2,601 research outputs found

    The potato murrain on the European continent and the revolutions of 1848

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    The tale of the Irish Famine, 1845¿1849, following the outbreak of potato late blight, has been told repeatedly, but the parallel story of the Continental Famine, 1845¿1847, has not yet been recorded. The Continental Famine was caused by poor harvests of potatoes, due to the same late blight, but also of grain, due to frost, drought, rust, voles, inopportune rains, floods and hailstorms. The Continental Famine was enhanced by hoarding, speculation, and poor governance. Hunger was followed by infectious diseases. The demographic effects of hunger and diseases are difficult to disentangle. The number of excess deaths due to the Continental Famine cannot yet be determined with any precision, but clearly it approaches that of the Irish Famine. The harvest failures of 1845 and 1846 and the resulting famines came on top of rural pauperisation and urban discontent, and thus contributed to the revolutions of 1848 on the European Continent. The statement `an epidemic of potato late blight caused an epidemic of revolutions¿ is, perhaps, exaggerated but it contains a grain of truth

    The integrated concept of disease resistance; a new view including horizontal and vertical resistance in plants

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    Horizontal, uniform, race-non-specific or stable resistance can be discerned according to Van der Plank, from vertical, differential, race-specific or unstable resistance by a test in which a number of host genotypes (cultivars or clones) are tested against a number of pathogen genetypes traces of isolatest. If the total non-environmental variance in levels of resistance is due to main effects only differences between cultivars and differences between isolates) the resistance and the pathogen many (in the broad sense) are horizontal in nature. Vertical resistance and pathogenicity are characterized by the interaction between host and pathogen showing up as a variance compenent in this test due to interaction between cultivars and isolates. A host and pathogen model was made in which resistance and pathogenicity are governed by live polygenic loci. Within the host the resistance genes show additivity. Two models were investigated in model I resistance and pathogenicity genes operate in an additive way as envisaged by Van der Plank in his horizontal resistance. Model II is characterized by a gene-for-gene action between the polygenes of the host and those of the pathogen. The cultivar isolate test in model I showed only main effect variance. Surprisingly, the variance in model II was also largely due to main effects. The contribution of the interaction to the variance uppeared so small, that it would be difficult to discern it from a normal error variance. So-called horizontal resistance can therefore be explained by a polygenic resistance, where the individual genes are vertical and operating on a gene-for-gene basis with virulence genes in the pathogen. The data reported so far support the idea that model II rather than model I is the realistic one. The two models also revealed that populations with a polygenic resistance based on the gene-for-gene action have an increased level of resistance compared with the addition model, while its stability as far as mutability of the pathogen is concerned, is higher compared to those with an additive gene action. Mathematical studies of Mode too support the gene-for-gene concept. The operation of all resistance and virulence genes in a natural population is therefore seen as one integrated system. All genes for true resistance in the host population, whether they are major or minor genes are considered to interact in a gene-for-gene way with virulence genes either major or minor, in the pathogen population. The models revealed other important aspects. Populations with a polygenic resistance based on a gene-for-gene action have an increased level of resistance compared to populations following the addition model. The stability, as far as mutability of the pathogen is concerned, is higher in the interaction model than in the addition model. The effect of a resistance gene on the level of resistance of the population consists of its effect on a single plant times its gene frequency in the population. Due to the adaptive forces in both the host and the pathogen population and the gene-for-gene nature of the gene action an equilibrium develops that allows all resistance genes to remain effective although their corresponding virulence genes are present. The frequencies of the resistance and virulence genes are such that the effective frequencies of resistance genes tend to be negatively related to the magnitude of the gene effect. This explains why major genes often occur at low frequencies, while minor genes appear to be frequent. It is in this way that the host and the pathogen, both as extremely variable and vigorous populations, can co-exist. Horizontal and vertical resistance as meant by Van der Plank therefore do not represent different kinds of resistances, they represent merely polygenic and oligogenic resistances resp. In both situations the individual host genes interact specifically with virulence genes in the pathogen. Van der Plank's test for horizontal resistance appears to be a simple and sound way to test for polygenic inheritance of resistance. The practical considerations have been discussed. The agro-ecosystems should be made as diverse as possible. Multilines, polygenic resistance, tolerance, gene deployment and other measures should be employed, if possible in combination

