| Malassezia species are members of the human cutaneous commensal flora, at the same time a kind of lipiphilic opportunistic pathogen. Malassezia can cause pityriasis versicolor, follicolitis, onychomycosis, fungemia, peritonitis and ostathritis, and it is close to dandruff, seborrhoeic dermatitis, atopic dermatitis and psoriasis, but the pathogenisis is not clear. The use of intravenous fat emulsions appears to have altered the epidemiology and pathogenic mechanism of malassezia infection. In the last 20 years, more and more researchers study on systemic infection with malassezia. Most reports of systemic infection with malassezia happened on premature neonates with serious underlying diseases, having central or peripheral catheters inserted, receiving parenteral nutrition (including lipid emulsions) through the catheter. Adults immunosuppressed and with severe gastrointestinal diseases are also at high risk for systemic malassezia infection. There are non-classic systemic malassezia infection reports in recent years, such as systemic infection without parenteral nutrition and lipid emulsions, systemic infection of lipid-independent M.sympodialis and systemic infection in adult withoutunderlying diseases. To date, no study was reported on systemic infection in immunosuppressed animal model, only M. furfur M. sympodialis and M. pachydermatis have been reported to cause systemic disease. We made mouse animal model of systemic infection with M. sympodialis, M. globosa and M. sloofiae, observed the infected mouse, researched deeply through histopathologic method and transmission electronic microscopy, and analyzed the pathogenic difference in different organs of these systemic infected mouse. The aim of this study is to clarify the mechanism, histopathological changes and ultrastructure changes of systemic malassezia infection, consequently provide information for clinical research of systemic infection with opportunistic pathogenetic fungi.Materials and methods:1 Forty KM mouse immunosuppressed by cyclophosphamide were divided into 4 groups randomly, 10 mouse in each group. Three tested groups were injected venously with 20% lipid emulsions 0.2ml and 1 X 108 spores/ml M. sympodialis M. globosa and M. sloofiae liquid 0.2ml separately to make animal model of systemic infection. One control group were injected venously with 20% lipid emulsions 0.2ml and physiological saline solution 0.2ml.2 Hematoxylin and eosin stain periodic acid-Schiff stain and transmission electronic microscopy were used to examine the pathogenetic fungus histopathological and ultrastructural changes in heart lung liver spleen and kidney of infected mouse dead or killed.3 Statistical tool: SPSS 10.0 software system. Rank test was used to analyze the data. There is a significance when P<0.05.Results:1 All the infected mouse lost weight at different degree and died in 9 days at different speed after being injected venously with malassezia spore liquid. While themouse in contrast only lost weight for 3 to 5 days, then recovered, and no one died until the end of the experiment.2 Focus or diffuse spores in heart lung liver spleen and kidney, even hyphae in liver and spleen were observd. There was a significant difference in infectious condition between different organs (P<0.01), and lung, liver, spleen, heart, kidney in turn from severe to mild. When each organ was compared with others, there was a significant difference between lung and other organs, liver and other organs, spleen and other organs (P<0.01), but no significant difference between heart and kidney (P>0.05).3 Degeneration and necrosis granuloma inflammatory cells infiltration infectious exudates neutrophilic leukocytosis spore thrombus and other thrombus in heart lung liver spleen and kidney of infected mouse were observed. There was a significant difference in histopathological change between different organ (P<0.01), and liver, lung, heart, spleen, kidney in turn from severe to mild. There was a significant difference between each organ...
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