Chromoblastomycosis (CBM) — Disease Characteristics Research Report

Executive summary (current understanding)

Chromoblastomycosis (CBM) is a chronic implantation/subcutaneous mycosis caused by melanized (dematiaceous) fungi introduced via traumatic transcutaneous inoculation, producing slowly progressive, polymorphic skin/subcutaneous lesions and disability; diagnosis is defined by the presence of muriform (Medlar/sclerotic/“copper penny”) bodies on microscopy/histopathology. CBM is a WHO-designated neglected tropical disease (NTD) and a skin-NTD, but global burden estimates remain uncertain because surveillance and access to diagnostics/treatment are limited. (smith2024aglobalchromoblastomycosis pages 2-3, smith2024aglobalchromoblastomycosis pages 1-2)

1. Disease information

1.1 Definition/overview

• CBM is an implantation mycosis acquired when melanized filamentous fungi enter the skin through traumatic injury; it is chronic, granulomatous, and predominantly involves skin and subcutaneous tissues. (smith2024aglobalchromoblastomycosis pages 2-3, martinelli2024treatmentresistantchromoblastomycosissuccessfully pages 2-5)
• Diagnostic hallmark: thick-walled, pigmented, septate muriform (Medlar/sclerotic) bodies in clinical specimens (scrapings/biopsy). (smith2024aglobalchromoblastomycosis pages 2-3, smith2025chromoblastomycosisandphaeohyphomycotic pages 1-3)

1.2 Key identifiers and controlled vocabularies (available from retrieved sources)

Table: This table summarizes the key classification terms, disease identifiers, and synonym information for chromoblastomycosis using only evidence available in the cited context. It is useful for normalizing a disease knowledge-base entry and documenting where identifier gaps remain.

Notes on identifier gaps: ICD-11, MONDO, and Orphanet IDs were not found in the retrieved full texts; additional retrieval from those specific terminologies would be required rather than inference. (smith2024aglobalchromoblastomycosis pages 2-3, smith2024aglobalchromoblastomycosis pages 1-2)

1.3 Synonyms and alternative names

• “Chromomycosis” appears as a synonym/umbrella term in a ClinicalTrials.gov observational study that includes “Chromomycosis” as a condition keyword and “Chromoblastomycosis” as a keyword. (NCT06523998 chunk 1)

1.4 Evidence source type

Evidence summarized below comes from: - Aggregated disease-level strategy/gap-analysis for WHO NTD roadmap implementation. (smith2024aglobalchromoblastomycosis pages 2-3, smith2024aglobalchromoblastomycosis pages 1-2) - Regional retrospective clinical series (French Guiana; Peru) and administrative hospitalization analyses (US). (valentin2024chromoblastomycosisinfrench pages 1-2, sanchezdiaz2025chromoblastomycosisinperu pages 1-2, smith2025chromoblastomycosisandphaeohyphomycotic pages 3-5) - Mechanistic studies in vitro and in murine experimental models, and review-level immunology synthesis. (ferreira2025il18productionis pages 1-2, zhong2024roleofdectin1 pages 1-2, lionakis2023immuneresponsesto pages 9-10)

2. Etiology

2.1 Primary causal factors

• Cause: infection by dematiaceous (melanized) fungi, acquired after traumatic inoculation from environmental reservoirs (soil, plants, decaying wood; splinters/thorns). (martinelli2024treatmentresistantchromoblastomycosissuccessfully pages 2-5, smith2025chromoblastomycosisandphaeohyphomycotic pages 1-3)
• Common etiologic genera/species described in recent sources include Fonsecaea (F. pedrosoi, F. monophora, F. nubica), Cladophialophora (C. carrionii), Phialophora (P. verrucosa), and Rhinocladiella (R. aquaspersa). (smith2025chromoblastomycosisandphaeohyphomycotic pages 1-3, sanchezdiaz2025chromoblastomycosisinperu pages 1-2)

