Biophysicochemical characterization of Pyocin SA189 produced by Pseudomonas aeruginosa SA189

Abstract Pseudomonas aeruginosa, in spite of being a ubiquitous organism (as it is found in soil, water, and humans), is also an opportunistic pathogen. In order to maintain its diversity in the community, it produces various toxic proteins, known as, bacteriocins. In the present study, pyocin SA189, which is a bacteriocin produced by P. aeruginosa SA189 (isolated from a clinical sample) was characterized. P. aeruginosa SA189, as identified by the conventional and 16S rRNA gene amplification, produced pyocin SA189 of molecular weight of 66 k Da. The pyocin showed antimicrobial activity against several clinically relevant Gram-positive and Gram-negative bacteria and was substantially stable for wide ranges of temperature and pH. Furthermore, the pyocin also retained its biological activity upon treatment with metal ions, organic solvents, and various proteolytic and lipolytic enzymes. The data from the growth kinetics indicated that the maximum bacteriocin production occurred in the late log phase. Overall, our results signify the potential of pyocin SA189 as a bio-control agent.

Study of Pseudomonas aeruginosa causing ventilator associated pneumonia.

Ps. aeruginosa is a frequent and prominent cause of nosocomial pneumonia especially in persons on assisted ventilation in the intensive care units. In a year long surveillance of ventilator associated pneumonia (VAP) we isolated 42 strains from broncho alveolar lavage samples collected and processed from 102 patients. By pyocin typing 40 of the 42 strains could be typed into 39 types but this designation changed each time the test was repeated. SDS-PAGE analysis of the whole cell proteins grouped the 42 strains of Ps. aeruginosa into 20 groups. After ribotyping, using an 18 mer DIG labelled oligonucleotide to the conserved region of 16S rRNA gene, the strains were designated into 18 types. The major type contained 8 isolates, but there was no clustering of isolates, indicating that each infecting strain was acquired separately and not from a common source. It would, therefore, appear that cross infection with a single clone was not the predominant mode of Ps. aeruginosa infection causing VAP in our ICU.