Infection DOI 10.1007/s15010-015-0757-y
CASE REPORT
Necrotizing mycosis due to Verruconis gallopava in an immunocompetent patient Christian Geltner · Sieglinde Sorschag · Birgit Willinger · Thomas Jaritz · Zoran Saric · Cornelia Lass‑Flörl
Received: 23 November 2014 / Accepted: 24 February 2015 © Springer-Verlag Berlin Heidelberg 2015
Abstract Verruconis gallopava is a dematiaceous mould usually causing saprophytic infection in immunosuppressed host. Only a few cases have been published even in immunocompromised states. We present a rare case of pulmonary involvement in an immunocompetent patient with recurrent disease. The mid-aged woman had no evidence of any disease causing impaired immune response. Recurrent disease shows pulmonary infiltrates and symptoms of allergic bronchopulmonary mycosis. We describe an emerging pathogen that has been found in an immunocompetent host. Eradication was not possible despite the use of several different antifungal drugs. Further recurrence of infection in the described patient is probable.
Introduction Dematiaceous moulds as well as non-Aspergillus fumigatus species are increasingly recognized as opportunistic pathogens in immunocompromised hosts [1]. Verruconis
C. Geltner (*) · T. Jaritz · Z. Saric Department of Pulmonology, Klinikum Klagenfurt am Wörthersee, Feschnigstr. 11, AT 9020 Klagenfurt, Austria e-mail: [email protected]; [email protected] S. Sorschag Institute of Laboratory Diagnostics and Microbiology, Klinikum Klagenfurt, Klagenfurt, Austria
gallopava, a dematiaceous fungus found in soil and decaying vegetation, causes infections of the central nervous system and the lower respiratory tract in immunologically impaired patients [2, 3]. The principal portal of entry and also the most common site of infection is the lower respiratory tract. V. gallopava has been reported to cause brain abscesses and encephalitis in birds and other animals. In humans, most cases of infection occur either in transplant recipients [4–8] or in patients with hematologic malignancies receiving chemotherapies [9, 10]. In solid organ transplant recipients, V. gallopava infections mainly occur in lung and liver transplants. Shoham et al. [1] described 12 cases of V. gallopava infections in transplant recipients. A single-centre case study in solid organ transplants has been published by Quereshi et al. [11]. Nearly all patients with brain involvement died, whereas a majority of patients with lung manifestation survived. Augmented immunosuppressive therapies were given in most of the reported cases. Only very few reports of V. gallopava infections in immunocompetent patients have been published. A case of a wood pulp worker treated by surgery [12] and a single case of a respiratory infection in an immunocompetent host [13] have been published earlier. No serological or antigen diagnostic tests are available to detect this fungus. Diagnosis is based on morphology, growth properties, and molecular biology analysis of the isolate. Recently, the taxonomy of the genus has been re-evaluated, and the most relevant species, Ochroconis gallopava, was transferred to the new genus Verruconis [14].
