Effect of antivenin dose on outcome from crotalid envenomation: 218 dogs (1988–2006)

Objective – To determine whether the dose of antivenin administered is associated with a difference in survival of crotalid‐envenomated dogs. A secondary objective was to determine whether other covariables affect survival. Design – Retrospective study (1988–2006). Setting – Private referral center and university small animal teaching hospital. Animals – Two hundred and eighteen dogs with evidence of crotalid envenomation and treatment with equine‐derived antivenin. Interventions – Administration of antivenin. Measurements and Main Results – Patient signalment, physical and clinicopathologic data at time of presentation, treatments, complications of antivenin therapy, length and cost of hospitalization, and outcome were recorded. Confidence intervals were determined for the difference in median number of vials administered and for median dosage for patients that lived versus died. Penalized logistic regression was performed to evaluate the effect of other covariables on survival. The median age of affected dogs was 3 years (range 6 w–12 y) with a median weight of 25.7 kg (range 1.95–86.4 kg). The median number of antivenin vials administered was 1.0 (range 1.0–10.0). Acute and chronic reactions were reported in 7% (16/218) and 0.9% (2/218) of dogs, respectively. Nine of 218 dogs (4.1%) died. The median number of vials administered to the nonsurvivors and survivors were 2.0 (range 1–5 vials) and 1.0 (range 1–10 vials), respectively. The median number of vials received was significantly different in dogs that died versus those that lived (P<0.05). Increased heart rate (P=0.02) and petechiation (P=0.04) were associated with decreased likelihood of survival, while diphenhydramine (P=0.02) and fluoroquinolone (P=0.046) administration was associated with increased likelihood of survival. The median duration of hospitalization was 1.0 day (range 2 h–22 d). The median cost of hospitalization was US$1592.00 (range US$267.20–US$6738.00). Conclusion – The administration of more vials of antivenin is potentially associated with negative outcome; however, a causal relationship has not been established. Controlled, prospective studies are needed to optimize antivenin administration.     

Early investigations into the infection courts used by <Emphasis Type="Italic">Neonectria fuckeliana</Emphasis> to enter <Emphasis Type="Italic">Pinus radiata</Emphasis> stems

Nectria flute canker is a disease of Pinus radiata stems caused by the pathogen Neonectria fuckeliana occurring in the southern parts of New Zealand. In Northern Hemisphere countries where N. fuckeliana is endemic, it is commonly found in Picea and Abies spp. Open wounds, dead attached branches and branch stubs have been identified as the primary infection courts. Although in New Zealand the development of Nectria flute canker disease is associated with pruned branch stubs, recent studies suggest that this is not the only possible entry method as the fungus has been found in trees prior to pruning. Three field trials were established to examine the potential infection mechanisms for N. fuckeliana in P. radiata in New Zealand; including stem wounds and branch stubs. The difference between inoculations into the stem and into branch wood was clear. Inoculation of deep stem wounds resulted in the greatest fluting with 76% of trees inoculated developing cankers. Inoculation directly into stubs resulted in only small stem depressions that occurred in 17% of cases and the fungus was largely contained within the branch trace. Tree response to inoculation with either ascospores or conidia of the Acremonium anamorph gave similar results in terms of canker development and fungal spread within the stem. Tree response to inoculation was highly variable however: in one study 6% of trees did not respond to inoculation at all, while 26% produced severe cankers regardless of inoculation method. A more thorough understanding of the infection mechanisms of N. fuckeliana will contribute to the development of better disease management protocols to prevent infection and disease development in future plantation stock.     

