Trichosporon asahii fungaemia in an adult patient with acute … · 2012. 3. 20. · Revista Român ă de Medicin ă de Laborator Vol. 12, Nr. 3, Septembrie 2008 Trichosporon asahii

Revista Română de Medicină de Laborator Vol. 12, Nr. 3, Septembrie 2008

Trichosporon asahii fungaemia in an adult patient withacute lymphoblastic leukaemia and viral hepatitis C.

A Case Report

Fungemie cu Trichosporon asahii la o pacientă adultă cu leucemie acutălimfoblastică şi hepatită virală C. Prezentare de caz

Annamária Földes1∗, Doina-Veronica Bilca1, Judit Beáta Köpeczi2, ErzsébetBenedek 2, István Benedek 2,3, Enikı Farkas1, Edit Székely1,4

1. Mureş County Emergency Hospital Clinics, Central Clinical Laboratory, Department ofMicrobiology;

2. Clinic of Haematology and Bone Marrow Transplantation, Târgu-Mureş;3. U.M.Ph. Târgu-Mureş, Department of Medical Semiology;

4. U.M.Ph. Târgu-Mureş, Department of Microbiology

Abstract

T. asahii is an emerging fungal pathogen that causes severe invasive diseases, particularly in immuno-compromised hosts. We report the case of a 45-year-old woman T.M. who was first diagnosed with non-Hodgk-in’s lymphoma (NHL) with B cells, but later pre-B acute lymphoblastic leukaemia (ALL) and viral hepatitis Cwere confirmed. After conventional cytostatic chemotherapy the patient achieved only partial haematological re-mission and she developed two periods of severe marrow aplasia. During the second period she became severelyill, with high fever (38-39°C), and we isolated T. asahii from three sets of consecutive blood culture. The identi-fication of the fungus was based on culture and microscopic characteristics, urease production and confirmed byusing API Candida (BioMérieux) and Vitek 2 Compact System. The patient became afebrile after 12 days of anti-fungal therapy (6 days of fluconazole followed by voriconazole) associated with antibiotic therapy. Severe mar-row aplasia persisted and her general condition deteriorated progressively. After 5 days of afebrility she de-veloped signs of an acute abdominal syndrome and died of cardiac arrest. Invasive trichosporonosis should notbe overlooked, particularly in neutropenic febrile patients with acute leukaemia; those received aggressive cyto-static and broad-spectrum antibiotic therapy. This case suggests the importance of identification and antifungalsusceptibility testing of T. asahii for the application of an adequate treatment.

Key words: Trichosporon asahii, blood culture, severe marrow aplasia, imunodepression, voriconazole

*Address for correspondence: Annamária Földes, Str. Victoriei 69/14, Baia Mare, Jud. Maramureş, 430072Tel.: 0751200852, E-mail:[email protected] of institute: Mureş County Emergency Hospital Clinics, Central Clinical Laboratory, Department ofMicrobiology, Str. Gh. Marinescu nr. 50, Târgu-Mureş, Romania

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Rezumat

Trichosporon asahii este un fung oportunist emergent care provoacă infecŃii invazive severe, în specialla persoane imunodeprimate. Redăm cazul pacientei T.M. în vârstă de 45 ani, diagnosticată iniŃial histopatolo-gic cu limfom malign non-Hodgkin (LMNH) cu celule mari B, dar la care s-a confirmat ulterior prin imunofeno-tipare leucemie acută limfoblastică (LAL) pre-B. Totodată s-a identificat serologic şi hepatită virală C. Postchi-mioterapie citostatică convenŃională s-a obŃinut doar o remisie hematologică parŃială, pacienta dezvoltând douăfaze de aplazie medulară severă, ultima fiind acompaniată de sindrom febril (38-39°C) şi de izolarea T. asahiidin 3 seturi succesive de hemoculturi. Identificarea micromicetului s-a realizat pe baza caracterelor de cultură,microscopice, producŃiei de urează, alături de API Candida (BioMérieux) şi Vitek 2 Compact System. Pacienta adevenit afebrilă după 12 zile de terapie antifungică (fluconazol 6 zile, ulterior voriconazol) asociată cu antibiote-rapie cu spectru larg. Aplazia medulară severă a persistat. După 5 zile de afebrilitate, pe fondul unei stări gene-rale alterate progresiv a dezvoltat semne de abdomen acut chirurgical şi a decedat prin stop cardio-respirator.Trichosporonoza invazivă este un diagnostic ce nu trebuie omis la pacienŃii imunodeficitari febrili, mai ales ceicu leucemii acute şi neutropenie, care au beneficiat de chimioterapie citostatică agresivă şi antibioterapie cuspectru larg. Cazul prezentat sugerează importanŃa identificării şi testării susceptibilităŃii in vitro a T. asahii laantifungice în scopul instituirii unei conduite terapeutice adecvate.