    An update on environmental mastitis: challenging perceptions

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    Environmental mastitis is the most common and costly form of mastitis in modern dairy herds where contagious transmission of intramammary pathogens is controlled through implementation of standard mastitis prevention programmes. Environmental mastitis can be caused by a wide range of bacterial species, and binary classification of species as contagious or environmental is misleading, particularly for Staphylococcus aureus, Streptococcus uberis and other streptococcal species, including Streptococcus agalactiae. Bovine faeces, the indoor environment and used pasture are major sources of mastitis pathogens, including Escherichia coli and S. uberis. A faeco-oral transmission cycle may perpetuate and amplify the presence of such pathogens, including Klebsiella pneumoniae and S. agalactiae. Because of societal pressure to reduce reliance on antimicrobials as tools for mastitis control, management of environmental mastitis will increasingly need to be based on prevention. This requires a reduction in environmental exposure through bedding, pasture and pre-milking management and enhancement of the host response to bacterial challenge. Efficacious vaccines are available to reduce the impact of coliform mastitis, but vaccine development for gram-positive mastitis has not progressed beyond the “promising” stage for decades. Improved diagnostic tools to identify causative agents and transmission patterns may contribute to targeted use of antimicrobials and intervention measures. The most important tool for improved uptake of known mastitis prevention measures is communication. Development of better technical or biological tools for management of environmental mastitis must be accompanied by development of appropriate incentives and communication strategies for farmers and veterinarians, who may be confronted with government-mandated antimicrobial use targets if voluntary reduction is not implemented

    Multilocus sequence typing of a global collection of pasteurella multocida isolates from cattle and other host species demonstrates niche association

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    Background- Pasteurella multocida causes disease in many host species throughout the world. In bovids, it contributes to bovine respiratory disease (BRD) and causes haemorrhagic septicaemia (HS). Previous studies have suggested that BRD-associated P. multocida isolates are of limited diversity. A multilocus sequence typing (MLST) scheme for P. multocida was used to determine whether the low levels of diversity reported are due to the limited discriminatory power of the typing method used, restricted sample selection or true niche association. Bovine respiratory isolates of P. multocida (n = 133) from the UK, the USA and France, collected between 1984 and 2008 from both healthy and clinically affected animals, were typed using MLST. Isolates of P. multocida from cases of HS, isolates from other host species and data from the MLST database were used as comparison. Results - Bovine respiratory isolates were found to be clonal (ISA 0.45) with 105/128 belonging to clonal complex 13 (CC13). HS isolates were not related to bovine respiratory isolates. Of the host species studied, the majority had their own unique sequence types (STs), with few STs being shared across host species, although there was some cross over between porcine and bovine respiratory isolates. Avian, ovine and porcine isolates showed greater levels of diversity compared to cattle respiratory isolates, despite more limited geographic origins. Conclusions - The homogeneity of STs of bovine respiratory P. multocida observed, and the differences between these and P. multocida subpopulations from bovine non-respiratory isolates and non-bovine hosts may indicate niche association

    ‘Next-Generation’ surveillance: an epidemiologists’ perspective on the use of molecular information in food safety and animal health decision-making

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    Advances in the availability and affordability of molecular and genomic data are transforming human health care. Surveillance aimed at supporting and improving food safety and animal health is likely to undergo a similar transformation. We propose a definition of ‘molecular surveillance’ in this context and argue that molecular data are an adjunct to rather than a substitute for sound epidemiological study and surveillance design. Specific considerations with regard to sample collection are raised, as is the importance of the relation between the molecular clock speed of genetic markers and the spatiotemporal scale of the surveillance activity, which can be control- or strategy-focused. Development of standards for study design and assessment of molecular surveillance system attributes is needed, together with development of an interdisciplinary skills base covering both molecular and epidemiological principles

    Use of on-farm data to guide treatment and control mastitis caused by Streptococcus uberis

