Abstract
We characterized two bacteriophages, ΦFG02 and ΦCO01, against clinical isolates of Acinetobacter baumannii and established that the bacterial capsule is the receptor for these phages. Phage-resistant mutants harboured loss-of-function mutations in genes responsible for capsule biosynthesis, resulting in capsule loss and disruption of phage adsorption. The phage-resistant strains were resensitized to human complement, beta-lactam antibiotics and alternative phages and exhibited diminished fitness in vivo. Using a mouse model of A. baumannii infection, we showed that phage therapy was effective.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acinetobacter Infections / microbiology*
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Acinetobacter Infections / therapy*
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Acinetobacter baumannii / drug effects
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Acinetobacter baumannii / genetics
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Acinetobacter baumannii / virology*
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Animals
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Anti-Bacterial Agents / pharmacology*
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Bacterial Capsules / virology
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Bacteriophages / physiology*
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Complement System Proteins / pharmacology
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Disease Models, Animal
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Drug Resistance, Bacterial
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Female
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Humans
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Loss of Function Mutation
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Mice
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Mice, Inbred BALB C
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Microbial Sensitivity Tests
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Phage Therapy*
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beta-Lactamase Inhibitors / pharmacology
Substances
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Anti-Bacterial Agents
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beta-Lactamase Inhibitors
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Complement System Proteins