Bordetella pertussis: Difference between revisions
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==Pathology== | ==Pathology== | ||
Humans are its only host. Pertussis is a severe, highly contagious respiratory disease characterized by outbursts of coughing followed by “whooping” sound during breathing in. Often vomiting takes place with discharge of sticky mucus. The bacteria are transmitted directly from person to person and are most contagious in its early stage of the disease. The symptoms of pertussis are similar to a common cold: runny nose, sneezing, mild cough, and low-grade fever. [1] | |||
''Bordetella pertussis'' has several virulence factors, one of which is the adenylate cyclase toxin (CyaA). It is the agent that causes whooping cough. CyaA invades eukaryotic cells by a calcium-dependent mechanism in which the CyaA catalytic domain is directly moved across the target cell’s plasma membrane. CyaA contains a series of a Gly-and Asp-rich nonapeptide repeats of the prototype GGXG(N/D)DX(L/I/F)X (where X can be any amino acid). This prototype is a characteristic of the repeat in toxin for the bacterial cytolysins family.[2] Another major virulence factor that is secreted by ''Bordetella pertussis'' is the pertussis toxin (PT). Pertussis toxin ADP ribosylates mammalian G(i) proteins and is a key component in the early stages of the respiratory infection. PT targets respiratory tract macrophages in promoting the infection. [5] Furthermore, like any infection, attachment to epithelial cells is a major factor in colonization. The filamentous hemagglutinin (FHA) is the virulence factor mediating adhesion to host cells. [11] | |||
==Application to Biotechnology== | ==Application to Biotechnology== |
Revision as of 10:00, 4 June 2007
A Microbial Biorealm page on the genus Bordetella pertussis
Classification
Higher order taxa
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Betaproteobacteria
Order: Burkholderiales
Family: Alcaligenaceae
Genus: Bordetella
Species: B. pertussis
Species
Bordetella pertussis
Other Names: “Haemophilus pertussis” (Pribram 1933) “Bacterium tussis-convulsivae” (Lehmann and Neumann 1927) "Hemophilus pertussis" (Bergey et al. 1923), and "Microbe de la coqueluche" Bordet and Gengou 1906. [10]
NCBI: Taxonomy |
Description and significance
Bordetella pertussis is a small, Gram-negative, coccoid bacterium about the size of 0.8 µm by 0.4 µm. It is an encapsulated immotile aerobe that does not make spores. Bordetella pertussis produces a number of virulence factors, including pertussis toxin, adenylate cyclase toxin, filamentous hemagglutinin, and hemolysin. It cannot survive in the environment; it must reside in a host either in small groups or singly. It grows at an optimal temperature of 35-37ºC. [1]
Bordetella pertussis is a strict human pathogen that is the causative agent of pertussis (whooping cough). Its natural habitat is in the human respiratory mucosa. Whooping Cough, or pertussis, is a respiratory infection in which a “whooping” sound is produced when the sufferer breathes. Pertussis kills an estimated 300,000 children annually, most of which occur in developing countries. [6]
Genome structure
Bordetella pertussis strain Tohama I has its complete genome sequenced. The genome consists of 1 circular chromosome with 4,086,189 nucleotides (3867 genes). Approximately 67% of the genome is GC rich and its coding density is 82% (1056 bp/gene). [10]
The IncP-1 beta plasmid pBP136 from Bordetella pertussis is also sequenced. It contains 41,268 bp nucleotides and carries 46 ORFs. Two of the ORFs have similar genes with unknown function to a plant pathogen called “Xylella fastidiosa”. pBP136 plasmid do not contain any accessory genes that code for antibiotics, mercury resistance, or xenobiotic degradation. Its role in the bacteria is unclear and is still under investigation. [9]
Cell structure and metabolism
Bordetella pertussis is an aerobe and thus utilizes aerobic respiration as its metabolism. Bordetella pertussis is also a Gram negative bacterium so its cell structure would consist of an outer membrane, an inner membrane and a periplasmic space with a thin peptidoglycan layer in between. On its outer membrane, Bordetella pertussis has unusual lipoopolysaccharides (LPS), endotoxins that are unlike other Gram-negative bacterium. It is different in that it contains two forms differing in its phosphate composition of the lipid portion of the LPS. This form is designated Lipid X, instead of the usual Lipid A form. The role of the unusual LPS is not fully understood in the pathogenesis of pertussis. [8]
Ecology
Humans are its only host. The B. pertussis bacterium resides in the upper air pathways, mostly the trachea and the bronchi. The pathogen is transmitted from person to person through droplets of respiratory secretions that are either coughed or sneezed into the air by an infected person. Without its host’s respiratory mucus, the pathogen cannot be sustained in the environment. [12]
Pathology
Humans are its only host. Pertussis is a severe, highly contagious respiratory disease characterized by outbursts of coughing followed by “whooping” sound during breathing in. Often vomiting takes place with discharge of sticky mucus. The bacteria are transmitted directly from person to person and are most contagious in its early stage of the disease. The symptoms of pertussis are similar to a common cold: runny nose, sneezing, mild cough, and low-grade fever. [1]
Bordetella pertussis has several virulence factors, one of which is the adenylate cyclase toxin (CyaA). It is the agent that causes whooping cough. CyaA invades eukaryotic cells by a calcium-dependent mechanism in which the CyaA catalytic domain is directly moved across the target cell’s plasma membrane. CyaA contains a series of a Gly-and Asp-rich nonapeptide repeats of the prototype GGXG(N/D)DX(L/I/F)X (where X can be any amino acid). This prototype is a characteristic of the repeat in toxin for the bacterial cytolysins family.[2] Another major virulence factor that is secreted by Bordetella pertussis is the pertussis toxin (PT). Pertussis toxin ADP ribosylates mammalian G(i) proteins and is a key component in the early stages of the respiratory infection. PT targets respiratory tract macrophages in promoting the infection. [5] Furthermore, like any infection, attachment to epithelial cells is a major factor in colonization. The filamentous hemagglutinin (FHA) is the virulence factor mediating adhesion to host cells. [11]
Application to Biotechnology
Current Research
References
Edited by Linda Wang a student of Rachel Larsen and Kit Pogliano