B. Willinger Division of Clinical Microbiology, Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria
Case report
C. Lass‑Flörl Division of Hygiene and Microbiology, Medical University Innsbruck, Innsbruck, Austria
We report the case of a 54-year-old female presenting with dyspnoea on exertion, fatigue, cough and episodes
13
C. Geltner et al. Fig. 1 V. gallopava on standard medium. Specimen Bronchoalveolar lavage. Incubation on solid and liquid Sabouraud Dextrose Agar (30 °C) showed fungal growths after 3 days
Fig. 2 V. gallopava in microscopic view. Bronchoalveolar lavage with Gram stain (magnification ×630). Fungal elements appear as hyalin, thick, and septated mycelial fragments with 3–5 µm in diameter
of sporadic fever. She had previous treatments for pneumonia and bronchitis with conventional antibiotics. Due to recurrent disease bronchoscopy was performed and the microbiological specimen revealed infection with V. gallopava. In previous history, at least five episodes of pulmonary infiltrates were reported and presented as left lower lobe pneumonia. At the time of first detection of the fungal infection she showed signs of asthma as well as of allergic mycosis. Laboratory analysis showed elevation of the white blood cell count, CRP and IgE 1466 kU/l. Specific IgE, aspergillus IgG, panfungal PCR (Mycoreal Fungi®; Ingenetix, Vienna, Austria) and detection of galactomannan (Platelia Aspergillus®, BioRad, Vienna, Austria) were negative. Transbronchial biopsy and BAL revealed fungi in standard cultures (Fig. 1), and microscopic examinations of the cultured species were performed (Fig. 2). Identification was performed by sequence analysis of the ITS 2 region using an automated sequence analyzer (ABI Prism 310, Genetic Analyzer; Applied Biosystems, California, USA) and was assessed by a search for homology with GenBank sequences using the BLAST search program. Sequence similarity with V. gallopava was 99 % and, therefore, considered to be the correct identification (GenBank accession number: 169659269/AB125284.4). Antifungal susceptibility testing was done using the European Committee on Antimicrobial Susceptibility Testing (EUCAST) [15] criteria. MICs obtained were 0.19 µg/ml for caspofungin,
13
0.016 µg/ml for anidulafungin, 0.023 µg/ml for micafungin, 0.016 µg/ml for itraconazole, 0.008 µg/ml for each, voriconazole and posaconazole and 0.019 µg/ml for amphotericin B. In computer tomography and chest X-ray, infiltrates were located mostly in the left lower lobe. At the same time coughing, asthma and persisting infiltrates were detected, during which sputum cultures revealed the presence of V. gallopava. Voriconazole was given as first-line therapy intravenously and switched to oral treatment after 2 weeks. Infiltrates regressed and the patient felt much better. Treatment was stopped due to several of side effects of voriconazole such as bronchospasm, nausea, vomiting, weight loss and sleeplessness. During the following months she developed various episodes of recurrent disease, with symptoms correlating to allergic fungal disease (similar to allergic bronchopulmonary aspergillosis, ABPA) and infiltrates being present in the left lower lobe. The course of the patient’s disease and its treatment is shown in Table 1. Evaluation of the patient for immunosuppression revealed no pathological findings. Protein electrophoresis, IgG and IgM levels, IgG subclass analyses were within the reference ranges. PCR for CMV, EBV and HSV showed negative results. The patient showed no history of haematological, oncological disease or any signs of chronic infection.
Coughing
The pulmonary symptoms were managed using intravenous liposomal amphotericin for another 2 weeks, followed by inhaled amphotericin B, which led to several side effects but no complete eradication of the fungus. 6 weeks after treatment episodes microbiological specimens were again positive for V. gallopava. A therapy with oral itraconazole was started, which was well tolerated by the patient. This treatment was continued for 3 months. After stopping oral medication the disease recurred quickly. Disease relapse usually occurred within 4–8 weeks after discontinuation of the antimycotic therapy. Typical symptoms were cough, dyspnoea on exertion, nausea, fatigue and unspecific flu-like syndromes. In most cases infiltrates and consolidation could be detected radiologically. Sputum and/or bronchial lavage showed cultural growth of V. gallopava.