Cuvinte cheie: Trichosporon. asahii, hemocultură, aplazie medulară severă, imunodepresie, voriconazol

Introduction

The incidence of invasive fungal infec-tions in immunocompromised patients, particu-larly those with haematological malignancieshas risen over the last two decades, mainly as aresult of the increased use of intensive cytotoxictherapy, allogeneic blood stem cell transplanta-tion, immunosuppressive therapy7 and broad-spectrum antibiotics. In this context, we parti-cipate in a diversification of species involved infungaemia, with the decrease of Candida albic-ans strains and the increase of non-albicans spe-cies of Candida and the species of other genus:Trichosporon, Cryptococcus, Malassezia etc.2

Invasive trichosporonosis is an uncom-mon disease and it most frequently affects im-munocompromised hosts21, especially thosewith neutropenia or marrow aplasia. The pro-gnosis of trichosporonosis is poor and most fre-quently fatal.3, 7, 19

Trichosporon genus includes more than25 species, but only 6 of them are recognized aspotential human pathogens: T. asahii, T. as-teroides, T. cutaneum, T. inkin, T. ovoides andT. mucoides. 2 T. asahii and T. mucoides havebeen isolated from a few patients with white

piedra, but they are usually associated withdeep-seated infections. T. asteroides and T. cu-taneum seem to be linked with superficial infec-tions, while T. ovoides and T. inkin are involvedin white piedra of the scalp and pubic area, re-spectively.8

T. asahii is an emerging opportunisticfungal pathogen and it is included in phylumBasidiomycota, order Sporidiales. This fungalagent is commonly found in soil, water, butmay also be a part of the normal human and an-imals flora of the oral cavity, digestive tract andskin.4,6

In immunocompetent patients T. asahiiinduces white piedra, onychomycosis, glossitis,esophagitis, meningitis, urinary tract infectionsetc.2, 15, 16, 17

In this paper we report the case of anadult patient with pre-B ALL and viral hepatitisC, who developed an episode of fungaemiawith T. asahii during a period of severe marrowaplasia.

Case Report

From the summer 2007 a 45-year-old

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woman, T. M., presented a progressive tumourin the right coxofemural region. In January2008 an incisional biopsy of the tumour tissuewas performed at the Clinic of Orthopaedy,Târgu-Mureş. The histopathologic and immun-ohistochimic examinations diagnosed NHLwith B cells.

In January 2008 the patient was admit-ted to the Clinic of Haematology and BloodMarrow Transplantation at Târgu-Mureş. Themovements of her right hip joint were painfuland restricted. Physical examination revealedthe pallor of the skin, mucosas, and a tumour of

20x30 cm in the right coxofemural region. Thesize of liver and spleen was within normal lim-its and no lymphadenopathy was detected.

Pelvis X-ray showed osteolytic lesionsin the 1/3 proximal end of the right femur. Noskull modifications were observed radiologic-ally.

Laboratory parameters, at the time ofadmission to hospital, were as follows: leuko-cyte count: 8170/µL (82% neutrophils, 1% eos-inophils, 0% basophils, 4% monocytes, 13%lymphocytes), haemoglobin: 11g/dL, haemato-crit: 34.3%, platelets: 449000/µL, erythrocyte

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Figure 1. Flowcitometry demonstrates 65,11% blasts with the following antigenic profile: CD19+, CD20+(33%), CD22+, CD10+ (70%), CD33+ (90%), CD34+, HLA-DR+, CD13+ (61%), CD 11c + (35%).


sedimentation rate (ESR): 110/150, fibrinogen:682 mg%, AST: 20 U/L, ALT: 25 U/L, serumtotal bilirubin: 0.34 mg/dL, serum direct biliru-bin: 0,11mg/dL, LDH: 276 U/L, serum irron:11.66 µmol/L. Bone marrow examination de-tected the infiltration of bone marrow withatypical cells, some of them in group disposi-tion. Cellular series were poorly represented,but the maturation process of the cells was rel-ativeely good.

