Skip to content
How It Works
Explore
Ask a Question Resources Pricing
Who It's For
Patients
Decode results, prep for appointments, weigh options.
Caregivers & advocates
Carry the research load for someone you love.
Providers & clinicians
Resources for patients in your practice.
Log In Sign Up
PubMed This is a summary of 25 peer-reviewed journal articles Updated
Dermatology · Chromoblastomycosis

Understanding Chromoblastomycosis

At a Glance

Chromoblastomycosis is a slow-growing fungal infection acquired when dark-walled fungi enter the skin through a minor injury. Because it can resemble warts or other skin conditions, a deep biopsy may be needed to confirm it and assess long-term complications.

If you have spent years searching for an answer to a persistent, slow-growing skin condition, your frustration is valid. Chromoblastomycosis (also known as chromomycosis) is a chronic fungal infection that is notoriously difficult to identify in its early stages [1][2]. Because it begins as a small, painless bump and can take a decade or more to fully develop, many patients go through multiple incorrect diagnoses before finding the right care [3][4].

The Biology of Persistence

The infection begins when specific types of fungi, known as dematiaceous (melanized or dark-walled) fungi, are accidentally pushed into the skin through minor trauma [5]. This often happens via a splinter, a thorn, or a small cut while gardening or farming [6][7]. Chromoblastomycosis is acquired directly from the environment and is generally not passed from person to person.

Once inside the warm environment of your body, the fungus undergoes a remarkable transformation. It stops growing as a typical mold and turns into muriform cells (also called sclerotic bodies or Medlar bodies) [5]. These thick-walled, chestnut-brown cells are the “parasitic” form of the fungus and are the key to its survival:

  • Melanin Protection: The dark pigment (melanin) in the fungal walls is believed to protect the fungus from the body’s natural immune defenses, contributing to its treatment resistance [8][9].
  • Immune Evasion: The structure of the muriform cells allows them to resist being destroyed by white blood cells. They can even dampen the signals your immune system uses to coordinate an attack [10].
  • Chronic Inflammation: Because the body cannot easily clear these cells, it remains in a state of constant, low-level inflammation, leading to the characteristic skin changes seen over time [11][12].

Common Causes and Geographic Hotspots

While there are several types of fungi that can cause this condition, a few are responsible for the vast majority of cases globally:

  • Fonsecaea pedrosoi: The most common cause worldwide, typically found in humid, tropical rainforest environments like the Amazon basin [13][14].
  • Cladophialophora carrionii: Often found in drier, more arid regions, including parts of Africa, Australia, and Central America [15].
  • Fonsecaea nubica and Fonsecaea monophora: Frequently identified in southern China and other parts of Asia [16][17].

The World Health Organization (WHO) classifies chromoblastomycosis as a neglected tropical disease, reflecting the fact that it primarily affects people in rural, agricultural communities in South and Central America, Africa, and Asia [18][13].

Why Diagnosis Takes So Long

It is common for a diagnosis to take years [1][2]. This delay usually happens for several reasons:

  1. Slow Progression: The infection grows so slowly that many people do not seek medical help until the lesion becomes large or bothersome [5].
  2. Clinical Mimics: Chromoblastomycosis can look like many other skin conditions, including common warts, psoriasis, or even some types of skin cancer [19][20].
  3. Specialized Testing: Standard skin swabs or basic cultures often fail to grow the fungus. Confirming the diagnosis usually requires specialized techniques, such as a deep skin biopsy where a pathologist looks for the characteristic brown muriform cells under a microscope using special stains [21][22].

Understanding the Risks of Chronic Infection

If left untreated for many years, the constant inflammation can lead to complications. The most common is fibrosis (scarring), which can cause the skin to become thick and hard [5]. In some cases, this can lead to lymphedema (swelling due to blocked lymph vessels) or restricted movement if the infection is near a joint [23][2]. In rare instances of chronic infection, the prolonged inflammation can lead to the development of a type of skin cancer called squamous cell carcinoma [24][25]. Identifying and treating the infection is the best way to prevent these long-term issues.

Common questions in this guide

What is chromoblastomycosis?
Chromoblastomycosis is a chronic fungal infection of the skin caused by dark-walled fungi that enter through a minor injury. It usually develops slowly and can produce persistent, changing skin lesions.
How does someone get chromoblastomycosis, and can it spread between people?
The fungi live in the environment and can enter the skin through a splinter, thorn, or small cut, often during gardening or farming. The infection is generally not spread from person to person.
Why can chromoblastomycosis be mistaken for other skin conditions?
It often begins as a small, painless bump and changes slowly over years. It may resemble a wart, psoriasis, or some skin cancers, so specialized testing is usually needed rather than relying on appearance alone.
What test is used to confirm chromoblastomycosis?
A clinician may examine a scraping or another sample, but confirmation usually requires a deep skin biopsy. A pathologist looks for brown, thick-walled muriform cells, also called sclerotic or Medlar bodies, using microscopy and special stains.
What complications can untreated chromoblastomycosis cause?
Long-term inflammation can cause fibrosis, which makes the skin thick and hard, and may block lymph vessels, causing swelling. Infection near a joint can limit movement, and rarely chronic infection can contribute to squamous cell carcinoma, a type of skin cancer.
Which specialists may help diagnose chromoblastomycosis?
A dermatologist often evaluates the skin lesions, while an infectious disease specialist may help manage the fungal infection. A pathologist examines biopsy tissue to look for the characteristic fungal cells.

