Difference between revisions of "Bordetella bronchiseptica"
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==Application to Biotechnology==
==Application to Biotechnology==
Revision as of 06:56, 5 June 2007
Bordetella bronchiseptica A Microbial Biorealm page on the genus Bordetella bronchiseptica
Higher order taxa
Domain; Phylum; Class; Order; family [Others may be used. Use NCBI link to find]
Bordetella bronchiseptica is a minute, gram-negative rod-shaped coccobacilli about .5-1 micrometers in diameter and 5 micrometers in length. It may or may not have a flagella, dependent on environmental stimuli. Optimal growth temperature is 35-37° C.  Though it is commonly known to colonize in respiratory tracts of animals, it can also withstand surviving long-term in the environment, a trait that separates it from its most common relatives (noted below). It can also be cultured on various media and has demonstrated rapid growth on blood-free peptone agar. [1,4]
This aerobic species was first isolated and identified by Ferry in 1910 as Bacillus bronchicanis, recovered from respiratory tracts of dogs infected with distemper. Ferry also isolated it later (1912-1913) from the respiratory tracts of guinea pigs, monkeys, and other animals and subsequently changed the name to Bacillus bronchiseptica. The organism would go through at least four more name changes before Moreno-Lopez founded and described the genus Bordetella (After the first man to isolate the pertussis-causing organism, Jules Bordet). The name was then settled to be Bordetella bronchiseptica. [4,9] Bordetella bronchiseptica is mostly closely related to Bordetella pertussis and Bordetella parapertussis, both of which is believed to have risen originally from Bordtella bronchiseptica. It is believed that the species diverged 3.5 million years ago through decay of the Bordetella brochiseptica genome, as seen through a large-scale gene loss of the two subsequent species. [1,9] Due to its effect on mammals such as domestic pets (cats and dogs) and lab animals, Bordetella bronchiseptica has been closely studied. It has also had its genome sequenced, primarily to derive data in comparison to its relative Bordetella pertussis, which causes whooping cough in humans. 
Bordetella bronchiseptica has a circular chromosome consisting of approximately 5,338,400 base pairs. It has one or more medium to large-sized plasmids dependent on the strain, and it is unknown at the time if these encode for anything useful. A small labile plasmid is found in most strains and is believed to be crucial in inferred antibiotic resistance. Of the circular chromosome, 68.07% of the composition are GC complements. It is believed to have 5,007 coding sequences with an average gene size of 978 base pairs. There are 3 rRNA operons as well as 55 tRNA operons. Analysis of the genome shows that there has been horizontal DNA transfer as apparent by the anomalous GC content. About 3,000 genes are shared by its closest relatives, B.pertussis and B. parapertussis. Its larger genome size compared to B. pertussis and B. parapertussis is believed to be crucial in coding for extra features suce as its capsule.
Cell structure and metabolism
Bordetella bronchiseptica may or may not have a flagella dependent on if environment stimuli signals for need of motility. When present, the flagella is most commonly observed to be a left-handed triple helix with an average diameter of approximately 13.8 nm. In some cases, the flagella may be up to 18 to 22 nm thick, consisting of braided structures of 5 to 6 individual strands.  Other unique structures include a 5-layered cell wall. The first 3 layers give the organism a lobulated surface contour appearance. The walls have channels between the lobules which are within a 10-20nm wide range. 
The inner cell membrane which surrounds the cytoplasm is tri-laminar. Inside, the cytoplasm matrix is rich in ribosomes.  The nuclear zone of Bordetella bronchiseptica contains DNA present in a network of fibers and undefined bodies. The whole organism seems to be encapsulated in a polysaccharide capsule , enabling it to survive in the environment whereas its two closest relatives which lack the capsule cannot. The organism seems also to contain genes that encode pili. While its genome does encode complete pathways for biosynthesis of needed intermediates, Bordetella bronchiseptica and the genus Bordetella in general do not use sugars as a carbon source. As expected, the genes encoding for enzymes normally present in this pathway (such as phosophofructokinase, glucokinase, fructose1,6-bisphophate, etc.) are absent form the genome. However, genes encoding the gluconeogenesis are present, suggesting that sugars such as glucose can be made. Though genes are present that encode for the TCA cycle are present, it is believed to be non-functional from a study’s observations in which Acetyl-Coenzyme A and oxaloacetate did not give rise to alpha-ketoglutarate.  This may be due to an evolutionary remnant.
Infections in domestic dogs, swine, and laboratory animals have led to a huge economic loss through veterinary costs, disfigurement, loss in sales, vaccine research and development, drug costs, etc. Bordetella bronchiseptica colonizes the tracheal area and often times induces other respiratory illnesses by making the host more susceptible to them. Inflammation may occur as a result to the LPS antigen. In the wild, infections may help keep population numbers stable. [4,10]
Bordetella bronchiseptica has a broad mammalian host range, including swine, dogs, cats, and assorted rodents. Whereas it can infect humans, it is thought to be rare with the exception of immuno-compromised individuals. Host symptoms are present in a various array dependent on the species and may include coughing, sneezing, pyrexia, nasal discharge, submandibular lymphadenomegaly, dyspnea and cyanosis. Bordetella bronchiseptica is most known for causing “kennel cough” in dogs and brochopnemonia in cats. [2,8] Bordetella bronchiseptica and related bordetellae generally colonizes areas of the respiratory tract. There are multiple adhesions such as pertactin, tracheal colonization factor, fimbraiae, and filamentous hemagglutinin (FHA).  Toxins include tracheal cytotoxin, dermonecrotic toxin and adenylate cyclase-hemolysin. The primary well-understood mechanism for dominant attachment into host cells involves the FHA binding directly to the ciliary membrane host-receptor glycospingolipids. Other modes of attachment and other toxins are able to be expressed at-will determined on environmental factors. This is commonly regulated by a two-component regulatory system called BvgA/S. BvgS,a histidine kinase sensor on the inner membrane, will auto-phosphorylate before phosphorylating the BvgA protein. This will activate transcription for certain genes required for virulence by binding to their promoter sites. [2,5,8,10] Important virulence factors are the polysaccharide capsule mentioned previously, a Type-III secretion system, as well as the O-antigen domain of the organism’s lipopolysaccharide (LPS), and flagella. A capsule enables the organism to survive long-term in the environment and also provides a defensive barrier from the host. The Type-III secretion system is a means of exporting virulence factors into the cell, but the exact mechanism is unknown as effectors secreted have not yet been identified. The O-antigen of the cell surface glycolipid LPS is crucial in evading the host’s innate acquired immunity. O-antigen terminal sugar residues vary in pattern and modifications. The flagella is crucial in motility. [3,4,6] Though generally non-lethal, persistent symptoms mad lead to more serious infections and can ultimately lead to death. Most infected animals show clinical signs of recovery within 10 days.
Application to Biotechnology
Does this organism produce any useful compounds or enzymes? What are they and how are they used?
Enter summaries of the most recent research here--at least three required
[Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.
Edited by student of Rachel Larsen and Kit Pogliano