Estimates of Avian Mortality Attributed to Vehicle Collisions in Canada

Although mortality of birds from collisions with vehicles is estimated to be in the millions in the USA, Europe, and the UK, to date, no estimates exist for Canada. To address this, we calculated an estimate of annual avian mortality attributed to vehicular collisions during the breeding and fledging season, in Canadian ecozones, by applying North American literature values for avian mortality to Canadian road networks. Because owls are particularly susceptible to collisions with vehicles, we also estimated the number of roadkilled Barn owls (Tyto alba) in its last remaining range within Canada. (This species is on the IUCN red list and is also listed federally as threatened; Committee on the Status of Endangered Wildlife in Canada 2010, International Union for the Conservation of Nature 2012). Through seven Canadian studies in existence, 80 species and 2,834 specimens have been found dead on roads representing species from 14 orders of birds. On Canadian 1 and 2-lane paved roads outside of major urban centers, the unadjusted number of bird mortalities/yr during an estimated 4-mo (122-d) breeding and fledging season for most birds in Canada was 4,650,137 on roads traversing through deciduous, coniferous, cropland, wetlands and nonagricultural landscapes with less than 10% treed area. On average, this represents 1,167 birds killed/100 km in Canada. Adjusted for scavenging, this estimate was 13,810,906 (3,462 dead birds/100 km). For barn owls, the unadjusted number of birds killed annually on 4-lane roads during the breeding and fledging season, within the species geographic range in southern British Columbia, was estimated as 244 owls and, when adjusted for scavenging and observer bias (3.6 factor), the total was 851 owls.

Avian mortalities due to transmission line collisions: a review of current estimates and field methods with an emphasis on applications to the Canadian electric network

Birds are vulnerable to collisions with human-made fixed structures. Despite ongoing development and increases in infrastructure, we have few estimates of the magnitude of collision mortality. We reviewed the existing literature on avian mortality associated with transmission lines and derived an initial estimate for Canada. Estimating mortality from collisions with power lines is challenging due to the lack of studies, especially from sites within Canada, and due to uncertainty about the magnitude of detection biases. Detection of bird collisions with transmission lines varies due to habitat type, species size, and scavenging rates. In addition, birds can be crippled by the impact and subsequently die, although crippling rates are poorly known and rarely incorporated into estimates. We used existing data to derive a range of estimates of avian mortality associated with collisions with transmission lines in Canada by incorporating detection, scavenging, and crippling biases. There are 231,966 km of transmission lines across Canada, mostly in the boreal forest. Mortality estimates ranged from 1 million to 229.5 million birds per year, depending on the bias corrections applied. We consider our most realistic estimate, taking into account variation in risk across Canada, to range from 2.5 million to 25.6 million birds killed per year. Data from multiple studies across Canada and the northern U.S. indicate that the most vulnerable bird groups are (1) waterfowl, (2) grebes, (3) shorebirds, and (4) cranes, which is consistent with other studies. Populations of several groups that are vulnerable to collisions are increasing across Canada (e.g., waterfowl, raptors), which suggests that collision mortality, at current levels, is not limiting population growth. However, there may be impacts on other declining species, such as shorebirds and some species at risk, including Alberta’s Trumpeter Swans (Cygnus buccinator) and western Canada’s endangered Whooping Cranes (Grus americana). Collisions may be more common during migration, which underscores the need to understand impacts across the annual cycle. We emphasize that these estimates are preliminary, especially considering the absence of Canadian studies.

Extinction processes in hotspots of avian biodiversity and the targeting of pre-emptive conservation action

Hot spots of endemism are regarded as important global sites for conservation as they are rich in threatened endemic species and currently experiencing extensive habitat loss. Targeting pre-emptive conservation action to sites that are currently relatively intact but which would be vulnerable to particular human activities if they occurred in the future is, however, also valuable but has received less attention. Here, we address this issue by using data on Endemic Bird Areas (EBAs). First, we identify the ecological factors that affect extinction risk in the face of particular human activities, and then use these insights to identify EBAs that should be priorities for pre-emptive conservation action. Threatened endemic species in EBAs are significantly more likely to be habitat specialists or relatively large-bodied than non-threatened species, when compared across avian families. Increasing habitat loss causes a significant increase in extinction risk among habitat specialists, but we found no evidence to suggest that the presence of alien species/human exploitation causes a significant increase in extinction risk among large-bodied species. This suggests that these particular human activities are contributing to high extinction risk among habitat specialists, but not among large-bodied species. Based on these analyses, we identify 39 EBAs containing 570 species (24% of the total in EBAs) that are not currently threatened with severe habitat loss, but would be ecologically vulnerable to future habitat loss should it occur. We show that these sites tend to be poorly represented in existing priority setting exercises involving hot spots, suggesting that vulnerability must be explicitly included within these exercises if such sites are to be adequately protected.

