Ultrastructural changes related to the lymph node haemorrhages in acute African swine fever

Carrasco, L.; Lara, F. Chacón-M. de; Mulas, J. Martı́n de las; Gómez-Villamandos, J.C.; Sierra, M. A.; Villeda, C. J.; Wilkinson, Philip

doi:10.1016/s0034-5288(97)90190-9

Cited by 25 publications

(19 citation statements)

References 20 publications

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“…In addition, six and seven days after inoculation with the Malawi'83 isolate, scattered myeloid cells which were morphologically similar to immature neutrophils, and a few mature neutrophils showed diffuse immunoreactivity with the vp 73 mAb. This finding supports previous reports of viral antigens in neutrophils (Colgrove and others 1969, Pérez and others 1994, Rodriguez and others 1996a), and of viral replication in mature and immature neutrophils both in vitro (Casal and others 1984) and in vivo (Carrasco and others 1996b).…”

Section: Methodssupporting

confidence: 92%

Double‐labelling immunohistochemical study of megakaryocytes in African swine fever

et al. 1997

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Bone marrow samples from pigs infected with the highly virulent Malawi'83 or moderately virulent Dominican Republic (DR'78) isolates of African swine fever virus were studied by means of a double labelling immunohistochemical technique which stained the major structural protein VP73 of the virus and megakaryocytes simultaneously. In pigs infected with the highly virulent Malawi'83 isolate, 2.2 per cent of megakaryocytes were VP73+ five days after inoculation, and at six and seven days 2.5 and 9.5 per cent of megakaryocytes were VP73+. Some infected and uninfected megakaryocytes showed pyknosis and karyorrhexis, particularly at seven days after inoculation. However, in comparison with uninfected pigs, the number of megakaryocytes decreased only at seven days after inoculation. In pigs infected with the moderately virulent DR'78 isolate, only 0.2 per cent of megakaryocytes were VP73+ at eight days after inoculation. However, at eight, nine and 10 days after inoculation the total number of megakaryocytes was significantly lower (P < 0.01) than in control uninfected pigs, and the majority of the megakaryocytes showed signs of cell death such as pyknosis and karyorrhexis. The fact that this greater destruction of megakaryocytes was associated with the lower rate of infection of this cell type suggests that indirect damage to megakaryocytes is an additional mechanism of thrombocytopenia in acute and subacute African swine fever.

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Section: Methodssupporting

confidence: 92%

Double‐labelling immunohistochemical study of megakaryocytes in African swine fever

et al. 1997

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“…Affected animals die in shock, usually 1 week after fever begins and foam is generally observed around the mouth and nose (Sierra et al, 1990;Carrasco et al, 1996aCarrasco et al, , 2002. Affected pigs show erythema, which particularly affects the skin of the ears, tail, distal extremities, chest, abdomen and perianal area.…”

Section: Transmission Route Location and Date Of Occurrencementioning

confidence: 99%

“…The virus infects monocytes and macrophages (Malmquist and Hay, 1960), but infection of T or B lymphocytes has never been observed (Minguez et al, 1988). The virus also replicates in endothelial cells (Carrasco et al, 1996a), hepatocytes, renal tubular epithelial cells (G omez-Villamandos et al, 1995a) and neutrophils. After initial replication in these primary sites, ASFV spreads through the blood or the lymphatic system, where it persists for long periods of time in the absence of neutralizing antibodies and moves towards secondary sites of replication.…”

Section: Introductionmentioning

confidence: 99%

An Update on the Epidemiology and Pathology of African Swine Fever

Sánchez-Vizcaíno

Mur

Gómez-Villamandos

et al. 2015

Journal of Comparative Pathology

337

360

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“…The diffuse activation of the blood coagulation system, and subsequent development of disseminated intravascular coagulation (DIC) also has been demonstrated as the cause of haemorrhages in African swine fever (ASF) and other viral haemorrhagic diseases. In these cases, DIC has been attributed to activation of endothelial cells, as it coincides with the appearance of haemorrhages, observed from the first stages of the disease, and not with the virus replication in the endothelial cells, which has been observed only in the final stages of the disease and in a small proportion of cells (Gomez-Villamandos et al, 1995a;Carrasco et al, 1997b). The reported presence of activated endothelial cells in ASF (Gomez-Villamandos et al, 1995a;Carrasco et al, 1997b) is similar to that observed in HC: proliferation and enlargement of the endothelial cells that might, eventually, occlude the vascular lumen (Trautwein, 1988).…”

Section: Discussionmentioning

confidence: 89%

Characterization of Lesions Caused by a South American Virulent Isolate (‘Quillota’) of the Hog Cholera Virus

Quezada

Cayo

Carrasco

et al. 2000

Journal of Veterinary Medicine, Series B

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In this study, macroscopic and histopathological lesions produced by a virulent South American isolate ('Quillota') of hog cholera virus were studied. The virus was inoculated in doses of 10(5)TCID50 in each of 35 pigs of 20 kg live weight. The animals were slaughtered from 4 to 18 days post-inoculation. The presence of virus antigens in lymphatic tissue was confirmed by both direct immunofluorescence and Avidin-Biotin-Peroxidase techniques in formalin-embedded tissue samples. Histological sections were stained with haematoxylin-eosin and Mallory's phosphotungstic acid haematoxylin methods. The 'Quillota' isolate used in this study caused a disease characterized by vascular lesions (splenic infarcts, haemorrhages in the lymph nodes and the urinary system and disseminated microthrombosis), and necrosis of lymphocytes, particularly in the B-areas of the lymphoid organs, lesions that are characteristic of the acute form of the disease. Other lesions observed were a non-purulent meningoencephalitis, the necrosis of the epithelial cells of tonsils, the presence of fibrin nets in the red pulp and a marked thickening of the alveolar septa.

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Ultrastructural changes related to the lymph node haemorrhages in acute African swine fever

Cited by 25 publications

References 20 publications

Double‐labelling immunohistochemical study of megakaryocytes in African swine fever

Double‐labelling immunohistochemical study of megakaryocytes in African swine fever

An Update on the Epidemiology and Pathology of African Swine Fever

Characterization of Lesions Caused by a South American Virulent Isolate (‘Quillota’) of the Hog Cholera Virus

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