Genetic diversification of an invasive honey bee ectoparasite across sympatric and allopatric host populations.

Invasive parasites are major threats to biodiversity. The honey bee ectoparasite, Varroa destructor, has shifted host and spread almost globally several decades ago. This pest is generally considered to be the main global threat to Western honey bees, Apis mellifera, although the damages it causes are not equivalent in all its new host's populations. Due to the high virulence of this parasite and the viruses it vectors, beekeepers generally rely on acaricide treatments to keep their colonies alive. However, some populations of A. mellifera can survive without anthropogenic mite control, through the expression of diverse resistance and tolerance traits. Such surviving colonies are currently found throughout the globe, with the biggest populations being found in Sub-Saharan Africa and Latin America. Recently, genetic differences between mite populations infesting surviving and treated A. mellifera colonies in Europe were found, suggesting that adaptations of honey bees drive mite evolution. Yet, the prevalence of such co-evolutionary adaptations in other invasive populations of V. destructor remain unknown. Using the previous data from Europe and novel genetic data from V. destructor populations in South America and Africa, we here investigated whether mites display signs of adaptations to different host populations of diverse origins and undergoing differing management. Our results show that, contrary to the differences previously documented in Europe, mites infesting treated and untreated honey bee populations in Africa and South America are genetically similar. However, strong levels of genetic differentiation were found when comparing mites across continents, suggesting ongoing allopatric speciation despite a recent spread from genetically homogenous lineages. This study provides novel insights into the co-evolution of V. destructor and A. mellifera, and confirms that these species are ideal to investigate coevolution in newly established host-parasite systems

Diversity and Global Distribution of Viruses of the Western Honey Bee, Apis mellifera

Funding: This research was permitted and funded by the COLOSS network (https://coloss.org/).Peer reviewedPublisher PD

Evolutionarily diverse origins of deformed wing viruses in western honey bees

Novel transmission routes can allow infectious diseases to spread, often with devastating consequences. Ectoparasitic varroa mites vector a diversity of RNA viruses, having switched hosts from the eastern to western honey bees (Apis cerana to Apis mellifera). They provide an opportunity to explore how novel transmission routes shape disease epidemiology. As the principal driver of the spread of deformed wing viruses (mainly DWV-A and DWV-B), varroa infestation has also driven global honey bee health declines. The more virulent DWV-B strain has been replacing the original DWV-A strain in many regions over the past two decades. Yet, how these viruses originated and spread remains poorly understood. Here, we use a phylogeographic analysis based on whole-genome data to reconstruct the origins and demography of DWV spread. We found that, rather than reemerging in western honey bees after varroa switched hosts, as suggested by previous work, DWV-A most likely originated in East Asia and spread in the mid-20th century. It also showed a massive population size expansion following the varroa host switch. By contrast, DWV-B was most likely acquired more recently from a source outside East Asia and appears absent from the original varroa host. These results highlight the dynamic nature of viral adaptation, whereby a vector's host switch can give rise to competing and increasingly virulent disease pandemics. The evolutionary novelty and rapid global spread of these host-virus interactions, together with observed spillover into other species, illustrate how increasing globalization poses urgent threats to biodiversity and food security

Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

Summary Background Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. Methods We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung’s disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. Findings We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung’s disease) from 264 hospitals (89 in high-income countries, 166 in middleincome countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in lowincome countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≤0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. Interpretation Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between lowincome, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

Selección bidireccional de Apis mellifera (Hymenoptera: Apidae) para aumento de la resistencia y la susceptibilidad a la nosemosis

La nosemosis es una enfermedad que afecta las funciones digestivas de las abejas melíferas causada por los microsporidios Nosema apis y Nosema ceranae. En Uruguay la única especie detectada es N. ceranae. Para determinar si la incidencia de N. ceranae en las colonias tiene un componente genético se realizó una selección bidireccional para aumento de la resistencia y la susceptibilidad a este parásito sin control de la paternidad. Las colonias fueron evaluadas en una forestación de Eucalyptus grandis en otoño. La infección de las colonias se determinó como 1) el porcentaje de abejas pecoreadoras infectadas y 2) el número promedio de esporas por campo en 10 campos. El trabajo se inició con 138 colonias y se evaluaron dos generaciones de 30 y 63 colonias. La respuesta a la selección fue muy limitada, solo en la primera generación las colonias de la línea resistente presentaron menos esporas por abejas que las colonias de la línea susceptible (19,6 ± 5,8 y 26,8 ± 10,4, respectivamente, W = 41,5; P = 0.03). Esto indicaría que la resistencia a la nosemosis está fuertemente afectada por el ambiente. Futuros esfuerzos para aumentar la resistencia de las abejas a N. ceranae a través de mejora genética deberán incluir el control de la paternidad

Short communication: Natural molecules for the control of Paenibacillus larvae, causal agent of American foulbrood in honey bees (Apis mellifera L.)

