Evolution of Salmonella enterica Virulence via Point Mutations in the Fimbrial Adhesin

Whereas the majority of pathogenic Salmonella serovars are capable of infecting many different animal species, typically producing a self-limited gastroenteritis, serovars with narrow host-specificity exhibit increased virulence and their infections frequently result in fatal systemic diseases. In our study, a genetic and functional analysis of the mannose-specific type 1 fimbrial adhesin FimH from a variety of serovars of Salmonella enterica revealed that specific mutant variants of FimH are common in host-adapted (systemically invasive) serovars. We have found that while the low-binding shear-dependent phenotype of the adhesin is preserved in broad host-range (usually systemically non-invasive) Salmonella, the majority of host-adapted serovars express FimH variants with one of two alternative phenotypes: a significantly increased binding to mannose (as in S. Typhi, S. Paratyphi C, S. Dublin and some isolates of S. Choleraesuis), or complete loss of the mannose-binding activity (as in S. Paratyphi B, S. Choleraesuis and S. Gallinarum). The functional diversification of FimH in host-adapted Salmonella results from recently acquired structural mutations. Many of the mutations are of a convergent nature indicative of strong positive selection. The high-binding phenotype of FimH that leads to increased bacterial adhesiveness to and invasiveness of epithelial cells and macrophages usually precedes acquisition of the non-binding phenotype. Collectively these observations suggest that activation or inactivation of mannose-specific adhesive properties in different systemically invasive serovars of Salmonella reflects their dynamic trajectories of adaptation to a life style in specific hosts. In conclusion, our study demonstrates that point mutations are the target of positive selection and, in addition to horizontal gene transfer and genome degradation events, can contribute to the differential pathoadaptive evolution of Salmonella

Global lake responses to climate change

Climate change is one of the most severe threats to global lake ecosystems. Lake surface conditions, such as ice cover, surface temperature, evaporation and water level, respond dramatically to this threat, as observed in recent decades. In this Review, we discuss physical lake variables and their responses to climate change. Decreases in winter ice cover and increases in lake surface temperature modify lake mixing regimes and accelerate lake evaporation. Where not balanced by increased mean precipitation or inflow, higher evaporation rates will favour a decrease in lake level and surface water extent. Together with increases in extreme-precipitation events, these lake responses will impact lake ecosystems, changing water quantity and quality, food provisioning, recreational opportunities and transportation. Future research opportunities, including enhanced observation of lake variables from space (particularly for small water bodies), improved in situ lake monitoring and the development of advanced modelling techniques to predict lake processes, will improve our global understanding of lake responses to a changing climate

Influence of macronutrient composition of commercial diets on circulating leptin and adiponectin concentrations in overweight dogs

Leptin and adiponectin play important roles in obesity-related inflammation and comorbidities. Previous research suggests that alterations in dietary macronutrient composition can modify circulating leptin and adiponectin concentrations in people, but limited research on this subject has been performed in dogs. This study investigated the effects of commercial high protein (HP), high fat (HF) and high carbohydrate medium protein (HCMP) diets on baseline (T-1 ) concentrations, post-prandial peak concentrations and total release in a ten-hour time span of leptin and adiponectin in dogs, when compared to a maintenance high carbohydrate low protein (HCLP) diet. Thirty-six overweight dogs were fed the HCLP diet in a one-week control period, after which the animals were assigned to one of three groups. In three four-week periods, each group was fed all test diets in a different sequence. At the last day of each period, blood was sampled at one hour before feeding (T-1 ) and at three (T3 ), six (T6 ) and nine (T9 ) hours after feeding. Feeding caused peak leptin concentrations at T6 and T9 (p < .001). No significant post-prandial change in adiponectin concentrations was found (p = .056). The HP diet resulted in lower leptin peak concentrations (p = .004) and AUCT-1-T9 (p = .01), but none of the diets influenced baseline leptin concentrations (p = .273). Baseline adiponectin concentrations were lower for the HF diet (p = .018) and HCMP (p < .001), and the HP, HF and HCMP AUCT-1-T9 (p < .001) were lower compared with the HCLP diet. Female dogs had lower adiponectin baseline concentrations (p = .041) and AUCT-1-T9 (p = .023) than male dogs. In conclusion, the HP diet was associated with the lowest post-prandial peak leptin concentration and the least decrease in adiponectin release, suggesting that a HP diet may improve immune-metabolic health and post-prandial satiety in overweight dogs