Immunohistochemical demonstration of African horse sickness viral antigen in tissues of experimentally infected equines

Wohlsein, P.; Pohlenz, Joachim; Salt, Jeremy; Hamblin, C.

doi:10.1007/978-3-7091-6823-3_7

Cited by 8 publications

(57 citation statements)

References 5 publications

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“…Wohlsein et al [136] have shown that in experimentally infected horses with the peracute form of disease antigen is found primarily in the cardio-vascular and lymphatic systems, and to lesser extent throughout the body. In animals with horse sickness fever antigen is concentrated in the spleen, with lesser amounts elsewhere.…”

Section: Pathogenesismentioning

confidence: 99%

“…The main locations of antigen were endothelial cells suggesting them to be a primary target of the virus and large cells of the red pulp of the spleen. The presence of antigen in large mononuclear cells, resembling phagocytic cells, and surrounding lymphoid follicles suggests that these cells might also be involved in virus replication and in the transport of viral protein to the lymphoid follicles [136].…”

Section: Pathogenesismentioning

confidence: 99%

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African horse sickness

2004

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-African horse sickness virus (AHSV) causes a non-contagious, infectious insect-borne disease of equids and is endemic in many areas of sub-Saharan Africa and possibly Yemen in the Arabian Peninsula. However, periodically the virus makes excursions beyond its endemic areas and has at times extended as far as India and Pakistan in the east and Spain and Portugal in the west. The vectors are certain species of Culicoides biting midge the most important of which is the AfroAsiatic species C. imicola. This paper describes the effects that AHSV has on its equid hosts, aspects of its epidemiology, and present and future prospects for control. The distribution of AHSV seems to be governed by a number of factors including the efficiency of control measures, the presence or absence of a long term vertebrate reservoir and, most importantly, the prevalence and seasonal incidence of the major vector which is controlled by climate. However, with the advent of climatechange the major vector, C. imicola, has now significantly extended its range northwards to include much of Portugal, Spain, Italy and Greece and has even been recorded from southern Switzerland. Furthermore, in many of these new locations the insect is present and active throughout the entire year. With the related bluetongue virus, which utilises the same vector species of Culicoides this has, since 1998, precipitated the worst outbreaks of bluetongue disease ever recorded with the virus extending further north in Europe than ever before and apparently becoming endemic in that continent. The prospects for similar changes in the epidemiology and distribution of AHSV are discussed.

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Section: Pathogenesismentioning

confidence: 99%

Section: Pathogenesismentioning

confidence: 99%

African horse sickness

2004

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“…Virus isolation at the World Reference Centre for AHSV and BTV in South Africa confirmed the presence of AHSV-4 in the lung and spleen. Typical positive staining 52,53 was observed in target cells of selected target organs. One hundred reference positive control sections were stored in the form of paraffin tissue sections in closed, labeled slide boxes in the IHC laboratory in the Section of Pathology, Department of Paraclinical Sciences, Faculty of Veterinary Science, University of Pretoria (DPS; Onderstepoort, South Africa).…”

Section: Selection Of Casesmentioning

confidence: 91%

“…37,38 The antiserum was derived by immunizing rabbits with purified AHSV particles. 9,19,52,53 After analysis of all the IHC results obtained using the Hamblin antiserum, the results were compared with those obtained using an anti-AHSV mAb, designated 1F1, 50 on tissues from selected cases to determine whether the mAb could also detect all serotypes of AHSV in horse tissues and whether it would be less likely to cross-react with non-AHSV epitopes in those tissues. The 1F1 mAb has not yet been validated for use in IHC.…”

Section: Anti-ahsv Antibodiesmentioning

confidence: 99%

“…The tissues were fixed in 10% neutral buffered formalin for 24-48 hr, in accordance with approved methods. 17,37,38,52,53 The available spleen, lung, and heart tissue samples from each test case were embedded in a single wax block, sectioned, and mounted according to a standard operating procedure. 1 In some cases, a few extra tissues were also present in the tissue block.…”

Section: Tissue Fixation and Processingmentioning

confidence: 99%

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Standardization and Validation of an Immunoperoxidase Assay for the Detection of African Horse Sickness Virus in Formalin-Fixed, Paraffin-Embedded Tissues

et al. 2009

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Abstract. An immunoperoxidase assay for the detection of African horse sickness virus (AHSV) in formalin-fixed tissues is a valuable tool in the study of the pathogenesis of the disease, as well as a useful addition to existing diagnostic tests when only preserved tissues are available. An assay that uses Hamblin antiserum in a basic avidin-biotin complex detection system was standardized and validated in accordance with the guidelines of the American Association of Veterinary Laboratory Diagnosticians Subcommittee on Standardization of Immunohistochemistry. Using 128 positive cases of African horse sickness confirmed by viral isolation and serotyping and 119 negative cases from countries where the disease has never occurred, diagnostic sensitivity and diagnostic specificity were 100% in the prime target tissues of heart and lung. There was no variation in the ability of the assay to detect all 9 serotypes of AHSV, and there was no cross-reactivity with other orbiviruses in formalin-fixed tissues. The only cross-reactivity observed was in the lungs of 2 negative cases infected with Rhodococcus equi. The assay gave good results on tissues that had been fixed in formalin for up to 365 days. Nonspecific staining was minimal provided that the standard procedures for processing and staining tissues were followed. Good immunohistochemical results were also obtained on samples fixed as long as 24 hr after death. The assay, therefore, provides a robust diagnostic tool for detection of AHSV in formalin-fixed tissues, provided the analysis is done by an experienced pathologist.

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Endothelial cells as active participants in veterinary infections and inflammatory disorders

Behling‐Kelly

Czuprynski

2007

Anim. Health. Res. Rev.

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Endothelial cells were once viewed as relatively inert cells lining the vasculature. They are now recognized as active and responsive regulators of coagulation, platelet adhesion, fluid homeostasis, wound healing, leukocyte extravasation and vascular tone. Endothelial cells play a key role in the host response to infectious agents by regulating leukocyte trafficking, producing inflammatory cytokines and presenting antigen in association with major histocompatibility class II (MHC II) molecules. A number of infectious agents have a tropism for endothelial cells. Infection of endothelial cells can promote thrombosis, vascular leakage, and increased adherence and emigration of leukocytes. Furthermore, activation of a systemic inflammatory response, in the absence of direct endothelial cell infection, can also lead to endothelial cell dysfunction. The purpose of this review is to highlight the interactions between endothelial cells and infectious or inflammatory agents that contribute to coagulation disturbances, vasculitis and edema. A select group of viral and bacterial pathogens will be used as examples to demonstrate how endothelial cell dysfunction contributes to the pathogenesis of infectious and inflammatory disorders.

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Immunohistochemical demonstration of African horse sickness viral antigen in tissues of experimentally infected equines

Cited by 8 publications

References 5 publications

African horse sickness

African horse sickness

Standardization and Validation of an Immunoperoxidase Assay for the Detection of African Horse Sickness Virus in Formalin-Fixed, Paraffin-Embedded Tissues

Endothelial cells as active participants in veterinary infections and inflammatory disorders

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