Small hive beetles, Aethina tumida, are vectors of Paenibacillus larvae

The transmission of honeybee pathogens by free-flying pests, such as small hive beetles (=SHB), would be independent of bees and beekeepers and thereby constitute a new challenge for pathogen control measures. Here we show that larval and adult SHB become contaminated with Paenibacillus larvae spores when exposed to honeybee brood combs with clinical American foulbrood (=AFB) symptoms in the laboratory. This contamination persists in pupae and newly emerged adults. After exposure to contaminated adult SHB, honeybee field colonies showed higher numbers of P. larvae spores in worker and honey samples after five weeks. Despite these results, the rather low number of P. larvae spores on adult SHB suggests that clinical AFB outbreaks are not likely. However, even small spore numbers can be sufficient to spread P. larvae. Therefore, our data clearly show that SHB are vectors of P. larvae. We suggest considering the role of SHB in AFB control in areas where both pests are established.

Enumerating constrained elementary flux vectors of metabolic networks

The concept of elementary vector is generalised to the case where the steady-state space of the metabolic network is not a flux cone but is a general polyhedron due to further inhomogeneous constraints on the flows through some of the reactions. On one hand, this allows to selectively enumerate elementary modes which satisfy certain optimality criteria and this can yield a large computational gain compared with full enumeration. On the other hand, in contrast to the single optimum found by executing a linear program, this enables a comprehensive description of the set of alternate optima often encountered in flux balance analysis. The concepts are illustrated on a metabolic network model of human cardiac mitochondria.

Climate change and infectious diseases of wildlife: Altered interactions between pathogens, vectors and hosts

Infectious diseases result from the interactions of host, pathogens, and, in the case of vector-borne diseases, also vectors. The interactions involve physiological and ecological mechanisms and they have evolved under a given set of environmental conditions. Environmental change, therefore, will alter host-pathogen-vector interactions and, consequently, the distribution, intensity, and dynamics of infectious diseases. Here, we review how climate change may impact infectious diseases of aquatic and terrestrial wildlife. Climate change can have direct impacts on distribution, life cycle, and physiological status of hosts, pathogens and vectors. While a change in either host, pathogen or vector does not necessarily translate into an alteration of the disease, it is the impact of climate change on the interactions between the disease components which is particularly critical for altered disease risks. Finally, climate factors can modulate disease through modifying the ecological networks host-pathogen-vector systems are belonging to, and climate change can combine with other environmental stressors to induce cumulative effects on infectious diseases. Overall, the influence of climate change on infectious diseases involves different mechanisms, it can be modulated by phenotypic acclimation and/or genotypic adaptation, it depends on the ecological context of the host-pathogen-vector interactions, and it can be modulated by impacts of other stressors. As a consequence of this complexity, non-linear responses of disease systems under climate change are to be expected. To improve predictions on climate change impacts on infectious disease, we suggest that more emphasis should be given to the integration of biomedical and ecological research for studying both the physiological and ecological mechanisms which mediate climate change impacts on disease, and to the development of harmonized methods and approaches to obtain more comparable results, as this would support the discrimination of case-specific versus general mechanisms

Molecular and macromolecular alterations of recombinant adenoviral vectors do not resolve changes in hepatic drug metabolism during infection.

In this report we test the hypothesis that long-term virus-induced alterations in CYP occur from changes initiated by the virus that may not be related to the immune response. Enzyme activity, protein expression and mRNA of CYP3A2, a correlate of human CYP3A4, and CYP2C11, responsive to inflammatory mediators, were assessed 0.25, 1, 4, and 14 days after administration of several different recombinant adenoviruses at a dose of 5.7 x 1012 virus particles (vp)/kg to male Sprague Dawley rats. Wild type adenovirus, containing all viral genes, suppressed CYP3A2 and 2C11 activity by 37% and 39%, respectively within six hours. Levels fell to 67% (CYP3A2) and 79% (CYP2C11) of control by 14 days (p