2.2 Risk factors (human / environmental)

• Occupational/outdoor exposure and rural work: French Guiana series: 74% outdoor occupations and 87% male. (valentin2024chromoblastomycosisinfrench pages 2-4)
• Trauma history: French Guiana series: reported initial trauma in 39.1%. (valentin2024chromoblastomycosisinfrench pages 2-4)
• Endemicity and geography: CBM is endemic in tropical/subtropical regions of Latin America, Africa, Asia, and the Caribbean; uncommon in the US but can occur (e.g., gardening exposure). (martinelli2024treatmentresistantchromoblastomycosissuccessfully pages 2-5)
• Comorbidity/immunosuppression: CBM can affect immunocompetent and immunosuppressed individuals; immunosuppression can be associated with severe/treatment-resistant disease (e.g., tacrolimus). (smith2024aglobalchromoblastomycosis pages 2-3, martinelli2024treatmentresistantchromoblastomycosissuccessfully pages 2-5)

2.3 Protective factors

• No validated genetic protective variants were identified in the retrieved sources.
• Proposed/operational protective measures (behavioral/environmental) are described under Prevention (Section 13). (smith2024aglobalchromoblastomycosis pages 6-7)

2.4 Gene–environment interactions

Direct gene–environment interaction data were not identified in the retrieved clinical literature; strategy-level sources highlight traumatic inoculation and environmental reservoirs as key drivers and mention candidate host predisposition loci (Section 4/8). (smith2024aglobalchromoblastomycosis pages 2-3)

3. Phenotypes (clinical manifestations)

3.1 Core cutaneous phenotypes and frequencies (recent observational series)

French Guiana (1955–2023; published Feb 2024): lesion types included cicatricial 21.7%, verrucous 21.7%, nodular 13%, tumoral 4.3%, plaque 4.3%, mixed 34.8%; severity: mild 13%, moderate 52.2%, severe 30.4%; symptoms: pruritus 26.1%, pain 17.4%. (valentin2024chromoblastomycosisinfrench pages 4-7, valentin2024chromoblastomycosisinfrench pages 2-4)

Peru (2011–2024; published Aug 2025): plaque-like and verrucous forms 38% each; tumoral and cicatricial 15% each; pruritus 84%, pain 30%; 30% reported functional limitations affecting work. (sanchezdiaz2025chromoblastomycosisinperu pages 1-2)

Anatomic distribution: lower limb predominance is consistent across series (e.g., 78.3% in French Guiana; 53% in Peru). (valentin2024chromoblastomycosisinfrench pages 2-4, sanchezdiaz2025chromoblastomycosisinperu pages 1-2)

3.2 Severity/staging

• Both French Guiana and Peru series used the Queiroz-Telles severity grading (mild/moderate/severe) based on lesion size/extent (e.g., mild: single plaque/nodule <5 cm; severe: >15 cm or multiple non-adjacent areas). (valentin2024chromoblastomycosisinfrench pages 2-4, valentin2024chromoblastomycosisinfrench pages 1-2)

3.3 Complications and quality-of-life impact

• Strategy paper lists major complications: tissue fibrosis, lymphedema, secondary bacterial infections, squamous cell carcinoma, ankylosis, ectropium; risk-factor magnitude is considered poorly quantified globally. (smith2024aglobalchromoblastomycosis pages 4-6)
• French Guiana series observed long-term complications in 13% (functional limitation, elephantiasis/lymphedema, and squamous cell carcinoma requiring amputation). (valentin2024chromoblastomycosisinfrench pages 2-4)
• CBM is described as causing decreased quality of life, stigma, and disability in WHO-aligned strategy framing. (smith2024aglobalchromoblastomycosis pages 3-4)

