Bordetella pertussis in Canada: Difference between revisions
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B.pertussis is an aerobic gram negative bacterium that does not produce spores. Due to its lack of flagella, it is also immotile. It resides in the phylum Proteobacteria, class Betaproteobacteria, order Burkholderiales, and family Alcaligenaceae. Because it is an aerobe, it utilizes aerobic respiration. Therefore, the bacterium consists of an electron transport chain on its membrane, and is considered a chemoheterotroph. Like other gram negative bacteria, it possesses an inner and outer membrane, with a thin peptidoglycan cell wall in between. This cell wall is attached to the outer membrane via lipoproteins. Like other gram negatives, the outer membrane of B.pertussis is coated with LPS (lipopolysachharides), which are long sugar linked and lipid-anchored polysaccharides coating the outer membrane. LPS are endotoxins, meaning that they are toxic to host (or potentially other bacteria) cells when detached from the bacteria. However, B.pertussis consists of very unusual LPS compared to other gram negatives. Namely, it contains two forms of LPS that have a different phosphate composition than standard Lipid A form LPS. | B.pertussis is an aerobic gram negative bacterium that does not produce spores. Due to its lack of flagella, it is also immotile. It resides in the phylum Proteobacteria, class Betaproteobacteria, order Burkholderiales, and family Alcaligenaceae. Because it is an aerobe, it utilizes aerobic respiration. Therefore, the bacterium consists of an electron transport chain on its membrane, and is considered a chemoheterotroph. Like other gram negative bacteria, it possesses an inner and outer membrane, with a thin peptidoglycan cell wall in between. This cell wall is attached to the outer membrane via lipoproteins. Like other gram negatives, the outer membrane of B.pertussis is coated with LPS (lipopolysachharides), which are long sugar linked and lipid-anchored polysaccharides coating the outer membrane. LPS are endotoxins, meaning that they are toxic to host (or potentially other bacteria) cells when detached from the bacteria. However, B.pertussis consists of very unusual LPS compared to other gram negatives. Namely, it contains two forms of LPS that have a different phosphate composition than standard Lipid A form LPS. | ||
Bordetella pertussis does not necessarily cause whooping cough by itself, but rather produces toxins that do so. Among producing pertussis toxin, filamentous hemagglutinin, and hemolysin, B.pertussis produces the adenylate cyclase toxin (CyaA) – a direct causative agent of Whooping Cough. CyaA invades eukaryotic cells by a calcium-dependent mechanism in which the CyaA catalytic domain is directly moved across the target cells plasma membrane. CyaA has a series of G and D rich polypeptide residues, which is a characteristic repeat for similar toxins. B.pertussis attaches to host cells via the virulence factor P.69 pertactin, which is an extracellularly exposed domain of a membrane protein expressed by B.pertussis – and targets the adhesion to mammalian cells. It consists of an RGD tripeptide motif which attaches to various sites on mammalian adhesion proteins (some include fibronectin, vitronectin, and fibrinogen). In addition to this, the filamentous hemagglutinin (FHA) also helps mediate cell adhesion, and contains similar motifs as P.69 pertactin. Once attached, B.pertussis is able to transfer CyaA to the target host cell. | |||
The pertussis toxin (PT), also produced by B.pertussis, is known to also be an important factor in whooping cough respiratory infections. PT catalyzes ADP-ribosylation of the alpha subunit of G(i) proteins, preventing the exchange of GDP-GTP, thus blocking the inhibition of adenylyl cyclase by G(i). This will destroy the ciliated epithelial cells that normally would sweep away mucus, and without this ciliated action, vigorous coughing is needed to clear the tract. This coughing is painful, and also is what spreads the highly contagious B.pertussis to others. | |||
The Tahoma 1 strain of B.pertussis has its entire genome sequenced – it is 1 circular chromosome 4,086,189 nucleotides long (3867 genes), of which about 67% of the entire genome is GC rich. | |||
Link to MicrobeWiki Page: Bordetella pertussis | Link to MicrobeWiki Page: Bordetella pertussis | ||
Revision as of 20:53, 26 August 2009
Introduction
Briefly introduce your topic here.
