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 ~  Abstract
 ~  Case Report
 ~  Mycological inve...
 ~  Description of t...
 ~  PCR amplificatio...
 ~  In vitro antifun...
 ~  Broth microdilut...
 ~  E test method
 ~  Discussion
 ~  Acknowledgement
 ~  References

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Year : 2004  |  Volume : 22  |  Issue : 1  |  Page : 16-22

Trichosporon asahii as an emerging etiologic agent of disseminated trichosporonosis: A case report and an update

Department of Medical Mycology, Vallabhbhai Patel Chest Institute, University of Delhi, New Delhi - 110 007, India

Correspondence Address:
Department of Medical Mycology, Vallabhbhai Patel Chest Institute, University of Delhi, New Delhi - 110 007, India

 ~ Abstract 

PURPOSE: To report a fatal case of disseminated trichosporonosis caused by Trichosporon asahii in a patient with acute myeloblastic leukemia (AML) and to present an update on systemic trichosporonosis with special reference to India. METHODS: The diagnosis was based on repeated demonstration of budding yeast cells and arthroconidia by direct microscopic examination of sputum and by isolation of T. asahii in culture of sputum and blood. The update is largely based upon literature search in Medline and Review of Medical and Veterinary Mycology. RESULTS: A 41-year-old male presented with acute myeloblastic leukemia, cough and fever. He had received cytotoxic drug therapy, broad spectrum antibiotics and was neutropenic. Trichosporon asahii was repeatedly demonstrated in his sputum by direct microscopy and culture, and also isolated from blood. It was identified by appropriate morphological and physiological characteristics viz., arthroconidium formation, diazonium blue B reaction, urease activity and assimilation of carbon and nitrogen compounds. The identification was confirmed by PCR amplification and direct DNA sequencing of internally transcribed spacer (ITS) 1 and ITS2 of rDNA. CONCLUSION: With greater awareness of etiologic significance of T.asahii, trichosporonosis is likely to be recognised more frequently than apparent from the available published reports.

How to cite this article:
Chowdhary A, Ahmad S, Khan Z U, Doval D C, Randhawa H S. Trichosporon asahii as an emerging etiologic agent of disseminated trichosporonosis: A case report and an update. Indian J Med Microbiol 2004;22:16-22

How to cite this URL:
Chowdhary A, Ahmad S, Khan Z U, Doval D C, Randhawa H S. Trichosporon asahii as an emerging etiologic agent of disseminated trichosporonosis: A case report and an update. Indian J Med Microbiol [serial online] 2004 [cited 2020 Dec 4];22:16-22. Available from:

The basidiomycetous yeast, Trichosporon Behrend, is a medically important genus that includes the causative agents of white piedra in immunocompetent hosts and disseminated infections in immunocompromised hosts. Disseminated infection due to Trichosporon species is one of the emerging mycoses in neutropenic patients, particularly when they are treated for haematological malignancy with cytotoxic and immunosuppressive therapy.[1],[2] Until recently, most of Trichosporon isolates originating from clinical material were designated as T. beigelii or T. cutaneum. In 1992, Gueho et al proposed a significant taxonomic revision of Trichosporon.[3] Subsequently, Sugita and colleagues[4] expanded upon the proposals recognizing 17 species and 5 varieties in the genus which included 6 species implicated in various human infections. Of these, T. asahii and T. mucoides are involved in deep seated infections whereas T. asteroides, T. ovoides and T. cutaneum are responsible for white piedra or other superficial infections. The sixth species, T. inkin, has been reported in superficial as well as disseminated infections.[5] Recently Moylett et al[6]have added T. pullulans to the list of emerging pathogenic species of Trichosporon. They reported two cases of T. pullulans infection in patients with chronic granulomatous disease and reviewed five additional cases from literature.
The name T. beigelii, widely used in earlier medical literature, has recently been discarded because no authentic culture or adequate description of this species was available. It is believed that most cases of trichosporonosis attributed previously to T. beigelii and T. cutaneum were probably caused by T. asahii which is now emerging as an important life threatening opportunistic systemic pathogen, especially in granulocytopenic and immunocompromised hosts.[7] Besides, it has been implicated as a cause of hypersensitivity pneumonitis in Japan.[8]
Trichosporonosis is usually an insidious disease and its diagnosis is likely to be missed, particularly in developing countries, because of a general lack of awareness and lack of acquaintance with the salient diagnostic features of the etiologic agent. In an earlier study of yeasts and yeast like fungi associated with foodstuffs undertaken in this laboratory in 1978, Mishra[9] isolated T.cutaneum and T. pullulans from milk, meat, butter and coarsely ground gram seeds. He also isolated T. capitatum currently classified as Geotrichum capitatum from sputum of a patient with bronchopulmonary disorders. In a related experimental study on the pathogenicity of some of these yeast like fungi for cortisone treated mice, Khan et al[10] reported macroscopic and microscopic lesions in their brain, heart, kidney, liver, lung and spleen due to T. cutaneum with a mortality of 38%. However, barring a few sporadic case reports, there is no information on the prevalence of disseminated trichosporonosis in India.[5],[11],[12],[13],[14] In this communication we report a fatal case of infection caused by Trichosporon asahii in a patient with acute myeloblastic leukemia (AML) along with an update on disseminated trichosporonosis with special reference to India.