Origin of avian genome size and structure in non-avian dinosaurs

Avian genomes are small and streamlined compared with those of other amniotes by virtue of having fewer repetitive elements and less non-coding DNA(1,2). This condition has been suggested to represent a key adaptation for flight in birds, by reducing the metabolic costs associated with having large genome and cell sizes(3,4). However, the evolution of genome architecture in birds, or any other lineage, is difficult to study because genomic information is often absent for long-extinct relatives. Here we use a novel bayesian comparative method to show that bone-cell size correlates well with genome size in extant vertebrates, and hence use this relationship to estimate the genome sizes of 31 species of extinct dinosaur, including several species of extinct birds. Our results indicate that the small genomes typically associated with avian flight evolved in the saurischian dinosaur lineage between 230 and 250 million years ago, long before this lineage gave rise to the first birds. By comparison, ornithischian dinosaurs are inferred to have had much larger genomes, which were probably typical for ancestral Dinosauria. Using comparative genomic data, we estimate that genome-wide interspersed mobile elements, a class of repetitive DNA, comprised 5 - 12% of the total genome size in the saurischian dinosaur lineage, but was 7 - 19% of total genome size in ornithischian dinosaurs, suggesting that repetitive elements became less active in the saurischian lineage. These genomic characteristics should be added to the list of attributes previously considered avian but now thought to have arisen in non-avian dinosaurs, such as feathers(5), pulmonary innovations 6, and parental care and nesting

Alterations in receptor binding properties of recent human influenza H3N2 viruses are associated with reduced natural killer cell lysis of infected cells

Natural killer (NK) cell recognition of influenza virus-infected cells involves hemagglutinin (HA) binding to sialic acid (SA) on activating NK receptors. SA also acts as a receptor for the binding of influenza virus to its target host cells. The SA binding properties of H3N2 influenza viruses have been observed to change during circulation in humans: recent isolates are unable to agglutinate chicken red blood cells and show reduced affinity for synthetic glycopolymers representing SA-alpha-2,3-lactose (3'SL-PAA) and SA-alpha-2,6-N-acetyl lactosamine (6'SLN-PAA) carbohydrates. Here, NK lysis of cells infected with human H3N2 influenza viruses isolated between 1969 and 2003 was analyzed. Cells infected with recent isolates (1999 to 2003) were found to be lysed less effectively than cells infected with older isolates (1969 to 1996). This change occurred concurrently with the acquisition of two new potential glycosylation site motifs in RA. Deletion of the potential glycosylation site motif at 133 to 135 in HA1 from a recent isolate partially restored the agglutination phenotype to a recombinant virus, indicating that the HA-SA interaction is inhibited by the glycosylation modification. Deletion of either of the recently acquired potential glycosylation sites from HA led to increased NK lysis of cells infected with recombinant viruses carrying modified HA. These results indicate that alterations in RA glycosylation may affect NK cell recognition of influenza virus-infected cells in addition to virus binding to host cells.

Short report: human metapneumovirus in children with influenza-like illness in Yucatan, Mexico

The present study suggests that human metapneumovirus (hMPV) is an important cause of community acquired respiratory infections in children. We report the detection of hMPV in a pediatric population with influenza-like illness in the subtropical area of Yucatan in Mexico. Our data also shows that hMPV circulates in the community with other respiratory pathogens.

Variation in the ability of human influenza A viruses to induce and inhibit the IFN-beta pathway

We investigated the ability of a selection of human influenza A viruses, including recent clinical isolates, to induce IFN-beta production in cultured cell lines. In contrast to the well-characterized laboratory strain A/PR/8/34, several, but not all, recent isolates of H3N2 viruses resulted in moderate IFN-beta stimulation. Through the generation of recombinant viruses, we were able to show that this is not due to a loss of the ability of the NS1 genes to suppress IFN-beta induction; indeed, the NS1 genes behaved similarly with respect to their abilities to block dsRNA signaling. Interestingly, replication of A/Sydney/5/97 virus was less Susceptible to pre-treatment with IFN-alpha than the other viruses. In contrast to the universal effect on dsRNA signaling, we noted differences in the effect of NS1 proteins on expression of interferon stimulated genes and also genes induced by a distinct pathway. The majority of NS1 proteins blocked expression From both IFN-dependent and TNF-dependent promoters by an apparent post-transcriptional mechanism. The NS1 gene of A/PR/8/34 NS1 did not confer these blocks. We noted striking differences in the Cellular localization of different influenza A virus NS1 proteins during infection, which might explain differences in biological activity. (C) 2005 Elsevier Inc. All rights reserved.

Post dispersal weed seed predation by avian and non-avian predators

Seed predation by avian and non-avian predators was quantified in the boundaries and cropped areas of cereal fields by presenting known quantities of seed with and without exclusion cages. Predator encounter-rates with the dishes exceeded 99%. Birds removed on average 6.7% seed from the dishes during the seven-day trials compared to 51% by non-avian predators. A comparison was made of the causal factors responsible for predation of Avena fatua, Chenopodium album and Cirsium arvense seeds. A. fatua seeds were preyed most heavily by both avian and non-avian predators. Seed removal by birds was greater in the cropped area than in the field boundary, non-avian predators being generally more active in the field boundary. Seed predation by birds was greater in spring than in any other season, whilst losses to other animals were greater during autumn and winter. Although, birds were not the main seed predators in cereal fields, they may contribute to weed seed depletion, of relevance to reduced-input farming systems where herbicides use is restricted.

