Fonsecaea monophora
| Fonsecaea monophora | |
|---|---|
Scientific classification  | |
| Kingdom: | Fungi |
| Division: | Ascomycota |
| Class: | Eurotiomycetes |
| Order: | Chaetothyriales |
| Family: | Herpotrichiellaceae |
| Genus: | Fonsecaea |
| Species: | F. monophora |
| Binomial name | |
| Fonsecaea monophora (Moore and de Almeida(1936)) de Hoog, Vicente, Attili (2004) | |
| Type strain | |
| CBS 269.37, from a case of human chromoblastomycosis, S. America | |
| Synonyms | |
| |
Fonsecaea monophora is a species of ascomycete fungi in the family Herpotrichiellaceae and is a causative agent of chromoblastomycosis.[1][2] It is recognized by the World Health Organization as a neglected tropical disease.[3]
F. monophora was described as a separate species from F. pedrosoi by de Hoog et al. in 2004. [4]
Fonsecaea spp. are often recovered from environmental sources, including plants such as the babassu coconut.[5] Disease caused by this fungus is usually of traumatic origin.[6]
Microbiology
The colony morphology is described as being restricted, spreading moderately, lanose to velvety, and the top being olivaceous to black with the reverse being black.[2] The hyphae are septate and pale olivaceous. The conidiophores are erect, and can be either unbranched or branched, and are the same color as the hyphae or slightly darker. Conidiogenous cells are short-cylindrical, olivaceous, and arranged in loosely branched systems. The denticles have ellipsoidal, pale olivaceous conidia in short chains. Multi celled, sessile conidial chains similar to those found in the genus Cladophialophora can present.[2]
Morphologically, Fonsecaea pedrosoi and Fonsecaea monophora are very similar. F. monophora typically have slightly longer conidial chains and slightly shorter denticles than F. pedrosoi.[2] The two species cannot be distinguished physiologically, and sequencing of the internal transcribed spacer or D1/D2 region of ribosomal DNA is needed for identification.[7] The absence of growth with inulin as sole carbon source, absence of fermentation, intolerance of 10% NaCl, tolerance of cycloheximide and absence of acid and extracellular DNAse production are traits shared by both species, as well as other melanized fungi belonging to the order Chaetothyriales.[2][8]
In histopathology, a characteristic feature of chromoblastomycosis is the presence of Medlar bodies (also known as muriform cells), aggregations of spherical, pigmented fungal cells.[9]
Clinical Relevance
F. monophora is a causative agent of human chromoblastomycosis, and it is typically more opportunistic and neurotropic than F. pedrosoi. F. monophora has been isolated from brain abscesses, cervical lymph nodes, and bile, while F. pedrosoi appears to be associated strictly with chromoblastomycosis.[6][10] Because of the similarities between the two species and the inability to distinguish them phenotypically, some cases attributed to F. pedrosoi may actually have been caused by F. monophora. Molecular methods are necessary for definite species identification.[10]
The most common symptom experienced in CNS infection by F. monophora were headaches, which were typically accompanied by focal neurologic deficits and symptoms of increased intracranial pressure in several cases.[10] In chromoblastomycosis, disease is usually characterized by polymorphic skin lesions and muriform cells in granulomatous and suppurative tissue.[9][11]
For treatment, a combined approach with both early surgical intervention and combination treatment with antifungals vastly improves patient outcome. Therapy for F. monophora infection is challenging because there is no consensus regarding a treatment of choice.[6][10] Outcomes are greatly variable and are dependent on the site of infection, lesion size, the etiological agent, and the patient's health status.[6][12] In cases of chromoblastomycosis, F. monophora has been demonstrated to be sensitive to voriconazole, itraconazole, ketoconazole and terbinafine, but resistant to fluconazole and amphotericin B.[9][11] Voriconazole has been used to successfully treat a case of CNS infection by F. monophora.[13]
In a study involving 137 F. monophora isolates, the epidemiological cutoff values were; 2 μg/mL for itraconazole, 0.25 μg/mL for voriconazole and isavuconazole,1 μg/mL for posaconazole, and 0.5 μg/mL for terbinafine. [14] Amphotericin B and flucytosine did not have epidemiological cutoff values set due to bimodal distribution.
References
- ↑ "Fonsecaea monophora". NCBI. Retrieved 2026-05-27.
- 1 2 3 4 5 De Hoog, G. S.; Attili-angelis, D.; Vicente, V. A.; Gerrits Van Den Ende, A. H. G.; Queiroz-telles, F. (2004). "Molecular ecology and pathogenic potential of Fonsecaea species". Medical Mycology. 42 (5): 405–416. doi:10.1080/13693780410001661464. ISSN 1369-3786. PMID 15552642.
- ↑ "Ending the neglect to attain the Sustainable Development Goals: A road map for neglected tropical diseases 2021–2030". www.who.int. Retrieved 2026-07-22.
- ↑ de Hoog, G. S.; Attili-Angelis, D.; Vicente, V. A.; Gerrits Van Den Ende, A. H. G.; Queiroz-Telles, F. (2004-10-01). "Molecular ecology and pathogenic potential of Fonsecaea species". Medical Mycology. 42 (5): 405–416. doi:10.1080/13693780410001661464. ISSN 1369-3786. PMID 15552642.
