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Year : 2010  |  Volume : 28  |  Issue : 4  |  Page : 409-411

Thyroid abscess due to Scedosporium apiospermum

1 Department of Microbiology, Manipal Super Speciality Hospitals, Near Varadhi, Tadepalli, Vijayawada - 522 501, India
2 Department of General Medicine, Manipal Super Speciality Hospitals, Near Varadhi, Tadepalli, Vijayawada - 522 501, India
3 Department of Microbiology, Dr. Pinnamaneni Siddhartha Institute of Medical Sciences & Research Foundation, Chinoutpalli, Gannavaram Mandal, Krishna District - 521 286, Andhra Pradesh, India

Date of Submission13-May-2010
Date of Acceptance11-Aug-2010
Date of Web Publication20-Oct-2010

Correspondence Address:
P Sireesha
Department of Microbiology, Manipal Super Speciality Hospitals, Near Varadhi, Tadepalli, Vijayawada - 522 501
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0255-0857.71859

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 ~ Abstract 

We report a case of thyroid abscess caused by Scedosporium apiospermum in a patient with cirrhosis of liver and autoimmune haemolytic anaemia. To date, there are no reports of isolation of this fungus from thyroid abscess.

Keywords: Scedosporium apiospermum, thyroid abscess

How to cite this article:
Sireesha P, Manoj Kumar C H, Setty C R. Thyroid abscess due to Scedosporium apiospermum. Indian J Med Microbiol 2010;28:409-11

How to cite this URL:
Sireesha P, Manoj Kumar C H, Setty C R. Thyroid abscess due to Scedosporium apiospermum. Indian J Med Microbiol [serial online] 2010 [cited 2021 Mar 7];28:409-11. Available from:

 ~ Introduction Top

Scedosporium is a filamentous fungus which occasionally causes infections in humans. It is a cosmopolitan filamentous fungus which is commonly isolated from rural soils, polluted water, composts, and manure of cattle. Scedosporium apiospermum, the asexual state of Pseudallescheria boydii, is increasingly recognised as an opportunistic pathogen. Either of these two forms can be isolated from clinical specimens. S. apiospermum was first described as a human pathogen in 1911 by Saccardo from a case of mycetoma. [1],[2]

 ~ Case Report Top

A 48-year-old male patient, clerk by occupation, presented with history of fever and swelling in the neck, of 15 days duration. He gave history of joint pains and backache on and off since 6 months. He was diagnosed elsewhere to have cirrhosis of liver and autoimmune haemolytic anaemia 3 months back, for which he was on steroids. There was history of blood transfusions as well for the same condition. There is no history of diabetes mellitus, hypertension or asthma or any history of coronary heart disease. On physical examination, the patient was febrile. He was looking pale and had splenomegaly. Rest of the physical examination was normal. There were no signs of liver failure. A swelling of 5 × 4 cm in the front side of the neck which moved with deglutition and was not associated with any tenderness was noted. The swelling was more to the right [Figure 1]. There was no lymphadenopathy.
Figure 1: Swelling of the thyroid gland

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His hemoglobin was 8.8 g/dl, total count was 10,300/mm 3 with a neutrophil count of 6200/mm 3 . The erythrocyte sedimentation rate (ESR) was 65 mm/hour. Other biochemical parameters were as follows: bilirubin 4.4 mg/dl, direct 1.2 mg/dl, indirect 2.0 mg/dl, aspartate transaminase (AST) 47 U/l, alanine transaminase (ALT) 35 U/l, alkaline phosphatase 190 U/l, serum proteins 7.4 g/dl, albumin 2.8 g/dl and globulin 4.6 g/dl. Rheumatoid arthritis factor was 40 IU and C-reactive protein was 48 mg/dl. Direct coomb's test was positive. Anti nuclear antibodies and anti ds-DNA antibodies were negative. HIV was nonreactive and HBs Ag negative. Computed tomography (CT) scan of the thyroid revealed an enlarged right lobe, which measured 6 × 4 cm with central necrosis and peripheral enhancing component. CT guided aspiration of pus from thyroid swelling was done and sent for microbiological investigations.

