Rodriguez-Prieto V.,Complutense University of Madrid |
Vicente-Rubiano M.,Complutense University of Madrid |
Sanchez-Matamoros A.,Complutense University of Madrid |
Rubio-Guerri C.,Complutense University of Madrid |
And 11 more authors.
Epidemiology and Infection | Year: 2014
In this globalized world, the spread of new, exotic and re-emerging diseases has become one of the most important threats to animal production and public health. This systematic review analyses conventional and novel early detection methods applied to surveillance. In all, 125 scientific documents were considered for this study. Exotic (n = 49) and re-emerging (n = 27) diseases constituted the most frequently represented health threats. In addition, the majority of studies were related to zoonoses (n = 66). The approaches found in the review could be divided in surveillance modalities, both active (n = 23) and passive (n = 5); and tools and methodologies that support surveillance activities (n = 57). Combinations of surveillance modalities and tools (n = 40) were also found. Risk-based approaches were very common (n = 60), especially in the papers describing tools and methodologies (n = 50). The main applications, benefits and limitations of each approach were extracted from the papers. This information will be very useful for informing the development of tools to facilitate the design of cost-effective surveillance strategies. Thus, the current literature review provides key information about the advantages, disadvantages, limitations and potential application of methodologies for the early detection of new, exotic and re-emerging diseases. © 2014 Cambridge University Press. Source
Smither S.J.,UK Defence Science and Technology Laboratory |
Nelson M.,UK Defence Science and Technology Laboratory |
Eastaugh L.,UK Defence Science and Technology Laboratory |
Laws T.R.,UK Defence Science and Technology Laboratory |
And 4 more authors.
International Journal of Experimental Pathology | Year: 2013
Marburg virus causes a highly infectious and lethal haemorrhagic fever in primates and may be exploited as a potential biothreat pathogen. To combat the infection and threat of Marburg haemorrhagic fever, there is a need to develop and license appropriate medical countermeasures. To determine whether the common marmoset (Callithrix jacchus) would be an appropriate model to assess therapies against Marburg haemorrhagic fever, initial susceptibility, lethality and pathogenesis studies were performed. Low doses of virus, between 4 and 28 TCID50, were sufficient to cause a lethal, reproducible infection. Animals became febrile between days 5 and 6, maintaining a high fever before succumbing to disease between 8 and 11 days postchallenge. Typical signs of Marburg virus infection were observed including haemorrhaging and a transient rash. In pathogenesis studies, virus was isolated from the animals' lungs from day 3 postchallenge and from the liver, spleen and blood from day 5 postchallenge. Early signs of histopathology were apparent in the kidney and liver from day 3. The most striking features were observed in animals exhibiting severe clinical signs, which included high viral titres in all organs, with the highest levels in the blood, increased levels in liver function enzymes and blood clotting times, decreased levels in platelets, multifocal moderate-to-severe hepatitis and perivascular oedema. © 2013 Crown copyright. International Journal of Experimental Pathology © 2013 International Journal of Experimental Pathology. Source
Nelson M.,UK Defence Science and Technology Laboratory |
Nelson M.,University of Surrey |
Salguero F.J.,Animal Health Veterinary Laboratories Agency |
Dean R.E.,UK Defence Science and Technology Laboratory |
And 4 more authors.
International Journal of Experimental Pathology | Year: 2014
Glanders and melioidosis are caused by two distinct Burkholderia species and have generally been considered to have similar disease progression. While both of these pathogens are HHS/CDC Tier 1 agents, natural infection with both these pathogens is primarily through skin inoculation. The common marmoset (Callithrix jacchus) was used to compare disease following experimental subcutaneous challenge. Acute, lethal disease was observed in marmosets following challenge with between 26 and 1.2 × 108 cfu Burkholderia pseudomallei within 22-85 h. The reproducibility and progression of the disease were assessed following a challenge of 1 × 102 cfu of B. pseudomallei. Melioidosis was characterised by high levels of bacteraemia, focal microgranuloma progressing to non-necrotic multifocal solid lesions in the livers and spleens and multi-organ failure. Lethal disease was observed in 93% of animals challenged with Burkholderia mallei, occurring between 5 and 10.6 days. Following challenge with 1 × 102 cfu of B. mallei, glanders was characterised with lymphatic spread of the bacteria and non-necrotic, multifocal solid lesions progressing to a multifocal lesion with severe necrosis and pneumonia. The experimental results confirmed that the disease pathology and presentation is strikingly different between the two pathogens. The marmoset provides a model of the human syndrome for both diseases facilitating the development of medical countermeasures. © 2014 Company of the International Journal of Experimental Pathology (CIJEP). Source
Mill A.C.,Northumbria University |
Rushton S.P.,Northumbria University |
Shirley M.D.F.,Northumbria University |
Smith G.C.,Animal Health Veterinary Laboratories Agency |
And 3 more authors.
Environmental Microbiology | Year: 2014
Summary: American foulbrood (AFB), caused by Paenibacillus larvae, is the most damaging bacterial brood disease of the honeybee (Apis mellifera), causing colony deaths on all continents where honeybees are managed. AFB has been a persistent problem in the UK for over 70 years, with a fluctuating number of cases discovered annually. Once diseased colonies are identified, they are destroyed to reduce pathogen spread. We investigated the pattern of AFB cases recorded over the period 1994 to 2012 using spatial-statistical approaches, with a view to identifying the nature of spread across England and Wales. Our results indicated that AFB exhibits significant spatial aggregation at distances from 10 to 30km, with aggregations lasting between 1 and 5 years. Kernel smoothing indicated areas of elevated relative risk in different years, and these were further detailed by spatial-scan statistics. We identified disease clusters and successfully estimated their size, location and duration. The majority of clusters did not persist in all years, indicating that management measures may lead to localized extinction of the disease. Whilst less common, persistent clusters likely indicate potential endemic or exotic risk points. The application of robust epidemiological approaches to improve the control of AFB is discussed. © 2013 Crown copyright. Environmental Microbiology published by Society for Applied Microbiology and John Wiley & Sons Ltd. Source
Jeffrey M.,Animal Health Veterinary Laboratories Agency |
McGovern G.,Animal Health Veterinary Laboratories Agency |
Chambers E.V.,Roslin Institute |
King D.,Roslin Institute |
And 7 more authors.
Brain Pathology | Year: 2012
Gerstmann-Sträussler-Scheinker (GSS) P102L disease is a familial form of a transmissible spongiform encephalopathy (TSE) that can present with or without vacuolation of neuropil. Inefficient disease transmission into 101LL transgenic mice was previously observed from GSS P102L without vacuolation. However, several aged, healthy mice had large plaques composed of abnormal prion protein (PrP d). Here we perform the ultrastructural characterization of such plaques and compare them with PrP d aggregates found in TSE caused by an infectious mechanism. PrP d plaques in 101LL mice varied in maturity, with some being composed of deposits without visible amyloid fibrils. PrP d was present on cell membranes in the vicinity of all types of plaques. In contrast to the unicentric plaques seen in infectious murine scrapie, the plaques seen in the current model were multicentric and were initiated by protofibrillar forms of PrP d situated on oligodendroglia, astrocytes and neuritic cell membranes. We speculate that the initial conversion process leading to plaque formation begins with membrane-bound PrP C but that subsequent fibrillization does not require membrane attachment. We also observed that the membrane alterations consistently seen in murine scrapie and other infectious TSEs were not present in 101LL mice with plaques, suggesting differences in the pathogenesis of these conditions. © 2011 The Authors and Crown copyright (AHVLA); Brain Pathology © 2011 International Society of Neuropathology. Source