Habitat fragmentation matters more than habitat loss: The case of host-parasite interactions.

While ecologists agree that habitat loss has a substantial negative effect on biodiversity it is still very much a matter of debate whether habitat fragmentation has a lesser effect and whether this effect is positive or negative for biodiversity. Here, we assess the relative influence of tropical forest loss and fragmentation on the prevalence of vector-borne blood parasites of the genera Plasmodium and Haemoproteus in six forest bird species. We also determine whether habitat loss and fragmentation are associated with a rise or fall in prevalence. We sample more than 4000 individual birds from 58 forest sites in Guadeloupe and Martinique. Considering 34 host-parasite combinations independently and a fine characterization of the amount and spatial configuration of habitat, we use partial least square regressions to disentangle the relative effects of forest loss, forest fragmentation, landscape heterogeneity, and local weather conditions on spatial variability of parasite prevalence. Then we test for the magnitude and the sign of the effect of each environmental descriptor. Strikingly, we show that forest fragmentation explains twice as much of the variance in prevalence as habitat loss or landscape heterogeneity. In addition, habitat fragmentation leads to an overall rise in prevalence in Guadeloupe, but its effect is variable in Martinique. Both habitat loss and landscape heterogeneity exhibit taxon-specific effects. Our results suggest that habitat loss and fragmentation may have contrasting effects between tropical and temperate regions and that inter-specific interactions may not respond in the same way as more commonly used biodiversity metrics such as abundance and diversity.

The Nocardia cyriacigeorgica GUH-2 genome shows ongoing adaptation of an environmental Actinobacteria to a pathogen's lifestyle.

BACKGROUND: Nocardia cyriacigeorgica is recognized as one of the most prevalent etiological agents of human nocardiosis. Human exposure to these Actinobacteria stems from direct contact with contaminated environmental matrices. The full genome sequence of N. cyriacigeorgica strain GUH-2 was studied to infer major trends in its evolution, including the acquisition of novel genetic elements that could explain its ability to thrive in multiple habitats. RESULTS: N. cyriacigeorgica strain GUH-2 genome size is 6.19 Mb-long, 82.7% of its CDS have homologs in at least another actinobacterial genome, and 74.5% of these are found in N. farcinica. Among N. cyriacigeorgica specific CDS, some are likely implicated in niche specialization such as those involved in denitrification and RuBisCO production, and are found in regions of genomic plasticity (RGP). Overall, 22 RGP were identified in this genome, representing 11.4% of its content. Some of these RGP encode a recombinase and IS elements which are indicative of genomic instability. CDS playing part in virulence were identified in this genome such as those involved in mammalian cell entry or encoding a superoxide dismutase. CDS encoding non ribosomal peptide synthetases (NRPS) and polyketide synthases (PKS) were identified, with some being likely involved in the synthesis of siderophores and toxins. COG analyses showed this genome to have an organization similar to environmental Actinobacteria. CONCLUSION: N. cyriacigeorgica GUH-2 genome shows features suggesting a diversification from an ancestral saprophytic state. GUH-2 ability at acquiring foreign DNA was found significant and to have led to functional changes likely beneficial for its environmental cycle and opportunistic colonization of a human host.

Genome sequence of the human- and animal-pathogenic strain Nocardia cyriacigeorgica GUH-2.

The pathogenic strain Nocardia cyriacigeorgica GUH-2 was isolated from a fatal human nocardiosis case, and its genome was sequenced. The complete genomic sequence of this strain contains 6,194,645 bp, an average G+C content of 68.37%, and no plasmids. We also identified several protein-coding genes to which N. cyriacigeorgica's virulence can potentially be attributed.

Serotypes A1 and A2 of Mannheimia haemolytica are susceptible to genotypic, capsular and phenotypic variations in contrast to T3 and T4 serotypes of Bibersteinia (Pasteurella) trehalosi.

Mannheimia haemolytica and Bibersteinia (Pasteurella) trehalosi are the most common bacterial isolates that cause pulmonary diseases in ruminants worldwide. The disease is determined by specific serotypes found in cattle and small ruminants. The molecular epidemiology of strains involved in disease is important in the control of outbreaks as well as in the preparation of vaccines. This study aimed to detect the instability and variations of bacterial strains that may affect the analysis of epidemic strains, or the stability of vaccinal strains. Eight strains of M. haemolytica belonging to serotypes A1 and A2 and three B. trehalosi strains of the T3 and T4 serotypes were used. Strains were subjected to pulsed field gel electrophoresis (PFGE) and capsular and phenotypic typing at each round of a total of 50 successive subcultures. Remarkable stability was found in all selected strains of B. trehalosi in contrast to M. haemoltyica, in which strains of both serotypes showed pattern variations produced by PFGE and capsular and phenotypic analysis. Objective criteria for M. haemolytica and B. trehalosi typing are consequently addressed.

PrP(d) accumulation in organs of ARQ/ARQ sheep experimentally infected with BSE by peripheral routes.

To study the pathogenesis of bovine spongiform encephalopathy infection in small ruminants, two Lacaune sheep with the AA136RR154QQ171 and one with the AA136RR154RR171 genotype for the prion protein, were inoculated with a brain homogenate from a French cattle BSE case by peripheral routes. Sheep with the ARQ/ARQ genotype are considered as susceptible to prion diseases contrary to those with the ARR/ARR genotype. The accumulation of disease-associated prion protein (PrP(d)) was analysed by biochemical and immunohistochemical methods. No PrP(d) accumulation was detected in samples from the ARR/ARR sheep 2 years post inoculation. In the two ARQ/ARQ sheep that had scrapie-like clinical symptoms, PrP(d) was found in the central, sympathetic and enteric nervous systems and in lymphoid organs. Remarkably, PrP(d) was also detected in some muscle types as well as in all peripheral nerves that had not been reported previously thus revealing a widespread distribution of BSE-associated PrP(d) in sheep tissues.

Kinetics and metabolic specificities of Vero cells in bioreactor cultures with serum-free medium.

The aim of this study was to understand the metabolism kinetics of Vero cells grown on microcarriers in bioreactors in serum-free medium (SFM). We sought to determine what nutrients are essential for Vero cells and how they are consumed. Contrary to glucose and to most of the amino acids, glutamine and serine were very quickly depleted in this medium and can be supposed to be responsible for cell apoptosis. Lactate and ammonium ions did not reach toxic levels for Vero cells. We payed more attention to the lactate metabolism. Usually we observed that after about 2 days lactate was consumed in serum-containing media, but its concentration plateaud in SFM. Moreover, the addition of serum in SFM provoked lactate consumption and the rate of glucose and glutamine consumption was twice as high as in the SFM not supplemented with serum. The depletion of glutamine and serine and the metabolic deviations leading to a shortage of intermediate products required for other metabolic pathways probably contribute to the lower cell yield and higher cell death rate in SFM.