images in clinical medicineT h e n e w e ng l a n d j o u r na l o f m e dic i n e n engl j med 356;24 www.nejm.org june 14, 2007 e25 A 53-year-old man with crohn's disease, short-bowel syndrome that required total parenteral nutrition, a history of recurrent catheter infections, hypertension, chronic renal insufficiency, and mitral regurgitation presented with fevers of 2 weeks' duration. He had elevated liver enzyme levels (aspartate aminotransferase, 45 U per liter; alanine aminotransferase, 97 U per liter; alkaline phosphatase, 679 U per liter; and total bilirubin, 7.3 mg per deciliter [125 µmol per liter]). Abdominal ultrasonography and endoscopic retrograde cholangiopancreatography showed no abnormalities. Blood was obtained for culture, and the patient was discharged while receiving intravenous levofloxacin. He returned after 5 days because of continued fevers, with temperatures as high as 102°F (39°C). A peripheral-blood smear showed intracellular and extracellular budding yeasts that were 2 to 4 µm in diameter with Wright's stain (Panel A, arrows) and Gram's stain (Panel B, arrow), some with collarettes, along with cocci that were gram-positive (Panel B, arrowhead). Although initial blood cultures grew only coagulase-negative staphylococci, the fungus Malassezia furfur grew on subculture with lipid supplementation. The patient was subsequently treated with amphotericin B, daptomycin, and vancomycin with clinical improvement. Repeat lipid-supplemented fungal cultures 2 months later were negative. Infection with M. furfur is associated with the use of intravenous lipid supplementation, and the diagnostic evaluation requires such supplementation as well. As seen in this case, the peripheral-blood smear remains a valuable diagnostic tool.
was isolated from sterile specimens with increasing frequency over a several-month period despite a paucity of clinical evidence suggesting true infections. However, a health care-associated outbreak was strongly considered due to growth patterns in the microbiology laboratory that were more consistent with true infection than environmental contamination. Therefore, an extensive investigation was performed to identify its cause. With the exception of one case, patient clinical courses were not consistent with true invasive fungal infections. Furthermore, no epidemiologic link between patients was identified. Rather, extensive environmental sampling revealed in an anaerobic holding jar in the clinical microbiology laboratory, where anaerobic plates were prereduced and held before inoculating specimens. grows poorly under anaerobic conditions. Thus, we postulate that anaerobic plates became intermittently contaminated. Passaging from intermittently contaminated anaerobic plates to primary quadrants of aerobic media during specimen planting yielded a colonial growth pattern typical for true specimen infection, thus obscuring laboratory contamination. A molecular evaluation of the isolates confirmed a common source for pseudo-outbreak cases but not for the one true infection. In line with Reason's model of organizational accidents, active and latent errors coincided to contribute to the pseudo-outbreak. These included organism factors (lack of growth in anaerobic conditions obscuring plate contamination), human factors (lack of strict adherence to plating order, leading to only intermittent observation of aerobic plate positivity), and laboratory factors (novel equipment). All of these variables should be considered when evaluating possible laboratory-based pseudo-outbreaks.
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