Characterization of recombinant influenza B viruses with key neuraminidase inhibitor resistance mutations

Objectives and methods: An influenza B virus plasmid-based rescue system was used to introduce site-specific mutations, previously observed in neuraminidase (NA) inhibitor-resistant viruses, into the NA protein of six recombinant viruses. Three mutations observed only among in vitro selected zanamivir-resistant influenza A mutants were introduced into the B/Beijing/1/87 virus NA protein, to change residue E116 to glycine, alanine or aspartic acid. Residue E116 was also mutated to valine, a mutation found in the clinic among oseltamivir-resistant viruses. An arginine to lysine change at position 291 (292 N2 numbering) mimicked that seen frequently in influenza A N2 clinical isolates resistant to oseltamivir. Similarly, an arginine to lysine change at position 149 (152 in N2 numbering) was made to reproduce the change found in the only reported zanamivir-resistant clinical isolate of influenza B virus. In vitro selection and prolonged treatment in the clinic leads to resistance pathways that require compensatory mutations in the haemagglutinin gene, but these appear not to be important for mutants isolated from immunocompetent patients. The reverse genetics system was therefore used to generate mutants containing only the NA mutation. Results and conclusions: With the exception of a virus containing the E116G mutation, mutant viruses were attenuated to different levels in comparison with wild-type virus. This attenuation was a result of altered NA activity or stability depending on the introduced mutation. Mutant viruses displayed increased resistance to zanamivir, oseltamivir and peramivir, with certain viruses displaying cross-resistance to all three drugs.

The M1 matrix protein controls the filamentous phenotype of influenza A virus

We show that most isolates of influenza A induce filamentous changes in infected cells in contrast to A/WSN/33 and A/PR8/34 strains which have undergone extensive laboratory passage and are mouse-adapted. Using reverse genetics, we created recombinant viruses in the naturally filamentous genetic background of A/Victoria/3/75 and established that this property is regulated by the M1 protein sequence, but that the phenotype is complex and several residues are involved. The filamentous phenotype was lost when the amino acid at position 41 was switched from A to V, at the same time, this recombinant virus also became insensitive to the antibody 14C2. On the other hand, the filamentous phenotype could be fully transferred to a virus containing RNA segment 7 of the A/WSN/33 virus by a combination of three mutations in both the amino and carboxy regions of the M1 protein. This observation suggests that an interaction among these regions of M1 may occur during assembly. (C) 2004 Elsevier Inc. All rights reserved.

Reduced incorporation of the influenza B virus BM2 protein in virus particles decreases infectivity

BM2 is the fourth integral membrane protein encoded by the influenza B virus genome. It is synthesized late in infection and transported to the plasma membrane from where it is subsequently incorporated into progeny virus particles. It has recently been reported that BM2 has ion channel activity and may be the functional homologue of the influenza A virus M2 protein acting as an ion channel involved in viral entry. Using a reverse genetic approach it was not possible to recover virus which lacked BM2. A recombinant influenza B virus was generated in which the BM2 AUG initiation codon was mutated to GUG. This decreased the efficiency of translation of BM2 protein such that progeny virions contained only 1/8 the amount of BM2 seen in wild-type virus. The reduction in BM2 incorporation resulted in a reduction in infectivity although there was no concomitant decrease in the numbers of virions released from the infected cells. These data imply that the incorporation of sufficient BM2 protein into influenza B virions is required for infectivity of the virus particles. (C) 2004 Elsevier Inc. All rights reserved.

Extinction processes in hot spots of avian biodiversity and the targeting of pre-emptive conservation action

Hot spots of endemism are regarded as important global sites for conservation as they are rich in threatened endemic species and currently experiencing extensive habitat loss. Targeting pre-emptive conservation action to sites that are currently relatively intact but which would be vulnerable to particular human activities if they occurred in the future is, however, also valuable but has received less attention. Here, we address this issue by using data on Endemic Bird Areas (EBAs). First, we identify the ecological factors that affect extinction risk in the face of particular human activities, and then use these insights to identify EBAs that should be priorities for pre-emptive conservation action. Threatened endemic species in EBAs are significantly more likely to be habitat specialists or relatively large-bodied than non-threatened species, when compared across avian families. Increasing habitat loss causes a significant increase in extinction risk among habitat specialists, but we found no evidence to suggest that the presence of alien species/human exploitation causes a significant increase in extinction risk among large-bodied species. This suggests that these particular human activities are contributing to high extinction risk among habitat specialists, but not among large-bodied species. Based on these analyses, we identify 39 EBAs containing 570 species (24% of the total in EBAs) that are not currently threatened with severe habitat loss, but would be ecologically vulnerable to future habitat loss should it occur. We show that these sites tend to be poorly represented in existing priority setting exercises involving hot spots, suggesting that vulnerability must be explicitly included within these exercises if such sites are to be adequately protected.