Molecular characterization of boscalid- and penthiopyrad-resistant isolates of Didymella bryoniae and assessment of their sensitivity to fluopyram

BACKGROUND: Didymella bryoniae has a history of developing resistance to single‐site fungicides. A recent example is with the succinate‐dehydrogenase‐inhibiting fungicide (SDHI) boscalid. In laboratory assays, out of 103 isolates of this fungus, 82 and seven were found to be very highly resistant (B^VHR) and highly resistant (B^HR) to boscalid respectively. Cross‐resistance studies with the new SDHI penthiopyrad showed that the B^VHR isolates were only highly resistant to penthiopyrad (B^VHR‐P^HR), while the B^HR isolates appeared sensitive to penthiopyrad (B^HR‐P^S). In this study, the molecular mechanism of resistance in these two phenotypes (B^VHR‐P^HR and B^HR‐P^S) was elucidated, and their sensitivity to the new SDHI fluopyram was assessed. RESULTS: A 456 bp cDNA amplified fragment of the succinate dehydrogenase iron sulfur gene (DbSDHB) was initially cloned and sequenced from two sensitive (B^S‐P^S), two B^VHR‐P^HR and one B^HR‐P^S isolate of D. bryoniae. Comparative analysis of the DbSDHB protein revealed that a highly conserved histidine residue involved in the binding of SDHIs and present in wild‐type isolates was replaced by tyrosine (H277Y) or arginine (H277R) in the B^VHR‐P^HR and B^HR‐P^S variants respectively. Further examination of the role and extent of these alterations showed that the H/Y and H/R substitutions were present in the remaining B^VHR‐P^HR and B^HR‐P^S variants respectively. Analysis of the sensitivity to fluopyram of representative isolates showed that both SDHB mutants were sensitive to this fungicide as the wild‐type isolates. CONCLUSION: The genotype‐specific cross‐resistance relationships between the SDHIs boscalid and penthiopyrad and the lack of cross‐resistance between these fungicides and fluopyram should be taken into account when selecting SDHIs for gummy stem blight management. Copyright © 2011 Society of Chemical Industry     

Membrane fusion intermediates via directional and full assembly of the SNARE complex

Cellular membrane fusion is thought to proceed through intermediates including docking of apposed lipid bilayers, merging of proximal leaflets to form a hemifusion diaphragm, and fusion pore opening. A membrane-bridging four-helix complex of soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) mediates fusion. However, how assembly of the SNARE complex generates docking and other fusion intermediates is unknown. Using a cell-free reaction, we identified intermediates visually and then arrested the SNARE fusion machinery when fusion was about to begin. Partial and directional assembly of SNAREs tightly docked bilayers, but efficient fusion and an extended form of hemifusion required assembly beyond the core complex to the membrane-connecting linkers. We propose that straining of lipids at the edges of an extended docking zone initiates fusion.     

Regional astrocyte allocation regulates CNS synaptogenesis and repair

Astrocytes, the most abundant cell population in the central nervous system (CNS), are essential for normal neurological function. We show that astrocytes are allocated to spatial domains in mouse spinal cord and brain in accordance with their embryonic sites of origin in the ventricular zone. These domains remain stable throughout life without evidence of secondary tangential migration, even after acute CNS injury. Domain-specific depletion of astrocytes in ventral spinal cord resulted in abnormal motor neuron synaptogenesis, which was not rescued by immigration of astrocytes from adjoining regions. Our findings demonstrate that region-restricted astrocyte allocation is a general CNS phenomenon and reveal intrinsic limitations of the astroglial response to injury.     

Modeling regional-scale habitat of forest birds when land management guidelines are needed but information is limited

Conservation planning at broad spatial scales facilitates coherence between local land management and objectives set at the state or provincial level. Habitat suitability models are commonly used to identify key areas for conservation planning. The challenge is that habitat suitability models are data hungry, which limits their applicability to species for which detailed information exists, but managers need to address the needs of all at-risk species. We propose a modeling approach useful for regional-scale conservation planning that accommodates limited species knowledge, and identifies what managers should aim for at the local scale. For twenty at-risk bird species, we built models to identify potential habitat using both literature information and empirical data. Species occupancy within potential habitat depends on the presence of intrinsic elements, which we identified for each species so that managers can enhance these elements as appropriate. For most species, the estimated amount of habitat needed to meet population targets was <10% of the mapped potential habitat, with notable exceptions for Northern Goshawk (Accipiter gentilis; 100%), Brown Thrasher (Toxostoma rufum; 63.7%), and Veery (Catharus fuscescens; 17.9%). Model validation showed that interior forest species models performed best. Our modeling framework allowed us to build potential habitat models to various endpoints for different species, depending on the information available, and revealed a number of species for which basic natural history data are missing. Our potential habitat models provide regional perspective and guide local habitat management, and assist in identifying research priorities.     

