West Nile Virus Positive Blood Donation and Subsequent Entomological Investigation,Austria, 2014

The detection of West Nile virus (WNV) nucleic acid in a blood donation from Vienna, Austria, as well as in Culex pipiens pupae and egg rafts, sampled close to the donor’s residence, is reported. Complete genomic sequences of the human- and mosquito-derived viruses were established, genetically compared and phylogenetically analyzed. The viruses were not identical, but closely related to each other and to recent Czech and Italian isolates, indicating co-circulation of related WNV strains within a confined geographic area. The detection of WNV in a blood donation originating from an area with low WNV prevalence in humans (only three serologically diagnosed cases between 2008 and 2014) is surprising and emphasizes the importance of WNV nucleic acid testing of blood donations even in such areas, along with active mosquito surveillance programs.     

Effects of Lead Pollution on Ammonia Parkinsoniana (Foraminifera): Ultrastructural and Microanalytical Approaches

The responses of Ammonia parkinsoniana (Foraminifera) exposed to different concentrations of lead (Pb) were evaluated at the cytological level. Foraminifera-bearing sediments were placed in mesocosms that were housed in aquaria each with seawater of a different lead concentration. On the basis of transmission electron microscopy and environmental scanning electron microscopy coupled with energy dispersive spectrometer analyses, it was possible to recognize numerous morphological differences between untreated (i.e., control) and treated (i.e., lead enrichment) specimens. In particular, higher concentrations of this pollutant led to numerical increase of lipid droplets characterized by a more electron-dense core, proliferation of residual bodies, a thickening of the organic lining, mitochondrial degeneration, autophagosome proliferation and the development of inorganic aggregates. All these cytological modifications might be related to the pollutant-induced stress and some of them such as the thickening of organic lining might suggest a potential mechanism of protection adopted by foraminifera.Key words: Foraminifera, pollution, ultrastructure, mesocosm     

Contributions to the knowledge of oribatid mites (Acari,Oribatida) of Indonesia. 3. The genus Galumna (Galumnidae) with description of a new subgenus and seven new species

Seven new species of oribatid mites of the genus Galumna are described from litter and soil materials of Sumatra, Indonesia. A new subgenus, Galumna (Atypicogalumna) subgen. n., is proposed; it differs from all galumnid genera and subgenera by the simultaneous presence of porose areas and sacculi on the notogaster (vs. either porose areas or sacculi present). Galumna (Galumna) calva Starý, 1997 is recorded for the first time in the Oriental region, and Galumna (Galumna) sabahna Mahunka, 1995 is recorded for the first time in the Indonesian fauna.     

Coral population dynamics across consecutive mass mortality events

Annual coral mortality events due to increased atmospheric heat may occur regularly from the middle of the century and are considered apocalyptic for coral reefs. In the Arabian/Persian Gulf, this situation has already occurred and population dynamics of four widespread corals (Acropora downingi, Porites harrisoni, Dipsastrea pallida, Cyphastrea micropthalma) were examined across the first‐ever occurrence of four back‐to‐back mass mortality events (2009–2012). Mortality was driven by diseases in 2009, bleaching and subsequent diseases in 2010/2011/2012. 2009 reduced P. harrisoni cover and size, the other events increasingly reduced overall cover (2009: ?10%; 2010: ?20%; 2011: ?20%; 2012: ?15%) and affected all examined species. Regeneration was only observed after the first disturbance. P. harrisoni and A. downingi severely declined from 2010 due to bleaching and subsequent white syndromes, while D. pallida and P. daedalea declined from 2011 due to bleaching and black‐band disease. C. microphthalma cover was not affected. In all species, most large corals were lost while fission due to partial tissue mortality bolstered small size classes. This general shrinkage led to a decrease of coral cover and a dramatic reduction of fecundity. Transition matrices for disturbed and undisturbed conditions were evaluated as Life Table Response Experiment and showed that C. microphthalma changed the least in size‐class dynamics and fecundity, suggesting they were ‘winners’. In an ordered ‘degradation cascade’, impacts decreased from the most common to the least common species, leading to step‐wise removal of previously dominant species. A potentially permanent shift from high‐ to low‐coral cover with different coral community and size structure can be expected due to the demographic dynamics resultant from the disturbances. Similarities to degradation of other Caribbean and Pacific reefs are discussed. As comparable environmental conditions and mortality patterns must be expected worldwide, demographic collapse of many other coral populations may soon be widespread.     

