scholarly journals Patogenesis dan virulensi Burkholderia pseudomallei penyebab melioidosis dan Burkholderia cepacia sebagai patogen oportunis

2021 ◽  
Vol 4 (1) ◽  
pp. 27-36
Author(s):  
Conny Riana Tjampakasari

Diantara genus Burkholderia terdapat dua spesies yang menjadi perhatian dalam bidang kesehatan, yaitu B. pseudomallei dan  B. cepacia.   Kedua bakteri ini menyebabkan masalah klinis yang berbeda.  Penyakit melioidosis kerap disebabkan oleh  B.pseudomallei, sedangkan  B. cepacia complex (Bcc) seringkali ditemukan pada pasien cystic fibrosis (CF). Burkholderia pseudomallei merupakan kelompok bakteri patogen intracellular Gram negatif, memiliki bentuk seperti peniti. Demikian pula  B. cepacia  merupakan kelompok bakteri Gram negatif basil, tidak dapat membentuk spora, bersifat aerobik, katalase dan oksidase positif, serta mempunyai flagel polar multitrik.  Meskipun jalur patogenesis kedua  bakteri ini sedikit berbeda, faktor virulensi yang dimiliki oleh kedua spesies ini hampir sama. B. pseudomallei memiliki kemampuan untuk menginfeksi berbagai jenis sel dan menghindari respon imun manusia. Bakteri  ini masuk melalui kulit atau selaput lendir dan bereplikasi di sel epitel. Di dalam sel inang, bakteri bergerak dengan menginduksi polimerisasi aktin inang,  mendesak dinding membran membentuk tonjolan yang meluas ke sel lain. Tonjolan ini menyebabkan sel tersebut  bergabung, membentuk sel raksasa berinti (multinucleated giant cell /MNGC). MNGC akan membentuk plak sebagai tempat bagi bakteri untuk bereplikasi. Setelah memasuki saluran pernafasan pasien penderita CF, B. cepacia menempel pada permukaan sel mukosa ataupun sel epitel inang.  Lapisan mukus yang menebal pada paru mendukung efikasi antimikrobia dan meningkatkan respon inflamasi. Kemampuan untuk melewati barier epitelial dan menemukan akses ke aliran darah hanya dimiliki oleh strain kelompok ini karena patogen lain yang ditemukan pada pasien CF tidak menyebabkan bakteremia. Faktor virulensi bertugas  membantu proses invasi sel inang oleh bakteri patogen. Secara umum, kedua spesies ini memiliki jenis faktor virulensi yang sama, diantaranya adalah  intracellular survival, quorum sensing, adherence factor, sistem sekresi, LPS dan EPS,  biofilm, toksin dan resistensi antimikrobia.

2020 ◽  
Vol 64 (2) ◽  
pp. 87-98 ◽  
Author(s):  
Pitchaipillai Sankar Ganesh ◽  
Sivakumar Vishnupriya ◽  
Jamuna Vadivelu ◽  
Vanitha Mariappan ◽  
Kumutha M. Vellasamy ◽  
...  

2008 ◽  
Vol 190 (15) ◽  
pp. 5339-5352 ◽  
Author(s):  
Ludovic Vial ◽  
François Lépine ◽  
Sylvain Milot ◽  
Marie-Christine Groleau ◽  
Valérie Dekimpe ◽  
...  

ABSTRACT 4-Hydroxy-2-alkylquinolines (HAQs), especially 3,4-dihydroxy-2-heptylquinoline (Pseudomonas quinolone signal) and its precursor, 4-hydroxy-2-heptylquinoline, are attracting much attention, mainly because of their role as signaling molecules in Pseudomonas aeruginosa. The pqsABCDE operon is centrally involved in their biosynthesis. The presence of a homologous operon in Burkholderia pseudomallei and B. thailandensis was recently reported. Thus, we have investigated the abilities of 11 Burkholderia species to produce HAQ-like molecules by liquid chromatography/mass spectrometry. We have identified 29 different HAQ derivatives produced by the only three Burkholderia species where a pqsABCDE homologue was found among available sequenced Burkholderia species genomes, including B. ambifaria, a member of the Burkholderia cepacia complex. In contrast with those of P. aeruginosa, Burkholderia HAQs typically bear a methyl group, hence their designation as 4-hydroxy-3-methyl-2-alkylquinolines (HMAQs). We identified three families of HMAQs with a saturated or unsaturated alkyl chain at the 2′ position, in contrast with the 1′ position of P. aeruginosa, including one with an N-oxide group. Furthermore, the operon in these species contains two more genes downstream of the pqsE homologue, resulting in the hmqABCDEFG operon. While the inactivation of hmqA inhibits the production of HMAQs, the methylation of the quinoline ring requires a putative methyltransferase encoded by hmqG. Interestingly, hmqA or hmqG mutations increase the production of acyl homoserine lactones and, consequently, phenotypes under the control of quorum sensing in B. ambifaria: antifungal activity, siderophore production, and proteolytic activity. These results indicate that only HAQs bearing a methyl group (HMAQs) are involved in quorum-sensing regulation.


2014 ◽  
Vol 14 (1) ◽  
pp. 98 ◽  
Author(s):  
Gianluca Pegoraro ◽  
Brett P Eaton ◽  
Ricky L Ulrich ◽  
Douglas J Lane ◽  
Jenifer F Ojeda ◽  
...  

