Water, a frequent vehicle for the transmission of viruses, may permit their survival, but many environmental factors will have an adverse effect on the viral population. Risk evaluation requires identification of these factors and assessment of the inactivation rate of infectious viruses. A higher temperature means a faster reduction of the viral population, as do increased sunlight, higher antimicrobial concentration, or higher oxygen levels. Another documented impact is linked to the presence of indigenous microbial populations: virus survival is higher in sterile water. Environmental factors inactivate viruses through direct or indirect action on one part of the viral structure: genome, capsid, or envelope if present. Viral populations also have resistance mechanisms, generally involving physical shielding from adverse effects; such protective behaviors include aggregation, adhesion, or internalization inside living structures. Because of these phenomena, inactivation kinetics may deviate from traditional log-linear shapes. It is therefore important to account for all factors that may impact on survival, to carefully design experiments to ensure sufficient data, and to select the right modelling approach. Comparison between studies is difficult. It is suggested that laboratory studies include standard conditions of water, and analyze the impact of different factors as precisely as possible. Larger studies in natural environments, though more difficult, are also much needed.
One hundred one strains of Listeria monocytogenes isolated from seafood and cheese industry samples and from patients with listeriosis were assessed using a microtiter plate method for adhesion to polystyrene and stainless steel surfaces. The adhesion rate for these strains ranged from 3.10 to 35.29% with an inoculum of 8 x 10(8) cells per well. A strong correlation was found between adhesion to polystyrene and stainless steel microtiter plates, indicating that the intrinsic ability of L. monocytogenes to adhere to inert surfaces is stronger than the influence of the surface's physicochemical properties. The clinical strains were less adherent to inert surfaces than were the industrial strains. By integrating other factors such as location of the industrial strains, contamination type of the clinical strains, serotype, and pulsotype into the analysis, some weak but significant differences were noted. For the industrial isolates, the number of cells attached to both surfaces differed significantly depending on whether they were isolated from food or food-processing environments in the seafood and cheese industry. For clinical isolates, sporadic strains exhibited greater adhesion to polystyrene than did epidemic strains. Strains belonging to the pulsed-field gel electrophoretype clusters A and M (lineages II and I, respectively) were less able to adhere to polystyrene and stainless steel than were strains in the more common clusters.
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