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ever, similar data were not available from studies of liver transplant patients [4]. Our study found that the incidence of TB among TSTpositive patients who did not receive prophylaxis was 1,585.3 cases per 100,000 person-years. TST-positive liver transplant candidates and recipients may benefit from prophylaxis for TB. Sandra V. Chaparro, Jose G. Montoya, Emmet B. Keeffe, Jeanne T. Rhee, and Peter M. Small Divisions of Infectious Diseases and Gastroenterology, Department of Medicine, and Division of Epidemiology, Department of Health Research and Policy, Stanford University School of Medicine, Stanford, California
Candida (Torulopsis) glabrata Septic Arthritis Candida (Torulopsis) glabrata is an emerging nosocomial pathogen that frequently infects the bloodstream, abdomen, and genitourinary system [1]. To our knowledge, C. glabrata septic arthritis of a native joint has not been previously reported. We report a case of septic arthritis that occurred 31 months after an episode of C. glabrata fungemia. A 34-year-old male patient with liver cirrhosis due to alcoholism and infections with hepatitis B and C viruses underwent orthotopic liver transplantation on 7 April 1994. Six days later, he developed C. glabrata fungemia that lasted for 7 days. Echocardiography and CT of the abdomen failed to reveal a source. He received 1,520 mg of amphotericin B and did well. The postoperative period was also complicated by left internal jugular catheter–associated thrombosis and Staphylococcus aureus bacteremia that was treated with intravenous vancomycin for 6 weeks. He did well for .2 years, but on 11 November 1996, he developed left hip and groin pain, especially with weight bearing. The pain worsened over the next 4 days, and he presented to the hospital. He denied antecedent trauma to the hip, fever, chills, night sweats, and weight loss. His only medications were cyclosporine (100 mg daily) and prednisone (5 mg daily). He had a temperature of 38.6°C. Physical examination demonstrated mild left groin tenderness and severe pain with passive and active hip movement. Results of laboratory studies were normal except for a Westergren sedimentation rate of 97 mm/h. An MRI of the hip revealed bilateral stage 0 avascular necrosis and a large left hip effusion. Aspiration of the joint yielded turbid fluid, and the patient underwent surgical debridement; gross pus was found in the left hip, but he had no articular cartilage damage. Gram staining of the pus showed only a few polymorphonuclear cells, but cultures of the fluid and tissue yielded C. glabrata. The macrobroth dilution method revealed an
Reprints or correspondence: Dr. David L. Longworth, Department of Infectious Disease, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44195 (
[email protected]). Clinical Infectious Diseases 1999;29:208 –9 © 1999 by the Infectious Diseases Society of America. All rights reserved. 1058 – 4838/99/2901– 0036$03.00
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References 1. Ridzon R, Onorato IM. Infection in organ-transplant recipients [letter]. N Engl J Med 1998;339:1245. 2. Bass JB, Farer LS, Hopewell PC, et al. Treatment of tuberculosis and tuberculosis infection in adults and children. Am J Respir Crit Care 1994;149:1359 –74. 3. Higgins RM, Cahn AP, Porter D, et al. Mycobacterial infections after renal transplantation. Q J Med 1991;78:145–53. 4. Singh N, Paterson DL. Mycobacterium tuberculosis infection in solid-organ transplant recipients: impact and implications for management. Clin Infect Dis 1998;27:1266 –77.
