İnfeksiyon: Yarada Biyofilm Oluşumu ve Engellenmesi
Özet
Yarada biyofilm, mikroorganizmaların canlı veya cansız yüzeylere geri dönüşümsüz tutunarak ekstrasellüler polimerik yapıda bir matriks (EPS) içinde oluşturduğu topluluktur. Kronik yaraların yaklaşık %78.2'sinde bulunan biyofilm, yara iyileşmesini geciktiren ve yarayı tek başına kronikleştiren kritik bir faktördür. Biyofilm oluşumu; planktonik hücrelerin yapışması, quorum sensing (QS) ile iletişim kurarak gen değişimi yapması, EPS üretimi, olgunlaşma ve bakterilerin ayrılarak yeni döngü başlatması olmak üzere beş dinamik aşamada gerçekleşir. Bakterilerin yapışması dakikalar içinde olurken, biyofilm 2-4 günde olgunlaşır. Biyofilm engellenmesinde; hücreler arası iletişimi bozan QS inhibitörleri, yüzeye yapışmayı önleyen anti-adezinler, sortaz inhibitörleri ile laktoferrin kullanılmaktadır. Ayrıca nonsteroid anti-inflamatuar ajanlar ve antimikrobiyal peptitler de oluşumu baskılar. Biyofilm tedavisinde ise tek başına bir yöntem yetersiz olup multidisipliner "biyofilm odaklı yara tedavisi" uygulanır. EPS matrisi ve düşük metabolik aktivite nedeniyle biyofilmler antibiyotiklere karşı 10 ila 1000 kat daha dirençlidir. Tedavide en önemli strateji cerrahi, mekanik, enzimatik veya biyolojik (maggot) yöntemlerle yapılan tekrarlı debridmandır. Debridman sonrası biyofilmin yeniden oluşmasını engellemek amacıyla daptomisin, tigesiklin gibi nüfuz edebilen antibiyotikler ile hipokloröz asit, PHMD, iyod ve bal gibi etkili topikal antiseptikler kombine edilir.
Biofilm in wounds is a community of microorganisms that irreversibly adhere to living or non-living surfaces and proliferate within an extracellular polymeric substance (EPS) matrix. Found in approximately 78.2% of chronic wounds, biofilm is a critical factor that delays wound healing and renders the wound chronic on its own. Biofilm formation progresses through five dynamic stages: accumulation of planktonic cells, communication via quorum sensing (QS) to develop resistance through gene exchange, high EPS production, maturation, and detachment of bacteria to restart the cycle. While bacterial attachment occurs within minutes, the biofilm matures within 2 to 4 days. Strategies to prevent biofilm include QS inhibitors that disrupt intercellular communication, anti-adhesins, sortase inhibitors, and lactoferrin that block surface adherence. Additionally, nonsteroidal anti-inflammatory drugs and antimicrobial peptides suppress its formation. For biofilm treatment, a single modality is insufficient, necessitating a multidisciplinary "biofilm-based wound care" approach. Due to the EPS matrix and low metabolic activity, biofilms are 10 to 1000 times more resistant to antibiotics. The most crucial strategy in treatment is repeated debridement performed through surgical, mechanical, enzymatic, or biological (maggot) methods. To prevent the rapid regrowth of biofilm post-debridement, penetrable antibiotics such as daptomycin and tigecycline are combined with effective topical antiseptics including hypochlorous acid, PHMD, iodine, and honey.
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