Abstract
The increasing prevalence of infections caused by multidrug-resistant Klebsiella pneumoniae necessitates the development of alternative therapies. Here, we isolated, characterized, and sequenced a K. pneumoniae bacteriophage (SH-KP152226) that specifically infects and lyses K. pneumoniae capsular type K47. The phage SH-KP152226 contains a genome of 41,420 bp that encodes 48 predicted proteins. Among these proteins, Dep42, the gene product of ORF42, is a putative tail fiber protein and hypothetically possesses depolymerase activity. We demonstrated that recombinant Dep42 showed specific enzymatic activities in the depolymerization of the K47 capsule of K. pneumoniae and was able to significantly inhibit biofilm formation and/or degrade formed biofilms. We also showed that Dep42 could enhance polymyxin activity against K. pneumoniae biofilms when used in combination with antibiotics. These results suggest that combination of the identified novel depolymerase Dep42, encoded by the phage SH-KP152226, with antibiotics may represent a promising strategy to combat infections caused by drug-resistant and biofilm-forming K. pneumoniae.
Highlights
Klebsiella pneumoniae is an opportunistic bacterial pathogen that causes a wide range of nosocomial infections
The Multilocus sequence typing (MLST) results indicated that all five K47-type, all three K64-type, and one K38-type isolates belonged to the ST11 type (Table 1)
As type K47 and type K64 were the predominant carbapenemresistant Klebsiella pneumoniae (CRKP) strains in China (66.1 and 18.3%, respectively) (Liu et al, 2017) and type ST11 was the most prevalent CRKP strain (Qi et al, 2011), it is not surprising that all strains of types K47 and K64 in this study belonged to the ST11 type (Table 1)
Summary
Klebsiella pneumoniae is an opportunistic bacterial pathogen that causes a wide range of nosocomial infections. It widely colonizes the human mouth, skin, respiratory tract, and digestive tract under normal physiological conditions. One of the crucial pathogenic factors of K. pneumoniae is the capsular polysaccharide (CPS), which either exists on the surface of the bacterial cells or is released to the surrounding environment as an exopolysaccharide. The extracellular polysaccharide (EPS) released by K. pneumoniae may contribute to biofilm formation (Li et al, 2014), which confers high tolerance against antimicrobial agents to the bacteria and potentially leads to severe persistent infections (Anderl et al, 2000; Dowd et al, 2008). Due to the inherent tolerance of biofilms to antimicrobial agents, there is a growing need for the development of alternate strategies to control biofilm-associated infections (Ansari et al, 2014)
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