Interactive effects of elevation,species richness and extreme climatic events on plant–pollinator networks

Plant–pollinator interactions are essential for the functioning of terrestrial ecosystems, but are increasingly affected by global change. The risks to such mutualistic interactions from increasing temperature and more frequent extreme climatic events such as drought or advanced snow melt are assumed to depend on network specialization, species richness, local climate and associated parameters such as the amplitude of extreme events. Even though elevational gradients provide valuable model systems for climate change and are accompanied by changes in species richness, responses of plant–pollinator networks to climatic extreme events under different environmental and biotic conditions are currently unknown. Here, we show that elevational climatic gradients, species richness and experimentally simulated extreme events interactively change the structure of mutualistic networks in alpine grasslands. We found that the degree of specialization in plant–pollinator networks (H2′) decreased with elevation. Nonetheless, network specialization increased after advanced snow melt at high elevations, whereas changes in network specialization after drought were most pronounced at sites with low species richness. Thus, changes in network specialization after extreme climatic events depended on climatic context and were buffered by high species richness. In our experiment, only generalized plant–pollinator networks changed in their degree of specialization after climatic extreme events. This indicates that contrary to our assumptions, network generalization may not always foster stability of mutualistic interaction networks.     

Temporal Dynamics of Powdery Mildew (Oidium neolycopersici) and its Effects on the Host Growth Dynamics of Tomato

Controlled glasshouse experiments were conducted to investigate the temporal progress of powdery mildew and its effects on host dynamics of tomato, without and with one fungicide application. Healthy tomato transplants (5‐ to 6‐week old) were artificially inoculated with powdery mildew, and disease progress as well as host growth were monitored in both fungicide sprayed and unsprayed treatments and compared with non‐inoculated plants. Actual disease severity on a plant basis increased in unsprayed plants reaching maximum severity in the proportionate range of 0.53–0.83. One fungicide spray significantly reduced the maximum disease severity by two‐ to fourfolds. Despite adjustments for defoliation, declines in the proportion of disease severity between successive assessments were evident. Whereas the estimated growth rates of diseased plants were significantly lower than that of healthy plants, no significant differences were observed in the maximum leaf area formed of inoculated and non‐inoculated plants. A considerable effect of the powdery mildew epidemics was manifested through hastened shrivelling and defoliation of diseased leaves within the tomato canopy. An average of 18–29% and 40–52% of leaves had abscised from the plant canopy at the last date of assessment in sprayed and non‐sprayed plants, respectively. Accordingly, defoliation accounted for 14–33.3% and 58.3–63.1% losses in leaf area of sprayed and non‐sprayed plants, respectively. Duration of healthy leaf area and yield of inoculated plants were also significantly reduced by powdery mildew epidemics.     

Noise affects the shape of female preference functions for acoustic signals

The shape of female mate preference functions influences the speed and direction of sexual signal evolution. However, the expression of female preferences is modulated by interactions between environmental conditions and the female's sensory processing system. Noise is an especially relevant environmental condition because it interferes directly with the neural processing of signals. Although noise is therefore likely a significant force in the evolution of communication systems, little is known about its effects on preference function shape. In the grasshopper Chorthippus biguttulus, female preferences for male calling song characteristics are likely to be affected by noise because its auditory system is sensitive to fine temporal details of songs. We measured female preference functions for variation in male song characteristics in several levels of masking noise and found strong effects of noise on preference function shape. The overall responsiveness to signals in noise generally decreased. Preference strength increased for some signal characteristics and decreased for others, largely corresponding to expectations based on neurophysiological studies of acoustic signal processing. These results suggest that different signal characteristics will be favored under different noise conditions, and thus that signal evolution may proceed differently depending on the extent and temporal patterning of environmental noise.     

