Candida infection in oral lesions of kaposi sarcoma

Abstract
Background Oral candidiasis is the most common infection of the oral mucosa of HIV-seropositive patients, although its frequency is rapidly decreasing with the advent of highly active antiretroviral therapy (HAART). Many questions regarding its complex pathogenesis remain unanswered. The diagnosis is usually established with non-invasive techniques such as mucosal smears. Oral lesions of HIV-associated Kaposi sarcoma (HIV-KS) are routinely biopsied and frequently show secondary infection with Candida albicans or other Candida species. Aims and objectives The aim of this investigation was to determine the frequency and histomorphology of secondary Candidal infection of the surface epithelium of oral HIV-associated KS lesions (HIV-KS), which are routinely biopsied in HIV infected patients. Materials and methods Haematoxylin and eosin (HE), and Periodic Acid-Schiff (PAS) stains of 133 cases of oral Kaposi sarcoma diagnosed between the period 2003 and 2007 within the Division of Oral Pathology were examined histologically for intensity and morphology of Candidal colonisation, depth of invasion, number of organisms, epithelial reactions and associated inflammatory response. The depth of Candidal invasion and severity of infection were correlated with the available CD4 T cell counts of HIV seropositive patients at the time of biopsy. Results Almost forty one percent (40.62%) of all oral HIV-KS cases were secondarily infected with Candida species. The intensity varied from an isolated single pseudohyphus to matted colonies of vegetative yeasts and psuedohyphae. Whilst in most cases the organisms did not invade beyond the parakeratin layer, pseudohyphae were noted extending into the stratum spinosum in 2 cases, and a single case showed a pseudohyphus within the lamina propria. A further 2 cases showed pseudohyphae growing in the pyogenic membrane. Neutrophilic permeation of the epithelium and Munro micro-abscess formation, features commonly associated with Candidal infection, were frequently present even in the absence of Candidal infection. Candidal organisms were often present in the absence of inflammation. Conclusion Oral lesions of HIV-KS are commonly secondarily infected with large numbers of Candidal organisms. The morphological characteristics of secondary Candidal infection within the surface epithelium of HIV-KS lesions suggest an altered pathogenetic pathway. Further studies are necessary in this regard.
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