter bethesdensis

Description and significance

Granulibacter bethesdensis is a new speices discovered in 2006. It has distinctive phylogenetic and phenotypic characteristics. Phylogentic analysis on 16S rRNA indicated that Granulibacter bethesdensis shared most similarities with organisms in Acetobacteraceae family, but no species or strains of Acetobacteraceae are similar to Granulibacter bethesdensis: it has similarity ranges from 95.4% with Gluconacetobacter liquefaciens to 86.0% with Stella humosa; analysis of internal transcribed spacer (ITS) region showed that Granulibacter bethesdensis has similarity range from 55.3% with Gluconobacter albidus to 42.9% with Rhodospirillium rubum; analysis of recA gene sequence showed that Granulibacter bethesdensis has similarity ranges from 80.6% with Acetobacter estunensis to 71.4% with Rhodobacter sphaeroides, and 90.8% with Acetobacter orleanensis to 75.0% with Rhodobacter sphaeroides (1). Moreover, Granulibacter bethesdensis has four distinguished phenotypic characteristics. Unlike other acetic acid bacteria, Granulibacter bethesdensis is able to use methanol as a sole carbon source, produce weak acid from glucose, and has yellow pigmentation and a higher optimal growth temperature (1). It is a rod-shaped, thermophilic, aerobic, gram-negative, catalase-positive and oxidase-negative pathogenic bacterium, which contributes to chronic granulomatous disease (CGD)(2). CGD is a rare inherited disease caused by abnormal phagocytic cells in immune system; CGD causes repeated bacterial infections and development of tissue granulomas.

Genome structure

Granulibacter bethesdensis has 2498 genes, 2437 proteins, 2708355 nucleotides, 61 structural RNAs, 59% GC content, 0 pseudogene, 91% coding, and circular DNA (3).

Cell structure and metabolism

Granulibacter bethesdensis is usually found in soil and plants, and rarely in human. It produces weak acetic acid by oxidizing glucose and ethanol but can't oxidize lactose, mannitol, sucrose, maltose or xylose (1);It oxidizes lactate and acetate to carbon dioxide and water, and uses methanol as a sole carbon source. There are two major fatty acids: 1) a straight-chain unsaturated acid, 50% of total cellular fatty acid 2)C16:0, 17% of total cellular fatty acid (1). Granulibacter bethesdensis produces acetic acid better with a lower concentration of CaCO3 in ethanol-CaCO3 agar plates (1).

Ecology

Contributions of Granulibacter bethesdensis have not been studied thoroughly. Like many other organisms in Acetobacteraceae family, Granulibacter bethesdensis is a ubiquitous environmental organism, and causes biodegradation of organic waste. Many organisms in Acetobacteraceae family are found in soil and associated with plants, and Asaia bogorensis is the only known organism that causes human disease in this family other than Granulibacter bethesdensis (4). Granulibacter bethesdensis is able to break down ethanol, methanol and formaldehyde to produce non-toxic products, such as carbon dioxide, water and weak acetic acid (1,2).

Pathology

The discovery of the mechanisms about how Granulibacter bethesdensis causes chronic granulomatous disease (CGD) needs further research investigations. CGD is caused by a defect in any of the 4 subunits of the NADPH oxidase, which affects the ability of phagocytes to generate antimicrobial reactive oxygen intermediates (5). It is thought that catalase-positive pathogens causes CGD by depriving the CGD phagocytes of the oxidative metabolites to use against them (2,5,6). However, the narrow list of catalase-positive bacteria that cause CGD suggest that there might be other mechanism beyond catalase (2). Recent research showed that Granulibacter bethesdensis has low virulence and is not fatal;it causes fever, plympahdenitis, and weight loss over almost six months in a patient with X-linked CGD (2).

Application to Biotechnology

The ability of Granulibacter bethesdensis to oxidize ethanol and glucose to produce weak acetic acid in the presence of air may be exploited in vinegar production and wine fermentation (2). It may be used as microbial fuel cell, and production of purified polypeptide enzymes for industrial use.

Current Research

One of the current main researches is to study the epidemiology and pathogenicity of Granulibacter bethesdensis (2). Granulibacter bethesdensis genome sequence contributed to predicting relatedness to other bacteria (7). Some scientists proposed the studies of the high-level resistance of Granulibacter bethesdensis to many antibiotics, and find out if the resistance is intrinsic of the bacteria or induced by antibiotic therapies (4).

References

1. David E. Greenberg1,, Stephen F. Porcella2,, Frida Stock3, Alexandra Wong3, Patricia S. Conville3, Patrick R. Murray3, Steven M. Holland1 and Adrian M. Zelazny3 . "Granulibacter bethesdensis gen. nov., sp. nov., a distinctive pathogenic acetic acid bacterium in the family Acetobacteraceae".International Journal of Systematic and Evolution Microbiology 56 (November 2006), 2609-2616. http://ijs.sgmjournals.org/cgi/content/full/56/11/2609.

2. David E Greenberg,1 Li Ding,1 Adrian M Zelazny,2 Frida Stock,2 Alexandra Wong,2 Victoria L Anderson,1 Georgina Miller,3 David E Kleiner,4 Allan R Tenorio,5 Lauren Brinster,3 David W Dorward,6 Patrick R Murray,2 and Steven M Holland1. "A Novel Bacterium Associated with Lymphadenitis in a Patient with Chronic Granulomatous Disease". PLoS Pathog. 2006 April; 2(4): e28. Published online 2006 April 14. doi: 10.1371/journal.ppat.0020028. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16617373

3. KEGG, April 2007, Kyoto Encyclopedia of Genes and Genomes, http://www.genome.jp/kegg

4. David Fredricks and Lalita Ramakrishnan. "The Acetobacteraceae: Extending the Spectrum of Human Pathogens". PLoS Pathog. 2006 April; 2(4): e36. Published online 2006 April 28. doi: 10.1371/journal.ppat.0020036

5. Meischl C, Roos D. "The molecular basis of chronic granulomatous disease". Springer Semin Immunopathol. 1998;19(4):417-34

6. Segal BH, Leto TL, Gallin JI, Malech HL, Holland SM. "Genetic, biochemical, and clinical features of chronic granulomatous disease". 2000 May; 79(3):170-200.

7. Daniel R. Zeigler. "Gene sequences useful for predicting relateness of whole genomes in bacteria". International Journal of Systemic and Evolutionary Microbiology. 2003, 1893-1900.

Edited by student of Rachel Larsen and Kit Pogliano

Edited KMG