Cases reported "Disease Models, Animal"

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1/3. Clinical and experimental mycotic corneal ulcer caused by aspergillus fumigatus and the effect of oral ketoconazole in the treatment.

    aspergillus fumigatus was isolated from a case of keratomycosis. The patient, a 12-year-old boy presented with large corneal ulcer with hypopyon. The direct microscopic examination of scrapings revealed hyaline, septate mycelium. in vitro some antimycotics (amphotericin b,5-fluorocytosine, oxiconazole, amorolfine and ketoconazole) were tested against A. fumigatus by agar dilution method. ketoconazole with minimum inhibitory concentration of 30 micrograms/ml after 11 days of incubation was most effective against A. fumigatus. Experimental corneal ulcer was produced by injecting intralamellary spore suspension (2.5 x 10(6) c.f.u.) into the right eyes of previously immunosuppressed albino and black wild types of rabbits. The extent of ocular infection was graded up to 32 days. Histopathologic examination showed infiltration and large destruction of corneal stroma. Oral ketoconazole therapy exhibited partial response followed by relapse. The black type of rabbit appeared more suitable as an animal model for mycotic keratitis.
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2/3. Autoimmune hematologic diseases associated with infraclinical systemic lupus erythematosus in four patients. A human equivalent of the NZB mice.

    In four patients with a diagnosis of autoimmune hemolytic anemia or idiopathic thrombocytopenic purpura antinuclear antibodies and circulating immune complexes (Clq-BA test) have developed at some time in their history. Renal biopsy material was assayed with different methods. Immunofluorescence studies revealed granular deposits of immunoglobulin g (IgG), immunoglobulin m (IgM) and third component of complement (C3). Upon optic microscopy, three patients had mild mesangial proliferation, one a focal glomerulonephritis. Upon electron microscopy, all patients exhibited mesangial and/or subendothelial deposits. The patients have been followed for 18 to 37 years since the beginning of their disease. There has been no clinical evidence of systemic lupus erythematosus (SLE), although they present in their glomeruli immunologic and anatomic features compatible with this disease. These patients seem to be a human equivalent of the black NZB mouse which presents immunohematologic disorders and some biologic markers of SLE without having a full clinical picture of SLE.
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3/3. Acute episodic hemolysis in the African black rhinoceros as an analogue of human glucose-6-phosphate dehydrogenase deficiency.

    Sudden episodes of massive hemolysis have become the most common cause of death among captive black rhinoceroses, and there is evidence that they occur in the wild as well. We have observed radically unique enzyme and metabolite profiles in normal rhinoceros erythrocytes compared to humans and other mammals, including marked deficiencies of intracellular adenosine triphosphate (ATP), catalase, adenosine deaminase, and other enzymes involved in glycolysis, glutathione cycling, and nucleotide metabolism. Minimal concentrations of ATP appear to impair effective acceleration of hexosemonophosphate shunt activity in response to oxidants by restricting substrate generation at the hexokinase step. Antioxidant defenses are further compromised by catalase deficiency, which may be a general characteristic of rhinoceros erythrocytes, perhaps related to the common occurrence of severe mucocutaneous ulcerative disease. It is proposed that erythrocyte ATP deficiency in rhinoceroses may be an evolutionary adaptation conferring selective advantage against common hemic parasites, comparable to the role of human glucose-6-phosphate dehydrogenase (G-6-PD) deficiency in falciparum malaria.
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