Routine culture media, i.e., blood agar, chocolate agar and MacConkey agar, were inoculated. Wet mount preparation revealed plenty of WBCs and no bacteria, but thin branching septate filaments suggestive of fungi were noticed. KOH wet mount was done which showed similar fungal filaments. Gram staining picture showed plenty of pus cells and no organisms. Acid fast staining was negative for acid fast bacilli. Two sets of Sabouraud's Dextrose Agar (SDA) tubes were inoculated. One set was incubated at room temperature and other at 37°C. Before the report was ready, the patient was discharged on antibiotics with advice for follow-up after 1 week.

At the end of 48 hours, there was no bacterial growth. After 72 hours, there was filamentous fungal growth on chocolate agar [Figure 2], blood agar and SDA, which on further incubation showed dark coloured reverse pigmentation. Slide culture technique was done to identify the fungus. Lactophenol cotton blue preparation showed septate hyaline hyphae (2-4 μm in diameter), conidiophores and conidia. The conidia were unicellular and oval in shape; some of them were pale brown. They were truncate at their base and were found singly on the conidiophores and it was identified as S. apiospermum [Figure 3]. The fungus was inoculated on cornmeal agar to look for the teleomorph (sexual) stage P. boydii of S. apiospermum. However, the present isolate did not show the sexual stage.
Figure 2: Cottony grayish white colonies of S. apiospermum on chocolate agar on third day

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Figure 3: Lactophenol cotton blue preparation showing septate hyphae with unicellular oval conidia, born singly at the end of the conidiophore (×400)

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The patient returned after 1 week with no improvement in his condition. Since by this time the earlier specimen was positive for fungus, repeat CT guided aspiration of the thyroid abscess was done to confirm the aetiology. The pus was subjected to the same above-mentioned microbiological investigations. The fungus with similar microscopic and colony morphology was isolated again. The direct microscopic and culture examinations were negative for bacteria including mycobacteria.

This time, the patient was started on voriconazole 400 mg twice daily. After 1 week of voriconazole treatment, the patient's liver enzymes were elevated. Hence, the drug was stopped for a period of 2 weeks and restarted with 200 mg twice daily dose with regular monitoring of liver and kidney functions. The follow-up of the patient showed clinical improvement in the thyroid swelling.

 ~ Discussion Top

S. apiospermum is a ubiquitous saprophytic ascomycetous fungus found in soil, sewage, contaminated water and manure of farm animals. In recent years, it has been shown to be pathogenic for both immunocompetent and immunosuppressed patients. The genus Scedosporium contains two species: S. apiospermum and Scedosporium prolificans. P. boydii is the teleomorph (sexual stage) of S. apiospermum. There is no sexual stage for S. prolificans. [1]

In immunocompetent individuals, this filamentous fungus can gain entry into cutaneous and subcutaneous tissues due to trauma or surgical implantation and causes infections like solitary ulcers, infiltrative erythematous plaques or nodules [3] and white grain mycetoma. [4] This fungus can be a coloniser of previously damaged bronchopulmonary tree due to tuberculosis with cavities, cystic fibrosis or bronchiectatic lungs of any aetiology. It can also produce invasive pulmonary disease. [1],[5] It is also known to cause infections like sinusitis, keratitis, arthritis, lymphadenitis, endophthalmitis, [6] meningoencephalitis, endocarditis, [7] pneumonia and brain abscess due to penetrating trauma or surgery. Sinopulmonary and central nervous system infections have been associated with near drowning in waters polluted with this fungus. [8],[9] In certain circumstances, it can also invade blood vessels, causing thrombosis and perineural areas along the nerve sheath. [6]

This fungus can produce opportunistic infections in immunocompromised individuals like those with advanced human immunodeficiency virus (HIV) infection, primary immunodeficiencies [mainly chronic granulomatous disease (CGD) and Job's syndrome], or haematological malignancies, as well as stem cell transplantation recipients. The most important risk factors are prolonged, profound neutropenia and corticosteroid therapy and the commonest sites involved are lungs and soft tissues, with occasional extension to bones. [1]