3.4 Suggested HPO terms (non-exhaustive; based on phenotypes evidenced above)

• Verrucous skin lesion (HPO suggestion: HP:0100804 “Verrucous skin lesion”) (sanchezdiaz2025chromoblastomycosisinperu pages 1-2, valentin2024chromoblastomycosisinfrench pages 4-7)
• Cutaneous plaque (HP:0011124 “Plaque”) (sanchezdiaz2025chromoblastomycosisinperu pages 1-2, valentin2024chromoblastomycosisinfrench pages 4-7)
• Skin nodule (HP:0001484 “Skin nodule”) (sanchezdiaz2025chromoblastomycosisinperu pages 1-2, valentin2024chromoblastomycosisinfrench pages 4-7)
• Pruritus (HP:0000989) (sanchezdiaz2025chromoblastomycosisinperu pages 1-2, valentin2024chromoblastomycosisinfrench pages 4-7)
• Pain (HP:0012531) (sanchezdiaz2025chromoblastomycosisinperu pages 1-2, valentin2024chromoblastomycosisinfrench pages 4-7)
• Lymphedema/elephantiasis (HP:0001004 “Lymphedema”) (valentin2024chromoblastomycosisinfrench pages 2-4, smith2024aglobalchromoblastomycosis pages 4-6)
• Squamous cell carcinoma of the skin (HP:0006735 “Squamous cell carcinoma”) (valentin2024chromoblastomycosisinfrench pages 2-4, smith2024aglobalchromoblastomycosis pages 4-6)

4. Genetic / molecular information (human and fungal)

4.1 Human susceptibility genetics (current evidence status)

• A 2024 global strategy paper cites HLA-A29 and CARD9 as examples of genetic predisposing factors discussed in the CBM context. (smith2024aglobalchromoblastomycosis pages 2-3)
• No Mendelian “causal gene” for CBM was established in the retrieved clinical series; evidence is currently framed as susceptibility/predisposition rather than a monogenic etiology. (smith2024aglobalchromoblastomycosis pages 2-3)

4.2 Human immunologic markers (host response)

• Human lesion immunopathology (Dec 2023) emphasizes T-cell infiltration and immunoregulatory/exhaustion pathways, reporting PD-1/PD-L1 positivity in all samples and cytokine patterns that can favor chronic infection (e.g., increased IL-10/IL-17 associated with muriform cells). (cavallone2023newimmunologicalmarkers pages 6-9)

4.3 Fungal molecular determinants (virulence and persistence)

• Melanin is repeatedly implicated as a virulence factor; strategy framing links melanin to protection from host oxidative/nitrosative stresses and facilitation of transformation into thick-walled muriform bodies resistant to immunity and antifungals. (smith2024aglobalchromoblastomycosis pages 2-3)
• In vitro macrophage study (Sep 2024) supports a mechanistic role where fungal melanin hinders Dectin-1 binding and reduces phagocytosis/killing and proinflammatory responses. (zhong2024roleofdectin1 pages 1-2)
• Fungal functional genomics: transformation tools and a Fonsecaea pedrosoi trpB knockout system were developed to enable gene-function studies in CBM agents, relevant for future target validation. (favilla2023expandingthetoolbox pages 1-2, favilla2023expandingthetoolbox pages 12-13)

4.4 Ontology suggestions

• GO biological process suggestions: “inflammasome complex assembly”, “interleukin-18 production”, “T helper 1 type immune response”, “phagocytosis”, “fungal cell wall organization” (ferreira2025il18productionis pages 1-2, zhong2024roleofdectin1 pages 1-2, smith2024aglobalchromoblastomycosis pages 2-3)
• CL cell-type suggestions: macrophage; neutrophil; CD4-positive, alpha-beta T cell; CD8-positive, alpha-beta T cell (ferreira2025il18productionis pages 1-2, cavallone2023newimmunologicalmarkers pages 6-9)

5. Environmental information

• Reservoirs/exposure contexts: fungi are environmental and can be associated with thorn/prick injuries and certain plants; the 2024 strategy highlights plant associations (e.g., Mimosa pudica) and climate sensitivity of causative fungi. (smith2024aglobalchromoblastomycosis pages 4-6)

