Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MELIOIDOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 811 records · Page 45Linked to original sources
PubMed1991

Antibody to Pseudomonas pseudomallei exotoxin in sheep exposed to natural infection.

Specific antibody to Pseudomonas pseudomallei exotoxin was detected in sheep sera exposed to natural infection. An enzyme-linked immunosorbent assay (ELISA) was used. Serum antitoxin was present in 49.3% of sera obtained from a flock of sheep naturally exposed to P. pseudomallei infection. Among these sera, 17.0% gave titers of 10,000. In contrast, serum antitoxin was present in only 6.0% of sera collected from sheep kept on a melioidosis-free farm. The ELISA reactivity of all positive sera could be completely absorbed with purified P. pseudomallei exotoxin. Similarly, preincubation of the exotoxin-coated wells with specific antiserum inhibited the ELISA reactivity of sheep sera. The results indicate that exotoxin is produced in vivo during infection by P. pseudomallei.

Animals↗
PubMed2006

Development of a polymerase chain reaction assay for the specific identification of Burkholderia mallei and differentiation from Burkholderia pseudomallei and other closely related Burkholderiaceae.

Burkholderia mallei and Burkholderia pseudomallei, the etiologic agents responsible for glanders and melioidosis, respectively, are genetically and phenotypically similar and are category B biothreat agents. We used an in silico approach to compare the B. mallei ATCC 23344 and B. pseudomallei K96243 genomes to identify nucleotide sequences unique to B. mallei. Five distinct B. mallei DNA sequences and/or genes were identified and evaluated for polymerase chain reaction (PCR) assay development. Genomic DNAs from a collection of 31 B. mallei and 34 B. pseudomallei isolates, obtained from various geographic, clinical, and environmental sources over a 70-year period, were tested with PCR primers targeted for each of the B. mallei ATCC 23344-specific nucleotide sequences. Of the 5 chromosomal targets analyzed, only PCR primers designed to bimA(Bm) were specific for B. mallei. These primers were used to develop a rapid PCR assay for the definitive identification of B. mallei and differentiation from all other bacteria.

Bacterial Typing Techniques↗
PubMed2005

Type III secretion system cluster 3 is required for maximal virulence of Burkholderia pseudomallei in a hamster infection model.

Burkholderia pseudomallei, the etiological agent of melioidosis, is an animal pathogen capable of inducing a highly fatal septicemia. B. pseudomallei possesses three type III secretion system (TTSS) clusters, two of which (TTSS1 and TTSS2) are homologous to the TTSS of the plant pathogen Ralstonia solanacearum, and one (TTSS3) is homologous to the Salmonella SPI-1 mammalian pathogenicity island. We have demonstrated that TTSS3 is required for the full virulence of B. pseudomallei in a hamster model of infection. We have also examined the virulence of B. pseudomallei mutants deficient in several putative TTSS3 effector molecules, and found no significant attenuation of B. pseudomallei virulence in the hamster model.

Animals↗
PubMed2005

Rapid presumptive identification of Burkholderia pseudomallei with real-time PCR assays using fluorescent hybridization probes.

Burkholderia pseudomallei (the etiologic agent of melioidosis) can cause pyogenic or granulomatous lesions in almost any organ. Septicemia has a case fatality rate of >40%. Early diagnosis and appropriate antibiotic therapy are crucial for survival, but cultivation, biochemical identification, and conventional PCR of B. pseudomallei are time consuming. We established real-time PCR assays using fluorescent hybridization probes targeting the 16S rDNA, the flagellin C (fliC) and the ribosomal protein subunit S21 (rpsU) genes. The test sensitivity and specificity were assessed with a representative panel of 39 B. pseudomallei, 9 B. mallei, 126 other Burkholderia strains of 29 species, and 45 clinically relevant non-Burkholderia organisms. The detection limit for the 16S rDNA, fliC, and rpsU assay was 40, 40, and 400 genome equivalents per reaction, however, in spiked blood samples it was 300, 300, and 3000, respectively. Specificity, positive and negative predictive value of the assays was 100%. In conclusion, we recommend the use of the 16S rDNA and/or fliC real-time PCR assays for the rapid identification of B. mallei and B. pseudomallei in positive blood cultures or from suspicious bacterial colonies.

