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Biomedical subjects

L H Paasch

Publications and source records attributed to L H Paasch.

8 recordsLinked to original sources
PubMed2005

Haematological and histological findings in Leghorn chickens infected with infectious bursal disease virus strain 73688.

In the present study, specific-pathogen-free, 2-week-old Leghorn chickens were experimentally infected with strain 73688 of infectious bursal disease virus (IBDV) in order to evaluate haematological and histological changes that might suggest a pathomechanism for haemorrhages in this disease. At 96 hours post infection (hpi) a significant increase in prothrombin time was detected in the absence of visible lesions in myeloid bone marrow tissue and of significant thrombocytopenia. The aforementioned findings suggest alteration of the secondary coagulation mechanisms and not a direct effect of virus on thrombocytes or its precursors.

Animals↗
PubMed2005

Thrombocytopenia in Newcastle disease: haematological evaluation and histological study of bone marrow.

A Newcastle disease virus (NDV) isolated in Mexico and called Chimalhuacan strain was characterised by gene F restriction enzyme analysis and found to be a genotype II velogenic virus. Haematological evaluations and histological studies of bone marrow were conducted on chickens experimentally infected with the Chimalhuacan virus and on control chickens. Within 72 hours post infection (hpi), a 50% decrease in thrombocyte and monocyte counts and a complete cellular depletion in bone marrow islands were evident in the infected group. These findings suggest that the Chimalhuacan strain of NDV causes an early and severe damage of the haematopoietic cells including thrombocyte precursors, which might explain the marked thrombocytopenia detected in early stages of this disease.

Animals↗
PubMed2005

Haematological and histological findings in birds experimentally infected with highly pathogenic H5N2 avian influenza virus.

Experimental infection of specific-pathogen-free (SPF) Leghorn chickens with a highly pathogenic H5N2 avian influenza virus produced cellular hyperplasia in the bone marrow at 36 hours post infection (hpi) and haematological evidence of monocytosis, thrombocytopenia and heterophilia was also detected. An early, significant and progressive haematological change was thrombocytopenia starting at 24 hpi without an increase of prothrombin time. The findings suggest that highly pathogenic avian influenza virus interferes only with the primary haemostatic mechanisms by consumption of thrombocytes, while the secondary haemostatic mechanisms remain intact.

Animals↗
PubMed1979

Pathological studies in experimental Candida endocarditis.

Mycotic endocarditis was produced in rabbits by indwelling intracardiac catheters filled with a suspension of Candida albicans. Grossly, cardiac lesions consisted of massive fungoid valvular vegetations and/or "sleeve thrombi" surrounding the catheter. Microscopically, platelet-fibrin aggregates were observed to be loosely attached to the valvular cusps. With time, the vegetations became organized and more firmly attached against the endocardium. Also observed was a heavy neutrophylic collar often containing Candida cells which infiltrate the subendothelial tissues of the valvular cusps. Sterile endocardial lesions were produced by retained catheters. The lesions consisted of discrete, glistening, hemispherical nodules in the right heart; and similar elevated plaques on the mural endocardium of the left ventricle. Microscopically, these lesions consisted of fibrous connective tissues devoid of inflammatory cells. The lesions in the left ventricle were more extensive, extending into the myocardium.

Animals↗
PubMedDate not supplied

Ultrastructural glomerular changes in experimental infection with the classical swine fever virus.

Ultrastructural studies of glomerular changes were performed on 16 pigs experimentally infected with a highly virulent strain of the classical swine fever virus. Our observations revealed the thickening of glomerular basement membranes, swelling of endothelial cells and cytoplasmic vacuolization within podocytes containing abundant viral particles. An early viral infection of podocytes was suggested as the cause of selective swelling of the foot processes of these cells with the consequent obliteration of the glomerular urinary spaces. To our knowledge this is the first report of ultrastructural evidence of classical swine fever virions infecting glomerular podocytes.

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