Burkholderia mallei: Difference between revisions
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==Cell Structure, Metabolism and Life Cycle== | ==Cell Structure, Metabolism and Life Cycle== | ||
B. mallei exhibits distinctive cellular features that contribute to its pathogenicity and survival in various host environments. Burkholderia mallei cells are typically coccobacilli, measuring approximately 1.5–3.0 μm in length and 0.5–1.0 μm in diameter, with rounded ends. Unlike its motile counterpart B. pseudomallei, Burkholderia mallei is nonmotile. As discussed earlier the cell wall of Burkholderia mallei is Gram-negative, characterized by an outer membrane containing lipopolysaccharides (LPS) that contribute larg;y to its pathogenic properties and interaction with host cells. Burkholderia mallei usually produces a thick capsule composed of polysaccharides which serves as a virulence factor protecting the bacterium from host immune defenses and its survival in the host environment. | |||
Burkholderia mallei uses a wide diverse range of metabolic pathways to obtain energy and essential nutrients for its growth and survival. Burkholderia mallei is aerobically metabolically active, relying on aerobic respiration for energy production. The bacterium utilizes organic compounds as carbon and energy sources, including sugars, amino acids, and fatty acids, which are catabolized through various metabolic pathways such as the tricarboxylic acid (TCA) cycle and glycolysis. Burkholderia mallei possesses nitrogen-fixing capabilities, allowing it to convert atmospheric nitrogen into ammonia through nitrogenase enzymes. This ability enhances its adaptability to nitrogen-limiting environments and contributes to its growth in diverse ecological niches. | |||
The life cycle of Burkholderia mallei involves complex interactions with host cells and the environment, facilitating its replication and spread. Burkholderia mallei infects host cells, primarily epithelial cells and macrophages, through mechanisms such as adhesion, invasion, and intracellular survival. The bacterium employs virulence factors, including adhesins and secretion systems, to establish infection and evade host immune responses. Once inside host cells, Burkholderia mallei establishes intracellular replication niches, where it replicates and proliferates using host cellular machinery and nutrients. The bacterium manipulates host cell signaling pathways and immune responses to create a favorable environment for its survival and propagation. Burkholderia mallei eventually triggers host cell lysis, leading to the release of progeny bacteria into the extracellular environment. The bacterium may also disseminate through cell-to-cell spread or form biofilm communities in host tissues, contributing to chronic infections and disease persistence. | |||
Understanding the cell structure, metabolism, and life cycle of Burkholderia mallei is crucial for elucidating its pathogenic mechanisms and developing targeted interventions for glanders. Insights into the bacterium's metabolic pathways and virulence strategies provide opportunities for the development of novel therapeutics and vaccines to combat infections caused by this medically important pathogen. | |||
==Ecology and Pathogenesis== | ==Ecology and Pathogenesis== | ||
Revision as of 22:29, 24 April 2024
Classification
Domain: Bacteria
Phylum: Pseudomonadota
Class: Betaproteobacteria
Order: Burkholderiales
family: Burkholderiaceae
genus: Burkholderia
Species
Burkholderia mallei
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NCBI: Taxonomy |
Genus species
Description and Significance
Burkholderia mallei is a Gram-negative, bipolar, aerobic bacterium, a human and animal pathogen of genus Burkholderia causing glanders; the Latin name of this disease (malleus) gave its name to the species causing it. It is closely related to B. pseudomallei, and by multilocus sequence typing it is a subspecies of B. pseudomallei.[1] B. mallei evolved from B. pseudomallei by selective reduction and deletions from the B. pseudomallei genome.[2] Unlike B. pseudomallei and other genus members, B. mallei is nonmotile; its shape is coccobacillary measuring some 1.5–3.0 μm in length and 0.5–1.0 μm in diameter with rounded ends.