Aim of study: To evaluate the potential bactericidal activity of natural molecules against Paenibacillus larvae. Moreover, we investigated if molecules that exhibit antimicrobial activity were able to inhibit the proteolytic activity of the bacterium.Area of study: Isolates S1 and S2 were from Balcarce, Buenos Aires province, strain S3 from Rio Cuarto, Cordoba province, strain S4 from Concordia, Entre Rios province, strain S5 and S8 from Necochea, Buenos Aires, strain S6 and S7 from Mar del Plata, Buenos Aires, strain S9 from Modena, Italy and strain S10 from Emilia Reggio, Italy.Material and methods: Bacterial isolates identification was carried out by amplification of a specific 16S rRNA gene fragment of P. larvae using primers PL5 and PL4. Screening of the antimicrobial activity of thirteen molecules against four P. larvae isolates was conducted by the agar diffusion technique. The antimicrobial activity of selected molecules was evaluated by broth microdilution method.Main results: Menadione, lauric acid, monoglyceride of lauric acid and naringenin showed antimicrobial activity against ten P. larvae isolates. Menadione and lauric acid showed the strongest activities, with minimum inhibitory concentration mean values ranging 0.78-3.125 µg/mLand 25-50 µg/mL, respectively.Research highlights: Those concentrations are feasible to be applied at field level, and constitute promissory candidates to be evaluated using in vivo larval models

Lactobacillus kunkeei strains decreased the infection by honey bee pathogens Paenibacillus larvae and Nosema ceranae

Due to their social behaviour, honey bees can be infected by a wide range of pathogens including the microsporidia Nosema ceranae and the bacteria Paenibacillus larvae. The use of probiotics as food additives for the control or prevention of infectious diseases is a widely used approach to improve human and animal health. In this work, we generated a mixture of four Lactobacillus kunkeei strains isolated from the gut microbial community of bees, and evaluated its potential beneficial effect on larvae and adult bees. Its administration in controlled laboratory models was safe for larvae and bees; it did not affect the expression of immune-related genes and it was able to decrease the mortality associated to P. larvae infection in larvae and the counts of N. ceranae spores from adult honey bees. These promising results suggest that this beneficial microorganism's mixture may be an attractive strategy to improve bee health. Field studies are being carried out to evaluate its effect in naturally infected colonies.Fil: Arredondo, Daniela. Instituto de Investigaciones Biológicas Clemente Estable. Departamento de Microbiología; UruguayFil: Castelli, Luisina. Instituto de Investigaciones Biológicas Clemente Estable. Departamento de Microbiología; UruguayFil: Porrini, Martín Pablo. Universidad Nacional de Mar del Plata. Facultad de Cs.exactas y Naturales. Instituto de InvestIgaciones Biologicas. Departamento de Biologia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mar del Plata. Instituto de Investigaciones Biológicas. Universidad Nacional de Mar del Plata. Facultad de Ciencias Exactas y Naturales. Instituto de Investigaciones Biológicas; ArgentinaFil: Garrido, Paula Melisa. Universidad Nacional de Mar del Plata. Facultad de Ciencias Exactas y Naturales. Departamento de Biología; ArgentinaFil: Eguaras, Martin Javier. Universidad Nacional de Mar del Plata. Facultad de Ciencias Exactas y Naturales. Departamento de Biología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mar del Plata. Instituto de Investigaciones Biológicas. Universidad Nacional de Mar del Plata. Facultad de Ciencias Exactas y Naturales. Instituto de Investigaciones Biológicas; ArgentinaFil: Zunino Abirad, Pablo Miguel. Instituto de Investigaciones Biológicas Clemente Estable. Departamento de Microbiología; UruguayFil: Antunez, Karina. Instituto de Investigaciones Biológicas Clemente Estable. Departamento de Microbiología; Urugua