Inhaled amphotericin for 3 month
Discussion
RLL right lower lobe, LLL left lower lobe, CT computer tomography
Dyspnoea, cough, infiltrates, fatigue
August 2013
February 2013
January 2014
V. gallopava (sputum)
V. gallopava (bronchoscopy)
Neutropenia, nausea
Neutropenia, nausea
Liposomal amphotericin (Ambisome) 14 days 5 mg/kg i.v. Liposomal amphotericin (Ambisome) 14 days 5 mg/kg V. gallopava (sputum)
Itraconazole 200 mg bid, 12 weeks
Infiltrate, diffuse symptoms of chronic disease, weight loss Infiltrate, diffuse symptoms of chronic disease, weight loss Dyspnoea, cough, fatigue December 2012
V. gallopava (sputum)
Dizziness, nausea, sleeplessness Stopped for leucopenia, renal insufficiency V. gallopava (bronchoscopy)
Cough, dizziness, nausea
Voriconazole 200 mg bid i.v., 14 days Liposomal amphotericin for 6 days (amphocil) Cough, infiltrates LLL Cough, asthma, consolidation LLL November 2012 December 2012
May 2012
June 2011
August 2012
V. gallopava (bronchoscopy) No
Fever, coughing, nausea,
Voriconazole 7 days bid i.v., p.o. 200 mg bid 8 weeks No V. gallopava (sputum)
No
No Aminopenicillin for 10 days hemophilus (sputum)
Consolidations middle lobe, reticular opacities RLL, IGE 1455 Bronchiectasis, consolidation middle lobe, bronchoscopy putrid secretion Bronchiectasis, coughing, sputum green, CT: opacities ML and RLL CT: idem, bronchoscopy putrid June 2009
Microbiology (specimen) Symptoms Period
Table 1 Course of disease: an overview of symptoms and antifungal treatment
Treatment
Side effects
Necrotizing mycosis due to V. gallopava
In this case, we show that a normally non-pathogenic mould can cause various symptoms of necrotizing mycosis and allergic bronchopulmonary mycosis. Previous reports show infections in immunocompromised hosts especially in solid organ transplants. In our patient with normal immune system V. gallopava eradication was not possible despite the use of various antifungal drugs. The in vitro testing of drug enhances the use of voriconazole and amphotericin B. Both drugs were not tolerated by the patient for longer time periods. In two recently published studies, different drug susceptibilities were found; Giraldo et al. [16] described terfenadine and micafungin to be the most active drugs in a retrospective analysis of 51 specimens, whereas anidulafungin and posaconazole have the lowest MICs in other study [17]. Combining all results available for susceptibility testing and findings in the literature, we found that posaconazole and voriconazole were the antimycotic drugs with the best overall activity in our V. gallopava isolate. All these drugs had limited tolerance, which complicated the treatment and did not achieve complete eradication of the mould and infection control. It is worth mentioning that V. gallopava can cause disease similar to ABPA. ABPA (allergic bronchopulmonary aspergillosis) is hypersensitivity pulmonary disease usually associated with inflammatory destruction of airways in response to Aspergillus allergens [18]. Thus, chronic airway colonization with Aspergillus induces strong inflammatory responses with high IgE levels [19]. Aspergillusspecific and other filamentous fungi antigen, IgE-mediated type I hypersensitivity reactions and specific IgG-mediated type III hypersensitivity reactions play central roles in the pathogenesis of allergic bronchopulmonary mycosis (ABPM). These pathognomonic symptoms also occurred in
13
C. Geltner et al.
variable intensity in our patient and reflect good immune response. Necrotizing inflammation and tissue invasion, however, are signs of extensive impairment of immune competence and is typically seen in organ transplant recipients. The recurrence of disease in our patient started with non-specific symptoms mostly seen in ABPM followed by consolidation and later the more invasive phenotype.
Conclusion We describe an immunocompetent host with recurrent disease and infection with V. gallopava, previously described mainly in immunocompromised hosts. Symptoms were non-specific and recurrent infiltrates were common. Up to now, eradication has not been possible despite the use of various antifungal drugs. In vitro susceptibility was performed and showed the fungus to be in vitro highly susceptible against the various drugs tested. Conflict of interest None for this case report.
References 1. Shoham S, Pic-Aluas L, Taylor J, Cortez K, Rinaldi MG, Shea Y, Walsh TJ. Transplant-associated Ochroconis gallopava infections. Transpl Infect Dis. 2008;10:442–8. 2. Rossmann SN, Cernoch PL, Davis JR. Dematiaceous fungi are an increasing cause of human disease. Clin Infect Dis. 1996;22:73–80. 3. Singh N, Chang FY, Gayowski T, Marino IR. Infections due to dematiaceous fungi in organ transplant recipients: case report and review. Clin Infect Dis. 1997;24:369–74. 4. Meriden Z, Marr KA, Lederman HM, Illei PB, Villa K, Riedel S, Caroll KC, Zhang SX. Ochroconis gallopava infection in a patient with chronic granulomatous disease: case report and review of the literature. Med Mycol. 2012;50:883–9. 5. Mayer N, Bastani B. A case of pulmonary cavitary lesion due to Dactylaria constricta var. gallopava in a renal transplant patient. Nephrology. 2009;14:262. 6. Burns KEA, Ohori NP, Iacono AT. Dactylaria gallopava infection presenting as a pulmonary nodule in a single-lung transplant recipient. J Heart Lung Transplant. 2000;19:900–2. 7. Mancini MC, McGinnis MR. Dactylaria infection of a human being: pulmonary disease in a heart transplant recipient. J Heart Lung Transpl. 1992;11:827–30.