 ~ Case Report Top

The patient was a 41-year-old male who had been diagnosed as a case of AML in Rajiv Gandhi Cancer Institute and Research Center, Delhi. After complete remission for several months following administration of a high dose of cytosine arabinoside regimen, he had relapse of AML with fever and cough, necessitating readmission in October 2001. Upon physical examination he was found to be anaemic, severely ill, dyspnoeic at rest, and had pyrexia of 101F. His haemoglobin was 6.6gm/dL, leukocyte count 11000/mL, platelets 42000/mL and absolute neutrophil count 1300/mL. Bone marrow aspiration revealed infiltration with megaloblasts, indicating relapse of AML. Chest X-ray showed diffuse interstitial infiltrates in both lung fields. Re-induction chemotherapy was initiated with daunorubicin and cytosine arabinoside regimen. Amikacin 400 mg, twice daily and both ceftazidime 1gm and vancomycin 500 mg every 6 hours, were started after blood cultures were done. The empirical cover with antibiotics for one week had no benefit, and he remained febrile. Blood cultures for aerobic pathogens during this period were negative. Despite continuation on broad spectrum antibiotics, his persistent fever spiked to 103F and his leukocyte count decreased to 1200/mL. In November 2001, a generalized fungal infection was suspected and he was referred to the Department of Medical Mycology, V.P. Chest Institute, for investigation of a possible deep seated fungal infection.

 ~ Mycological investigations Top

Three consecutive freshly expectorated sputum specimens were collected for direct microscopy and culture for fungus from the patient after he thoroughly rinsed his oropharyngeal cavity with sterile distilled water. The material was cultured on routine mycological media including Sabouraud dextrose agar (SDA) supplemented with chloramphenicol and on the same medium containing cycloheximide. One set of inoculated slants was incubated at 28C and the second at 37C for up to 4 weeks. Three sets of blood culture were done at 37C on brain heart infusion broth. Subcultures from the broth were done on plates of SDA supplemented with chloramphenicol and on the same medium containing cycloheximide after 48 and 72 hours of incubation. The plates were incubated both at 28C and 37C.
Direct microscopic examination of KOH wet mounts of sputum specimens showed mainly budding yeast cells and a few arthroconidia. All of the sputum specimens inoculated on SDA slants incubated at 28C and 37C yielded numerous colonies of a yeast like fungus in pure culture, that was subcultured and eventually identified as Trichosporon asahii. The same fungus was also isolated from blood culture on SDA plates after 72 hours of incubation. The species identification of T. asahii was based upon verification of its salient diagnostic morphological and physiological characteristics, employing the standard techniques.[15] The formation of sarcinae was examined in slide cultures on 50% glucose peptone agar. The isolate was also tested for (i) sensitivity to cycloheximide (ii) growth at 37C, 42C and 45C on SDA (iii) diazonium blue B color reaction (iv) urease activity on Christensen's urea medium (v) carbohydrate and nitrogen assimilation profiles as determined by the Vitek 2 (bioMerieux) yeast identification system.[16] In addition, PCR amplification and direct DNA sequencing of internally transcribed spacer (ITS) 1 and 2 of rDNA of the blood isolate was done.