How much compensation do we need? Replacement ratio estimates for Swiss dry grassland biotopes

Development pressure on reserve networks in densely populated countries may lead to the decision to allow for replacement compensation. Replacement ratios used for specifying replacement compensation are usually based on expert judgment. In contrast, we propose a method to estimate replacement ratios based on the set covering framework. The method is applied to presence-absence data of vascular plants of the dry grassland inventory of Switzerland. For the replacement of 60% of a patch’s high conservation value species by the same vegetation type (“in-kind” compensation), the estimated replacement ratios are <5 for most vegetation types. These ratios are comparable with replacement ratios usually used in practice. Our replacement ratio estimates for replacement by another vegetation type (“out-of-kind” compensation) are considerable higher than proposed by the literature. For oligotroph dry grassland associations, the replacement rations are extremely high, so that these associations have to be considered irreplaceable. The estimated replacement ratios provide a good starting point for designing compensation measures for unavoidable losses in a reserve system. However, additional biodiversity conservation goals should be considered when designing replacement compensation in practice.     

Management of advanced regeneration in secondary forests of the Brazilian Amazon

Gap formation is a critical process for plant establishment that may be absent or infrequent in second-growth forests, negatively influencing their ability to become diverse mature forest. I simulated treefall gaps within a 10-year-old secondary forest established on a clear-cut area, because cut areas may have a greater potential for economic exploitation than areas used for pastures and shifting cultivation. I explored the effects of varying degrees of canopy opening on the growth of plants already established as advanced regeneration. Five intensities of canopy opening were created: total removal (100%), 80–90%, 50–60%, 20–30% and a 0% control. Only trees >5 cm DBH were cut. The established plant community was diverse, and comprised 37 families and 126 species and morpho-species, of which 72% had some use reported in the literature. I found that the canopy opening treatments resulted in very little disturbance to the established seedling and sapling community, with no significant increase in mortality, but had a strong positive effect on their growth. Light levels reaching the understory were increased from 1% of incident photosynthetic active radiation in control plots to 35% in 100% canopy opening plots. During the first year, differences in plant growth were not significant, but by the second year, differential plant growth associated with canopy opening became evident. Most seedlings (51%) grew approximately 25 cm in height, and approximately one quarter grew more than 25 cm. Only 2.6% of the seedlings decreased in height, and 12% did not grow at all. Fifty percent canopy removal resulted in an almost threefold increase in plant height compared to control plots (0.52 ± 0.4 m and 0.20 ± 0.2 m, respectively), and was not significantly different from 80 or 100% removal. This indicates that intermediate levels of canopy removal had positive effects and total removal was unnecessary to stimulate the best growth responses. I conclude that regeneration of diverse mature forest can be accelerated under some conditions by partial removal of secondary forest canopy.     

Idiopathic acute onset myelopathy in cheetah (Acinonyx jubatus) cubs.

Numerous cases of ataxia, hind limb paresis, and paralysis have occurred in cheetah (Acinonyx jubatus) cubs over the past 10 yr within the European Endangered Species Program population, including 12 in mainland Europe, two in the British Isles, one in Namibia, and one in Dubai. The condition is the most important medical factor limiting European cheetah population growth. Eight cubs at the Salzburg Zoo, Austria, were affected. They demonstrated upper motor neuron lesions when alive and bilateral, symmetrical myelin degeneration of the spinal cord on necropsy. Ballooning of myelin sheaths surrounded mostly preserved axons, and no spheroids, characteristic of acute axonal degeneration, were found. Myelin loss markedly exceeded axonal degeneration. The syndrome's etiology is unclear, although viral, bacterial, parasitic, genetic, nutritional-metabolic, toxic, and physical causes have been considered.