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    Treatment of mastitis is the most common reason for use of antimicrobial agents in dairy cattle. The responsible use of antimicrobials could be strengthened by knowledge of predictors for cure, which would help to tailor treatment decisions. Ideally, to allow for widespread uptake, this would be achieved using data that are routinely available. To assess whether this is feasible in practice, farmers were invited to submit milk samples from mastitis cases to their veterinary practice for bacteriological culture. Among 624 culture-positive samples, 251 were positive for Streptococcus uberis. Using cow-level data, cases were classified as severe, first nonsevere, repeat, or subclinical. Additional data were collected at the cow level [somatic cell count (SCC), parity, lactation stage, milk yield, fat and protein contents, treatment] and at the herd level (housing, bedding, premilking teat disinfection, postmilking teat disinfection). Severe cases were overrepresented among heifers and animals in early lactation, and repeat cases were overrepresented in cows with 3 or more lactations. The probability of cure was higher among first- and second-parity animals than among older cows, and was higher in animals with a single elevated cow-level SCC than in animals with multiple high SCC records. Results obtained in the current study are similar to those previously described for Staphylococcus aureus mastitis. Thus, routinely available cow-level information can help to predict the outcome of antimicrobial treatment of the most common causes of gram-positive mastitis

    Pilot study into milk haptoglobin as an indicator of udder health in heifers after calving

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    Mastitis, inflammation of the mammary gland, is often caused by intramammary infection with bacterial organisms. It impacts on dairy cattle welfare, production, udder health and longevity in the herd. Current detection methods for mammary inflammation and infection all have limitations, particularly for on-farm diagnosis of non-clinical mastitis after calving. Acute phase proteins have been suggested as alternative early indicators of the disease and can potentially be used as cow-side test with results in real time. In this study, milk haptoglobin concentrations were investigated over the first week postpartum to explore haptoglobin's potential as indicator of udder health in dairy heifers. Haptoglobin concentration was highest on day 3 of lactation, and was positively correlated with somatic cell count, a commonly used marker of inflammation (rs=0.68). Haptoglobin level was also associated with bacteriological culture results, a key indicator of infection status, whereby median haptoglobin concentration on days 3 and 5 was higher in quarters that were infected at calving than quarters that were non infected at calving. Sensitivity and specificity of haptoglobin concentration as indicator of infection were low, both for lenient and strict culture-based definitions of intramammary infection (57 or 60% and 61 or 63%, respectively). Although haptoglobin was a poor biomarker for intramammary infection with coagulase negative staphylococci in heifers during the first week after calving, it may have value as an indicator of major pathogen infections, particularly in large scale dairy herds where pre-partum heifers are managed off-site

    Human streptococcus agalactiae strains in aquatic mammals and fish

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    <p>Background: In humans, Streptococcus agalactiae or group B streptococcus (GBS) is a frequent coloniser of the rectovaginal tract, a major cause of neonatal infectious disease and an emerging cause of disease in non-pregnant adults. In addition, Streptococcus agalactiae causes invasive disease in fish, compromising food security and posing a zoonotic hazard. We studied the molecular epidemiology of S. agalactiae in fish and other aquatic species to assess potential for pathogen transmission between aquatic species and humans.</p> <p>Methods: Isolates from fish (n = 26), seals (n = 6), a dolphin and a frog were characterized by pulsed-field gel electrophoresis, multilocus sequence typing and standardized 3-set genotyping, i.e. molecular serotyping and profiling of surface protein genes and mobile genetic elements.</p> <p>Results: Four subpopulations of S. agalactiae were identified among aquatic isolates. Sequence type (ST) 283 serotype III-4 and its novel single locus variant ST491 were detected in fish from Southeast Asia and shared a 3-set genotype identical to that of an emerging ST283 clone associated with invasive disease of adult humans in Asia. The human pathogenic strain ST7 serotype Ia was also detected in fish from Asia. ST23 serotype Ia, a subpopulation that is normally associated with human carriage, was found in all grey seals, suggesting that human effluent may contribute to microbial pollution of surface water and exposure of sea mammals to human pathogens. The final subpopulation consisted of non-haemolytic ST260 and ST261 serotype Ib isolates, which belong to a fish-associated clonal complex that has never been reported from humans.</p> <p>Conclusions: The apparent association of the four subpopulations of S. agalactiae with specific groups of host species suggests that some strains of aquatic S. agalactiae may present a zoonotic or anthroponotic hazard. Furthermore, it provides a rational framework for exploration of pathogenesis and host-associated genome content of S. agalactiae strains.</p&gt
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