Questions For You

Answer a question to get research tailored to you. Your answers are private.

Get notified when new evidence is published on Chromomycosis.

We monitor PubMed for new peer-reviewed studies on this topic and email a short summary when something meaningful changes.

Questions to Ask Your Doctor

Curated prompts to bring to your next appointment.

  1. 1.What diagnostic tests (such as a KOH scrape or a skin biopsy) will you use to confirm the presence of muriform cells?
  2. 2.Which specific fungus is causing my infection, and how does that influence our choice of treatment?
  3. 3.Based on the appearance and size of my lesions, do you classify this as a mild, moderate, or severe case?
  4. 4.Does my biopsy show any signs of secondary bacterial infection or other complications like squamous cell carcinoma?
  5. 5.How much experience does your team have in managing chromoblastomycosis, and is there a specialist you recommend I consult?
  6. 6.What is the expected timeline for my treatment, and how will we monitor if the fungus is being cleared?

References

References (25)
  1. 1

    Chromoblastomycosis in an Immunocompetent Child: A Case Report.

    Ullah M, Shahzad MK, Khan AM, Ramzan E

    Cureus 2025; (17(11)):e96406 doi:10.7759/cureus.96406.

    PMID: 41376728
  2. 2

    Chromoblastomycosis in Latin America and the Caribbean: Epidemiology over the past 50 years.

    Guevara A, Siqueira NP, Nery AF, et al.

    Medical mycology 2021; (60(1)) doi:10.1093/mmy/myab062.

    PMID: 34637525
  3. 3

    Clinical and demographic profile of chromoblastomycosis in a referral service in the midwest of São Paulo state (Brazil).

    Marques GF, Masuda PY, Sousa JM, et al.

    Anais brasileiros de dermatologia 2015; (90(1)):140-2.

    PMID: 25672318
  4. 4

    Implantation mycoses: A nationwide survey on diagnostic and treatment modalities in Nepal.

    Parajuli N, Kiran U, Shrestha R, et al.

    PLoS neglected tropical diseases 2026; (20(4)):e0014223 doi:10.1371/journal.pntd.0014223.

    PMID: 42008606
  5. 5

    Chromoblastomycosis.

    Queiroz-Telles F, de Hoog S, Santos DW, et al.

    Clinical microbiology reviews 2017; (30(1)):233-276 doi:10.1128/CMR.00032-16.

    PMID: 27856522
  6. 6

    Chromoblastomycosis in an Endemic Area of Brazil: A Clinical-Epidemiological Analysis and a Worldwide Haplotype Network.

    Santos DWCL, Vicente VA, Weiss VA, et al.

    Journal of fungi (Basel, Switzerland) 2020; (6(4)) doi:10.3390/jof6040204.

    PMID: 33022951
  7. 7

    Chromoblastomycosis in India: Review of 169 cases.

    Agarwal R, Singh G, Ghosh A, et al.

    PLoS neglected tropical diseases 2017; (11(8)):e0005534 doi:10.1371/journal.pntd.0005534.

    PMID: 28771470
  8. 8

    Melanin and chromoblastomycosis agents: Characterization, functions, and relation with antifungals.

    Koehler A, Heidrich D, Pagani DM, et al.

    Journal of basic microbiology 2021; (61(3)):203-211 doi:10.1002/jobm.202000664.

    PMID: 33576034
  9. 9

    Tricyclazole alleviates Fonsecaea pedrosoi-induced immune suppression of neutrophils by inhibiting DHN-melanin biosynthesis.

    Zheng C, Li W, Wang Y, et al.

    Frontiers in cellular and infection microbiology 2025; (15()):1697287 doi:10.3389/fcimb.2025.1697287.

    PMID: 41602105
  10. 10

    Impaired NLRP3 inflammasome activation by chitin underlies refractory chromoblastomycosis caused by Fonsecaea pedrosoi muriform cells.

    Chen Y, Qu Z, Xie Z, et al.

    Frontiers in immunology 2026; (17()):1843553 doi:10.3389/fimmu.2026.1843553.

    PMID: 42523712
  11. 11

    Neutrophil extracellular traps (NETs) and Th-2 dominant immune responses in chronic granulomatous chromobalstomycosis.

    Huang H, Li M, Luo M, et al.

    Medical mycology 2024; (62(2)) doi:10.1093/mmy/myae008.

