Primary cutaneous mucormycosis (zygomycosis) caused by Apophysomyces elegans.

A 53 year-old male diabetic presented with a month-old, painful ulcer with necrotic margins over the right thigh. Wound debridement was done twice and the ulcer showed recurrent growth of a white, cottony filamentous structure. Cutaneous mucormycosis was suspected and confirmed by histopathology and a culture isolate of Apophysomyces elegans . The patient was treated with liposomal amphotericin-B and itraconazole followed by partial thickness skin grafting, and then discharged after being prescribed posaconazole syrup for three weeks. Regular follow-up was done and during the last visit after six months following discharge, the ulcer was found to have healed well with no recurrence of the fungus.

Interaction of Mycobacterium avium complex with human respiratory epithelial cells.

Adherence of Mycobacterium avium complex (MAC) to human respiratory epithelial cells (HEp-2) induced 2 distinct modes of internalization. In the first, MAC induced ruffling of HEp-2 cell membrane and formation of surface projections securing the bacilli on the surface, and concurrent membrane depressions, beneath the sites of attachment of bacilli, resulted in internalization of the organisms. The second mode involved formation of membrane folds wrapping around the bacilli, followed by internalization. Two MAC proteins of approximately 31 kD and approximately 25 kD, respectively, were identified that mediated these interactions specific for HEp-2 cells. The N-terminal amino acid sequence of the 31-kD MAC protein displayed homology with the 21-kD hypothetical protein of Mycobacterium tuberculosis, and the 25-kD MAC protein showed homology with Mn-superoxide dismutase of MAC and Mycobacterium leprae. These 2 HEp-2 cell-specific MAC proteins may be involved in the interaction of MAC with epithelial cells.

Antimycobacterial activities of riminophenazines.

Riminophenazines were specifically developed as drugs active against Mycobacterium tuberculosis but extensive research over several decades has shown that these compounds are also active against many other mycobacterial infections, particularly those caused by Mycobacterium leprae and the Mycobacterium avium complex (MAC). Clofazimine, the lead compound in this series, is included in the regimens that are approved by the WHO for the treatment of leprosy and has contributed significantly to the control of that disease, particularly that caused by dapsone-resistant bacteria. Despite early problems, clofazimine has shown clinical efficacy in tuberculosis, in particular that caused by multiple drug resistant strains. Clofazimine does not induce resistance and also inhibits emergence of resistance to isoniazid in M. tuberculosis. The efficacy of clofazimine against MAC is more varied and the availability of better drugs has limited its use. Newer riminophenazines, such as B746 and B4157, not only showed increased anti-mycobacterial activity but also produced less skin pigmentation, which is the main drawback of this group of compounds. The most important virtues of riminophenazines, such as intracellular accumulation in mononuclear phagocytic cells, anti-inflammatory activity, a low incidence of drug resistance and slow metabolic elimination, make them attractive candidates for the treatment of mycobacterial infections. It is essential, however, to investigate the newer analogues clinically, while continuing the pursuit of alternate candidates that demonstrate higher anti-mycobacterial activity and lower rates of skin pigmentation.