6. Mechanism / pathophysiology

6.1 Causal chain (integrated)

1) Traumatic inoculation introduces melanized fungi into skin/subcutaneous tissue. (smith2024aglobalchromoblastomycosis pages 2-3) 2) Fungal adaptation includes formation of muriform cells with thickened pigmented cell walls, contributing to persistence and treatment refractoriness. (smith2024aglobalchromoblastomycosis pages 2-3) 3) Innate immune recognition is suboptimal in some models; a high-impact review describes modest CLR signaling via dectin-2/Mincle and failure to activate TLRs effectively, contributing to inadequate local inflammation. (lionakis2023immuneresponsesto pages 9-10) 4) Protective pathways include macrophage recognition/phagocytosis (e.g., Dectin-1-associated) and Th1/Th17 adaptive immunity; experimental work shows NLRP3→caspase-1→IL-18 supports Th1/IFN-γ-mediated fungal control. (ferreira2025il18productionis pages 1-2, zhong2024roleofdectin1 pages 1-2) 5) Chronicity may be reinforced by immunoregulatory/exhaustion mechanisms in human lesions (PD-1/PD-L1; IL-10/IL-17 patterns), impairing effective clearance. (cavallone2023newimmunologicalmarkers pages 6-9)

6.2 Recent mechanistic developments (2023–2024 prioritized)

• Immune exhaustion markers: PD-1/PD-L1 and altered cytokine landscapes in human CBM lesions (Dec 2023). (cavallone2023newimmunologicalmarkers pages 6-9)
• Melanin–CLR interference: melanin-dependent suppression of Dectin-1–mediated macrophage responses (Sep 2024). (zhong2024roleofdectin1 pages 1-2)

7. Anatomical structures affected

• Primary sites: skin and subcutaneous tissues, classically lower extremities (legs/feet). (valentin2024chromoblastomycosisinfrench pages 2-4, sanchezdiaz2025chromoblastomycosisinperu pages 1-2)
• Complication-associated structures: lymphatic system involvement (lymphedema/elephantiasis) and potential malignant transformation of skin; deeper involvement can occur (bone involvement described in SCC complication). (valentin2024chromoblastomycosisinfrench pages 2-4)

UBERON suggestions: skin of lower limb; subcutaneous adipose tissue; lymphatic vessel; (valentin2024chromoblastomycosisinfrench pages 2-4, sanchezdiaz2025chromoblastomycosisinperu pages 1-2)

8. Temporal development (natural history)

• Onset pattern: typically chronic/insidious after inoculation trauma. (smith2024aglobalchromoblastomycosis pages 2-3)
• Diagnostic delay and chronicity: median time to diagnosis 4 years in French Guiana; mean disease duration at diagnosis 10.7 years in Peru. (valentin2024chromoblastomycosisinfrench pages 2-4, sanchezdiaz2025chromoblastomycosisinperu pages 1-2)
• Progression: lesions can expand (e.g., large vegetating lesions) and complications become more likely with duration/severity. (smith2024aglobalchromoblastomycosis pages 4-6)

9. Inheritance and population

• Inheritance: not applicable as a primary cause (infectious implantation mycosis). Candidate susceptibility loci are discussed but not a defined inheritance pattern. (smith2024aglobalchromoblastomycosis pages 2-3)
• Epidemiology and demographics: summarized quantitatively in the table below.

Table: This table compiles recent quantitative epidemiology, demographics, diagnostic yield, and outcome data for chromoblastomycosis across regional studies and global strategy sources. It is useful for comparing burden estimates, diagnostic delays, and complications across settings.

