Table of Contents
- What is Chromoblastomycosis (Chromomycosis)?
- Causative agents of Chromoblastomycosis (Chromomycosis)
- Pathogenesis of Chromoblastomycosis (Chromomycosis)
- Clinical Features of Chromoblastomycosis (Chromomycosis)
- Diagnosis of Chromoblastomycosis (Chromomycosis)
- Clinical Diagnosis
- Laboratory Diagnosis
- Direct examination and microscopy
- Cultural Examination
- Histological Examination
- Molecular Identification of agents
- Immunological Examination
- Treatment of Chromoblastomycosis (Chromomycosis)
- Antifungal Resistance of causative agents of chromoblastomycosis
- Prevention and Control of chromoblastomycosis
What is Chromoblastomycosis (Chromomycosis)?
Chromoblastomycosis, also known as chromomycosis, is a chronic fungal illness of the epidermis and subcutaneous tissue produced by various dematiaceous fungi families.
- Aside from sporotrichosis and mycetoma, it is one of the most common subcutaneous fungus diseases.
- Dermateciuos fungi are pigmented fungus that produce dark pigments.
- The illness is characterized by slow-growing warty plaques and cauliflower-like tumors that may ulcerate.
- It primarily impacts immunocompromised people with weakened immune systems, making them vulnerable to fungus colonization and illness.
- The fungi have a type of traumatic implantation, which means that the fungi inoculate the skin as a result of injuries such as wounds or abrasions, exposing the skin to fungal infection.
- The illness primarily impacts adult agricultural laborers, but a few instances of infection in children have been recorded.
Causative agents of Chromoblastomycosis (Chromomycosis)
- Dematiaceous fungus induce chromomycosis.
- Dermatiaceous fungi are a diverse collection of molds that produce a variety of skin diseases such as phaeohyphomycosis, chromoblastomycosis, and eumycotic mycetoma.
- Fonsecaea pedrosoi, Phialophora spp, Cladophialophora bantiana, Rhinocladiella and Exophiala spp, Mudurella spp, Scedosporium prolificans, and Wangiella dermatitidis are among the pathogenic fungus in this category.
- Cladosporium carrionii, Phialophora verrucosa, and Fonsecaea pedrosoi are the most frequent etiologies of chromomycosis fungi, while Fonsacea compactum, Exophiala spinifera, Rhinocladiella aquaspersa, Exophiala jeanselmei, and Wangiella dermatitidis are the least prevalent.
- They are found in a variety of environments, including dirt, wood, and deceased decaying plant detritus.
- They are also widespread in warm and subtropical regions.
- Their cell membranes contain melanin, which decides the pigment of the spores.
- They multiply asexually by producing seeds called conidia.
- In mycological agar, they produce colonies that are usually brown to black in appearance.
Pathogenesis of Chromoblastomycosis (Chromomycosis)
- Fungi enter the epidermis through damage from vegetative materials such as thorns or splinters, causing a granulomatous reaction on the skin.
- Most fungal infections are silent (oligosymptomatic) for several years before symptoms emerge.
- Localized pain and increased itching define the intermediate stage of the disease, which advances to severe disease associated with edema and secondary bacterial infection, which may restrict bodily movements and activities.
- The chronic illness causes chronic lymphoedema and the development of ankylosis and non-invasive squamous cell cancer, which can render the patient disabled.
General manifestations will also include:
- The epidermis produces pseudoepitheliomatous proliferation, while the dermis produces granuloma linked with epithelioid cells and Langhans giant cells.
- Fungal components appear as dark septate celled sclerotic bodies.
- Medlar bodies, muriform bodies, and copper coins are examples of sclerotic cella.
- These bodies, which appear as dark spots on the surface lesions, are ejected trans-epidermally.
Risk factors of infection
- Patients with weakened immune systems, such as diabetics, who have cutaneous abrasions
- Patients undergoing medicinal treatments
- Patients who have been injured or have had surgery
- Agricultural laborers who suffer from skin itching (abrasions) caused by vegetation
Virulence factors of dematiaceous fungi
- The presence of melanin in the cell walls of dematiaceous fungi provides a protective benefit by scavenging free radicals and hypochlorite, which are generated by phagocytic cells.
- Melanin may also attach to hydrolytic enzymes, stopping phagocytic cells from acting on the plasma membrane of fungal cells.
- Melanin provides pigment to the fungal spores and hyphae generated during the fungi's germination and reproduction. This causes the fungi to become pigmented, resulting in colored skin lesions and cutaneous symptoms.
