Supplemental feeding drives endoparasite infection in wild boar in Western Spain.

Wildlife population management is thought to destabilize existing host-parasite equilibriums in opposing directions, that is, it may increase parasite success or host resilience once infection takes place. This process is of special importance for species such as the wild boar (Sus scrofa) that are managed for game purposes throughout much of Europe. However, little is known about how this practices influcences either gastrointestinal or pulmonary parasitism in the wild boar. Twelve hunting estates were chosen in order to study the relationship of management measures (feeder density, wild boar abundance, the ratio of wild boar per feeder and the percentage of sclerophyllous vegetation) and host factors (age and sex) with gastrointestinal and pulmonary parasite aggregation, richness, infection probability and intensity of infection. Parasitological analyses from 300 wild boar gastrointestinal and 269 respiratory tracts were performed for this purpose. A set of general linear models with combinations of the explanatory variables was built and the model with the smallest Akaike Information Criterion was selected as the best. The feeder density increased gastrointestinal parasite traits (richness, infection probability and intensity of infection), probably due to the contamination of feeding sites with infective parasite forms. Pulmonary parasite traits, on the other hand, were only influenced by host sex and age class, and parasite aggregation was as expected for a wild population. Managers should be aware of the consequences on parasitism when implementing supplemental feeding in hunting estates.

Effect of cattle on Salmonella carriage, diversity and antimicrobial resistance in free-ranging wild boar (Sus scrofa) in northeastern Spain.

Salmonella is distributed worldwide and is a pathogen of economic and public health importance. As a multi-host pathogen with a long environmental persistence, it is a suitable model for the study of wildlife-livestock interactions. In this work, we aim to explore the spill-over of Salmonella between free-ranging wild boar and livestock in a protected natural area in NE Spain and the presence of antimicrobial resistance. Salmonella prevalence, serotypes and diversity were compared between wild boars, sympatric cattle and wild boars from cattle-free areas. The effect of age, sex, cattle presence and cattle herd size on Salmonella probability of infection in wild boars was explored by means of Generalized Linear Models and a model selection based on the Akaike's Information Criterion. Prevalence was higher in wild boars co-habiting with cattle (35.67%, CI 95% 28.19-43.70) than in wild boar from cattle-free areas (17.54%, CI 95% 8.74-29.91). Probability of a wild boar being a Salmonella carrier increased with cattle herd size but decreased with the host age. Serotypes Meleagridis, Anatum and Othmarschen were isolated concurrently from cattle and sympatric wild boars. Apart from serotypes shared with cattle, wild boars appear to have their own serotypes, which are also found in wild boars from cattle-free areas (Enteritidis, Mikawasima, 4:b:- and 35:r:z35). Serotype richness (diversity) was higher in wild boars co-habiting with cattle, but evenness was not altered by the introduction of serotypes from cattle. The finding of a S. Mbandaka strain resistant to sulfamethoxazole, streptomycin and chloramphenicol and a S. Enteritidis strain resistant to ciprofloxacin and nalidixic acid in wild boars is cause for public health concern.

Missense mutation of the COQ2 gene causes defects of bioenergetics and de novo pyrimidine synthesis.

Coenzyme Q(10) (CoQ(10)) deficiency has been associated with an increasing number of clinical phenotypes that respond to CoQ(10) supplementation. In two siblings with encephalomyopathy, nephropathy and severe CoQ(10) deficiency, a homozygous mutation was identified in the CoQ(10) biosynthesis gene COQ2, encoding polyprenyl-pHB transferase. To confirm the pathogenicity of this mutation, we have demonstrated that human wild-type, but not mutant COQ2, functionally complements COQ2 defective yeast. In addition, an equivalent mutation introduced in the yeast COQ2 gene also decreases both CoQ(6) concentration and growth in respiratory-chain dependent medium. Polyprenyl-pHB transferase activity was 33-45% of controls in COQ2 mutant fibroblasts. CoQ-dependent mitochondrial complexes activities were restored in deficient fibroblasts by CoQ(10) supplementation, and growth rate was restored in these cells by either CoQ(10) or uridine supplementation. This work is the first direct demonstration of the pathogenicity of a COQ2 mutation involved in human disease, and establishes yeast as a useful model to study human CoQ(10) deficiency. Moreover, we demonstrate that CoQ(10) deficiency in addition to the bioenergetics defect also impairs de novo pyrimidine synthesis, which may contribute to the pathogenesis of the disease.