10. Diagnostics

10.1 Standard diagnostic concept

• Confirmatory diagnosis relies on identification of muriform bodies on KOH direct microscopy and/or histopathology. (smith2024aglobalchromoblastomycosis pages 4-6, valentin2024chromoblastomycosisinfrench pages 4-7)

10.2 Diagnostic modalities (real-world implementation)

Table: This table summarizes the main diagnostic modalities used for chromoblastomycosis, what each test detects, and the quantitative evidence available from recent studies. It is useful for comparing real-world diagnostic yield and understanding how microscopy, pathology, culture, and newer adjunctive tools fit together in practice.

10.3 Visual diagnostic evidence (recent; 2024)

Cropped figures from a 2024 French Guiana series illustrate KOH microscopy fumagoid cells and histopathology “copper penny” bodies in tissue. (valentin2024chromoblastomycosisinfrench media 4ac5c53a, valentin2024chromoblastomycosisinfrench media f433a202, valentin2024chromoblastomycosisinfrench media 91754828)

10.4 Differential diagnosis

• Clinical differentials noted include squamous cell carcinoma, tuberculosis cutis verrucosa, and other deep fungal or atypical mycobacterial infections. (ariani2023clinicalandmycological pages 6-9, martinelli2024treatmentresistantchromoblastomycosissuccessfully pages 2-5)

11. Outcome / prognosis

• CBM is described as curable when diagnosed early, but long treatment courses and relapse are common when diagnosis is delayed. (smith2024aglobalchromoblastomycosis pages 2-3, valentin2024chromoblastomycosisinfrench pages 9-10)
• Complications can include lymphedema/elephantiasis and squamous cell carcinoma (including amputations in severe cases). (valentin2024chromoblastomycosisinfrench pages 2-4, smith2024aglobalchromoblastomycosis pages 4-6)
• Hospitalization outcomes (US administrative dataset, 2016–2021): mean length of stay 9.9 days; in-hospital death 3%; lymphedema noted in 14% of chromoblastomycosis hospitalizations. (smith2025chromoblastomycosisandphaeohyphomycotic pages 1-3, smith2025chromoblastomycosisandphaeohyphomycotic pages 3-5)

12. Treatment

12.1 Current standard-of-care (practice patterns and evidence base)

• There are no universally standardized protocols; therapy is individualized based on lesion extent, pathogen, and feasibility of physical methods. (farid2025thecurrentlandscape pages 1-2)
• Recent clinical practice synthesis recommends surgery for recent/limited lesions and systemic itraconazole and/or terbinafine for broader disease, with combinations plus physical modalities often used. (valentin2024chromoblastomycosisinfrench pages 1-2, valentin2024chromoblastomycosisinfrench pages 9-10)

12.2 Treatments and outcomes (with MAXO/CHEBI suggestions)

Table: This table summarizes the main drug and procedural treatments reported for chromoblastomycosis, including typical dosing, outcome data, and implementation caveats from the retrieved context. It is useful for comparing first-line, adjunctive, and refractory-disease management options.

12.3 Recent developments / adjunctive strategies

• Imiquimod (TLR7 agonist) is highlighted mechanistically as a way to compensate for weak innate TLR activation in Fonsecaea infection models and is reported as a beneficial adjunct to antifungals in small case series/case reports. (lionakis2023immuneresponsesto pages 9-10, zheng2024successfulmanagementof pages 1-2, farid2025thecurrentlandscape pages 2-4)
• Photodynamic therapy (ALA-PDT) is reported as a possible adjunct with large lesion-size reductions in small studies. (farid2025thecurrentlandscape pages 2-4, valentin2024chromoblastomycosisinfrench pages 9-10)

13. Prevention

• The 2024 global strategy explicitly emphasizes primary prevention through personal protective equipment (e.g., gloves, shoes, appropriate clothing) and programmatic measures integrated with WASH and wound management, alongside capacity building for earlier recognition and access to diagnostics/treatment. (smith2024aglobalchromoblastomycosis pages 6-7)
• WHO-roadmap-aligned actions include establishing surveillance, improving access to affordable diagnostics and treatment, creating field manuals and training health care workers, and developing rapid diagnostics and more effective therapies. (smith2024aglobalchromoblastomycosis pages 2-3)

14. Other species / natural disease

No naturally occurring veterinary/chronic chromoblastomycosis burden in non-human species was identified in the retrieved sources. This section requires additional targeted veterinary literature retrieval.

