Publications

This chapter discusses the historical distribution of Avian metapneumoviruses (aMPV), molecular biology of aMPV isolates, pathobiology of aMPV, diagnostics and prevention of aMPV disease in turkey and poultry.

Resistance to respiratory disease in cattle requires host defense mechanisms that protect against pathogens which have evolved sophisticated strategies to evade them, including an altered function of pulmonary macrophages (M phi s) or the induction of inflammatory responses that cause lung injury and sepsis. The aim of this study was to clarify the mechanisms responsible for vascular changes occurring in the lungs of calves infected with bovine viral diarrhea virus (BVDV) and challenged later with bovine herpesvirus type 1 (BHV-1), evaluating the role of M phi s in the development of pathological lesions in this organ. For this purpose, pulmonary lesions were compared between co-infected calves and healthy animals inoculated only with BHV-1 through immunohistochemical (MAC387, TNF alpha, IL-1 alpha, iNOS, COX-2 and Factor-VIII) and ultrastructural studies. Both groups of calves presented important vascular alterations produced by fibrin microthrombi and platelet aggregations within the blood vessels. These findings were earlier and more severe in the co-infected group, indicating that the concomitance of BVDV and BHV-1 in the lungs disrupts the pulmonary homeostasis by facilitating the establishment of an inflammatory and procoagulant environment modulated by inflammatory mediators released by pulmonary M phi s. In this regard, the co-infected calves, in spite of presenting a greater number of IM phi s than single-infected group, show a significant decrease in iNOS expression coinciding with the presence of more coagulation lesions. Moreover, animals pre-inoculated with BVDV displayed an alteration in the response of pro-inflammatory cytokines (TNF alpha and IL-1), which play a key role in activating the immune response, as well as in the local cell-mediated response.

The National Equine Database (NED) contains information on the size and distribution of the horse population, but the data quality remains unknown. These data could assist with surveillance, research and contingency planning for equine infectious disease outbreaks. OBJECTIVES: 1) To assess the extent of obsolete and missing data from NED, 2) evaluate the extent of spatial separation between horse and owner location and 3) identify relationships between spatial separation and land use. Two questionnaires were used to assess data accuracy in NED utilising local authority passport inspections and distribution of questionnaires to 11,000 horse owners. A subset of 1010 questionnaires was used to assess horse-owner geographic separation. During 2005-2010, 17,048 passports were checked through local authority inspections. Of these, 1558 passports (9.1%; 95% confidence interval [CI] 8.7-9.5%) were noncompliant, with 963 (5.6%; 95% CI 5.3-6.0%) containing inaccurate information and 595 (3.5%; 95% CI 3.2-3.8%) classified as missing. Of 1382 questionnaires completed by horse owners, 380 passports were obsolete (27.5%; 95% CI 25.2-29.9%), with 162 (11.7%; 95% CI 10.0-13.4%) being retained for deceased horses and 218 (15.8%; 95% CI 13.9-17.7%) having incorrect ownership details. Fifty-three per cent (95% CI 49.9-56.1%) of owners kept their horse(s) at home and 92% (95% CI 90.3-93.7%) of horses resided within 10?km of their owners. Data from a small sample survey suggest the majority of data on NED are accurate but a proportion of inaccuracies exist that may cause delay in locating horses and contacting owners during a disease outbreak. The probability that horses are located in the same postcode sector as the owner's home address is larger in rural areas. Appropriate adjustment for population size, horse-owner spatial separation and land usage would facilitate meaningful use of the national horse population derived from NED for risk modelling of incursions of equine diseases into Great Britain.

Dendritic cells (DCs) are professional antigen-presenting cells with a critical role in the regulation of innate and adaptive immune responses and thus have been considered of great interest in the study of a variety of infectious diseases. The objective of this investigation was to characterize the in vivo distribution of DCs in bovine tissues by using potential DC markers to establish a basis for the study of DCs in diseased tissues. Markers evaluated included MHCII, CD208, CD1b, CD205, CNA.42, and S100 protein, the latter 2 being expressed by follicular dendritic cells whose origin and role are different from the rest of hematopoietic DCs. Paraffin wax-embedded tissues from 6 healthy Friesian calves were subjected to the avidin-biotin-peroxidase method, and the most appropriate fixatives, dilutions, and antigen retrieval pretreatments were studied for each of the primary antibodies. The most significant results included the localization of CD208-positive cells not only in the T zone of lymphoid organs but also within lymphoid follicles; CD1b-positive cells were mainly found in thymus and interfollicular areas of some lymph nodes; cells stained with anti-CD205 antibody were scarce, and their location was mainly in nonlymphoid tissues; and CNA.42- and S100 protein-positive cells localized in primary lymphoid follicles and light zones of germinal centers, although showing differences in the staining pattern. Furthermore, MHCII was established as one of the most sensitive markers for any DC of hematopoietic origin. These results increase our understanding of DC immunolabeling and will help in future DC studies of both healthy and diseased tissues.