Burkholderia pseudomallei↗
PubMed2005

A model of immunity to Burkholderia pseudomallei: unique responses following immunization and acute lethal infection.

Burkholderia pseudomallei, the etiological agent of melioidosis, causes significant mortality in endemic regions, but little is known regarding the immune mechanisms required for successful protective immunity. To establish a model of immunization that could be used to study this we screened a library of B. pseudomallei strains for immunogenicity in mice. BALB/c mice were immunized with test strains, and 2 weeks later were given a lethal challenge (LC) of virulent B. pseudomallei. Among 49 strains tested, a single strain, CL04, exhibited strong immunoprotective capacity. Interestingly, CL04 had been cultured from a patient with chronic colonization of B. pseudomallei, which is a rare phenomenon. Mice immunized with 0.1 x LD50 (5 x 10(3) CFU) of CL04 had significantly better survival and lower bacterial loads after LC compared to naïve controls. Dose-response analysis demonstrated more robust immunity after higher immunizing doses, and bacterial inactivation by gamma irradiation diminished the protective effect, indicating a requirement for viable organism for immunity. CL04-induced immunity was demonstrated both in B. pseudomallei-susceptible BALB/c and -resistant C57BL/6 mice. We investigated the gene profile of CL04-induced immunity by analyzing responses to immunization using cDNA microarray. Unique responses involving granulocyte macrophage colony stimulating factor (GM-CSF), the proapoptotic regulator Bad and cyclin-dependent kinase (CDK5) were detected in immunized mice, but these responses were absent in naïve-LC mice. Further, responses differed between mouse strains, indicating dependence on host genetic background. This model will be useful in identifying elements of the immune response required for successful adaptive immunity against B. pseudomallei.

Animals↗
PubMedDate not supplied

Burkholderia pseudomallei invasion and activation of epithelial cells requires activation of p38 mitogen-activated protein kinase.

Burkholderia pseudomallei is a causative agent of melioidosis. This gram-negative bacterium is able to survive inside the macrophages and also able to invade non-phagocytic cells including epithelial cells. Interaction of pathogenic bacteria to the host cells is frequently associated with activation of mitogen-activated protein (MAP) kinases signaling activity. In this study, we demonstrated that B. pseudomallei stimulated p38 MAP kinase of human alveolar lung epithelial cell line (A549). Phosphorylation of p38 was observed after 15 min, attained a maximal level at 60 min after the infection. A specific inhibitor of p38 phosphorylation, SB 203580, was able to inhibit invasion of this bacterium into the cells suggesting that invasion of B. pseudomallei required activation of p38. In contrast, wortmannin which is a specific inhibitor of phosphoinositide 3-kinase (PI3-kinase) failed to inhibit the invasion. Moreover, SB 203580 can also interfere with IkappaBalpha degradation and IL-8 mRNA expression, indicating that the phosphorylation of p38 occurred upstream of NF-kappaB activation. Cytochalasin D, an inhibitor of actin polymerization needed for internalisation of bacteria, did not have any effect on the phosphorylation of p38. These results indicate that B. pseudomallei stimulate phosphorylation of p38 making by initial contact with the cell surface components and do not require internalisation and interaction with intracellular cytoplasmic components of the cells.

Androstadienes↗
PubMed2005

Virulence of Burkholderia pseudomallei does not correlate with biofilm formation.