- ↑ Voidaleski, Morgana Ferreira; Gomes, Renata Rodrigues; Azevedo, Conceição de Maria Pedrozo e Silva de; Lima, Bruna Jacomel Favoreto de Souza; Costa, Flávia de Fátima; Bombassaro, Amanda; Fornari, Gheniffer; Cristina Lopes da Silva, Isabelle; Andrade, Lucas Vicente; Lustosa, Bruno Paulo Rodrigues; Najafzadeh, Mohammad J.; de Hoog, G. Sybren; Vicente, Vânia Aparecida (2020-11-17). "Environmental Screening of Fonsecaea Agents of Chromoblastomycosis Using Rolling Circle Amplification". Journal of Fungi. 6 (4): 290. doi:10.3390/jof6040290. ISSN 2309-608X. PMC 7712894. PMID 33212756.
- 1 2 3 4 Najafzadeh, Mohammad J.; Badali, Hamid; Illnait-Zaragozi, Maria Teresa; De Hoog, G. Sybren; Meis, Jacques F. (2010). "In Vitro Activities of Eight Antifungal Drugs against 55 Clinical Isolates of Fonsecaea spp". Antimicrobial Agents and Chemotherapy. 54 (4): 1636–1638. doi:10.1128/AAC.01655-09. ISSN 0066-4804. PMC 2849378. PMID 20086140.
- ↑ Najafzadeh, M. J.; Sun, J.; Vicente, V.; Xi, L.; van den Ende, A. H. G. Gerrits; de Hoog, G. S. (2010-09-01). "Fonsecaea nubica sp. nov, a new agent of human chromoblastomycosis revealed using molecular data". Medical Mycology. 48 (6): 800–806. doi:10.3109/13693780903503081. ISSN 1369-3786. PMID 20302550.
- ↑ de Hoog, G. S.; Gerrits van den Ende, A. H. G.; Uijthof, J. M. J.; Untereiner, W. A. (1995-03-01). "Nutritional physiology of type isolates of currently accepted species ofExophiala andPhaeococcomyces". Antonie van Leeuwenhoek. 68 (1): 43–49. doi:10.1007/BF00873291. ISSN 1572-9699. PMID 8526480.
- 1 2 3 Oprea, Yasmine; Stringer, Thomas; Mattis, Daiva; Amin, Bijal; Mann, Ranon (2024). "Chromoblastomycosis Caused by Fonsecaea monophora Mimicking Lichen Planus". Cureus. 16 (2) e53863. doi:10.7759/cureus.53863. ISSN 2168-8184. PMC 10924668. PMID 38465023.
- 1 2 3 4 Gourav, Sudesh; Singh, Gagandeep; Pandey, Mragnayani; Rana, Bhaskar; Gupta, Sonakshi; Mishra, Himanshu; Xess, Immaculata (2024). "Molecular Identification of Fonsecaea monophora, Novel Agent of Fungal Brain Abscess". Emerging Infectious Diseases. 30 (6): 1232–1235. doi:10.3201/eid3006.240077. ISSN 1080-6059. PMC 11138971. PMID 38782016.
- 1 2 Yang, Y.-P.; Li, W.; Huang, W.-M.; Zhou, Y.; Fan, Y.-M. (2013). "Chromoblastomycosis caused by Fonsecaea: clinicopathology, susceptibility and molecular identification of seven consecutive cases in southern China". Clinical Microbiology and Infection. 19 (11): 1023–1028. doi:10.1111/1469-0691.12067. ISSN 1198-743X. PMID 23153454.
- ↑ Bonifaz, A.; Carrasco-Gerard, E.; Saúl, A. (2001). "Chromoblastomycosis: clinical and mycologic experience of 51 cases". Mycoses. 44 (1–2): 1–7. doi:10.1046/j.1439-0507.2001.00613.x. ISSN 0933-7407. PMID 11398635.
- ↑ Takei, H.; Goodman, J.C.; Powell, S.Z. (2007-01-01). "Cerebral phaeohyphomycosis caused by Cladophialophora bantiana and Fonsecaea monophora: report of three cases". Clinical Neuropathology. 26 (1): 21–27. doi:10.5414/NPP26021. ISSN 0722-5091. PMID 17290933.
- ↑ Smith, Dallas J.; van Beurden, Tijmen; Li, Yalong; Almeida-Paes, Rodrigo; Jacomel, Bruna; Vicente, Vania Aparecida; Lustosa, Bruno P. R.; Walter, Thiago Henrique; Neto, Elias Nunes Monteiro; Hallur, Vinaykumar; Paul, Diptanu; Paul, Nimmy; Li, Ruoyu; Lu, Sha; Kidd, Sarah E. (2026-06-25). "Establishment of epidemiological cutoff values against Fonsecaea monophora, an agent of chromoblastomycosis and cerebral phaeohyphomycosis". Journal of Clinical Microbiology. 0 e01846-25: e01846–25. doi:10.1128/jcm.01846-25. PMID 42345564.