Chromoblastomycosis caused by Exophiala spinifera.

We report the second case of chromoblastomycosis caused by Exophiala spinifera; this is the first known case in the United States. Examination of biopsied tissue showed thick-walled, internally septated, chestnut brown muriform cells (sclerotic bodies) within multinucleated giant cells present in the dermis that were characteristic of chromoblastomycosis. The individual cells within the muriform cells disarticulated from the outer wall of the parent cell and from each other to form endoconidia within the outer walls of the parent cells. After fracture of the outer walls, the endoconidia were released. This unique process of endoconidial formation in vivo for the propagation of muriform cells was observed for the first time. Initial treatment with itraconazole and 5-fluorocytosine followed by treatment with itraconazole and heat resulted in marked improvement in the patient's lesions. This infection reiterates the fact that the dematiaceous fungus E. spinifera, a well-known etiologic agent of phaeohyphomycosis, can cause more than one type of infection and supports earlier observations that chromoblastomycosis and phaeohyphomycosis represent extremes of a continuum of infections.

Efficacy of antibiotic-coated catheters in preventing subcutaneous Staphylococcus aureus infection in rabbits.

Vascular catheters coated with antiinfective compounds were evaluated as to their ability to prevent Staphylococcus aureus catheter infection in a rabbit model. Zones of inhibition of agar surface-plated S. aureus demonstrated the following hierarchy: dicloxacillin and clindamycin were each better than fusidic acid or chlorhexidine, which were better than ciprofloxacin, cefotaxime, or cefuroxime. In vivo half-lives of inhibitory activity for clindamycin and dicloxacillin were 5.6 and 17.7 h, respectively, with apparent first-order kinetics. Chlorhexidine disappeared in vivo with apparent two-compartment kinetics: first-compartment t1/2, 16.8 h; second-compartment t1/2, 115.6 h. In a rabbit model, dicloxacillin, clindamycin, fusidic acid, and chlorhexidine decreased the risk of infection compared with uncoated control catheters (P < .05). For dicloxacillin, clindamycin, and chlorhexidine, this was true even if the S. aureus inoculation was delayed 48 or 96 h after catheter implantation. These data suggest that vascular catheters with antiinfective coatings should be investigated further in hospitalized patients.

Vascular-access infections in hospitalized patients.

Vascular catheters are a common source of nosocomial infections, although many of these infections are potentially preventable. A long duration of catheterization, multiple catheter manipulations, the inexperience of some inserters, use of transparent plastic dressings, violations of aseptic technique, the use of multilumen catheters, and inadequate sterilization of reusable pressure transducers all increase the risk of these infections. The only interventions that have been proved to reduce the risk are standardized insertion and maintenance technique by an intravenous-therapy team, preinsertion skin preparation with chlorhexidine gluconate, and the use of topical antibiotics at the insertion site. The goal of the physician should be to prevent catheter infection, because the treatment of established infection can be difficult and costly. Treatment must be individualized for each patient on the basis of the clinical presentation and the causative organism.