15. Model organisms and experimental systems

• Murine experimental CBM models support roles for inflammasome signaling (NLRP3/caspase-1/IL-18) and Th1 responses in controlling fungal load. (ferreira2025il18productionis pages 1-2)
• In vitro macrophage systems (THP-1) have been used to study Dectin-1-dependent recognition and melanin-mediated immune evasion. (zhong2024roleofdectin1 pages 1-2)
• Fungal genetic tools: split-marker/biolistic transformation enabling targeted gene inactivation (e.g., ∆trpB) in F. pedrosoi expands functional genomics capacity for CBM agents. (favilla2023expandingthetoolbox pages 1-2, favilla2023expandingthetoolbox pages 12-13)

Clinical trials and real-world implementation (recent)

• ClinicalTrials.gov observational study: NCT06523998 (Completed). Official title: “Retrospective Descriptive Observational Study of the Epidemiological, Clinical and Therapeutic Profile of Patients With Rare Infections of Dermatological Interest … in Costa Rica From 2019–2023.” Posted 2024-07-29; completed 2024-05-24; enrollment 95. This study includes chromomycosis/chromoblastomycosis among conditions and aims to characterize risk factors, diagnostics (culture/histology/molecular), and treatments. (NCT06523998 chunk 1)

Expert opinions and authoritative-source analysis (WHO/NTD roadmap implementation)

• The 2024 Global Chromoblastomycosis Working Group strategy argues that progress toward WHO roadmap targets is limited and highlights the need for surveillance systems, access to diagnostics/therapeutics, standardized case definitions, and integration into existing NTD infrastructure. (smith2024aglobalchromoblastomycosis pages 2-3, smith2024aglobalchromoblastomycosis pages 3-4)

Statistics (high-value recent quantitative findings)

• French Guiana (published 2024): median time to diagnosis 4 years; lower-limb involvement 78.3%; histopathology positivity 95.7%. (valentin2024chromoblastomycosisinfrench pages 2-4, valentin2024chromoblastomycosisinfrench pages 4-7)
• Peru (published 2025; cases through 2024): average disease duration 10.7 years; pruritus 84%; pain 30%; functional limitation 30%; cure 46%. (sanchezdiaz2025chromoblastomycosisinperu pages 1-2)
• US hospitalizations (published 2025; 2016–2021): 690 hospitalization estimates; in-hospital death 3%; comorbid diabetes 33%; lymphedema 14% among chromoblastomycosis hospitalizations. (smith2025chromoblastomycosisandphaeohyphomycotic pages 1-3, smith2025chromoblastomycosisandphaeohyphomycotic pages 3-5)

Direct quotes from abstracts (supporting key points)

• Global strategy paper abstract: “Chromoblastomycosis, an implantation mycosis, is a neglected tropical disease that causes decreased quality of life, stigma, and disability. The global burden of disease is unknown …” (smith2024aglobalchromoblastomycosis pages 3-4)
• US hospitalization study abstract: “An estimated 690 chromoblastomycosis and phaeohyphomycotic abscess-associated hospitalizations occurred during 2016–2021. … in-hospital death occurred in 3%.” (smith2025chromoblastomycosisandphaeohyphomycotic pages 1-3)

Limitations of this report (evidence gaps)

• Standard ontology IDs (MONDO, Orphanet, ICD-11) were not present in the retrieved full texts and were not inferred.
• Several treatment outcome metrics in the literature are derived from small series and heterogeneous regimens; high-quality randomized trials remain sparse.
• Some mechanistic and epidemiologic developments appear in 2025 publications; these were used where they reported uniquely quantitative metrics, while 2023–2024 sources were prioritized when available.

References

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