Inequalities in noise will affect urban wildlife

Understanding the extent to which systemic biases influence local ecological communities is essential for developing just and equitable environmental practices. With over 270 million people across the United States living in urban areas, understanding the socio-ecological consequences of racially-targeted zoning, such as redlining, provides crucial information for urban planning. There is a growing body of literature documenting the relationships between redlining and disparities in the distribution of environmental harms and goods, including inequities in green space cover and pollutant exposure. Yet, it remains unknown whether noise pollution is also inequitably distributed, and whether inequitable noise is an important driver of ecological change in urban environments. We conducted 1) a spatial analysis of urban noise to determine the extent to which noise overlaps with the distribution of redlining categories and 2) a systematic literature review to summarize the effects of noise on wildlife in urban landscapes. We found strong evidence that noise is inequitably distributed in cities across the United States, and that inequitable noise may drive complex biological responses across diverse urban wildlife. These findings lay a foundation for future research that advances acoustic and urban ecology by centering equity and challenging systems of oppression.Data can be viewed using any software that can open a .csv file. Code can be viewed using any software that can open a .txt file.Funding provided by: Colorado State UniversityCrossref Funder Registry ID: http://dx.doi.org/10.13039/100007235Award Number:Spatial Analysis of Urban Noise Pollution To evaluate noise exposure across HOLC redlining grades for 83 U.S. cities in our study, we acquired spatial data on the distribution of HOLC grades across U.S. cities from the Mapping Inequality Project. We also acquired data on road, rail, and aircraft noise (hereafter transportation noise models), from the U.S. Department of Transportation, National Transportation Noise Map 2018. The transportation noise models represent potential exposure to transportation noise reported on a decibel scale in a 30m x 30m pixel resolution. Here noise represents the average noise energy produced by road, rail, and aviation networks over a 24-hour period, measured in A-weighted decibels (dBA) (LAeq, 24h) at sampling locations deployed across a uniform grid in each city at an elevation of 1.5 m above ground level. Noise levels below 35 dBA are assumed to have minimal negative impacts to humans and the environment and thus are represented with null values in the transportation noise models. For each HOLC grade and each city, we used zonal statistics in ArcGIS Desktop v. 10.7 to calculate descriptive statistics (median, minimum, maximum, area) for the 30m x 30m pixels in the transportation noise models with non-null noise values (i.e., values > 35 dBA). We used the resulting zonal statistics estimates to calculate an area-corrected measure of excess noise: N = (r * Md)/a where N is excess noise in each HOLC grade (with units of dBA/900 m2); r is the area covered by the 30m x 30m pixels with noise values >35 dBA across all polygons of the same HOLC grade in each city; Md is the median transportation noise value (in dBA) for those same pixels; and a is the total area of all polygons of the same HOLC grade in each city. Literature Review Methodology To assess the effects of noise on wildlife in urban environments, we conducted a literature review using Thompson's ISI Web of Science and adapting the methods of Shannon et al. (2016). We adjusted Shannon et al. (2016) search criteria to include urban phrases, resulting in the following search terms (TS=(WILDLIFE OR ANIMAL OR MAMMAL OR REPTILE OR AMPHIBIAN OR BIRD OR FISH OR INVERTEBRATE) AND TS=(NOISE OR SONAR) AND TS=(CITY OR *URBAN OR METROPOLITAN)). We only selected papers published between 1990 and 23 June 2021 (i.e., the date we conducted our search) within the ISI Web of Science categories of 'Acoustics', 'Zoology', 'Ecology', 'Environmental Sciences', 'Ornithology', 'Biodiversity Conservation', 'Evolutionary Biology', and 'Marine Freshwater Biology'. This returned 691 peer-reviewed papers, which we filtered so only empirical studies focused on documenting the effects of anthropogenic noise on wildlife in urban or suburban ecosystems or the effects of urban noise on wildlife in rural environments were included in the final data set. We excluded reviews, meta-analyses, methods papers, and research that took place outside of urban or suburban areas where the noise was not explicitly denoted as urban (e.g., omitted studies that measured traffic noise by parks and reserves in rural areas). For the 241 articles previously analyzed in Shannon et al. (2016), one of our authors reviewed each paper to determine which studies were focused on urban noise. We also verified the noise levels that caused a significant biological response, noting each noise level if multiple responses were recorded. For any new articles published since the Shannon et al. (2016) dataset or those published between 1990 and 2013 but not reviewed by Shannon et al. (2016) (n = 96), two of our authors reviewed each paper to first determine which studies met our criteria and then compiled data on a number of variables of interest, including the noise levels and their resulting biological responses that were statistically significant. For this subset of papers, one author was randomly assigned a list of papers and then a second author was randomly assigned to assess the accuracy of the data collected by the first author. Any discrepancies were discussed as a group until an agreement was reached. Noise categories (environmental, transportation, industrial, multiple, other) were chosen for each paper by noting the explicitly stated source or description of urban noise described in the methodology. Noise levels and their units were reported for each paper, with only noise levels reported in decibels (dB) being used in data analysis. We recorded the sound metric used (i.e., SPL, SPL Max, Leq) for each paper and also recorded the weightings for each noise level