MIC of amphotericin B of 2 mg/mL and an MIC of fluconazole of 64 mg/mL. Blood cultures were negative. He received 2,500 mg of amphotericin B and did well. One year later, he was ambulating without difficulty and had taken up a hobby of biking. In May 1998, he complained of left hip and knee pain. Examination of an aspirate of the knee joint revealed sodium urate crystals, and roentgenograms of the left hip demonstrated stage 5 avascular necrosis. Biopsy of the hip joint showed only mild inflammation. Tissue and synovial fluid cultures were negative. Septic arthritis caused by fungal organisms is uncommon [2]. Infection is related to surgical contamination during joint surgery, intraarticular injections, and hematogenous spread [2]. However, despite the fact that C. glabrata accounts for up to 16% of nosocomial bloodstream infections (BSIs) [3], there have been no reports of C. glabrata septic arthritis, except for one case involving a prosthetic joint [4]. Our case illustrates three important points. First, dissemination and persistence of the infection occurred despite adequate doses of amphotericin B. Second, we believe that the joint was likely seeded at the time of prior fungemia, thus representing a long latent period between the original BSI and this rare complication of dissemination. Third, the infection progressed despite very little immunosuppression. The original BSI was treated with a cumulative dose of amphotericin B of .15 mg/kg. Despite this high dose, our patient developed septic arthritis 31 months later. A possible explanation may be that the C. glabrata isolate had reduced susceptibility to amphotericin B. Although the use of MICs in predicting the response of C. glabrata BSI to antifungal therapy has not been standardized, preliminary evidence suggests that an MIC of amphotericin B of .1 mg/mL may indicate resistance [5]. The MIC for the C. glabrata isolate from our patient was 2 mg/mL. It is possible that there was insufficient suppression of C. glabrata in the hip tissue despite the standard dose of amphotericin B given. Goodman et al. [4] described a patient who developed C. glabrata prosthetic hip infection 27 months after hip surgery. Their patient, however, had no documented episode of fungemia, and it is unclear whether this infection was a complication of hip surgery. Our patient developed symptoms of hip infection almost 3 years after BSI. We doubt that the hip infection was new and unrelated to prior fungemia. Blood cultures were negative at the time of septic arthritis, and evaluation for occult endocarditis was not revealing. Our case highlights the need to constantly monitor
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long-term complications of C. glabrata fungemia even in patients who have received traditionally adequate therapy. Tawanda Gumbo, Carlos M. Isada, George F. Muschler, and David L. Longworth Departments of Infectious Disease and Orthopedic Surgery, The Cleveland Clinic Foundation, Cleveland, Ohio References 1. Nguyen MH, Peacock JE, Morris AJ, et al. The changing face of candidemia: emergence of non-Candida albicans species and antifungal resistance. Am J Med 1996;100:617–23.
Rapid, Hot Chromotrope Stain for Detecting Microsporidia Microsporidia, intracellular protozoan parasites (phylum Microspora), have been recognized as agents of diarrhea and wasting in patients with AIDS [1–3]. Several time-consuming diagnostic staining procedures are in vogue, and because of the small size of the spores, considerable expertise is required to distinguish them from other fecal elements [4, 5]; transmission electron microscopy is still the gold standard for species identification, and reliable serological assays and fluorescein-labeled monoclonal antibody testing for identification are still under development and/or lacking. Recently, attempts have been made to improve staining by heating; however, the time needed to complete these procedures varies from 30 to 40 minutes [6, 7]. Our laboratory has extensively used the fluorescent Fungi-Fluor chitin stain (Polysciences, Warrington, PA) in a screening procedure [8] and the conventional and time-consuming Weber’s modified trichrome (chromotrope) stain procedure for confirmation [4]. To speed up the trichrome stain procedure for confirmation and archiving, fecal samples preserved in 10% formalin that were from 50 patients positive for microsporidia were tested by a new, rapid staining method. Smears were prepared from 10 to 20 mL of comminuted stool spread thinly over 1-in2 areas of three microscope slides, placed on a hot plate at 45°C for drying, and