 ~ Description of the Fungus Top

Colonies on SDA at 280C after 2 days of incubation were white, profusely wrinkled with an irregular margin, measuring 17 mm in diameter, and with 2 to 4 radial cracks in the agar medium [Figure - 1].
After 10 days of incubation, the colonies were raised with a highly convoluted central part, surrounded by a peripheral zone of radial prominent folds and measured 35 mm (average) in diameter. The cracks in the medium had widened and extended to the periphery of the culture plate. Microscopically, slide culture on 2% malt extract agar after 2 days of incubation at 28C revealed abundant rectangular arthroconidia, 3-4 mm wide and with rounded ends [Figure - 2].
Occasionally, lateral branches of disarticulating hyphae terminated in a conidium [Figure - 3]. No appressoria were observed. Slide cultures on 50% glucose peptone agar showed thick walled structures resembling chlamydoconidia [Figure - 4]. The isolate grew on SDA at 37C but not at 45C. It was resistant to 0.01% cycloheximide, hydrolysed urea and was diazonium blue B positive. It was identified as T. asahii on the basis of the afore-mentioned characteristics and its assimilation profile obtained with the Vitek 2 (bioMerieux) yeast identification system.[16]

 ~ PCR amplification and direct DNA sequencing Top

The identity of the blood isolate as T. asahii was confirmed by PCR amplification and direct DNA sequencing of ITS 1 and ITS2 of rDNA. The genomic DNA isolated from the cultures of T. asahii CBS 2530, T. asahii CBS 2479, T. faecalis CBS 4828, T. inkin CBS 5585, T. jiroveci CBS 6864 were used as reference for the amplification of rDNA in PCR. The DNA extracted from Candida albicans (ATCC 76615), C. parapsilosis (ATCC 10233), C. tropicalis (ATCC 750), C. glabrata (ATCC 15545), C. dubliniensis (type strain CD 36), Aspergillus fumigatus (ATCC 13073) Cryptococcus neoformans (ATCC 90112) was also included. The PCR amplification of rDNA was performed by following the method of Sugita et al[17] with minor modifications. While the forward primer was the same as that used by Sugita et al[17] the sequence of the reverse primer was derived from the 3'-end of the ITS2 region. This was achieved by downloading the ITS1-5sr RNA-ITS 2 segment of rDNA from several Trichosporon species and other fungi. The comparison of the sequences obtained was done by cluster W analysis. This primer combination is expected to amplify from the 5'-end of ITS1 to 3'-end of ITS2 including the intervening 5s rRNA of T. asahii subtypes only. The DNA sequences of the forward and reverse primers for the amplification of rDNA were: Forward (F): 5'-ggatcattagtgattg cctttata-3'; Reverse (R): 5'-GGATCATTAGTGAATTGCTCTTTGA-3'.
The amplification of target DNA was carried out in a total volume of 50 L containing 1x AmpliTaq PCR buffer I, 1 U AmpliTaq DNA polymerase, 10 pmole each of forward and reverse primers, 1 L of DNA extracted from culture and 0.1 mM of each dNTP. All reagents excluding primers were obtained from Perkin-Elmer Corp., Connecticut. PCR cycling was carried out in a Perkin-Elmer cycler (GeneAmp PCR system 2400) under the following conditions: denaturation at 94C for 1 min, annealing at 60C for 30 seconds and extension at 72C for 1 min. An initial denaturation step at 95C for 3 min and a final extension step at 72C for 10 min were also included. Amplification was performed for 30 cycles. The product (20 L) of PCR was detected by agarose gel electrophoresis.[18] The agarose gels were stained with ethidium bromide, visualized under ultraviolet light and photographed. The universal precautions suggested by Kwok and Higuchi[19] were followed to eliminate possible contamination of samples. Cross-contamination by aerosols of spores was reduced by physical separation of laboratory areas where organisms were cultured, sample DNA was isolated, PCR mixtures were prepared and PCR products were analyzed.
When PCR was performed with T. asahii specific primers listed above, specific amplification was obtained with genomic DNA isolated from the reference cultures of T. asahii CBS 2530, T. asahii CBS 2479, and T. faecalis CBS 4828 [Figure:5], Lanes 1, 3 and 4, respectively) while no amplification was obtained when genomic DNA from T. mucoides CBS 7625 [Figure:5], Lane 2), T. inkin CBS 5585 [Figure:5], Lane 5), T. jiroveci CBS 6864, C. albicans, C. parapsilosis, C. tropicalis, C. glabrata, C. dubliniensis, A. fumigatus and C. neoformans was used as template (data not shown). A single band of amplified product was obtained with the test isolate of T. asahii that corresponded to the reference isolates of T. asahii CBS 2530, CBS 2479, T. faecalis CBS 4828. The identity of the clinical isolate as T. asahii was further confirmed by direct DNA sequencing of the amplified product [Figure:5], Lane 6). The DNA sequence of ITS1 and ITS2 contained within the amplified DNA fragment matched perfectly with the corresponding sequences from T. asahii CBS 2530, and T. asahii CBS 2479, but not with other Trichosporon species or any other fungal species (data not shown).

