The detection of insertion sequences within the human pathogen Burkholderia pseudomallei which have been identified previously in Burkholderia cepacia

Mack, Kerri

doi:10.1016/s0378-1097(98)00104-9

Cited by 19 publications

(28 citation statements)

References 16 publications

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“…As Burkholderia cepacia can degrade toxic compounds in pesticides and is active against many soilborne pathogens, there has been interest in its use as a crop biological control agent (199). However, numerous insertion sequences within B. cepacia, including for some strains sequences identical to B. pseudomallei insertion sequences (284), and transposable genetic elements in B. pseudomallei (61) have been identified. This justifies concerns that widespread agricultural use of B. cepacia may be a hazard to human health, with the potential for more virulent B. cepacia bacteria to emerge following horizontal transmission of genetic elements (199).…”

Section: Environmental Microbiology and Epidemiologymentioning

confidence: 99%

Melioidosis: Epidemiology, Pathophysiology, and Management

2005

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Melioidosis, caused by the gram-negative saprophyte Burkholderia pseudomallei, is a disease of public health importance in southeast Asia and northern Australia that is associated with high case-fatality rates in animals and humans. It has the potential for epidemic spread to areas where it is not endemic, and sporadic case reports elsewhere in the world suggest that as-yet-unrecognized foci of infection may exist. Environmental determinants of this infection, apart from a close association with rainfall, are yet to be elucidated. The sequencing of the genome of a strain of B. pseudomallei has recently been completed and will help in the further identification of virulence factors. The presence of specific risk factors for infection, such as diabetes, suggests that functional neutrophil defects are important in the pathogenesis of melioidosis; other studies have defined virulence factors (including a type III secretion system) that allow evasion of killing mechanisms by phagocytes. There is a possible role for cell-mediated immunity, but repeated environmental exposure does not elicit protective humoral or cellular immunity. A vaccine is under development, but economic constraints may make vaccination an unrealistic option for many regions of endemicity. Disease manifestations are protean, and no inexpensive, practical, and accurate rapid diagnostic tests are commercially available; diagnosis relies on culture of the organism. Despite the introduction of ceftazidime- and carbapenem-based intravenous treatments, melioidosis is still associated with a significant mortality attributable to severe sepsis and its complications. A long course of oral eradication therapy is required to prevent relapse. Studies exploring the role of preventative measures, earlier clinical identification, and better management of severe sepsis are required to reduce the burden of this disease

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Section: Environmental Microbiology and Epidemiologymentioning

confidence: 99%

Melioidosis: Epidemiology, Pathophysiology, and Management

2005

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“…B. cepacia can degrade some toxic compounds in pesticides and herbicides, and can kill many soil-borne plant pathogens. However, rapid mutation and adaptation is considered likely, given the presence of numerous insertion sequences within B. cepacia [11], including, for some strains, sequences identical to B. pseudomallei insertion sequences [12]. This justifies concern that widespread agricultural use of B. cepacia may be a hazard to human health and, most particularly, for patients with cystic fibrosis (CF) [11].…”

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confidence: 99%

Melioidosis: an important cause of pneumonia in residents of and travellers returned from endemic regions

Currie¹

2003

Eur Respir J

166

171

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Melioidosis is endemic in South East Asia, Asia and northern Australia. Infection usually follows percutaneous inoculation or inhalation of the causative bacterium,Burkholderia pseudomallei, which is present in soil and surface water in the endemic region. While 20–36% of melioidosis cases have no evident predisposing risk factor, the vast majority of fatal cases have an identified risk factor, the most important of which are diabetes, alcoholism and chronic renal disease.Half of all cases present with pneumonia, but there is great clinical diversity, from localised skin ulcers or abscesses without systemic illness to fulminant septic shock with multiple abscesses in the lungs, liver, spleen and kidneys. At least 10% of cases present with a chronic respiratory illness (sick >2 months) mimicking tuberculosis and often with upper lobe infiltrates and/or cavities on chest radiography. As with tuberculosis, latency with reactivation decades after infection can also occur, although this is rare.Confirmation of diagnosis is by culture ofB. pseudomalleifrom blood, sputum, throat swab or other samples. Microbiology laboratories need to be informed of the possibility of melioidosis, as those not familiar with it can misidentify the organism. Antibiotic therapy is initial intensive therapy withi.v.ceftazidime or meropenem or imipenem +/− cotrimoxazole for ≥10 days, followed by eradication therapy with cotrimoxazole +/− doxycycline +/− chloramphenicol (first 4 weeks only) for ≥3 months.Melioidosis has been increasingly recognised in returning travellers in Europe and recently melioidosis and colonisation withB. pseudomalleihave been documented in cystic fibrosis patients visiting or resident in endemic areas.

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“…DNA was prepared from 100-ml cultures of B. pseudomallei in LB broth by a lysozyme, phenolchloroform extraction method [36] and digested with SacI restriction endonuclease. The digested DNA was purified with Microcon 100 (Millipore UK, Watford) spin columns and ligated with similarly pre-digested pUC19 plasmid DNA.…”

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confidence: 99%