Narrow-spectrum staining pattern of Pityrosporum.

BACKGROUND: Broad-spectrum fungal stains are used to detect fungal organisms, but narrow-spectrum stains can assist in fungal differential diagnosis. These stains include mucicarmine and Fontana-Masson (FM) for Cryptococcus, Alcian Blue for Cryptococcus and Blastomyces, Congo Red for Blastomyces and Coccidioides, and Ziehl-Neelsen for some examples of Blastomyces and Histoplasma. Pityrosporum is increasingly being recognized as a pathogen capable of significant cutaneous and systemic infections, but the narrow-spectrum staining pattern of Pityrosporum has not yet been systematically studied and reported. METHODS: Paraffin-embedded archival tissue from 10 skin biopsies containing Pityrosporum was stained with Alcian Blue, Congo Red, Ziehl-Neelsen acid-fast stain, and FM stain. In addition to the 60-min staining time, a modified FM stain with 15-, 30-, and 45-min staining times was also performed. RESULTS: All cases stained positive with Alcian Blue, Congo Red, and FM stains and negative with the Ziehl-Neelsen stain. The modified FM stain with the 15-min staining time showed significant staining in more than 50% of the cases. DISCUSSION: The narrow-spectrum staining pattern of Pityrosporum distinguishes it from Cryptococcus, Blastomyces, Candida, Histoplasma, and Coccidioides.

Helicobacter pylori infection and oncogene expressions in gastric carcinoma and its precursor lesions.

Although it is fairly well accepted that Helicobacter pylori infection plays a significant role in causing gastric cancer, the exact mechanisms involved in its pathogenesis are unclear. We have examined the relationship between H. pylori infection and oncogene expression in different stages of disease progression from precursor lesions to gastric carcinoma. We used Diff-Quik stain to diagnose H. pylori infection and immunohistochemical stains against c-erbB-2, p53, ras, c-myc, and bcl-2 to determine expression of oncogenes. H. pylori infection was found in all cases of chronic gastritis, atrophic gastritis, intestinal metaplasia, and early gastric carcinoma, and in 16 of 30 (53%) cases of advanced gastric carcinoma. Overexpression of c-erbB-2 was found in 2 (7%) cases of advanced gastric carcinoma, which were H. pylori negative. Suppressor gene, p53, was overexpressed in 3 (30%) cases of intestinal metaplasia, 2 (33%) cases of early gastric carcinoma, and 18 (60%) cases of advanced gastric carcinoma. Of these 18 p53-positive advanced gastric cancer cases, 11 (61%) were H. pylori positive. Expression of ras p21 was found in 4 (40%) cases of H. pylori-negative normal mucosa, 10 (100%) cases of chronic gastritis, 1 (10%) case of atrophic mucosa, 6 (60%) cases of intestinal metaplasia, 2 (33%) cases of nonneoplastic mucosa adjacent to early gastric carcinoma, and 7 (23%) nonneoplastic mucosa adjacent to advanced gastric carcinoma, all of which showed H. pylori. No evidence of expression of either c-myc or bcl-2 was detected in any of the above-mentioned samples. The data suggest that H. pylori infection may increase expression of ras p21 proteins and induce p53 suppressor gene mutation early in the process of gastric carcinogenesis.