Bacterial contamination of radiologist workstations: results of a pilot study.

PURPOSE: The aim of this study was to quantify and characterize bacterial contamination of radiologist workstations. METHODS: Dictation microphones and computer mice at the most frequently used radiologist workstations from 2 inpatient and 2 outpatient reading rooms at 2 teaching hospitals in 2 states were sampled for bacteria. Reference toilet seat and doorknob sampling was performed in the 4 restrooms nearest those reading rooms. One microphone and one mouse in each reading room were sampled again after quick disinfection with an inexpensive, commercially available antiseptic pad. Sampling was performed using direct trypticase soy agar plating, with sampled areas uniformly approximating 50 cm(2). Colonies were quantified and additionally characterized after 24 hours using mannitol salt agar and MacConkey agar. RESULTS: All sampled radiologist computer workstation and restroom sites were contaminated with bacteria. Mean colony counts were 69.4 ± 38.7 (range, 15-123) for microphones, 46.1 ± 58.1 (range, 1-173) for mice, 10.5 ± 9.7 (range, 1-22) for toilet seats, and 14.8 ± 16.0 (range, 1-36) for restroom doorknobs. Of all workstation sites, 64.3% (9 of 14) grew Staphylococcus aureus, and 21.4% (3 of 14) grew enteric organisms. Overall microphone and mouse bacterial contamination was significantly higher than that of nearby restroom toilets and doorknobs (57.8 ± 49.0 vs 12.6 ± 12.5, P = .005). Microphone and mouse bacterial counts were nearly completely eliminated after brief antiseptic swabbing (from 76.9 ± 53.2 to 0.3 ± 0.7, P = .002). CONCLUSIONS: Bacterial contamination of microphones and computer mice at radiologist workstations is common, with colonization significantly greater than nearby restroom toilet seats and doorknobs. Simple, rapid, and inexpensive disinfection techniques nearly completely eradicate workstation bacterial contamination. The clinical implications of colonization merits further study.

Defective expression of Tamm-Horsfall protein/uromodulin in COX-2-deficient mice increases their susceptibility to urinary tract infections.

Mice lacking a functional cyclooxygenase-2 (COX-2) gene develop abnormal kidneys that contain hypoplastic glomeruli and reduced proximal tubular mass, and they often die of renal failure. A comparison of kidney-specific gene expression between wild-type and COX-2-deficient mice by cDNA microarrays revealed that although more than 500 mRNAs were differentially expressed between the two strains of mice depending on their ages, the genes encoding pre-pro-epidermal growth factor (pre-pro-EGF) and Tamm-Horsfall protein (THP)/uromodulin were aberrantly expressed in the kidneys of COX-2 -/- mice at all stages of their development. Downregulation of EGF could potentially affect renal development, and THP/uromodulin gene has been implicated in abnormal kidney development and end-stage renal failure in humans. We assessed in detail mechanism of defective THP/uromodulin gene expression and its potential consequences in COX-2-deficient mice. Consistent with the microarray data, the steady-state levels of THP/uromodulin mRNA were severely reduced in the COX-2 -/- kidney. Furthermore, reduced expression of renal THP/uromodulin, as assessed by Western blot and immunohistological methods, was closely corroborated by a corresponding decline in the urinary secretion of THP/uromodulin in COX-2 -/- mice. Finally, we demonstrate that the bladders of COX-2 -/- mice, in contrast to those of the wild-type mice, are highly susceptible to colonization by uropathogenic Escherichia coli.

Both constitutive and inducible prostaglandin H synthase affect dermal wound healing in mice.

In an attempt to define the roles of prostaglandin H synthase 1 (PGHS-1, cyclooxygenase-1, COX-1) and prostaglandin H synthase 2 (PGHS-2, cyclooxygenase-2, COX-2) in wound healing, we investigated the healing of incisional dermal wounds in wild-type, PGHS-1 null, and PGHS-2 null mice. We measured tensile strength of the wounds, levels of PGHS-1 and PGHS-2 mRNA in the wound site, and histologic markers for the inflammatory, proliferative, and remodeling phases of wound healing. Although no gross visible differences were noted among healed wounds of the different mouse types, measurement of tensile strength showed that both PGHS-1 and PGHS-2 null wounds were weaker (75% and 70%, respectively) than wild-type wounds at 12 days after incision. At Day 8 the endothelial staining was 70% greater in the wounds of PGHS-2 null mice compared with their wild-type counterparts. In contrast at Day 12, staining for macrophages and myofibroblasts was less in PGHS-1 null wounds compared with wild-type and PGHS-2 null tissue. Compensatory expression of the alternate PGHS mRNA could be demonstrated by RT-PCR in the wounds of PGHS null mice on Days 1 and 4. We conclude that both PGHS-1 and PGHS-2 genes play distinct roles in the process of dermal wound healing.