 ~ In vitro antifungal susceptibility testing Top

The antifungal susceptibility testing of the isolate was determined by the broth microdilution method (document M27-A) as per recommendation of the National Committee for Clinical Laboratory Standards (NCCLS)[20] and by the E-test. The antifungals tested were amphotericin B and ketoconazole (Sigma), fluconazole and itraconazole (Ranbaxy Research Foundation).

 ~ Broth microdilution method Top

Briefly, stock solutions were diluted with RPMI 1640 tissue culture medium supplemented with glutamine (Sigma), buffered to a final pH 7 with 0.165 M MOPS (Sigma) and 1M NaOH and inoculated with saline suspension of the Trichosporon asahii isolate (104cfu/mL). For amphotericin B testing, the RPMI 1640 medium was supplemented with 2% glucose. The final concentrations were 0.125-64 mg/L for fluconazole, and 0.03-16 mg/L for amphotericin B, ketoconazole and itraconazole. The microtitre plates were incubated at 35C for 48 hrs. The MICs of azoles were read as the lowest concentration of the agent, which inhibited growth by 80%. For amphotericin B the MIC represented the lowest concentration of the drug that completely inhibited the growth. Suseptibilty break points were taken from Espinel-Ingroff et al.[21]

 ~ E test method Top

The in vitro antifungal susceptibility of the T. asahii isolate was determined by the E-test system (AB Biodisk, Sweden) according to the manufacturer's instructions. The RPMI 1640 medium with glutamine (Sigma) supplemented with 1.5% Bacto agar and 2% glucose was buffered to pH 7 with 0.165 M MOPS (Sigma). Cell suspension from 48 hour SDA cultures were prepared in sterile 0.85 % NaCl adjusted to the turbidity of a 1.0 MacFarland standard. The plates were incubated at 35C and read at 24 and 48 hours.
The MICs of antifungal drugs for T. asahii isolate obtained by broth microdilution method were; amphotericin B - 0.25g/mL, fluconazole - 4g/mL, itraconazole - 0.5g/mL and ketoconazole - 0.25g/mL. MICs values obtained by the E-test method were with in the range obtained by broth microdilution method and were; amphotericin B - 0.125g/mL, fluconazole - 4g/mL, itraconazole - 0.75g/mL and ketoconazole - 0.35g/mL. The isolate was resistant to 5-flucytosine as determined by E-test method only. Our strain had a MIC of 0.25mg/L (NCCLS method) in susceptible dose dependent range (0.25-0.5mg/L) against itraconazole.
Two weeks after admission of the patient, administration of amphotericin B was started at a dose of 1mg/kg per day. As he showed no improvement when reviewed 4 weeks later he was treated with oral itraconazole 400 mg a day. His condition deteriorated progressively and he died after 4 days.