13
8. Wang TK, Chiu W, Chim S, Chan TM, Wong SS, Ho PL. Disseminated Ochroconis gallopavum infection in a renal transplant recipient: the first reported case and a review of the literature. Clin Nephrol. 2003;60:415–23. doi:10.5414/CNP60415. 9. Sides EH, Benson JD, Padhye AA. Phaeohyphomycotic brain abscess due to Ochroconis gallopavum in a patient with malignant lymphoma of a large cell type. J Med Vet Mycol. 1991;29:317–22. 10. Fukushima N, Mannen K, Okamoto S, Shinogi T, Nishimoto K, Sueoka E. Disseminated Ochroconis gallopavum infection in a chronic lymphocytic leukemia: a case report and review of the literature on hematological malignancies. Intern Med. 2005;44:879–82. 11. Qureshi ZA, Kwak EJ, Nguyen MH, Silveira FP. Ochroconis gallopava: a dematiaceous mold causing infections in transplant recipients. Clin Transplant. 2012;26:E17–23. 12. Odell JA, Alvarez S, Cvitkovich DG, Cortese DA, McComb BL. Multiple lung abscesses due to Ochroconis gallopavum, a dematiaceous fungus, in a nonimmunocompromised wood pulp worker. Chest. 2000;118:1503–5. 13. Hollingsworth JW, Shofer S, Zaas A. Successful treatment of Ochroconis gallopavum infection in an immunocompetent host. Infection. 2007;35:367–9. 14. Samerpitak K, Van der Linde E, Choi HJ, Gerrits van den Ende AHG, Machouart M, Gueidan C, de Hoog GS. Taxonomy of Ochroconis, genus including opportunistic pathogens on humans and animals. Fungal Divers. 2014;65:89–126. doi:10.1007/ s13225-013-0253-6. 15. Lass-Flörl C, Mayr A, Perkhofer S, Hinterberger G, Hausdorfer J, Speth C, Fille M. Activities of antifungal agents against yeasts and filamentous fungi: assessment according to the methodology of the European Committee on Antimicrobial Susceptibility Testing. Antimicrob Agents Chemother. 2008;52:3637–41. doi:10.1128/AAC.00662-08 [Epub 2008 Aug 11]. 16. Giraldo A, Sutton DA, Samerpitak K, de Hoog GS, Wieder hold NP, Guarro J, Gené J. Occurrence of Ochroconis and Verruconis species in clinical specimens from the United States. J Clin Microbiol. 2014;52:4189–201. doi:10.1128/JCM.02027-14 [Epub 2014 Sep 17]. 17. Seyedmousavi S, Samerpitak K, Rijs AJM, Melchers WJG, Mouton JW, Verweij PE, de Hoog GS. Antifungal Susceptibility Patterns of Opportunistic Fungi in the Genera Verruconis and Ochroconis. Antimicrob Agents Chemother. 2014;58:3285–92. 18. Walsh TJ, Anaissie EJ, Denning DW, Herbrecht R, Kontoyian-nis DP, Marr KA, Morrison VA, Segal BH, Steinbach WJ, Stevens DA, Van Burik JA, Wingard JR, Patterson TF. Treatment of aspergillosis: clinical practice guidelines of the Infectious Diseases Society of America. Clin Infect Dis. 2008;46:327–60. 19. Fricker-Hidalgo H, Coltey B, Llerena C, Renversez JC, Grillot R, Pin I, Pelloux H, Pinel C. Recombinant allergens combined with biological markers in the diagnosis of allergic bronchopulmonary aspergillosis in cystic fibrosis patients. Clin Vaccine Immunol. 2010;17:1330–6. doi:10.1128/CVI.00200-10.
