The Burkholderia Taxonomy and Genomics
Burkholderia pseudomallei (Bp) belongs to the Burkholderia genus which contains over 40 species that inhabit a variety of ecological niches. The majority of species within this genus are non-pathogenic soil-dwelling bacteria, but a few species are highly pathogenic to humans and can result in severe disease [1]. This includes B. mallei, an obligate mammalian pathogen and the causative agent of glanders, which primarily affects horses and other solipeds and is highly virulent in humans. A clinically important species of Burkholderia is B. cenocepacia, which is a major cause of opportunistic infections in patients with cystic fibrosis [2, 3]. The genus also includes the Bp-like strain B. thailandensis, …show more content…
It is believed that these habitats are the primary reservoirs from which susceptible hosts acquire infections [14]. Infection results from percutaneous inoculation (e.g. by means of a penetrating injury or open wound), inhalation (e.g. during severe weather or as a result of a deliberate release), or ingestion (e.g. through contaminated food or water) [3]. Manifestations of disease are dependent on host pathogen interaction and extremely broad ranging from rapidly life-threatening sepsis to chronic low-grade infection. A common clinical picture associated with melioidosis is that of sepsis associated with bacterial dissemination to distant sites [9, 15, 16], frequently causing simultaneous pneumonia and liver and splenic abscesses [17]. Infection may also occur in bone, joints, skin, soft tissue, or the prostate [18-20] and can also cause blood disease, kidney disease, heart disease, and more [17]. This broad spectrum of clinical symptoms has earned Bp the nickname “The Great Mimicker”, since the clinical symptoms of melioidosis imitate those of many other diseases. Thus, differentiating between melioidosis and other acute and chronic bacterial infections, including tuberculosis, is often impossible which often leads to misdiagnosis and improper treatment [21] which is often fatal [3]. Confirmation of the …show more content…
The varying responses are anchored to heritable variation, which predisposes an individual to particular disease outcomes. It is possible to study each of the biochemical, cellular, and genetic factors in isolation in understanding melioidosis, but this strategy would clearly be challenging. Recent computational and technological advances have made it feasible to quantitatively survey hundreds or thousands of biological molecules, from DNA sequence variations to epigenetic marks to levels of transcripts, proteins and metabolites [51, 52]. Because it is also now possible to monitor transcript levels in a comprehensive fashion, integrating DNA variation, transcription, and phenotypic data has the potential to enhance identification of the associations between DNA variation and diseases like obesity and diabetes, as well as characterize those parts of the molecular networks that drive these diseases [52]. As such, we use a system genetics approach to identify and characterize genetic loci that contribute to resistance and/or susceptibility to
Burkholderia pseudomallei (Bp) belongs to the Burkholderia genus which contains over 40 species that inhabit a variety of ecological niches. The majority of species within this genus are non-pathogenic soil-dwelling bacteria, but a few species are highly pathogenic to humans and can result in severe disease [1]. This includes B. mallei, an obligate mammalian pathogen and the causative agent of glanders, which primarily affects horses and other solipeds and is highly virulent in humans. A clinically important species of Burkholderia is B. cenocepacia, which is a major cause of opportunistic infections in patients with cystic fibrosis [2, 3]. The genus also includes the Bp-like strain B. thailandensis, …show more content…
It is believed that these habitats are the primary reservoirs from which susceptible hosts acquire infections [14]. Infection results from percutaneous inoculation (e.g. by means of a penetrating injury or open wound), inhalation (e.g. during severe weather or as a result of a deliberate release), or ingestion (e.g. through contaminated food or water) [3]. Manifestations of disease are dependent on host pathogen interaction and extremely broad ranging from rapidly life-threatening sepsis to chronic low-grade infection. A common clinical picture associated with melioidosis is that of sepsis associated with bacterial dissemination to distant sites [9, 15, 16], frequently causing simultaneous pneumonia and liver and splenic abscesses [17]. Infection may also occur in bone, joints, skin, soft tissue, or the prostate [18-20] and can also cause blood disease, kidney disease, heart disease, and more [17]. This broad spectrum of clinical symptoms has earned Bp the nickname “The Great Mimicker”, since the clinical symptoms of melioidosis imitate those of many other diseases. Thus, differentiating between melioidosis and other acute and chronic bacterial infections, including tuberculosis, is often impossible which often leads to misdiagnosis and improper treatment [21] which is often fatal [3]. Confirmation of the …show more content…
The varying responses are anchored to heritable variation, which predisposes an individual to particular disease outcomes. It is possible to study each of the biochemical, cellular, and genetic factors in isolation in understanding melioidosis, but this strategy would clearly be challenging. Recent computational and technological advances have made it feasible to quantitatively survey hundreds or thousands of biological molecules, from DNA sequence variations to epigenetic marks to levels of transcripts, proteins and metabolites [51, 52]. Because it is also now possible to monitor transcript levels in a comprehensive fashion, integrating DNA variation, transcription, and phenotypic data has the potential to enhance identification of the associations between DNA variation and diseases like obesity and diabetes, as well as characterize those parts of the molecular networks that drive these diseases [52]. As such, we use a system genetics approach to identify and characterize genetic loci that contribute to resistance and/or susceptibility to