The patient received two cycles ofCHOP chemotherapy: Ciclophosphamide, Far-marubicine, Vincristine and Medrol for thetreatment of NHL.

In March 2008 she developed a severesyndrome of hepatocytolisis (AST: 1772 U/L,ALT: 3349 U/L, serum total bilirubin: 3.95mg/L, serum direct bilirubin: 1.59 mg/L, LDH:1026 U/L). For this reason she was transferredto the Clinic of Infectious Diseases, Târgu-Mureş, where antibodies against hepatitis C vir-us (HCV) were identified by ELISA serologicalmethod. She received hydroelectrolitic treat-ment associated with hepatoprotector agents.

In April 2008 the patient was readmit-ted to the Clinic of Haematology and BloodMarrow Transplantation, Târgu-Mureş. Hergeneral condition was severely deteriorated.She presented hepatosplenomegaly, and thehepatocytolisis syndrome was in moderate re-mission. The results of laboratory investigationsrevealed: leukocyte count: 59150/µL (peripher-al blood smear: 65% blasts, 15% neutrophils,0% eosinophils, 0% basophils, 1% monocytes,19% lymphocytes), haemoglobin: 6.2 g/dL,haematocrit: 19.5%, platelets: 28000/µL, ESR:50/98, fibrinogen: 174 mg%, AST: 170 U/L,ALT: 102 U/L, serum total bilirubin: 3.52mg/L, serum direct bilirubin: 0.98 mg/L, LDH:3171 U/L, serum iron: 48.16 µmol/L, prothrom-bin index: 82%, INR: 1.11, antibodies againstHCV positive (MEIA method). Immunopheno-typing of peripheral blood established the dia-gnosis of pre-B ALL with myeloid markers(Figure 1).

Cytogenetic examination confirmed thepresence of Philadelphia (Ph') chromosomet(9;22)(9q;22q). For this reason treatment wasinitiated with Glivec 4x100 mg/day in associa-tion with corticotherapy. Other complex cyto-genetic abnormalities such as: monosomy X,t(9;10)(p11;p11), deletion 16p- and t(2;5)(q3;q1) were demonstrated.

The conventional protocol of cytostaticchemotherapy ALL Ph+ BCR/ABL was admin-istred to the patient, but only a partial haemato-logical remission was achieved. During thechemotherapy two periods of severe marrowaplasia appeared with leukocyte count<1000/µL and neutrophils count <500/µL. Thefirst episode was in May 2008 (of 7 days dura-tion) and the second was in July 2008.

Between May and July 2008 a series ofbacteriological examinations were performedfrom the pharingeal exudate and lingual secre-tion. First Candida albicans was identified fol-lowed by C. krusei/ incospicua/ lambica, and fi-nally C. glabrata. In this period she receivedprolonged treatment with fluconazole 200 mg/day.

In July 2008 the patient was again hos-pitalized to the Clinic of Haematology andBlood Marrow Transplantation, Târgu-Mureş.She developed the second period of severe mar-row aplasia, which was accompanied with fever(temperature 38-39°C). We isolated T. asahiifrom three sets of consecutive blood cultures (inpure culture). She received broad-spectrum an-tibiotic therapy (Tienam, Zyvoxid) associatedwith fluconazole 200mg/day in the first 6 days,followed by voriconazole. She became afebrileafter 12 days of this combined treatment. Thepatient remained severely aplastic despite ad-ministrations of hematopoetic growth factors.Her general condition deteriorated progress-ively and after 5 days of afebrility presentedsigns of an acute abdominal syndrome. Surgicalintervention was not possible because of herpoor clinical condition and the laboratory para-meters that had profoundly alterated. Physical

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examination suggested the probability of an in-testinal perforation. She died of cardiac arrest.