CASE REPORT
Necrotizing mycosis due to Verruconis gallopava in an immunocompetent patient Christian Geltner · Sieglinde Sorschag · Birgit Willinger · Thomas Jaritz · Zoran Saric · Cornelia Lass‑Flörl
Received: 23 November 2014 / Accepted: 24 February 2015 © Springer-Verlag Berlin Heidelberg 2015
Abstract Verruconis gallopava is a dematiaceous mould usually causing saprophytic infection in immunosuppressed host. Only a few cases have been published even in immunocompromised states. We present a rare case of pulmonary involvement in an immunocompetent patient with recurrent disease. The mid-aged woman had no evidence of any disease causing impaired immune response. Recurrent disease shows pulmonary infiltrates and symptoms of allergic bronchopulmonary mycosis. We describe an emerging pathogen that has been found in an immunocompetent host. Eradication was not possible despite the use of several different antifungal drugs. Further recurrence of infection in the described patient is probable.
Introduction Dematiaceous moulds as well as non-Aspergillus fumigatus species are increasingly recognized as opportunistic pathogens in immunocompromised hosts [1]. Verruconis
C. Geltner (*) · T. Jaritz · Z. Saric Department of Pulmonology, Klinikum Klagenfurt am Wörthersee, Feschnigstr. 11, AT 9020 Klagenfurt, Austria e-mail: [email protected]; [email protected] S. Sorschag Institute of Laboratory Diagnostics and Microbiology, Klinikum Klagenfurt, Klagenfurt, Austria
gallopava, a dematiaceous fungus found in soil and decaying vegetation, causes infections of the central nervous system and the lower respiratory tract in immunologically impaired patients [2, 3]. The principal portal of entry and also the most common site of infection is the lower respiratory tract. V. gallopava has been reported to cause brain abscesses and encephalitis in birds and other animals. In humans, most cases of infection occur either in transplant recipients [4–8] or in patients with hematologic malignancies receiving chemotherapies [9, 10]. In solid organ transplant recipients, V. gallopava infections mainly occur in lung and liver transplants. Shoham et al. [1] described 12 cases of V. gallopava infections in transplant recipients. A single-centre case study in solid organ transplants has been published by Quereshi et al. [11]. Nearly all patients with brain involvement died, whereas a majority of patients with lung manifestation survived. Augmented immunosuppressive therapies were given in most of the reported cases. Only very few reports of V. gallopava infections in immunocompetent patients have been published. A case of a wood pulp worker treated by surgery [12] and a single case of a respiratory infection in an immunocompetent host [13] have been published earlier. No serological or antigen diagnostic tests are available to detect this fungus. Diagnosis is based on morphology, growth properties, and molecular biology analysis of the isolate. Recently, the taxonomy of the genus has been re-evaluated, and the most relevant species, Ochroconis gallopava, was transferred to the new genus Verruconis [14].