fixed in methanol for 1 minute before staining. Although the first two slides of all samples were processed with use of the fluorescent chitin stain [8] and Weber’s modified trichrome stain [4], respectively, the third slide was stained by the new method. These slides were placed on a hot plate at 45°C, covered with modified Gomori’s stain (Medical Chemical Corporation, Santa Monica, CA), and stained for 3 minutes; care was taken to prevent the stain from drying. The slides were individually removed, drained of extra stain, and then placed in a staining rack; the slides were decolorized in acetic acid–90% ethanol (three to four dips), rinsed briefly in 95% ethanol (five to 10 dips), dehydrated by placing in ethanol (1–2 minutes), xylene, or xylene substitute (1–2 minutes), and
This work was presented at the American Gastroenterological Association, Digestive Diseases Week held in May 1998 in New Orleans. Reprints or correspondence: Dr. O. George W. Berlin, Department of Epidemiology, UCLA School of Public Health, Los Angeles, California 900951772 (
[email protected]). Clinical Infectious Diseases 1999;29:209 © 1999 by the Infectious Diseases Society of America. All rights reserved. 1058 – 4838/99/2901– 0037$03.00
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2. Berkowitz ID, Robboy SJ, Karchmer AW, Kunz LJ. Torulopsis glabrata fungemia—a clinical pathological study. Medicine (Baltimore) 1979; 58:430 – 40. 3. Cuellar ML, Silveira LH, Espinoza LR. Fungal arthritis. Ann Rheum Dis 1992;51:690 –7. 4. Goodman JS, Seibert DG, Reahl E, Geckler RW. Fungal infection of prosthetic joints: a report of two cases. J Rheumatol 1983;10: 494 –5. 5. National Committee for Clinical Laboratory Standards. Reference method for broth dilution antifungal susceptibility testing of yeasts: approved standard. NCCLS document M27-A. Wayne, Pennsylvania: National Committee for Clinical Laboratory Standards, 1997.
air-dried before examination. Slides from all three staining procedures were evaluated by means of light microscopy by at least two trained laboratory personnel for confirmation. Control slides of Enterocytozoon bieneusi or Encephalitozoon intestinalis were included in all staining procedures. Microsporidia appeared as pink oval bodies in all 50 samples by this new procedure, and heating the stain speeded up its incorporation. Analysis of the three staining procedures showed that the new method is fast and can be completed within 10 minutes. Benefits of this new staining procedure include the following: reduction in the time from 120 minutes as in Weber’s method [4] to only 10 minutes, for a saving of at least 100 –110 minutes; the slides can be examined under a light microscope, thereby obviating the need for an expensive fluorescent microscope; all species of microsporidia can be stained and detected by this procedure; the stained slides can be archived for future reference; its performance is at least equal to those of the conventional and established techniques; and in the era of cost containment, this method saves valuable time and money, thereby maximizing laboratory efficiency and providing a faster turnaround time for diagnosis. O. G. W. Berlin, L. R. Ash, C. N. Conteas, and J. B. Peter UCLA School of Public Health and Kaiser Permanente Hospital, Los Angeles, and Specialty Laboratories, Santa Monica, California References 1. Canning EU, Hollister WS. Human infections with microsporidia. Rev Med Microbiol 1992;3:35– 42. 2. Curry A, Canning EU. Human microsporidiosis. J Infect 1993;27:229 –36. 3. Weber R, Bryan RT, Schwartz DA, Owen RE. Human microsporidial infections. Clin Microbiol Rev 1994;7:426 – 61. 4. Weber R, Bryan RT, Owen RL, Wilcox CM, Gorelkin L, Visvesvara GS. Improved light microscopical detection of microsporidia spores in stool and duodenal aspirates. N Engl J Med 1992;326:161–5. 5. Ryan NJ, Sutherland G, Coughan K, et al. A new trichrome-blue stain for detection of microsporidial species in urine, stool and nasopharyngeal specimens. J Clin Microbiol 1993;31:3264 –9. 6. Kokoskin E, Gyorkos TW, Camus A, Cedilotte L, Purtill T, Ward B. Modified technique for efficient detection of microsporidia. J Clin Microbiol 1994;32:1074 –5. 7. Moura H, Schwartz DA, Bornay-Llinares F, Sodre FC, Wallace S, Visvesvara GS. A new and improved “quick-hot gram-chromotrope” technique that differentially stains microsporidian species in clinical samples, including paraffin-embedded tissue sections. Arch Pathol Lab Med 1997;121:888–93. 8. Berlin OGW, Conteas CN, Porschen RK. Rapid epifluorescent technique to detect microsporidia. AIDS 1996;10:1175– 6.
