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  Table of Contents    
Year : 2011  |  Volume : 54  |  Issue : 2  |  Page : 415-417
Fungal characterization using polymerase chain reaction in patients with fungal sinusitis

1 Department of Pathology, Alborzi Clinical Microbiology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
2 Alborzi Clinical Microbiology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
3 Department of Otolaryngology, Shiraz University of Medical Sciences, Shiraz, Iran

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Date of Web Publication27-May-2011

How to cite this article:
Ashraf M J, Azarpira N, Badiee P, Khademi B, Shishegar M. Fungal characterization using polymerase chain reaction in patients with fungal sinusitis. Indian J Pathol Microbiol 2011;54:415-7

How to cite this URL:
Ashraf M J, Azarpira N, Badiee P, Khademi B, Shishegar M. Fungal characterization using polymerase chain reaction in patients with fungal sinusitis. Indian J Pathol Microbiol [serial online] 2011 [cited 2023 Jun 4];54:415-7. Available from:


Fungal infection is a cause of sinusitis and nowadays is increasingly implicated in the etio-pathology of rhino-sinusitis. Aspergillus spp., dematiaceous fungi, and zygomyces have been reported as etiological agents. Diabetes mellitus, hematological malignancy, primary immunodeficiency state, human immunodeficiency virus (HIV) infection, chronic renal failure, autoimmune diseases, and use of immunosuppressive drugs are the well-known predisposing factors. However, it has been reported in immunocompetent individuals with indolent course. [1] Five distinct histologic categories of fungal sinusitis (FS) have been described: allergic, noninvasive fungal colonization (mycetoma or "fungus ball"), chronic granulomatous, chronic invasive, and acute fulminant. [1] Allergic mucin with Charcot-Leyden crystals are common histologic features of allergic fungal sinusitis (AFS). Patients with chronic rhino-sinusitis commonly present with nasal polyps, inhalant atopy, and elevated total serum immunoglobulin E (IgE). This condition is believed to be an allergic reaction to aerosolized environmental fungi. In chronic noninvasive FS, the fungal balls (mycetoma) are easily seen by H and E staining, without any mucosal invasion. Chronic invasive FS revealed non-necrotizing granulomas with infiltration of eosinophils. In acute invasive FS, vascular invasion by fungal hyphae and thrombosis are present. It has an aggressive course with a high mortality rate. [1],[2]

The aim of this study was determine the etiology of FS in patients from Shiraz, a city in the south of Iran. In a review of pathology files of Khalili hospital affiliated to Shiraz University of Medical Sciences, from June 2008 to July 2009, five cases of FS were diagnosed based on histopathologic findings. The patients were evaluated in the ENT out-patient department. The medical history and clinical examination of them were suggestive of chronic rhinosinusitis. All of them had radiologically proven sinusitis. Rigid nasal endoscopy with swab and biopsy collection from middle meatus was done.

The pathological report of three patients revealed allergic mucin, Charcot-Leyden crystals, and degenerated fungal hyphae, with no evidence of fungal invasion [Figure 1]. The fourth case suffered from asthma and atopy. The histopathologic evaluation of sinus mucosa showed fungus ball without any relation to respiratory mucosa [Figure 2]. The final case was a known case of uncontrolled diabetes mellitus, which on histo-pathological examination showed necrosis with invasion of blood hyphae in nasal mucosa and blood vessels. The fungal culture was positive in two patients; however, the type of fungus was not determined.
Figure 1: Allergic mucin with Charcot-Leyden crystals and degenerated hyphae (H and E ×200)

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Figure 2: Mycetoma or fungus ball, aggregation of fungal hyphae (H and E ×200)

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In order to define the exact fungal pathogen, DNA was extracted from formalin-fixed, paraffin-embedded tissues, using a commercial kit (DNP, CinageneIran), a nd nested polymerase chain reaction (PCR) to detect DNA specific for Aspergillus species was carried out. [3] The PCR was positive in all the five patients.

AFS is the most common form of FS. This finding is in line with other studies [1] and differs from the findings of Chakrabarti et al. [4] and Panda et al. [5]

The Aspergillus spp. is the only isolated fungus in our study. The most common isolated fungus from South India was Aspergillus spp. [1],[5] Dematiaceous fungi such as Bipolaris spp. and Curvularia spp. were found to predominate AFS in North America. [6]

In Sudan, Saudi Arabia, Northern India and along the Atlantic coast of the USA, Aspergillus spp. are the most common etiological agents, [7],[8] whereas the dematiaceous fungi are the commonest in the southwest of the USA. [6]

The climatic and geographic conditions seem to be responsible for this difference. The weather in our area is hot and dry which is similar to the weather in India and Saudi Arabia., [7] In contrast, in the United States, the humidity facilitates the growth of dematiaceous fungi. Aspergillus spp. was isolated from the fungus ball. This is in concordance with other studies which report that Aspergillus is the most commonly isolated in mycetoma. [1] We have only one case of acute invasive FS, from which Aspergillus spp. was isolated. Our finding is in concordance with a report from India that Aspergillus flavus was the most common isolate. [7] Rhizopus spp. that belongs to zygomycete and Aspergillus spp. were the first and second reported causes of invasive form in South India. [1] In another study from North India, Rhizopus arrhizus and Candida albicans were found to be the causative agents. [4]

In conclusion, this is the first report of FS from South Iran. The etiological agents involved in different forms of FS seem to be similar from India and Saudi Arabia, but differ from Western countries.

The sample size was small and fungal culture was not carried out for all of them. Therefore, further studies with larger patient numbers from different geographic parts of Iran are needed to investigate the cause of FS in our country.

   References Top

1.Michael RC, Michael JS, Ashbee RH, Mathews MS. Mycological profile of fungal sinusitis: An audit of specimens over a 7-year period in a tertiary care hospital in Tamil Nadu. Indian J Pathol Microbiol 2008;51:493-6.   Back to cited text no. 1
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2.Azarpira N, Esfandiari M, Bagheri MH, Rakei S, Salari S. Cerebral aspergillosis presenting as a mass lesion. Braz J Infect Dis 2008;12: 349-51.  Back to cited text no. 2
3.Yamakami Y, Hashimoto A, Tokimatsu I, Nasu M. PCR detection of DNA specific for Aspergillus species in serum of patients with invasive aspergillosis. J Clin Microbiol 1996;34:2464-8.  Back to cited text no. 3
4.Chakrabarti A, Sharma SC, Chander J. Epidemiology and pathogenesis of paranasal sinus mycoses. Otolaryngol Head Neck Surg 1992;107:745-50.  Back to cited text no. 4
5.Panda NK, Sharma SC, Chakrabarti A, Mann SB. Paranasal sinus mycoses in north India. Mycoses 1998;41:281-6.  Back to cited text no. 5
[PUBMED] Shazo RD, Swaim RE. Diagnostic criteria for Allergic Fungal Sinusitis. J Allergy Clin Immunol 1995;96:24-35.   Back to cited text no. 6
7.Chakrabarti A, Sharma SC. Paranasal sinus mycoses. Indian J Chest Dis Allied Sci 2000;42:293-304.   Back to cited text no. 7
8.Al-Dousary SH. Allergic fungal sinusitis: radiological and microbiological features of 59 cases. Ann Saudi Med 2008;28:17-21.  Back to cited text no. 8
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Correspondence Address:
N Azarpira
Transplant Research Center, Nemazi Hospital, P.O.Box: 71935-1119, Shiraz University of Medical Sciences
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.81602

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