Megakaryocyte rupture for acute platelet needs

Circulating platelets were thought to arise solely from the protrusion and fragmentation of megakaryocyte cytoplasm. Now, Nishimura et al. (2015. J. Cell Biol. http://dx.doi.org/10.1083/jcb.201410052) show that platelet release from megakaryocytes can be induced by interleukin-1α (IL-1α) via a new rupture mechanism, which yields higher platelet numbers, occurs independently of the key regulator of megakaryopoiesis thrombopoietin, and may occur during situations of acute platelet need.Platelets, small anucleate cells that circulate in the blood stream, are essential for normal hemostasis but also play major roles in inflammation, immunity, wound healing, tumor metastasis, and the development and maintenance of lymph vessels (Leslie, 2010). Hence, reduced platelet numbers and/or impaired platelet function, as found in the context of numerous pathologies or upon pharmacological intervention, may have a negative impact on a large variety of physiological processes and under certain circumstances can become life threatening (Sachs and Nieswandt, 2007).Platelets are continuously produced by fragmentation of the cytoplasm of their giant polyploid precursors in the bone marrow, the megakaryocytes. Recent studies using intravital two-photon microscopy of the bone marrow confirmed the formation of long protrusions of megakaryocytes termed proplatelets in vivo, which extend into bone marrow sinusoids where larger cytoplasmic fragments, so-called preplatelets, are shed and further mature within the circulation ultimately giving rise to platelets (Junt et al., 2007; Zhang et al., 2012; Bender et al., 2014). Calculations of platelet consumption and production in humans and mice suggested that platelet production via proplatelet formation is sufficient to maintain platelet count in normal physiology (Kaufman et al., 1965; Junt et al., 2007). However, this mechanism may not be efficient enough to produce sufficient platelet numbers under conditions of increased platelet consumption, such as inflammation/infection, immune thrombocytopenia, or traumatic blood loss. In this issue, Nishimura et al. have now identified an interleukin-1α (IL-1α)–induced rupture-type mechanism for platelet production that yields ∼20-fold higher numbers of released platelet particles as compared with the classical mechanism of proplatelet formation during the same period of time (Fig. 1). This work provides for the first time an explanation of how megakaryocytes can maintain platelet mass equilibrium and quickly restore platelet numbers under pathological conditions associated with increased platelet turnover. Even though the platelets released by megakaryocyte rupture were mildly enlarged in size, they were functionally indistinguishable from proplatelet-derived platelets.Open in a separate windowFigure 1.Platelet production in normal physiology and upon acute platelet needs. In normal physiology (left), platelets are continuously produced by megakaryocytes via the classical process of proplatelet formation. Under these conditions, thrombopoietin (Thpo) drives megakaryopoiesis by signaling through its receptor c-Mpl, but Thpo is dispensable for proplatelet formation, which is a cell-autonomous process and presumably regulated by the vascular niche. Inhibition of Caspase-3 and a well-organized orchestration of microtubule dynamics (green) are prerequisites for proper proplatelet formation and protrusion into bone marrow sinusoids, where preplatelets are released and further mature within the circulation. Proplatelet formation is a rather slow process with low yields of platelets per period of time but is sufficient to compensate for the continuous loss of aged platelets. Under conditions of increased platelet loss or consumption (right), e.g., as a result of excessive blood loss or in the setting of infection/inflammation, this mechanism might not be sufficient to ensure appropriate platelet supply. Under these conditions, interleukin-1α (IL-1α) levels increase rapidly and trigger rupture-type platelet formation via its receptor IL-1R1 on megakaryocytes. IL-1α signaling leads to a deregulated expression and organization of β1-tubulin (green) as well as to the activation of Caspase-3, which in turn leads to a reduction of