B. Willinger Division of Clinical Microbiology, Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria
Case report
C. Lass‑Flörl Division of Hygiene and Microbiology, Medical University Innsbruck, Innsbruck, Austria
We report the case of a 54-year-old female presenting with dyspnoea on exertion, fatigue, cough and episodes
13
C. Geltner et al. Fig. 1 V. gallopava on standard medium. Specimen Bronchoalveolar lavage. Incubation on solid and liquid Sabouraud Dextrose Agar (30 °C) showed fungal growths after 3 days
Fig. 2 V. gallopava in microscopic view. Bronchoalveolar lavage with Gram stain (magnification ×630). Fungal elements appear as hyalin, thick, and septated mycelial fragments with 3–5 µm in diameter
of sporadic fever. She had previous treatments for pneumonia and bronchitis with conventional antibiotics. Due to recurrent disease bronchoscopy was performed and the microbiological specimen revealed infection with V. gallopava. In previous history, at least five episodes of pulmonary infiltrates were reported and presented as left lower lobe pneumonia. At the time of first detection of the fungal infection she showed signs of asthma as well as of allergic mycosis. Laboratory analysis showed elevation of the white blood cell count, CRP and IgE 1466 kU/l. Specific IgE, aspergillus IgG, panfungal PCR (Mycoreal Fungi®; Ingenetix, Vienna, Austria) and detection of galactomannan (Platelia Aspergillus®, BioRad, Vienna, Austria) were negative. Transbronchial biopsy and BAL revealed fungi in standard cultures (Fig. 1), and microscopic examinations of the cultured species were performed (Fig. 2). Identification was performed by sequence analysis of the ITS 2 region using an automated sequence analyzer (ABI Prism 310, Genetic Analyzer; Applied Biosystems, California, USA) and was assessed by a search for homology with GenBank sequences using the BLAST search program. Sequence similarity with V. gallopava was 99 % and, therefore, considered to be the correct identification (GenBank accession number: 169659269/AB125284.4). Antifungal susceptibility testing was done using the European Committee on Antimicrobial Susceptibility Testing (EUCAST) [15] criteria. MICs obtained were 0.19 µg/ml for caspofungin,
13
0.016 µg/ml for anidulafungin, 0.023 µg/ml for micafungin, 0.016 µg/ml for itraconazole, 0.008 µg/ml for each, voriconazole and posaconazole and 0.019 µg/ml for amphotericin B. In computer tomography and chest X-ray, infiltrates were located mostly in the left lower lobe. At the same time coughing, asthma and persisting infiltrates were detected, during which sputum cultures revealed the presence of V. gallopava. Voriconazole was given as first-line therapy intravenously and switched to oral treatment after 2 weeks. Infiltrates regressed and the patient felt much better. Treatment was stopped due to several of side effects of voriconazole such as bronchospasm, nausea, vomiting, weight loss and sleeplessness. During the following months she developed various episodes of recurrent disease, with symptoms correlating to allergic fungal disease (similar to allergic bronchopulmonary aspergillosis, ABPA) and infiltrates being present in the left lower lobe. The course of the patient’s disease and its treatment is shown in Table 1. Evaluation of the patient for immunosuppression revealed no pathological findings. Protein electrophoresis, IgG and IgM levels, IgG subclass analyses were within the reference ranges. PCR for CMV, EBV and HSV showed negative results. The patient showed no history of haematological, oncological disease or any signs of chronic infection.
Coughing
The pulmonary symptoms were managed using intravenous liposomal amphotericin for another 2 weeks, followed by inhaled amphotericin B, which led to several side effects but no complete eradication of the fungus. 6 weeks after treatment episodes microbiological specimens were again positive for V. gallopava. A therapy with oral itraconazole was started, which was well tolerated by the patient. This treatment was continued for 3 months. After stopping oral medication the disease recurred quickly. Disease relapse usually occurred within 4–8 weeks after discontinuation of the antimycotic therapy. Typical symptoms were cough, dyspnoea on exertion, nausea, fatigue and unspecific flu-like syndromes. In most cases infiltrates and consolidation could be detected radiologically. Sputum and/or bronchial lavage showed cultural growth of V. gallopava.