Burkholderia pseudomallei is the causative agent of melioidosis but currently the pathogenesis of the disease is still poorly understood. One of the virulent factors of gram-negative bacteria is the ability to produce biofilm to evade host defense. As B. pseudomallei has also been reported to develop the biofilm [1], in the present study, we therefore, quantified the biofilm formation in 50 strains of B. pseudomallei and compared with 50 strains of its avirulent counterpart Burkholderia thailandensis using a modified microtiter-plate test. The results showed that the quantity of biofilm produced by B. pseudomallei was statistically higher (P< 0.01) than that of B. thailandensis (means and SEs of the corrected OD630 were 2.17+/-0.29 and 0.59+/-0.05, respectively). Transmission electron micrographs of the B. pseudomallei strain with high biofilm formation exhibited microcolonies of bacterial cells surrounded by dense extracellular slime matrix comparing with only trace quantity in the low biofilm-producing strain or the biofilm mutants generated by Tn5-OT182 mutagenesis. However, no correlation could be observed between the biofilm formation and virulence, judging from the LD50 values in BALB/c mice. The data obtained with these naturally occurring Burkholderia species and the biofilm mutants are incompatible with the possibility that the biofilm plays a role in the pathogenesis of B. pseudomallei infection.

Animals↗
PubMed2001

Ribotyping of Burkholderia pseudomallei from clinical and soil isolates in Thailand.

Burkholderia pseudomallei is a soil saprophyte that causes melioidosis in humans and animals. Restriction fragment length polymorphism of the ribosomal DNA regions (ribotyping) were analyzed in 577 isolates comprising 371 clinical and 206 soil isolates collected throughout Thailand in 1997. A total of 77 distinct ribotype patterns consisting of 2-9 bands with sizes ranging from 2.8 to >23 kb were found. Twelve major ribotypes were identified of which types 3, 8 and 23 were commonly found (278/577, 48.2%) in both clinical (217/371, 58.5%) and environmental isolates (61/206, 29.6%). Three unique environmental types were found whereas a unique clinical type was not observed. Even though ribotypes show high heterogeneity in the rDNA region, the unique environmental patterns were clearly different from the clinical patterns as clearly seen by UPGMA dendrogram. Moreover, the three major types (types 3, 8 and 23) were discovered in nearly half of B. pseudomallei isolates. Subtyping of these major ribotypes in correlation with clinical profiles may help researchers to identify the virulence factor of the organism.

Arabinose↗
PubMed2000

Use of multiplex PCR patterns as genetic markers for Burkholderia pseudomallei.

A simple PCR-based typing method was developed to differentiate between strains of Burkholderia pseudomallei. Two pairs of primers, based on sequences from two specific DNA probes, were used to amplify the bacterial DNA by multiplex PCR. We evaluated the PCR method for epidemiological typing of B. pseudomallei and compared this with restriction fragment length polymorphism (RFLP) and random amplified polymorphic DNA (RAPD) methods. In RFLP, the DNA of B. pseudomallei was digested with HindIII and the pKKU-S23L was used as a probe while 5' GTTTCGCTCC 3' primer was used in RAPD. DNA was obtained from 37 B. pseudomallei environmental and clinical isolates from humans or animals. These isolates were also classified by their ability to assimilate L-arabinose. A total of 21 type patterns were identified by multiplex PCR. Among human and animal isolates, multiplex PCR revealed ten types, all of which were arabinose negative (Ara-), whereas six of the 11 types of environmental isolates were Ara-. There are two environmental patterns that also were found in clinical isolates. The RFLP technique showed 12 different types in the 37 isolates, and three of these contained both Ara+ and Ara- isolates. The RAPD technique revealed 33 different types in the 37 isolates. Multiplex PCR, therefore, is the genetic marker that best correlates with the ability of the organism to assimilate L-arabinose. Moreover, two types (M4, M15) correlated with disseminated septicemic melioidosis in the northeast Thailand. If a greater number of isolates are tested, the multiplex PCR technique may prove to be useful for rapid epidemiological typing of B. pseudomallei.