megakaryocyte membrane stiffness. Together, these processes lead to the formation of multiple membrane blebs that are predominantly released into bone marrow sinusoids to quickly replenish platelet numbers.The IL-1α procytokine is expressed in virtually all nonhematopoietic cells, but also in platelets, and is involved in inflammatory processes, modulation of immune responses, and hematopoiesis. IL-1α is released from damaged endothelial cells and activated platelets, where it triggers the recruitment of immune cells (Rider et al., 2013). As the work from Nishimura et al. (2015) indicates, this cytokine may also stimulate thrombopoiesis and rupture-type platelet release from megakaryocytes to compensate for platelet loss and restore platelet mass equilibrium. This could explain why supplementing cancer patients experiencing chemotherapy-induced thrombocytopenia with IL-1α accelerated platelet count recovery (Gordon and Hoffman, 1992; Smith et al., 1993). These findings are of particular importance when considering the development of IL-1α inhibitors to dampen inflammatory processes.The technical optimization of the temporal and spatial resolution of two-photon intravital microscopy in combination with an elegant series of experiments using a broad variety of knockout mouse models allowed Nishimura et al. (2015) to observe and characterize this alternative mechanism of platelet formation. The mechanism strongly resembles key features of FasL-induced apoptosis, including activation of Caspase-3, disorganization of the cytoskeleton, and membrane blebbing. However, in stark contrast to typical FasL-induced apoptosis, rupture-type platelet formation is relatively quick (within an hour vs. >80 min) and results in the release of a large number of phosphatidylserine-negative particles. These particles carry an increased content of β1-tubulin, which is reminiscent of disorganized α- and β-tubulin expression, and has not been described for apoptotic cells (Fig. 1). The increased formation of membrane blebs was accompanied by a reduction in megakaryocyte membrane stiffness that could be reverted by caspase inhibitors. The activation of Caspase-3 represents a central step in rupture-type platelet release, as Caspase-3–deficient megakaryocytes could not use this alternative pathway for platelet production. Future studies will be required to determine how IL-1α modulates megakaryocyte membrane stiffness and to identify the mechanisms that distinguish rupture-type platelet release from typical FasL-induced apoptosis.Nishimura et al. (2015) find that rupture-type platelet production occurs independently of thrombopoietin (Thpo), the key driver of thrombopoiesis, as rupture-type platelet production constituted the major source of circulating platelets in Thpo-deficient mice. This finding is in line with a study by Ng et al. (2014) showing that megakaryocyte-specific Thpo receptor (c-Mpl)–deficient mice presented a marked thrombocytosis despite the lack of Thpo stimulation during terminal thrombopoiesis. Unfortunately, IL-1α levels or the presence of rupture-type platelet biogenesis have not yet been assessed in c-Mpl–deficient mice or in patients suffering from congenital amegakaryocytic thrombocytopenia. In addition, it would be of particular interest to assess the contribution of IL-1α–induced rupture-type platelet release in human patients and also in mouse models reproducing inherited or idiopathic platelet disorders, such as the Wiskott–Aldrich syndrome, Gray-platelet syndrome, or immune thrombocytopenia.In conclusion, the novel rupture-type platelet release mechanism identified by Nishimura et al. (2015) will help to answer the long-standing question of how circulating platelet numbers are quickly restored under conditions of increased platelet consumption or loss. Furthermore, this finding may lead to the development of new drugs to modulate platelet turnover in humans, but we also need to carefully reconsider previous experimental data on megakaryopoiesis/platelet production to include the possible contribution of IL-1α–induced platelet release. Overall, the identification of a new mechanism of platelet production has advanced our understanding of platelet production and will certainly stimulate new research in the field of megakaryocyte biology.