Inhaled amphotericin for 3 month
Discussion
RLL right lower lobe, LLL left lower lobe, CT computer tomography
Dyspnoea, cough, infiltrates, fatigue
August 2013
February 2013
January 2014
V. gallopava (sputum)
V. gallopava (bronchoscopy)
Neutropenia, nausea
Neutropenia, nausea
Liposomal amphotericin (Ambisome) 14 days 5 mg/kg i.v. Liposomal amphotericin (Ambisome) 14 days 5 mg/kg V. gallopava (sputum)
Itraconazole 200 mg bid, 12 weeks
Infiltrate, diffuse symptoms of chronic disease, weight loss Infiltrate, diffuse symptoms of chronic disease, weight loss Dyspnoea, cough, fatigue December 2012
V. gallopava (sputum)
Dizziness, nausea, sleeplessness Stopped for leucopenia, renal insufficiency V. gallopava (bronchoscopy)
Cough, dizziness, nausea
Voriconazole 200 mg bid i.v., 14 days Liposomal amphotericin for 6 days (amphocil) Cough, infiltrates LLL Cough, asthma, consolidation LLL November 2012 December 2012
May 2012
June 2011
August 2012
V. gallopava (bronchoscopy) No
Fever, coughing, nausea,
Voriconazole 7 days bid i.v., p.o. 200 mg bid 8 weeks No V. gallopava (sputum)
No
No Aminopenicillin for 10 days hemophilus (sputum)
Consolidations middle lobe, reticular opacities RLL, IGE 1455 Bronchiectasis, consolidation middle lobe, bronchoscopy putrid secretion Bronchiectasis, coughing, sputum green, CT: opacities ML and RLL CT: idem, bronchoscopy putrid June 2009
Microbiology (specimen) Symptoms Period
Table 1 Course of disease: an overview of symptoms and antifungal treatment
Treatment
Side effects
Necrotizing mycosis due to V. gallopava
In this case, we show that a normally non-pathogenic mould can cause various symptoms of necrotizing mycosis and allergic bronchopulmonary mycosis. Previous reports show infections in immunocompromised hosts especially in solid organ transplants. In our patient with normal immune system V. gallopava eradication was not possible despite the use of various antifungal drugs. The in vitro testing of drug enhances the use of voriconazole and amphotericin B. Both drugs were not tolerated by the patient for longer time periods. In two recently published studies, different drug susceptibilities were found; Giraldo et al. [16] described terfenadine and micafungin to be the most active drugs in a retrospective analysis of 51 specimens, whereas anidulafungin and posaconazole have the lowest MICs in other study [17]. Combining all results available for susceptibility testing and findings in the literature, we found that posaconazole and voriconazole were the antimycotic drugs with the best overall activity in our V. gallopava isolate. All these drugs had limited tolerance, which complicated the treatment and did not achieve complete eradication of the mould and infection control. It is worth mentioning that V. gallopava can cause disease similar to ABPA. ABPA (allergic bronchopulmonary aspergillosis) is hypersensitivity pulmonary disease usually associated with inflammatory destruction of airways in response to Aspergillus allergens [18]. Thus, chronic airway colonization with Aspergillus induces strong inflammatory responses with high IgE levels [19]. Aspergillusspecific and other filamentous fungi antigen, IgE-mediated type I hypersensitivity reactions and specific IgG-mediated type III hypersensitivity reactions play central roles in the pathogenesis of allergic bronchopulmonary mycosis (ABPM). These pathognomonic symptoms also occurred in
13
C. Geltner et al.
variable intensity in our patient and reflect good immune response. Necrotizing inflammation and tissue invasion, however, are signs of extensive impairment of immune competence and is typically seen in organ transplant recipients. The recurrence of disease in our patient started with non-specific symptoms mostly seen in ABPM followed by consolidation and later the more invasive phenotype.
Conclusion We describe an immunocompetent host with recurrent disease and infection with V. gallopava, previously described mainly in immunocompromised hosts. Symptoms were non-specific and recurrent infiltrates were common. Up to now, eradication has not been possible despite the use of various antifungal drugs. In vitro susceptibility was performed and showed the fungus to be in vitro highly susceptible against the various drugs tested. Conflict of interest None for this case report.
References 1. Shoham S, Pic-Aluas L, Taylor J, Cortez K, Rinaldi MG, Shea Y, Walsh TJ. Transplant-associated Ochroconis gallopava infections. Transpl Infect Dis. 2008;10:442–8. 2. Rossmann SN, Cernoch PL, Davis JR. Dematiaceous fungi are an increasing cause of human disease. Clin Infect Dis. 1996;22:73–80. 3. Singh N, Chang FY, Gayowski T, Marino IR. Infections due to dematiaceous fungi in organ transplant recipients: case report and review. Clin Infect Dis. 1997;24:369–74. 4. Meriden Z, Marr KA, Lederman HM, Illei PB, Villa K, Riedel S, Caroll KC, Zhang SX. Ochroconis gallopava infection in a patient with chronic granulomatous disease: case report and review of the literature. Med Mycol. 2012;50:883–9. 5. Mayer N, Bastani B. A case of pulmonary cavitary lesion due to Dactylaria constricta var. gallopava in a renal transplant patient. Nephrology. 2009;14:262. 6. Burns KEA, Ohori NP, Iacono AT. Dactylaria gallopava infection presenting as a pulmonary nodule in a single-lung transplant recipient. J Heart Lung Transplant. 2000;19:900–2. 7. Mancini MC, McGinnis MR. Dactylaria infection of a human being: pulmonary disease in a heart transplant recipient. J Heart Lung Transpl. 1992;11:827–30.