Clinical Features of Chromoblastomycosis (Chromomycosis)
Chromoblastomycosis is characterized by:
- Small scarlet or grey lump that is solid.
- The bump develops gently at a rate of about 2mm per year.
- With centralized scarring, a dr warty lump or plaque forms.
- Elephantiasis occurs when the afflicted leg enlarges.
- The scarred lesion then develops new lesions around the scar, enabling it to spread to new itchy locations.
- Squamous cell cancer can form as a result of chromoblastomycosis infection.
Lesions caused by chromoblastomycosis diseases include:
1. Nodular tumors are mildly raised, relatively tender, and have a dull to pink violaceous growth with a smooth, verrucous, or scaly surface. They develop tumors progressively over time.
2. Tumoral lesions are tumor-like lumps that are prominent, papillomatous, and sometimes lobulated; 'cauliflower-like,' with epidermal detritus and crusts coating the surface partly or completely. They are more exuberant and mostly appear in the lower limbs.
3. Cicatricial tumors are non-elevated, with atrophic scarring and an increased peripheral expansion. They have focused on recovery. They have a circular, arciform, or serpiginous shape and can be found throughout the body.
4. Plaques are slightly raised lesions with infiltration that come in a variety of sizes and forms. They are brownish to violaceous in hue, have a scaly surface, and may have distinct fracture lines. They are most commonly located on the upper portions of the limbs.
5. Verracuous lesions are warty, dry hyperkeratosis lesions that are frequently located along the foot's border.
Diagnosis of Chromoblastomycosis (Chromomycosis)
Clinical Diagnosis
Clinical observation of lesions and differentiation from other characteristic lesions formed by other microbial agents and fungal agents as described above.
Laboratory Diagnosis
Specimen: Exudates from lesion, skin scrapings, crusts, aspirated detritus, and tissue pieces
Direct examination and microscopy
- Muriform (single or clustered) cells in clinical samples are 5 to 12 m in diameter, round to polyhedral (chestnut) in shape, thick-walled, dark pigmented, and have both horizontal and longitudinal cross-walls approximating a brick wall.
- Hematoxylin and eosin staining of tissue samples for examination of muriform cells.
- Stain with calcofluor white color
Cultural Examination
- Isolation of pigmented fungus spores using mycological and bacterial cultures, followed by detection of muriform cells using KOH wet mount.
- However, cultural methods are insufficient and unusual, necessitating a follow-up investigation with staining and microscopic techniques.
Histological Examination
- Tissue samples and biopsies are used to identify disease fragments such as granulomatous tissue elements and giant cells.
Agent Molecular Identification
- Fonsecaea species. were identified using duplex PCR targeting ribosomal DNA, and C. carrionii was identified using a particular oligonucleotide primer.
Immunological Examination
This can be used to detect antibody production against fungus antigens, such as an ELISA test using C. carrionii antigen AgSPP.
Treatment of Chromoblastomycosis (Chromomycosis)
- Treatment for Chromoblastomycosis involves physical therapy as well as topical and systemic antifungal drugs that have been shown to be successful.
- Surgery, thermotherapy, laser therapy, and photodynamic treatment (PDT), as well as antifungal medication combination therapies, are all examples of physical therapies.
- Antifungal medications such as itraconazole (ITZ), voriconazole (VCZ), PCZ, and isavuconazole are used. (ISA). Itraconazole is the first-line therapy for CBM, and Terbinafine is the second-most commonly used antifungal drug for CBM treatment.
- Combination treatment with systemic antifungal medications, such as itraconazole and terbinafine, has been used in the salvage therapy situation for patients with invasive refractory mycoses.
- Antifungal drugs, as well as physical therapies such as surgery, may be used in combination treatment.
- Adjuvant therapy, which combines antifungal medications with immunomodulant adjuvants, has also been used as a type of treatment in severe and refractory instances of infection. Imiquimod and (13)--polyglucoside have been used as adjuvants with itraconazole and terbinafine antifungals.
- Clinical, mycological, and histopathological factors must be used to evaluate BM therapy to guarantee the clearing of lesions and scars and the definitive healing of the illness.
Antifungal Resistance of causative agents of chromoblastomycosis
Chromoblastomycosis is a chronic fungus illness that has developed tolerance to standard antifungal treatments such as fluconazole and amphotericin B, necessitating the use of broad-spectrum antifungal agents such as itraconazole and terbinafine.
Prevention and Control of chromoblastomycosis
Due to the absence of chromoblastomycosis vaccines, it was recommended that protective apparel such as gloves, shoes, and clothes be worn to decrease the risk of infection by ubiquitously dematiaceous fungus, particularly in occupationally hazardous groups.