Animals↗
PubMed1998

Brain abscesses caused by Burkholderia pseudomallei.

Burkholderia pseudomallei is an important human pathogen in tropical areas, particularly South East Asia and Northern Australia. A fatal case of meliodosis presenting as brain abscesses is described. The patient deteriorated despite treatment and died 21 days after admission. Burkholderia pseudomallei was only isolated after administration of corticosteroids, whilst on treatment with antibiotics to which the organism later showed in vitro sensitivity. Magnetic resonance imaging was more sensitive than computed tomography in diagnosing early brainstem infection in this patient. Physicians working outside the endemic areas must be attuned to the possibility of melioidosis in any patient with an appropriate history of travel to endemic areas. The combination of striking early, extensive, confluent T2 hyperintensity with disproportionately small enhancing lesions may be characteristic of meliodosis.

Adult↗
PubMed1997

Polymerase chain reaction for the detection of Burkholderia pseudomallei.

Melioidosis is a potentially lethal infection of humans and animals in Southeast Asia and northern Australia. Current methods for detection of the causative organism, Burkholderia pseudomallei, lack both speed and sensitivity. We report the development of a highly sensitive polymerase chain reaction-based method that can detect as few as 35 colony-forming units of B. pseudomallei/mL in saline suspensions. This polymerase chain reaction test also detected the presence of B. pseudomallei DNA in culture-negative splenic tissue obtained from mice infected with the organism, but without clinical evidence of disease. Specificity has been confirmed using a variety of pathogenic and nonpathogenic organisms, including B. mallei, B. cepacia, and Pseudomonas species. The clinical usefulness of this test should be assessed prospectively and compared with conventional diagnostic techniques.

Animals↗
PubMed2002

Characterization of Burkholderia pseudomallei infection and identification of novel virulence factors using a Caenorhabditis elegans host system.

The environmental saphrophyte Burkholderia pseudomallei is the causative agent of melioidosis, a systemic, potentially life-threatening condition endemic to many parts of south-east Asia and northern Australia. We have used the soil nematode Caenorhabditis elegans as a model host to characterize the mechanisms by which this bacterium mounts a successful infection. We find that C. elegans is susceptible to a broad range of Burkholderia species, and that the virulence mechanisms used by this pathogen to kill nematodes may be similar to those used to infect mammals. We also find that the specific dynamics of the C. elegans-B. pseudomallei host-pathogen interaction can be highly influenced by environmental factors, and that nematode killing results at least in part from the presence of a diffusible toxin. Finally, by screening for bacterial mutants attenuated in their ability to kill C. elegans, we genetically identify several new potential virulence factors in B. pseudomallei. The use of C. elegans as a model host should greatly facilitate future investigations into how B. pseudomallei can interact with host organisms.

Animals↗
PubMed2001

Paraplegia secondary to Burkholderia pseudomallei myelitis: a case report.

Bacterial infection is an uncommon cause of acute paraplegia. A 42-year-old Aboriginal man presented to a remote health clinic in northern Australia with myelitis associated with Burkholderia pseudomallei. He was treated with analgesia and intravenous flucloxacillin, ceftriaxone, and gentamicin and transferred to our hospital, where an urgent T12-L1 laminectomy and decompression was performed. Urine culture confirmed B. pseudomallei infection (melioidosis). Abdominopelvic computed tomography revealed left prostatic lobe and right periprostatic abscesses, which were managed conservatively. The patient was given intravenous ceftazidime (8g/d) for 2 months, followed by oral sulfamethoxazole (1600mg) and trimethoprim (320mg) twice daily for 8 weeks. Magnetic resonance imaging 3 weeks after his admission confirmed transverse myelitis. His rehabilitation was complicated by his difficulty in adjusting to disability, by urinary retention and fecal incontinence, by communication barriers, and his isolation from a culture familiar to him. He returned to his community after 15 weeks, free of infection, with T10-11 paraplegia and an indwelling catheter.