Colonies of Scedosporium grow rapidly at 37°C and at room temperature as well within 48-72 hours. Maturation occurs within 5 days. The colonies are cottony white initially but become light brown to gray after a few days of incubation. The reverse appears white to gray. Cleistothecia (non-ostiolate ascocarps) formation may be stimulated on cornmeal agar or other nutrient deficient media; however, many isolates may fail to show this structure. Cleistothecia are yellow-brown to black, spherical, are mostly submerged in the agar and are composed of irregularly interwoven brown hyphae. When crushed, cleistothecia release numerous faintly brown, ellipsoidal ascospores of 4-5 × 7-9 μm in size. [1],[10] However, the present isolate did not show cleistothecia.

In vitro studies indicate that all azoles have significant antifungal activity, except fluconazole and ketoconazole, on S. apiospermum. Most potent in vitro activity was noticed with voriconazole. Terbinafine and 5-flucytosine did not exhibit any antifungal activity and amphotericin B showed only limited activity. Among the echinocandins, caspofungin was most active, followed by anidulafungin. [1]

In vitro antifungal activity was not determined for the present isolate but the patient has responded to voriconazole treatment. Thus, a rare case of thyroid abscess due to S. apiospermum in a patient with autoimmune haemolytic anaemia which has responded to voriconazole treatment is reported.

 ~ References Top

1.Cortez KJ, Roilides E, Quiroz-Telles F, Meletiadis J, Antachopoulos C, Knudsen T, et al. Infections caused by Scedosporium spp. Clin Microbiol Rev 2008;21:157-97.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Kwon-Chung KJ, Bennett JE. Pseudallescheriasis and scedosporium infections (allescheriosis, allescheriasis, petriellidiosis, monosporiosis, scedosporiosis). Medical Mycology. 2 nd ed. Philadelphia: Lea and Febiger; 1992. p. 678-94.  Back to cited text no. 2      
3.Torok L, Simon G, Csornai A, Tapai M, Torok I. Scedosporium apiospermum infection imitating lymphocutaneous sporotrichosis in a patient with myeloblastic monocytic leukemia. Br J Dermatol 1995;133:805-9.  Back to cited text no. 3      
4.Miyamoto T, Sasaoka R, Kawaguchi M, Ishioka S, Inoue T, Yamada NS. Scedosporium apiospermum skin infection: A case report and review of literature. J Am Acad Dermatol 1998;39:498-500.   Back to cited text no. 4      
5.Tamm M, Malouf M, Glanville A. Pulmonary scedosporium infection following lung transplantation. Transpl Infect Dis 2001;3:189-94.   Back to cited text no. 5  [PUBMED]  [FULLTEXT]  
6.Safdar A, Papadopoulos EB, Young JW. Breakthrough Scedosporium apiospermum (Pseudallescheria boydii) brain abscess during therapy for invasive pulmonary aspergillosis following high risk allogenic haemotopoietic stem cell transplantation. Scedosporiasis and recent advances in anti-fungal therapy. Transpl Infect Dis 2002;4:212-7.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.Verghese S, Padmaja P, Chellamma MT, Leelavathy S, Nayar P. Prosthetic valve endocarditis caused by Scedosporium apiospermum. Indian J Med Microbiol 2005;23:264-6.   Back to cited text no. 7  [PUBMED]  Medknow Journal  
8.Allan R, Tunkell. Brain abscess. Chapter 84. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases. 6 th ed. New York: Churchill Livingstone; 2005. p. 1150-63.  Back to cited text no. 8      
9.Acharya A, Ghimire A, Khanal B, Bhattacharya S, Kumari N, Kanungo R. Brain abscess due to Scedosporium apiospermum in a non immunocompromised child. Indian J Med Microbiol 2006;24:231-2.  Back to cited text no. 9  [PUBMED]  Medknow Journal  
10.Forbes AB, Sahm DF, Weissfeld AS. Diagnostic Microbiology. 12 th ed. St. Louis, Mo. Bailey and Scott's; 2007. p. 633.  Back to cited text no. 10      


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