Bordetella pertussis
Description of the microbe
The bacterium Bordetella Pertussis is the causative agent of Whooping Cough. This small bacterium (about .8um in length and .4um by width) cannot survive in the open environment, and therefore must reside in a host, and is considered pathogenic. This host is almost always a human, where its “natural” environment is said to be the mucus in the human respiratory tract. The optimum temperature of growth for B.pertussis is about 35-37C, which is the temperature inside a living human host.
B.pertussis is an aerobic gram negative bacterium that does not produce spores. Due to its lack of flagella, it is also immotile. It resides in the phylum Proteobacteria, class Betaproteobacteria, order Burkholderiales, and family Alcaligenaceae. Because it is an aerobe, it utilizes aerobic respiration. Therefore, the bacterium consists of an electron transport chain on its membrane, and is considered a chemoheterotroph. Like other gram negative bacteria, it possesses an inner and outer membrane, with a thin peptidoglycan cell wall in between. This cell wall is attached to the outer membrane via lipoproteins. Like other gram negatives, the outer membrane of B.pertussis is coated with LPS (lipopolysachharides), which are long sugar linked and lipid-anchored polysaccharides coating the outer membrane. LPS are endotoxins, meaning that they are toxic to host (or potentially other bacteria) cells when detached from the bacteria. However, B.pertussis consists of very unusual LPS compared to other gram negatives. Namely, it contains two forms of LPS that have a different phosphate composition than standard Lipid A form LPS.
Bordetella pertussis does not necessarily cause whooping cough by itself, but rather produces toxins that do so. Among producing pertussis toxin, filamentous hemagglutinin, and hemolysin, B.pertussis produces the adenylate cyclase toxin (CyaA) – a direct causative agent of Whooping Cough. CyaA invades eukaryotic cells by a calcium-dependent mechanism in which the CyaA catalytic domain is directly moved across the target cells plasma membrane. CyaA has a series of G and D rich polypeptide residues, which is a characteristic repeat for similar toxins. B.pertussis attaches to host cells via the virulence factor P.69 pertactin, which is an extracellularly exposed domain of a membrane protein expressed by B.pertussis – and targets the adhesion to mammalian cells. It consists of an RGD tripeptide motif which attaches to various sites on mammalian adhesion proteins (some include fibronectin, vitronectin, and fibrinogen). In addition to this, the filamentous hemagglutinin (FHA) also helps mediate cell adhesion, and contains similar motifs as P.69 pertactin. Once attached, B.pertussis is able to transfer CyaA to the target host cell.
The pertussis toxin (PT), also produced by B.pertussis, is known to also be an important factor in whooping cough respiratory infections. PT catalyzes ADP-ribosylation of the alpha subunit of G(i) proteins, preventing the exchange of GDP-GTP, thus blocking the inhibition of adenylyl cyclase by G(i). This will destroy the ciliated epithelial cells that normally would sweep away mucus, and without this ciliated action, vigorous coughing is needed to clear the tract. This coughing is painful, and also is what spreads the highly contagious B.pertussis to others.
The Tahoma 1 strain of B.pertussis has its entire genome sequenced – it is 1 circular chromosome 4,086,189 nucleotides long (3867 genes), of which about 67% of the entire genome is GC rich.
Link to MicrobeWiki Page: Bordetella pertussis http://microbewiki.kenyon.edu/index.php/Bordetella_pertussis
Description of the disease
Transmission of disease
How is it transmitted? Is there a vector (animal/insect)?
Prevention
Why is this disease a problem in Canada
Do lifestyle/environment/economics/political issues play a role?
What is being done to address this problem
Include anything being done by the local government or groups as well as efforts by non-local groups.
What else could be done to address this problem
Are there solutions that could be successful but haven't been implemented due to political or economic reasons? Are there successful efforts in other countries? Are there reasons why these efforts may or may not be successful in the country you've focused on? etc. etc.
References
Edited by Bryan Dieffenbach, Gorjan Hrustanovic, Patricia Lee and Andrew Chen, students of Rachel Larsen