    PMID: 38318638
  12. 12

    New Immunological Markers in Chromoblastomycosis-The Importance of PD-1 and PD-L1 Molecules in Human Infection.

    Cavallone IN, Belda W, de Carvalho CHC, et al.

    Journal of fungi (Basel, Switzerland) 2023; (9(12)) doi:10.3390/jof9121172.

    PMID: 38132773
  13. 13

    The global burden of chromoblastomycosis.

    Santos DWCL, de Azevedo CMPES, Vicente VA, et al.

    PLoS neglected tropical diseases 2021; (15(8)):e0009611 doi:10.1371/journal.pntd.0009611.

    PMID: 34383752
  14. 14

    Molecular Epidemiology of Agents of Human Chromoblastomycosis in Brazil with the Description of Two Novel Species.

    Gomes RR, Vicente VA, Azevedo CM, et al.

    PLoS neglected tropical diseases 2016; (10(11)):e0005102 doi:10.1371/journal.pntd.0005102.

    PMID: 27893750
  15. 15

    Global Spread of Human Chromoblastomycosis Is Driven by Recombinant Cladophialophora carrionii and Predominantly Clonal Fonsecaea Species.

    Deng S, Tsui CK, Gerrits van den Ende AH, et al.

    PLoS neglected tropical diseases 2015; (9(10)):e0004004 doi:10.1371/journal.pntd.0004004.

    PMID: 26496430
  16. 16

    Molecular identification of chromoblastomycosis clinical isolates in Guangdong.

    Fransisca C, He Y, Chen Z, et al.

    Medical mycology 2017; (55(8)):851-858 doi:10.1093/mmy/myw140.

    PMID: 28053146
  17. 17

    Identification of Chromoblastomycosis and Phaeohyphomycosis Agents through ITS-RFLP.

    Sousa GSM, De Oliveira RS, De Souza AB, et al.

    Journal of fungi (Basel, Switzerland) 2024; (10(2)) doi:10.3390/jof10020159.

    PMID: 38392831
  18. 18

    Treatment-Resistant Chromoblastomycosis Successfully Managed With Surgical Excision.

    Martinelli MB, Cockerell CJ, Cohen PR

    Cureus 2024; (16(11)):e73619 doi:10.7759/cureus.73619.

    PMID: 39677178
  19. 19

    The Role of Excision for Treatment of Chromoblastomycosis: A Cutaneous Fungal Infection Frequently Mistaken for Squamous Cell Carcinoma.

    Rolon AM, Tolaymat LM, Sokumbi O, Bodiford K

    Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.] 2023; (49(7)):649-653 doi:10.1097/DSS.0000000000003800.

    PMID: 37093678
  20. 20

    Chromoblastomycosis due to Fonsecaea monophora in a man with nephritic syndrome.

    Tan H, Xu Y, Lan XM, et al.

    Mycopathologia 2015; (179(5-6)):447-52 doi:10.1007/s11046-014-9856-z.

    PMID: 25575792
  21. 21

    The Diagnosis of Fungal Neglected Tropical Diseases (Fungal NTDs) and the Role of Investigation and Laboratory Tests: An Expert Consensus Report.

    Hay R, Denning DW, Bonifaz A, et al.

    Tropical medicine and infectious disease 2019; (4(4)) doi:10.3390/tropicalmed4040122.

    PMID: 31554262
  22. 22

    Chromoblastomycosis Presenting with Sporotrichoid Distribution and Bony Destruction: A Rare Presentation.

    Rao AG, Marepally N, Sindhu V, et al.

    Indian journal of dermatology 2023; (68(4)):450-454 doi:10.4103/ijd.ijd_664_22.

    PMID: 37822400
  23. 23

    An optimized Agrobacterium tumefaciens-mediated transformation system for random insertional mutagenesis in Fonsecaea monophora.

    Xiao X, Li Y, Qin J, et al.

    Journal of microbiological methods 2020; (170()):105838 doi:10.1016/j.mimet.2020.105838.

    PMID: 31926179
  24. 24

    Squamous cell carcinoma in chronic lesions of recalcitrant chromoblastomycosis. Study of ten patients treated at the Dermatological Center of Yucatán, Mexico.

    Calderón Quiroz ER, Torres Guerrero E, Proy Trujillo H, et al.

    Anais brasileiros de dermatologia 2026; (101(4)):501372 doi:10.1016/j.abd.2026.501372.

    PMID: 42235130
  25. 25

    Squamous cell carcinoma derived from chronic chromoblastomycosis in Brazil.

    Azevedo CM, Marques SG, Santos DW, et al.

    Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 2015; (60(10)):1500-4 doi:10.1093/cid/civ104.

    PMID: 25681378

This page explains how chromoblastomycosis develops, is diagnosed, and may cause complications for informational purposes only and does not constitute medical advice. A dermatologist or infectious disease specialist should interpret your symptoms and test results.