13
8. Wang TK, Chiu W, Chim S, Chan TM, Wong SS, Ho PL. Disseminated Ochroconis gallopavum infection in a renal transplant recipient: the first reported case and a review of the literature. Clin Nephrol. 2003;60:415–23. doi:10.5414/CNP60415. 9. Sides EH, Benson JD, Padhye AA. Phaeohyphomycotic brain abscess due to Ochroconis gallopavum in a patient with malignant lymphoma of a large cell type. J Med Vet Mycol. 1991;29:317–22. 10. Fukushima N, Mannen K, Okamoto S, Shinogi T, Nishimoto K, Sueoka E. Disseminated Ochroconis gallopavum infection in a chronic lymphocytic leukemia: a case report and review of the literature on hematological malignancies. Intern Med. 2005;44:879–82. 11. Qureshi ZA, Kwak EJ, Nguyen MH, Silveira FP. Ochroconis gallopava: a dematiaceous mold causing infections in transplant recipients. Clin Transplant. 2012;26:E17–23. 12. Odell JA, Alvarez S, Cvitkovich DG, Cortese DA, McComb BL. Multiple lung abscesses due to Ochroconis gallopavum, a dematiaceous fungus, in a nonimmunocompromised wood pulp worker. Chest. 2000;118:1503–5. 13. Hollingsworth JW, Shofer S, Zaas A. Successful treatment of Ochroconis gallopavum infection in an immunocompetent host. Infection. 2007;35:367–9. 14. Samerpitak K, Van der Linde E, Choi HJ, Gerrits van den Ende AHG, Machouart M, Gueidan C, de Hoog GS. Taxonomy of Ochroconis, genus including opportunistic pathogens on humans and animals. Fungal Divers. 2014;65:89–126. doi:10.1007/ s13225-013-0253-6. 15. Lass-Flörl C, Mayr A, Perkhofer S, Hinterberger G, Hausdorfer J, Speth C, Fille M. Activities of antifungal agents against yeasts and filamentous fungi: assessment according to the methodology of the European Committee on Antimicrobial Susceptibility Testing. Antimicrob Agents Chemother. 2008;52:3637–41. doi:10.1128/AAC.00662-08 [Epub 2008 Aug 11]. 16. Giraldo A, Sutton DA, Samerpitak K, de Hoog GS, Wieder hold NP, Guarro J, Gené J. Occurrence of Ochroconis and Verruconis species in clinical specimens from the United States. J Clin Microbiol. 2014;52:4189–201. doi:10.1128/JCM.02027-14 [Epub 2014 Sep 17]. 17. Seyedmousavi S, Samerpitak K, Rijs AJM, Melchers WJG, Mouton JW, Verweij PE, de Hoog GS. Antifungal Susceptibility Patterns of Opportunistic Fungi in the Genera Verruconis and Ochroconis. Antimicrob Agents Chemother. 2014;58:3285–92. 18. Walsh TJ, Anaissie EJ, Denning DW, Herbrecht R, Kontoyian-nis DP, Marr KA, Morrison VA, Segal BH, Steinbach WJ, Stevens DA, Van Burik JA, Wingard JR, Patterson TF. Treatment of aspergillosis: clinical practice guidelines of the Infectious Diseases Society of America. Clin Infect Dis. 2008;46:327–60. 19. Fricker-Hidalgo H, Coltey B, Llerena C, Renversez JC, Grillot R, Pin I, Pelloux H, Pinel C. Recombinant allergens combined with biological markers in the diagnosis of allergic bronchopulmonary aspergillosis in cystic fibrosis patients. Clin Vaccine Immunol. 2010;17:1330–6. doi:10.1128/CVI.00200-10.
