Micafungin, a potent inhibitor of 1,3-b-D-glucan synthase, has become the second available agent in the echinocandins class that is approved for use in clinical practice. This agent shares with caspofungin an identical spectrum of in vitro activity against Candida albicans, non-albicans species of Candida, and Aspergillus species, as well as several but not all pathogenic molds. If anything, its in vitro activity appears to be superior to that of caspofungin, although the clinical relevance of this observation is unclear. The clinical role of micafungin appears to be similar to that of caspofungin, although clinical data are still lacking at this stage, with initial approval only for treatment of esophageal candidiasis and prophylaxis in subjects with neutropenia. Pharmacokinetic and pharmacodynamic studies and reports of adverse effects and safety have reported similar but not identical results to those of other agents in the echinocandin class. Factors such as acquisition costs and the potential for resistance development may be more relevant to its widespread use than in vitro and in vivo data comparisons with caspofungin.The echinocandins are a novel class of antifungals. Caspofungin was the first echinocandin agent approved by the US Food and Drug Administration (FDA), and anidulafungin is currently in phase 3 development. Micafungin is a promising echinocandin that was recently approved by the FDA and has demonstrated activity against Candida and Aspergillus species. MECHANISM OF ACTIONMicafungin is a water-soluble antifungal agent (molecular weight, 1292.26 Da) that is derived from Coleoptioma empedri via enzymatic cleavage of the hexapeptide FR901370, a natural product of the fungus; the addition of a fatty N-acyl side chain improves its antifungal potency [1,2]. Micafungin acts in a concentration-dependent manner as a noncompetitive inhibitor of the formation of the enzyme 1,3-b-d glucan synthase, an enzyme necessary for synthesis of 1,3-b-d glucan, a glucose polymer crucial to the structure and integrity of the cell wall of several common fungal pathogens [3][4][5]. Fungal cells unable to synthesize this polysaccharide cannot maintain their shape and lack adequate rigidity to resist osmotic pressure, which results in fungal cell lysis. This mechanism is unique to the echinocandin class of antifungal agents and has the potential to be either additive or synergistic with polyenes and azoles. Glucan is essential not only to cell-wall structure and integrity but also to cell growth and division [6]. Micafungin demonstrates a prolonged concentration-dependent postantifungal effect.Most fungal cell walls contain chitin, a-or b-linked glucans, and a variety of mannoproteins, although the quantity and relative importance of each component varies among different fungal species-thus, the selective antifungal effect on echinocandins [7]. Of significance, the cell walls of zygomycetes and cryptococcus lack 1,3-b-d glucan, which explains the poor activity of echinocandins, including micafungin, against these fungi ...
We report the first case of Weissella confusa bacteremia in an allogeneic hematopoietic stem cell transplant patient. After engraftment and discharge, the patient returned with fever and graft failure and was started on an empiric regimen of aztreonam and vancomycin. A blood culture grew an alpha-hemolytic, gram-positive coccus forming pairs and chains, originally thought to be a viridans Streptococcus and a skin contaminant. The isolation of the organism from multiple blood cultures, and the presence of vancomycin resistance prompted identification and additional susceptibility testing. The RapID(™) Str panel, which has W. confusa in its database, provided multiple incorrect identifications. The MicroScan WalkAway 96 SI, using PC-20 or -29 panels, also did not identify this bacterium, because it is not in their database. The organism was identified as W. confusa by 16S rDNA sequencing. Antibiotic susceptibility determination by Etest revealed vancomycin resistance and daptomycin susceptibility. Therapy was changed to daptomycin, and the infection resolved. Additionally, W. confusa sepsis, with multiple positive blood cultures, developed in a patient in the burn unit at our medical center. The patient's blood cultures remained positive until vancomycin was discontinued and daptomycin therapy initiated. Infections with vancomycin-resistant, gram-positive cocci are emerging among immuno compromised hosts. Under appropriate circumstances, clinicians need to request that the laboratory perform susceptibility testing and accurate identification, by nucleic acid sequencing if necessary. Sequencing of 16S rDNA is an important tool in the accurate identification of unusual pathogens.
Achromobacter xylosoxidans is an uncommon nosocomial pathogen known to cause many serious infections. A 69-year-old woman with diabetes mellitus and chronic renal failure was admitted with pulmonary edema. The patient developed fever and pulmonary infiltrate with bilateral pleural effusions while she was on a respirator in the intensive care unit. Culture of sputum, pleural fluid and blood grew A. xylosoxidans. Bilateral chest tubes were inserted and the patient was treated for one month with piperacillin and trimethoprim-sulfamethoxazole. Gradual response, both clinically and radiologically, was noted after prolonged therapy. A review of the literature on infections due to A. xylosoxidans, the unique susceptibility pattern of the organism to various antibiotics and the use of combination therapy in Achromobacter infections are discussed.
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