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| COMMENTARY |
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| Year : 2021 | Volume
: 14
| Issue : 2 | Page : 234-235 |
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Chromoblastomycosis: A neglected tropical disease
Gitanjali Sarangi
Department of Microbiology, FMMCH, Balasore, Odisha, India
| Date of Web Publication | 3-Mar-2021 |
Correspondence Address:
Gitanjali Sarangi
Department of Microbiology, Fakir Mohan Medical College, Balasore, Odisha
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/mjdrdypu.mjdrdypu_73_19
How to cite this article:
Sarangi G. Chromoblastomycosis: A neglected tropical disease. Med J DY Patil Vidyapeeth 2021;14:234-5 |
Chromoblastomycosis (also known as “Fonseca's disease”) is a chronic fungal infection of the skin and subcutaneous tissue that usually follows the traumatic implantation of the etiologic agent.[1],[2] These agents are a group of dematiaceous (black-pigmented) fungi such as Fonsecaea compacta, Fonsecaea pedrosoi, Phialophora verrucosa, Cladophialophora carrionii, and Rhinocladiella aquaspersa and occasionally by Exophiala spinifera, Aureobasidium pullulans and Chaetomium funicola.[3],[4]
It occurs throughout the world but is more common in tropical or subtropical regions, with Madagascar and Brazil having the largest reported cases.[5] In India, such cases have been reported from the Sub-Himalayan belt and the coastal areas due to the hot, humid climate in the areas.[6],[7]
Most of the cases are seen in the middle age group, especially agricultural workers, and is rarely reported in children. 54%–55% of children had close relatives, who had chromoblastomycosis suggesting a familial predisposition.[5]
A literature review has shown that there is 47%–65% risk of inheritable susceptibility to chromoblastomycosis, supporting that genetic factor may play an important role in the development of the disease. Studies have shown that the susceptibility to chromoblastomycosis may be influenced by a gene located on chromosome 6, in the region of major histocompatibility complex, suggesting that individuals carrying human leukocyte antigen A-29 have a 10-fold increased risk of developing the disease than those lacking the gene.[5] More research needs to be done in this aspect.
Carrión described five morphological types of chromoblastomycosis consisting of nodular lesion, tumorous, verrucous lesion, plaques, and cicatricial lesion.[8] It begins slowly over months to years starting initially as a warty papule to hyperkeratotic, verrucous plaque. The lesion may be localized or sprade to the contiguous site causing satellite lesions. It can also present as ulcerative or sporotrichoid form. It heals with central atrophy and scarring.
Reports from India, Sri Lanka, Nepal, and also Central and South America show common involvement of the lower extremity. This may be due to frequent trauma to the lower extremity during agricultural work. Involvement of face and trunk is rare, but few cases have been reported.[9],[10] A very few cases of involvement of bone have also been reported, which may be due to either metastatic or contiguous spread to the bone.[5],[11]
The key elements in the diagnosis of this infection are taking a detailed history, clinical findings, and microscopic demonstration of pathognomonic sclerotic bodies, fungal culture, and tissue biopsy for histopathology. The condition has to be differentiated from some other clinical entities such as tuberculosis verrucosa cutis, leishmaniasis, sporotrichosis, blastomycosis, paracoccidioidomycosis, tertiary syphilis, and leprosy.[11]
The treatment of chromoblastomycosis is cryosurgery for small lesions, itraconazole for larger ones, and a combination of both in some cases.[12],[13]
In the 10th meeting of the Strategic and Technical Advisory Group for Neglected Tropical Disease in 2017, chromoblastomycosis has been added to Neglected Tropical Disease Portfolio. Chromoblastomycosis evolves slowly but affects the quality of life. Therefore, a high index of suspicion and prompt laboratory diagnosis will help in initiation of therapy at an early stage to prevent the complications.
| References | |  |
| 1. | Carrión AL. Chromoblastomycosis and related infections: New concepts, differential diagnosis, and nomenclatorial implications. Int J Dermatol 1975;14:27-32.  |
| 2. | Rippon JW. Chromoblastomycosis. In: Wonsiewicz M, editor. Medical Mycology the Pathogenic Fungi and Pathogenic Actinomycetes. 3 rd ed. Philadelphia: WB Saunders Company; 1988. p. 276-96. |
| 3. | Milam CP, Fenske NA. Chromoblastomycosis. Dermatol Clin 1989;7:219-25. |
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| 8. | Vollum DI. Chromomycosis: A review. Br J Dermatol 1977;96:454-8. |
| 9. | Pradhan SV, Talwar OP, Ghosh A, Swami RM, Shiva Raj KC, Gupta S. Chromoblastomycosis in Nepal: A study of 13 cases. Indian J Dermatol Venereol Leprol 2007;73:176-8. [ PUBMED] [Full text] |
| 10. | Bharti R, Malhotra SK, Bal MS, Sharma K. Chromoblastomycosis. Indian J Dermatol Venereol Leprol 1995;61:54-5. [ PUBMED] |
| 11. | Sania J, Saelah B, Shahbaz A. Chromoblastomycosis with skeletal involvement. A case report. J Pak Assoc Dermatol 2016;26:379-82. |
| 12. | Poirriez J, Breuillard F, Francois N, Fruit J, Sendid B, Gross S, et al. A case of chromomycosis treated by a combination of cryotherapy, shaving, oral 5-fluorocytosine and oral amphotericin B. Am J Trop Med Hyg 2000;63:61-3. |
| 13. | Tripathy S, Panda P. Chromoblastomycosis causing osteolytic lesion in foot. Med J DY Patil Vidyapeeth 2019;12:537-9 |
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