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Co-infected hosts, individuals that carry more than one infectious agent at any one time, have been suggested to facilitate pathogen transmission, including the emergence of supershedding events. However, how the host immune response mediates the interactions between co-infecting pathogens and how these affect the dynamics of shedding remains largely unclear. We used laboratory experiments and a modeling approach to examine temporal changes in the shedding of the respiratory bacterium Bordetella bronchiseptica in rabbits with one or two gastrointestinal helminth species. Experimental data showed that rabbits co-infected with one or both helminths shed significantly more B. bronchiseptica, by direct contact with an agar petri dish, than rabbits with bacteria alone. Co-infected hosts generated supershedding events of higher intensity and more frequently than hosts with no helminths. To explain this variation in shedding an infection-immune model was developed and fitted to rabbits of each group. Simulations suggested that differences in the magnitude and duration of shedding could be explained by the effect of the two helminths on the relative contribution of neutrophils and specific IgA and IgG to B. bronchiseptica neutralization in the respiratory tract. However, the interactions between infection and immune response at the scale of analysis that we used could not capture the rapid variation in the intensity of shedding of every rabbit. We suggest that fast and local changes at the level of respiratory tissue probably played a more important role. This study indicates that co-infected hosts are important source of variation in shedding, and provides a quantitative explanation into the role of helminths to the dynamics of respiratory bacterial infections. [ABSTRACT FROM AUTHOR]

The primary concern of PM2.5 (particle size of an aerodynamic diameter 2.5 micrometers or less) is its adverse health effects. As not all PM2.5 particles are equally toxic, a uniform PM2.5 mass control across the emitting sources may not provide the maximum health benefits. A new approach that apportions PM2.5 constituents, based on their toxicity and further realigns them into the sources, is developed and applied to Delhi city. In PM2.5, concentrations of 81 constituents in 11 apportioned sources were derived. Fourteen carcinogen constituents (Pb, Cr, Ni, Cd, As, Co and eight PAHs) were considered. The USEPA's CompTox was used to obtain the cancer threshold concentration (Cca) of the constituents. A product of constituent concentration and the inverse of Cca yielded constituent-wise cancer potential (CCPca). The source-wise cancer potential was 20% for diesel, 19% for road dust, 16% for coal power plant, 13% for municipal solid waste burning and 8% for gasoline vehicles. Among 14 carcinogen constituents, Cr accounted for 20% of mass but showed the maximum CCPca. The net incremental lifetime cancer risk (NILCR) for all sources was 4.2 × 10−4. Diesel showed the maximum NILCR at 8.5 × 10−5 and liquid petroleum gas lowest at 8.8 × 10−6. [ABSTRACT FROM AUTHOR]

Abstract Background The role of host immunity has been recognized as not only playing a fundamental role in the interaction between the host and pathogen but also in influencing host infectiousness and the ability to shed pathogens. Despite the interest in this area of study, and the development of theoretical work on the immuno-epidemiology of infections, little is known about the immunological processes that influence pathogen shedding patterns. Results We used the respiratory bacterium Bordetella bronchiseptica and its common natural host, the rabbit, to examine the intensity and duration of oro-nasal bacteria shedding in relation to changes in the level of serum antibodies, blood cells, cytokine expression and number of bacteria colonies in the respiratory tract. Findings show that infected rabbits shed B. bronchiseptica by contact up to 4.5 months post infection. Shedding was positively affected by number of bacteria in the nasal cavity (CFU/g) but negatively influenced by serum IgG, which also contributed to the initial reduction of bacteria in the nasal cavity. Three main patterns of shedding were identified: i- bacteria were shed intermittently (46% of individuals), ii- bacteria shedding fell with the progression of the infection (31%) and iii- individuals never shed bacteria despite being infected (23%). Differences in the initial number of bacteria shed between the first two groups were associated with differences in the level of serum antibodies and white blood cells. These results suggest that the immunological conditions at the early stage of the infection may play a role in modulating the long term dynamics of B. bronchiseptica shedding. Conclusions We propose that IgG influences the threshold of bacteria in the oro-nasal cavity which then affects the intensity and duration of individual shedding. In addition, we suggest that a threshold level of infection is required for shedding, below this value individuals never shed bacteria despite being infected. The mechanisms regulating these interactions are still obscure and more studies are needed to understand the persistence of bacteria in the upper respiratory tract and the processes controlling the intensity and duration of shedding.