Melioidosis: Perbedaan antara revisi

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Bakteri dapat memasuki tubuh lewat luka, hirupan, dan [[penelanan|menelan]] air yang tercemar.<ref name="Joost 2018"/> Penularan dari orang ke orang sangat jarang terjadi.<ref name="Yi 2014"/> Melioidosis adalah penyakit yang diakui terhadap hewan semisal kucing, anjing, kambing, domba, dan kuda. Sapi, kerbau, dan buaya dianggap relatif resisten terhadap melioidosis meskipun terus-menerus terpapar air dan tanah yang mengandung bakteri ini. Burung juga resisten terhadap melioidosis.<ref name="Gassiep 2020"/><ref name="Allen C 2005"/> [[Zoonosis|Penularan dari hewan ke manusia]] jarang terjadi.<ref name="Joost 2018"/><ref name="Yi 2014"/>
 
[[Klorinasi air|Klorinasi]] pasokan air yang tidak memadai dikaitkan dengan wabah ''Burkholderia pseudomallei'' di Australia Utara dan Barat. Bakteri ini juga ditemukan dalam pasokan air yang tidak diklorinasi di pedesaan Thailand. Cairan pengairan yang terkontaminasi dengan ''Burkholderia pseudomallei'' dikaitkan dengan infeksi luka [[infeksi nosokomial|nosokomial]] di rumah sakit.<ref name="Joost 2018"/> BasedBerdasarkan on[[pengurutan thekeseluruhan wholegenom]] genomebakteri sequencing of the bacteriaini, humansmanusia maymungkin playberperan adalam role in movingmemindahkan ''B.&nbsp;Burkholderia pseudomallei'' fromdari satu tempat placeke totempat placelain.<ref>{{cite journal | vauthors = Baker A, Pearson T, Price EP, Dale J, Keim P, Hornstra H, Greenhill A, Padilla G, Warner J | display-authors = 6 | title = Molecular phylogeny of Burkholderia pseudomallei from a remote region of Papua New Guinea | journal = PLOS ONE | volume = 6 | issue = 3 | pages = e18343 | date = March 2011 | pmid = 21483841 | pmc = 3069084 | doi = 10.1371/journal.pone.0018343 | bibcode = 2011PLoSO...618343B | doi-access = free }} {{open access}}</ref>
 
== Patogenesis ==
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Manakala ''Burkholderia pseudomallei'' dapat bertahan hidup dalam sel fagosit, sel-sel fagosit ini dapat membunuh ''Burkholderia pseudomallei'' melalui beberapa mekanisme. Makrofag yang diaktifkan oleh [[interferon gamma]] menaikkan daya bunuh terhadap ''Burkholderiapseudomallei'' melalui produksi [[sintase oksida nitrat]] yang dapat diinduksi. Pengasaman endosom dan degradasi bakteri juga mungkin, tetapi kapsul bakteri dan LPS membuat ''Burkholderia pseudomallei'' resisten terhadap degradasi lisosom. Setelah ''Burkholderia pseudomallei'' lolos ke sitosol inang, bakteri ini dapat dikenali oleh [[reseptor pengenal pola]] seperti [[reseptor mirip NOD]], sehingga memicu pembentukan [[inflamasom]] dan aktivasi [[kaspase 1]] yang menginduksi kematian sel inang oleh [[piroptosis]] dan aktivasi lebih lanjut dari sel inang. sistem kekebalan tubuh. Beberapa pertahanan inang sistemik juga berkontribusi kepada respons imun. ''Burkholderia pseudomallei'' memicu [[sistem komplemen]] dan kaskade [[penggumpalan darah]], namun kapsul bakteri yang tebal mencegah aksi kompleks serangan membran komplemen.<ref name="Joost 2018"/><ref name="Gassiep 2020"/>
 
AdditionalUnsur elementstambahan ofdari thesistem immuneimun systemdiaktifkan are activated by the hostoleh [[toll-likereseptor mirip receptortol]]s suchinang asseperti TLR2, TLR4, anddan TLR5 thatyang recognize themengenali [[pathogen-associatedpola molecularmolekul patternterkait patogen|conservedbagian-bagian piece]]sbakteri ofini theyang bacteriaterlindung suchdari kerusakan]] asseperti LPS anddan flagellaflagela. ThisAktivasi activationini resultsmenghasilkan in the production ofproduksi [[cytokinesitokin]]s such asseperti [[interleukin 1 beta]] (IL-1β) anddan [[interleukin -18]] (IL-18). IL-18 increases IFN production through [[natural killer cell]]s, while IL-1beta reduces the IFN production. These immune molecules drive the recruitment of other immune cells such as [[neutrophil]]s, [[dendritic cell]]s, [[B cell]]s, and [[T cell]]s to the site of infection. T cells seem to be particularly important for controlling ''B. pseudomallei''; T cell numbers are increased in survivors, and low T cell numbers are associated with a high risk of death from melioidosis. Despite this, HIV infection is not a risk factor for melioidosis. Although macrophages show deregulated [[cytokine]] responses in individuals with HIV infection, bacterial internalization and intracellular killing are still effective. People infected with ''B. pseudomallei'' develop antibodies against the bacteria, and people who live in endemic areas tend to have antibodies in their blood that recognize ''B. pseudomallei'', but the effectiveness of these antibodies at preventing melioidosis is unclear.<ref name="Joost 2018"/><ref name="Gassiep 2020"/>
 
''B. pseudomallei'' can remain latent in the human body from 19 to 29 years until it is reactivated during [[immunosuppression]] or stress response. The site of bacteria during latent infection and the mechanism by which they avoid immune recognition for years are both unclear. Amongst the mechanisms suggested are residing in the nucleus of the cell to prevent being digested, entering a stage of slower growth, antibiotic resistance, and genetic adaption to the host environment. [[Granuloma]]s (containing neutrophils, macrophages, lymphocytes, and multinucleated giant cells) formed at the infection site in melioidosis have been associated with latent infection in humans.<ref name="Joost 2018"/>