2011 ◽  
Vol 203 (3) ◽  
pp. 383-392 ◽  
Author(s):  
Suzanne A. McKeon ◽  
David T. Nguyen ◽  
Duber F. Viteri ◽  
James E. A. Zlosnik ◽  
Pamela A. Sokol

2002 ◽  
Vol 48 (8) ◽  
pp. 707-716 ◽  
Author(s):  
Shawn Lewenza ◽  
Michelle B Visser ◽  
Pamela A Sokol

Burkholderia cepacia and Pseudomonas aeruginosa are opportunistic pathogens that commonly cause pulmonary infections in cystic fibrosis patients and occasionally co-infect patients' lungs. Both organisms possess quorum-sensing systems dependent on N-acyl homoserine lactone (N-acyl-HSL). Cross-feeding assays demonstrated that P. aeruginosa and B. cepacia were able to utilize heterologous N-acyl-HSL signaling molecules. The ability of quorum-sensing genes from one species to complement the respective quorum-sensing mutations in the heterologous species was also examined. These studies suggest that B. cepacia CepR can use N-acyl-HSLs synthesized by RhlI and LasI and that P. aeruginosa LasR and RhlR can use N-acyl-HSLs synthesized by CepI. It is possible that a mixed bacterial population of B. cepacia and P. aeruginosa can coordinately regulate some of their virulence factors and influence the progression of lung disease due to infection with these organisms.Key words: quorum sensing, Burkholderia cepacia, Pseudomonas aeruginosa, cystic fibrosis.


2019 ◽  
Vol 20 (8) ◽  
pp. 1838 ◽  
Author(s):  
Scoffone ◽  
Trespidi ◽  
Chiarelli ◽  
Barbieri ◽  
Buroni

Cystic fibrosis (CF) is an autosomal recessive genetic disorder which leads to the secretion of a viscous mucus layer on the respiratory epithelium that facilitates colonization by various bacterial pathogens. The problem of drug resistance has been reported for all the species able to colonize the lung of CF patients, so alternative treatments are urgently needed. In this context, a valid approach is to investigate new natural and synthetic molecules for their ability to counteract alternative pathways, such as virulence regulating quorum sensing (QS). In this review we describe the pathogens most commonly associated with CF lung infections: Staphylococcus aureus, Pseudomonas aeruginosa, species of the Burkholderia cepacia complex and the emerging pathogens Stenotrophomonas maltophilia, Haemophilus influenzae and non-tuberculous Mycobacteria. For each bacterium, the QS system(s) and the molecules targeting the different components of this pathway are described. The amount of investigations published in the last five years clearly indicate the interest and the expectations on antivirulence therapy as an alternative to classical antibiotics.


mBio ◽  
2017 ◽  
Vol 8 (2) ◽  
Author(s):  
Linda T. Viberg ◽  
Derek S. Sarovich ◽  
Timothy J. Kidd ◽  
James B. Geake ◽  
Scott C. Bell ◽  
...  

ABSTRACT Cystic fibrosis (CF) is a genetic disorder characterized by progressive lung function decline. CF patients are at an increased risk of respiratory infections, including those by the environmental bacterium Burkholderia pseudomallei, the causative agent of melioidosis. Here, we compared the genomes of B. pseudomallei isolates collected between ~4 and 55 months apart from seven chronically infected CF patients. Overall, the B. pseudomallei strains showed evolutionary patterns similar to those of other chronic infections, including emergence of antibiotic resistance, genome reduction, and deleterious mutations in genes involved in virulence, metabolism, environmental survival, and cell wall components. We documented the first reported B. pseudomallei hypermutators, which were likely caused by defective MutS. Further, our study identified both known and novel molecular mechanisms conferring resistance to three of the five clinically important antibiotics for melioidosis treatment. Our report highlights the exquisite adaptability of microorganisms to long-term persistence in their environment and the ongoing challenges of antibiotic treatment in eradicating pathogens in the CF lung. Convergent evolution with other CF pathogens hints at a degree of predictability in bacterial evolution in the CF lung and potential targeted eradication of chronic CF infections in the future. IMPORTANCE Burkholderia pseudomallei, the causative agent of melioidosis, is an environmental opportunistic bacterium that typically infects immunocompromised people and those with certain risk factors such as cystic fibrosis (CF). Patients with CF tend to develop chronic melioidosis infections, for reasons that are not well understood. This report is the first to describe B. pseudomallei evolution within the CF lung during chronic infection. We show that the pathways by which B. pseudomallei adapts to the CF lung are similar to those seen in better-studied CF pathogens such as Pseudomonas aeruginosa, Staphylococcus aureus, and Burkholderia cepacia complex species. Adaptations include the accumulation of antibiotic resistance, loss of nonessential genes, metabolic alterations, and virulence factor attenuation. Known and novel mechanisms of resistance to three of the five antibiotics used in melioidosis treatment were identified. Similar pathways of evolution in CF pathogens, including B. pseudomallei, provide exciting avenues for more-targeted treatment of chronic, recalcitrant infections. IMPORTANCE Burkholderia pseudomallei, the causative agent of melioidosis, is an environmental opportunistic bacterium that typically infects immunocompromised people and those with certain risk factors such as cystic fibrosis (CF). Patients with CF tend to develop chronic melioidosis infections, for reasons that are not well understood. This report is the first to describe B. pseudomallei evolution within the CF lung during chronic infection. We show that the pathways by which B. pseudomallei adapts to the CF lung are similar to those seen in better-studied CF pathogens such as Pseudomonas aeruginosa, Staphylococcus aureus, and Burkholderia cepacia complex species. Adaptations include the accumulation of antibiotic resistance, loss of nonessential genes, metabolic alterations, and virulence factor attenuation. Known and novel mechanisms of resistance to three of the five antibiotics used in melioidosis treatment were identified. Similar pathways of evolution in CF pathogens, including B. pseudomallei, provide exciting avenues for more-targeted treatment of chronic, recalcitrant infections.


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