A method to quantify infectious airborne pathogens at concentrations below the threshold of quantification by culture.

In aerobiology, dose-response studies are used to estimate the risk of infection to a susceptible host presented by exposure to a specific dose of an airborne pathogen. In the research setting, host- and pathogen-specific factors that affect the dose-response continuum can be accounted for by experimental design, but the requirement to precisely determine the dose of infectious pathogen to which the host was exposed is often challenging. By definition, quantification of viable airborne pathogens is based on the culture of micro-organisms, but some airborne pathogens are transmissible at concentrations below the threshold of quantification by culture. In this paper we present an approach to the calculation of exposure dose at microbiologically unquantifiable levels using an application of the "continuous-stirred tank reactor (CSTR) model" and the validation of this approach using rhodamine B dye as a surrogate for aerosolized microbial pathogens in a dynamic aerosol toroid (DAT).

En aérobiologie, les études dose-réponse sont utilisées pour estimer le risque d'infection que représente pour un hôte susceptible l'exposition à une dose spécifique d'un agent pathogène en suspension dans l'air. Dans un environnement de recherche, les facteurs spécifiques à l'hôte et à l'agent qui affectent le continuum dose-réponse peuvent être tenus pour compte dans le design expérimental, mais l'obligation de déterminer précisément la dose d'agent pathogène à laquelle l'hôte a été exposée représente souvent un défi. Par définition, la quantification des agents pathogènes viables en suspension dans l'air est basée sur la culture des microorganismes, mais certains agents pathogènes aériens sont transmissibles à des concentrations inférieures au seuil de quantification par culture. Dans cet article nous présentons une approche pour le calcul de la dose d'exposition à des niveaux non-quantifiables microbiologiquement en utilisant une application du modèle de réaction en réservoir avec agitation continue (CSTR) et la validation de cette approche en utilisant le colorant rhodamine B comme substitut à des agents pathogènes microbiens mis en aérosol dans un tore dynamique (DAT).(Traduit par Docteur Serge Messier).

Effect of temperature and relative humidity on ultraviolet (UV 254) inactivation of airborne porcine respiratory and reproductive syndrome virus.

The objective of this research was to estimate the effects of temperature and relative humidity on the inactivation of airborne porcine reproductive and respiratory syndrome (PRRS) virus by ultraviolet light (UV(254)). Aerosols of PRRS virus were exposed to one of four doses of UV(254) under nine combinations of temperature (n=3) and relative humidity (n=3). Inactivation constants (k), defined as the absolute value of the slope of the linear relationship between the survival fraction of the microbial population and the UV(254) exposure dose, were estimated using the random coefficient model. The associated UV(254) half-life dose for each combination of environmental factors was determined as (log(10)2/k) and expressed as UV(254) mJ per unit volume. The effects of UV(254) dose, temperature, and relative humidity were all statistically significant, as were the interactions between UV(254) dose × temperature and UV(254) dose × relative humidity. PRRS virus was more susceptible to ultraviolet as temperature decreased; most susceptible to ultraviolet inactivation at relative humidity between 25% and 79%, less susceptible at relative humidity ≤ 24%, and least susceptible at ≥ 80% relative humidity. The current study allows for calculating the dose of UV(254) required to inactivate airborne PRRS virus under various laboratory and field conditions using the inactivation constants and UV(254) half-life doses reported therein.

Ultraviolet irradiation and the mechanisms underlying its inactivation of infectious agents.

We review the principles of ultraviolet (UV) irradiation, the inactivation of infectious agents by UV, and current applications for the control of microorganisms. In particular, wavelengths between 200 and 280 nm (germicidal UV) affect the double-bond stability of adjacent carbon atoms in molecules including pyrimidines, purines and flavin. Thus, UV inactivation of microorganisms results from the formation of dimers in RNA (uracil and cytosine) and DNA (thymine and cytosine). The classic application of UV irradiation is the inactivation of microorganisms in biological safety cabinets. In the food-processing industry, germicidal UV irradiation has shown potential for the surface disinfection of fresh-cut fruit and vegetables. UV treatment of water (potable and wastewater) is increasingly common because the process is effective against a wide range of microorganisms, overdose is not possible, chemical residues or by-products are avoided, and water quality is unaffected. UV has been used to reduce the concentration of airborne microorganisms in limited studies, but the technology will require further development if it is to gain wider application. For bioaerosols, the primary technical challenge is delivery of sufficient UV irradiation to large volumes of air, but the absence of UV inactivation constants for airborne pathogens under a range of environmental conditions (temperature, relative humidity) further compounds the problem.

Median infectious dose (ID50) of porcine reproductive and respiratory syndrome virus isolate MN-184 via aerosol exposure.

The median infectious dose (ID(50)) of porcine reproductive and respiratory syndrome (PRRS) virus isolate MN-184 was determined for aerosol exposure. In 7 replicates, 3-week-old pigs (n=58) respired 10l of airborne PRRS virus from a dynamic aerosol toroid (DAT) maintained at -4°C. Thereafter, pigs were housed in isolation and monitored for evidence of infection. Infection occurred at virus concentrations too low to quantify by microinfectivity assays. Therefore, exposure dose was determined using two indirect methods ("calculated" and "theoretical"). "Calculated" virus dose was derived from the concentration of rhodamine B monitored over the exposure sequence. "Theoretical" virus dose was based on the continuous stirred-tank reactor model. The ID(50) estimate was modeled on the proportion of pigs that became infected using the probit and logit link functions for both "calculated" and "theoretical" exposure doses. Based on "calculated" doses, the probit and logit ID(50) estimates were 1 × 10(-0.13)TCID(50) and 1 × 10(-0.14)TCID(50), respectively. Based on "theoretical" doses, the probit and logit ID(50) were 1 × 10(0.26)TCID(50) and 1 × 10(0.24)TCID(50), respectively. For each point estimate, the 95% confidence interval included the other three point estimates. The results indicated that MN-184 was far more infectious than PRRS virus isolate VR-2332, the only other PRRS virus isolate for which ID(50) has been estimated for airborne exposure. Since aerosol ID(50) estimates are available for only these two isolates, it is uncertain whether one or both of these isolates represent the normal range of PRRS virus infectivity by this route.