Microbiological investigations

Gram-stained direct smear from theblood cultures revealed yeast cells, blastoconi-dia and hyphae. The blood samples were cul-tured on routine media including sheep bloodagar, Sabouraud’s dextrose agar (SDA), chro-mogen media Candiselect 4 (BioRad) and in-cubated overnight at 37°C and 25°C. At boththese temperatures rapidly growing colonies ofyeast-like fungus were obtained in pure cul-tures. After 24 hours of incubation on sheepblood agar and SDA the smooth, punctiformand white coloured colonies appeared. On Can-diselect 4 we observed a weak growth; thecolonies were first mauve coloured, and after48 hours became green-turquoise. The coloniesgrew in size progressively after 2-3 days onSDA. They became white to cream colouredwith heaping at the centre. (Figure 2). Withtime, the centre of mature colonies becamecerebriform (wrinkled) and it was surroundedby a velvety and powdery zone (Figures 3, 4).The rest of colonies remained un-pigmented.

Gram-stained smear from a 24 hoursold culture illustrated true hyphae, blastoconi-dia, pseudohyphae and rectangulare arthro-conidia (Figure 5). After 48 hours later we ob-served a decrease in the number of blastoconi-dia, and 4 – 5 days later hyphea showed de-creasing trend while the arthroconidia becamepredominant (Figures 6, 7).

API Candida (BioMérieux) identifiedfungus as Trichosporon spp. 2 with 99% con-fidence value. This isolate was urease positiveand the germ-tube test was negative. Follow-uptest, using the Vitek 2 Compact System, identi-fied T. asahii.

Discussion

T. asahii has emerged as a life-threaten-ing opportunistic pathogen in immunocom-promised patients, but it has also been reportedto cause different types of infections in immun-ocompetent hosts, too.

Watson and Kallichurum reported thefirst case of disseminated trichosporonosis in1970.20

Our case presents some characteristics.In the first place we report an atypical debut ofALL in an adult patient, with osteoarticularmanifestations, osteolytic femural lesions andan aleukaemic blood picture, but with elevatedESR. In the second place, co-expression of my-eloid markers on pre-B lymphoblasts, the pres-ence of Ph’ chromosome and other complexecytogenetic modifications are a signal for a highrisk ALL. In the third place this case is suggest-ive for an invasive trichosporonosis which ap-pears during a severe marrow aplasia in a pa-tient with ALL and viral hepatitis C.

Invasive trichosporonosis was dia-gnosed most frequently in patients with acuteleukaemia.7 Most of the infected patients hadbeen treated with conventional cytotoxicchemotherapy, corticosteroids and broad-spec-trum antibiotics.7 The victim of Trichosporonspp. infection is the neutropenic patient, imply-ing that neutrophils are the most important de-fence cells against this fungus.10

Invasive trichosporonosis was definedas “proven” when one or more of the followingcriteria were met:

• blood cultures yielding Trichosporonspp. in patients with temporally related clinicalsigns and symptoms of infection,

• positive cerebrospinal fluid culture re-sults, or

• biopsy specimens that were culturepositive for Trichosporon spp. and presentedhistopathologic evidence of fungal growth char-acterized by minimal septate hyphal branching,blastoconidia and fragmentation of the myceli-

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Figure 2. Appearance of colonies on SDA after Figure 5. Gram-stained smear of 24 hours old

72 hours colonies showing: 1. blastoconidia, 2. arthroconidia, 3. pseudohyphae (1000x)

Figure 3. Morphological features of an isolate Figure 6. Gram-stained smear of 48 hours old colony on SDA after 4 days colonies showing: septate hyphae, arthroconidia (1000x)

Figure 4. Morphological features of an isolate Figure 7. Gram-stained smear from 5 days old colony on SDA after 5 days culture showing numerous arthroconidia, true hyphae that disarticulate into rectangular arthroconidia (1000x)

1

2

3


um in arthroconidia (definition published by theEuropean Organization for Research and Treat-ment of Cancer Invasive Fungal Infection Co-operative Group EORTC/IFICG and NationalInstitute of Allergy and Infectious Disease My-coses Study Group NIAID/MSG)1.