Adult↗
PubMed2004

Exploitation of host cells by Burkholderia pseudomallei.

Intracellular bacterial pathogens have evolved mechanisms to enter and exit eukaryotic cells using the power of actin polymerisation and to subvert the activity of cellular enzymes and signal transduction pathways. The proteins deployed by bacteria to subvert cellular processes often mimic eukaryotic proteins in their structure or function. Studies on the exploitation of host cells by the facultative intracellular pathogen Burkholderia pseudomallei are providing novel insights into the pathogenesis of melioidosis, a serious invasive disease of animals and humans that is endemic in tropical and subtropical areas. B. pseudomallei can invade epithelial cells, survive and proliferate inside phagocytes, escape from endocytic vesicles, form actin-based membrane protrusions and induce host cell fusion. Here we review current understanding of the molecular mechanisms underlying these processes.

Actins↗
PubMed1998

Potential misidentification of Burkholderia pseudomallei by API 20NE.

Biochemical confirmation of the identity of Burkholderia pseudomallei in Singapore previously relied on the API 20NE panel of tests. After introducing an alternative proprietary biochemical panel, the Microbact 24E (MedVet, Adelaide, Australia), we noted that the API panel identified some presumptive B. pseudomallei isolates as other species. We therefore compared the performance of the API 20NE against the Microbact 24E with 50 distinct clinical isolates of B. pseudomallei, after 24 hours and after five days incubation of primary cultures. The API panel correctly identified 40 isolates. Four results were unacceptable or uninterpretable. Six isolates were misidentified as other species; the commonest being Chromobacterium violaceum. One of these was again identified as C. violaceum by the repeat API panel. Fourteen isolates, including the six misidentified isolates and four isolate pairs from separate sources in four separate patients, were typed using PCR amplification of repetitive extragenic palindromic sequences (REPS). The isolates identified as C. violaceum appeared to have identical REPS patterns, suggesting that some of the errant API results may be due to a single locally prevalent strain of B. pseudomallei. A previous suggestion that C. violaceum may produce a melioidosis-like illness may therefore be due to laboratory misidentification of B. pseudomallei with the API 20NE biochemical test panel.

Bacterial Typing Techniques↗
PubMed1998

Neonatal meningitis and septicaemia caused by Burkholderia pseudomallei.

We report a case of meningitis and one of fatal septicaemia in neonates due to Burkholderia pseudomallei and review the literature on neonatal melioidosis. Pneumonia was the primary presentation and was complicated by shock in the latter case. The epidemiological findings suggest that the cases reported from Malaysia were community-acquired in contrast with those from the USA and Thailand.

Burkholderia pseudomallei↗
PubMed2005

Interaction between Burkholderia pseudomallei and the host immune response: sleeping with the enemy?

Melioidosis is an infectious disease endemic in tropical and subtropical areas but is most often described in Southeast Asia and northern Australia. It has increasingly gained attention in the Western Hemisphere because of its potential use as a biological weapon. Progress in our understanding of the virulence mechanisms of Burkholderia pseudomallei, the causative agent, has provided clues to the pathogenesis of the disease. The bacterium can remain latent in the body for long periods of time and also possesses mechanisms to evade the host immune response. The complex spectrum of clinical manifestations resulting from infection could reflect the various outcomes after the host immune response encounters the bacteria. The use of appropriate animal models of susceptibility will likely shed light on what determines the development of an acute, chronic, or latent infection.

Animals↗
PubMed2006

Computed tomography characteristics of Burkholderia pseudomallei liver abscess.

We report 3 cases of Burkholderia pseudomallei liver abscesses that have a characteristic "honeycomb" appearance on computed tomography scans. Such a finding should prompt physicians to include B. pseudomallei infection in the differential diagnoses of liver abscesses and consider initiation of empirical therapy for melioidosis in high-risk patients from areas of endemicity.

Adult↗