Genome Structure
Burkholderia mallei's genome exhibits distinctive features that differentiate it from other members of the Burkholderia genus. Unlike its closely related counterpart, B. pseudomallei which has a larger genome (around 7.3 Mb) size, B. mallei possesses a smaller genome with unique characteristics (around 3.5 mb). While B. pseudomallei has a larger genome size, Burkholderia mallei's genome is relatively smalle. Which can reflect selective reduction and deletions from the B. pseudomallei genome during its evolution into a specialized and unique pathogen. B. mallei's genome provides insights into its phylogenetic relationship with other members of the Burkholderias genus and related organisms. Multilocus sequence typing has classified Burkholderia mallei as a subspecies of B. pseudomallei due to clone reduction. Indicating a close evolutionary relationship. However, genomic analysis reveals distinct genetic differences between the two species, reflecting their differences in ecological niches and lifestyles as pathogens. Overall the genome is structured as being made up of 2 circular chromosomes each with their own designated roles. Chromosome one harbors essential genes for basic cellular functions while chromosome 2 contains genes associated with adaptation, virulence and pathogenicity. Understanding th genome structure of B. Mallei is crucial for dissecting its pathogenic mechanisms, evolutionary history and adaptation to its host environment. This is possible from comparative genomic analysis which provides strategies for diagnosis, treatment and prevention of infections caused by the pathogens.
Cell Structure, Metabolism and Life Cycle
B. mallei exhibits distinctive cellular features that contribute to its pathogenicity and survival in various host environments. Burkholderia mallei cells are typically coccobacilli, measuring approximately 1.5–3.0 μm in length and 0.5–1.0 μm in diameter, with rounded ends. Unlike its motile counterpart B. pseudomallei, Burkholderia mallei is nonmotile. As discussed earlier the cell wall of Burkholderia mallei is Gram-negative, characterized by an outer membrane containing lipopolysaccharides (LPS) that contribute larg;y to its pathogenic properties and interaction with host cells. Burkholderia mallei usually produces a thick capsule composed of polysaccharides which serves as a virulence factor protecting the bacterium from host immune defenses and its survival in the host environment.
Burkholderia mallei uses a wide diverse range of metabolic pathways to obtain energy and essential nutrients for its growth and survival. Burkholderia mallei is aerobically metabolically active, relying on aerobic respiration for energy production. The bacterium utilizes organic compounds as carbon and energy sources, including sugars, amino acids, and fatty acids, which are catabolized through various metabolic pathways such as the tricarboxylic acid (TCA) cycle and glycolysis. Burkholderia mallei possesses nitrogen-fixing capabilities, allowing it to convert atmospheric nitrogen into ammonia through nitrogenase enzymes. This ability enhances its adaptability to nitrogen-limiting environments and contributes to its growth in diverse ecological niches.
The life cycle of Burkholderia mallei involves complex interactions with host cells and the environment, facilitating its replication and spread. Burkholderia mallei infects host cells, primarily epithelial cells and macrophages, through mechanisms such as adhesion, invasion, and intracellular survival. The bacterium employs virulence factors, including adhesins and secretion systems, to establish infection and evade host immune responses. Once inside host cells, Burkholderia mallei establishes intracellular replication niches, where it replicates and proliferates using host cellular machinery and nutrients. The bacterium manipulates host cell signaling pathways and immune responses to create a favorable environment for its survival and propagation. Burkholderia mallei eventually triggers host cell lysis, leading to the release of progeny bacteria into the extracellular environment. The bacterium may also disseminate through cell-to-cell spread or form biofilm communities in host tissues, contributing to chronic infections and disease persistence.
Understanding the cell structure, metabolism, and life cycle of Burkholderia mallei is crucial for elucidating its pathogenic mechanisms and developing targeted interventions for glanders. Insights into the bacterium's metabolic pathways and virulence strategies provide opportunities for the development of novel therapeutics and vaccines to combat infections caused by this medically important pathogen.
Ecology and Pathogenesis
Habitat; symbiosis; biogeochemical significance; contributions to environment.
If relevant, how does this organism cause disease? Human, animal, plant hosts? Virulence factors, as well as patient symptoms.
References
Author
Page authored by _____, student of Prof. Jay Lennon at IndianaUniversity.