In our case fever was the only sign ofinfection associated with fungaemia. An Italianmulticenter retrospective study showed that in-vasive infection with Trichosporon spp. wasconfirmed by bloodcultures in 75% of patients.7

In most of the cases of fungaemia, focal or dis-seminated invasive tissue infection was docu-mented; less commonly fungaemia was associ-ated only with fever, which was unresponsiveto broad-spectrum antibiotics.7 Invasive tissueinfections were defined as focal when the in-volvement of a single organ site was provedand disseminated when two or more organswere involved.1 In our case necroptic examina-tion was not performed, therefore we could notexclude the involvement of different organs.

The source of human Trichosporon isbelieved to be the patient’s own endogeneusmycobiota. Mucosal colonisation, which maybe enhanced by antibiotic therapy and sub-sequent seeding of the bloodstream throughbreaks in the integrity of the surface, is con-sidered to be an early sequence in the patho-physiology of invasive disease.6

During the multiple hospitalizations,our patient had no central venous, gastric orvesical indwelling catheters, which could be apossible source of exogene colonization. A re-cent study demonstrated that only in 3% ofcases the infection with Trichosporon spp. wasrelated to a central venous catheter.7

In our patient we detected simultaneousT. asahii from bloodcultures and C. glabratafrom the pharingean exudate and lingual secre-tion. It is important to note that this episode offungaemia was not induced by this species ofCandida genus. Between May and June 2008our patient received prolonged treatment withfluconazole and this aspect suggests that this

antifungal agent did not offer protection againstan invasive trichosporonosis. Kromery et al. re-ported nosocomial breakthrough fungaemia dueto Trichosporon during itraconazole prophylax-is.9

The crude mortality in systemic tricho-sporonosis is about 80% in patients with per-sistent neutropenia.7, 19

It is important to note that trichosporo-nosis may appear similar to disseminated can-didiasis both in its clinical and histopathologicappearance.6 We performed differential dia-gnosis with other genus of fungus and otherspecies of Trichosporon. T. asahii differs fromCandida by colonies features, producing arthro-conidia, the biochimic profile and germ-tubetest negative. Geotrichum candidum is a specieswith similar colony findings, which is differen-tiated from Trichosporon by morphology (itproduces arthroconidia without blastoconidia)and by biochemical properties (urease produc-tion positive).

In vitro susceptibility findings can be auseful guide in selecting an adequate antifungaltherapy for trichosporonosis. In our situation,we could not test in vitro susceptibility to fluc-onazole, voriconazole, amphotericin B, itraco-nazole and 5-flucytosine. Echinocandins,caspofungin, anidulafungin and FK 463 havepractically no activity against Trichosporonisolates.5, 18

After microbiological identification offungus and consultation with relevant publica-tions, fluconazole was replaced with voricona-zole in the treatment administred to our patient.Although, in recent studies, the new triazoles:voriconazole, posaconazole and ravuconazolehave displayed potent in vitro activity againstisolates of T. asahii and other Trichosporonspp.14, but the resolution of infection in patientswith neutropenia is primarily dependent on re-covery from granulocytopenia.13 Wolf et al. re-ported Trichosporon isolates with multi-drugresistance to amphotericina B, 5-flucytosine,fluconazole and itraconazole.22

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Despite our patient became afebrileafter 12 days of combined treatment, the effic-acy of voriconazole must have been consideredwith some reservations:

• severe marrow aplasia persisted, • in the progress of disease negative

blood culture was not obtained, • the symptoms and signs of inflamma-

tion can be minimal or even absent in patientswith severe neutropenia.

The diagnosis of Trichosporon infec-tions relies on clinical suspicion and microbio-logical confirmation.

Conclusions

Invasive trichosporonosis should not beoverlooked, particularly in neutropenic febrilepatients with acute leukaemia, those receivedaggressive cytostatic and broad-spectrum anti-biotic therapy. This case suggests the import-ance of identification and antifungal susceptib-ility testing of T. asahii for the application ofan adequate treatment.

References

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Trichosporon asahii fungaemia in an adult patient with acute … · 2012. 3. 20. · Revista Român ă de Medicin ă de Laborator Vol. 12, Nr. 3, Septembrie 2008 Trichosporon asahii