Q-276. Mechanisms of Viricidal Action of the Polyhexamethylene Biguanides (PHMB)

F. Pinto1, J. Maillard1, S. Denyer1, P. McGeechan2;
1Cardiff Univ., Cardiff, UNITED KINGDOM, 2ArchChemicals, Manchester, UNITED KINGDOM.

Background - Annually, 4-10% of the hospitalized patients acquired infections, causing 5000 deaths in the UK and 17500-70000 in the USA, causing an estimated one billion pounds per year in the UK and between 17 and 25 billion dollars in the USA. The main cause of nosocomial infections is contamination of hospital equipments. Viruses are the most common pathogens responsible for ward closure after an outbreak. The use of biocides in disinfection procedures is an important preventive measure, although there is generally a lack of information on their viricidal efficacy. Biguanides are biocides that are heavily used for disinfection and antisepsis. It is accepted that these cationic biocides are generally more active against enveloped viruses as they are classed as membrane active agents. To understand better the interaction of biguanides against viruses, we investigated the activity and effect of polyhexamethylene biguanide-based disinfectants against MS2 and F116 bacteriophages used as virus models. Methods - To understand the interaction of PHMB with viruses, a number of protocols were used and validated, including standard suspension tests, SDS-page and electron microscopy (EM). Results - Vantocil and Cosmocil, both containing polyhexamethylene biguanides at 200 and 800 ppm, were found to reduce the viability of F116 and MS2, by 1-2 Log10 PFU/ml, respectively. Inactivation kinetic presented a “tailing off” curve, indicating a rapid initial inactivation followed by the persistence of a “more resistant subpopulations”. EM investigation and protein assay suggested that MS2 and F116 were structurally damaged by PHMBs. Furthermore, EM pictures and knowledge of the phage isoelectric point lead to the conclusion that hydrophobic forces during the treatment induced aggregation. Conclusion - PHMB interacted with the phage structure damaging the capsid. The limited viricidal activity could be the result of the formation of aggregates, which have been described as a form of viral resistance to biocides. The formation of aggregates and the low activity were both supported by EM and the tailing curve observed with the inactivation kinetic.