 ~ Discussion Top

Invasive infections by rare and new opportunistic fungal pathogens have recently emerged as a significant problem in treatment of immunocompromised hosts. Since the first report on disseminated trichosporonosis in a leukemic patient in 1970,[22] sporadic cases have been reported over the years.[23],[24],[25],[26],[27],[28],[29] In a global review, Walsh (1986)[1] reported that 55 of 67 trichosporonosis cases (82%) had an underlying neoplastic disease, especially leukemia and lymphoma which were present in 60% of the cases. A review of more recent English language literature revealed additional cases of disseminated trichosporonosis among patients with AIDS, malignancy, extensive burns, intravenous catheters, treatment with corticosteroids and heart valve surgery reported from the United states, Europe and Japan.[30],[31],[32],[33],[34],[35],[36],[37],[38]
Mathews and Prabhakar in 1995 reported a case of localized invasive trichosporonosis of CNS due to T. beigelii from India.[12] T. beigelii was isolated from CSF of the patient who died before antifungal therapy was initiated. Singh et al[11] in 1989 isolated T. beigelii from the gastric aspirate of 10 patients who had undergone endoscopy. The source of the fungus was traced to an immunocompromised patient who was on radiotherapy for carcinoma cervix, had undergone endoscopy and had grown T. beigelii from her gastric aspirate. The biopsy channel of the endoscope was found to be contaminated and was responsible for the pseudoepidemic. In 1998, the first fatal case of disseminated trichosporonosis caused by T. inkin was documented by Mussa et al.[5] The patient developed trichosporonosis as a complication of chronic granulomatous disease. The diagnosis was based upon direct microscopy and isolation in pure culture of T. inkin from aspirated material in lumbar region and lung. Recently Chakrabarti and coworkers[13] described a case of generalized lymphadenopathy caused by T. asahii in a patient with Job's syndrome. The fungus was demonstrated and isolated in pure culture from the cervical lymph nodes. Two cases of disseminated trichosporonosis attributed to T. beigelii based upon highly questionable evidence have been claimed by Chitra et al.[14]
Our case of disseminated fatal trichosporonosis had manifestations of pneumonia and fungaemia not responding to conventional antibacterial antibiotic therapy. This is in consonance with most of the reported cases of trichosporonosis, who invariably presented with persistent or recurrent fever and development of neutropenia following chemotherapy.[1],[24],[39] The etiological role of T. asahii in the case was unequivocally established by repeated demonstration of the fungus in sputum specimens supported by its isolation in culture from this material as well as from blood. The macroscopic and microscopic morphology of T. asahii was compatible with the standard description of the species. In order to further confirm the identity of the T. asahii isolate we subjected it for PCR amplification and direct DNA sequencing of rDNA.
The likely routes of infection in trichosporonosis are the respiratory tract, the alimentary tract and the urinary tract, which are known to be frequent sites of colonization, leading to haematogenous dissemination.[2] Persistent positive cultures from sputum and urine of immunocompromised patients may be the harbinger of progression to invasive trichosporonosis if neutropenia persists.
There is paucity of data on the susceptibility of T. asahii to antifungal agents. The fungus is known for varied susceptibility to amphotericin B (MIC 0.01to 4 mg/mL) and laboratory studies have shown that it is relatively resistant to this antifungal agent.[7],[40] Both sensitivity and resistance to 5 flucytosine has been reported.[7],[26] As for azoles, miconazole, itraconazole, ketoconazole and voriconazole had higher in vitro activity than amphotericin B.[21],[41],[42].
The results of treatment of disseminated trichosporonosis have been very poor, and the reported case fatality of patients with persistent neutropenia is high, with 70% of deaths attributed to fungal infection. Despite in vitro susceptibility of T.asahii to amphotericin B, our patient died. Although the MICs may suggest susceptibility, the minimal lethal concentrations against T. asahii indicates that amphotericin B is not fungicidal.[40] This explains the extremely high mortality of disseminated trichosporonosis in immunocompromised patients treated with amphotericin B. The resolution of infection in leukaemic patients with neutropenia is related primarily with recovery from granulocytopenia.
For want of pathognomonic clinical features, the diagnosis of disseminated trichosporonosis depends primarily upon clinical suspicion, to be followed by intensive mycological investigations. Enhanced knowledge of this organism as a potential pathogen, especially in the appropriate clinical setting i.e., in neutropenic patients, and greater acquaintance with its laboratory diagnostic aspects will lead to more frequent recognition of disseminated trichosporonosis.

 ~ Acknowledgement Top

Acknowledgement is made to the Indian National Science Academy, New Delhi, for their financial support (Honorary Senior Scientist position to HSR), and to the Kuwait University, Kuwait, for the research project grant Y M02/02 for molecular typing. 

 ~ References Top

1.Walsh TJ, Newman KR, Moody M, Wharton RC, Wade JC. Trichosporonosis in patients with neoplastic disease. Medicine 1986;65:268-279.  Back to cited text no. 1    
2.Herbrecht R, Koenig H, Waller J, Liu KL, Gueho E. Trichosporon infections: clinical manifestations and treatment. J Mycol Med 1993;3:129-136.  Back to cited text no. 2    
3.Gueho E, Smith MT, de Hoog GS, Billon-Grand G, Christen R, Batenburg-Van der Vegte WH. Contributions to a revision of the genus Trichosporon. Antonie van Leeuwenhoek 1992;61:289-316.  Back to cited text no. 3  [PUBMED]  
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2004 - Indian Journal of Medical Microbiology
Published by Wolters Kluwer - Medknow

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