  |
|
|
The term subcutaneous mycosis means a disease in which the pathogen, an exosaprophyte, penetrates the dermis or even deeper during or after a skin trauma. The lesions gradually spread locally without dissemination to deep organs. However, most fungi which cause subcutaneous mycoses can also occasion deep mycoses in patients with severe underlying abnormalities (via the respiratory tract). Mycologically, the pathogens of subcutaneous mycoses have only a few common characteristics and belong to very different taxonomic groups.
Subcutaneous mycoses occur exclusively or predominantly in the tropics. This is related on the one hand to the geographical distribution of the pathogens and the ecological factors that determine their saprophytic growth and sporulation, and on the other hand it is also the consequence of the medical underdevelopment in these regions. Imported or indigenous cases are only rarely found in Western Europe.
This chronic dermal/epidermal mycosis, also known as chromoblastomycosis, is characterised by vegetative and verrucal lesions, which occur predominantly on the lower limbs. In addition, erythematosquamous, nodular or ulcerating lesions are sometimes also found.
The pathogens are dark-walled fungi (Fonsecaea pedrosoi, Cladophialophora carrionii, etc.), which are saprophytes on plants and wood.
|
Microscopic examination of crusts in KOH shows the presence of irregular, 10-20 µm large, brown-walled elements with transverse septa, 'sclerotic cells'. The specific causative agent can only be identified by culture.
Many clinicians find chromomycosis very resistant to antifungal treatment.
Mycetomas are chronic, inflammatory swellings with numerous sinuses, caused by moulds or bacteria. The causative agent can be seen in the bloody or non-bloody pus, sometimes with the naked eye, in the form of granules. In 75% of cases, a mycetoma is localised on the foot (Madura foot). In addition to involvement of soft tissue, bone tissue is severely affected, with osteolysis on the one hand and hyperostosis on the other.
|
Mycetomas are caused by 2 totally different groups of organisms: the first are moulds, and the second are filamentous bacteria in the order Actinomycetales. In the first case they are referred to as eumycetomas, in the second as actinomycetomas. The difference is very important for therapy. All causative agents of fungal mycetoma are exosaprophytes that have penetrated deep into the tissue with a splinter of wood or a thorn. The limited geographical distribution of most pathogens and their natural history explain why mycetomas occur practically exclusively in the tropics.
The differential diagnosis between fungal and actinomycotic mycetomas is based on the examination of the granules and/or culture. The compact microcolonies of the causative agents differ from one another in terms of colour, shape, dimensions and composition. Black granules are always of fungal origin (e.g. Madurella mycetomatis); small red granules are specific for the actinomycotic Streptomyces pelletieri; whitish-yellow granules can be fungal or actinomycotic in nature.
In the direct examination of a crushed granule in KOH, the distinction between fungal and actinomycotic granules can be made on the basis of the presence or absence of true hyphal fragments.
Most information is obtained from the histological examination of a biopsy taken from around the path of a sinus. Vesicular or filamentous elements are seen in fungal granules (Gomori-Grocott stain). Only Madurella mycetomatis, the most common causative agent of eumycetoma, can be detected histologically by the presence of a brown cement. With the other moulds, identification should be made by culture. The actinomycotic granules are wholly or partially stained with haematoxylin: granules of Streptomyces species can be distinguished on the basis of their stain, their shape and dimensions. For Nocardia, cultures are necessary for identification.
Until recently, only surgical removal of the whole affected area was successful. Itraconazole yields the best results for the treatment of fungal mycetomas. Ketoconazole is an alternative. For actinomycetoma, the first choice treatment is combination treatment of 2 drugs, such as streptomycin with dapsone or cotrimoxazole. Amikacin can also be used as part of a combination treatment.
|
The classic presentation is the lymphocutaneous form. After an initial lesion, the inoculation chancre, subcutaneous nodules appear followed by ascending lymphangitis. The nodules progressively penetrate the skin and ulcerate. The most common localisations are the hand and the forearm. In addition to this typical lymphocutaneous form, there is also one with disseminated skin lesions, a local cutaneous form, often on the face, which according to some authors occurs in re-infections, and extracutaneous sporotrichosis with involvement of the mucous membranes, bone, muscles, lungs or systemic infection. Pulmonary localisations without involvement of other organs occur in endemic areas (South America) probably more than is thought. This chronic pulmonary disease is often taken for tuberculosis
.
Sporotrichosis is only caused by the mould, Sporothrix schenckii. It is an exosaprophyte on plants, wood and in the soil (peat moss). S. schenckii is a dimorphic mould. At 37°C and on rich nutrient media such as BHI, the yeast phase is obtained with oblong yeast cells.
In contrast to all other mycoses, the diagnosis of sporotrichosis is based not on the detection of the pathogen by direct or histological examination, but solely on culture. It involves collecting a small quantity of the milky pus from ulcerated lesions after the removal of the superficial crusts and then inoculating it onto a Sabouraud nutrient medium. Growth is obtained after a few days of incubation at 25°C and the typical asexual spore formation is easily identified.
Cutaneous forms
All forms
Systemic form
|
Zygomycosis is a term referring to infections with zygomycetes, and more specifically infections such as mucormycosis and entomophthoromycosis (synonyms of the latter are the tongue-twisting and jaw-breaking "rhino-entomophthoromycosis" and "rhino-entomophthoramycosis"). Rhino-entomophthoromycosis is a slowly progressing tropical infection of the subcutaneous tissue or paranasal sinuses caused by Conidiobolus coronatus or related species. Severe mutilations with grotesque deformation of the face can ensue. Histopathology will show fungal elements, granulomata and eosinophils. Culture will confirm the diagnosis. Azoles such as itraconazole should be tried as treatment, although there is insufficient clinical experience.
Basidiobolomycosis is often considered together with rhino-entomophthoromycosis. Basidiobolus ranarum affects subcutaneous tissue in areas such as buttocks, thighs, arms. Biopsy with culture is essential for diagnosis.
Lobomycosis is a very rare infection. It is a self-limited chronic fungal infection of the skin endemic in rural regions in South America and Central America. The prevalence of the disease is high among the Caiabi Indians of Brazil and among the Amoruas tribe of the Casanare state in Colombia. It was the Brazilian physician Jorge Lobo who in 1931 in Recife first described this infection. He gave the name keloidal blastomycosis. The condition was called Lobo disease in 1938, and in 1958, the name lobomycosis was applied.
The organism responsible for lobomycosis has yet to be cultured in vitro. The infection has been transmitted to several lab animals, including an armadillo, golden hamsters, mice and tortoises. Sequence analysis of ribosomal RNA (rRNA) obtained from dolphin skin lesions are highly homologous to rRNA sequences from the fungal genus Cladosporium. Three genera and one species name have been recommended: Loboa loboi (referring to Jorge Lobo), Paracoccidioides loboi because of its antigenic relationship to Paracoccidioides brasiliensis; and Lacazia loboi in deference to Lacaz, who contributed much to the knowledge of the disease. Other names are Glenosporella loboi and Blastomyces loboi. The final designation is pending successful culturing of the organism.
The natural reservoir of the pathogen is unknown. Its likely habitat is somewhere in the rural environment because the disease occurs in humans living in rural areas. Soil and vegetation seem to be likely sources of infection. Since the pathogen has been recovered from lobomycotic lesions of Tursiops truncatus ("bottlenose dolphins") in Florida and in the Bay of Biscay in Europe
, an aquatic reservoir seems likely. A case of dolphin-to-human transmission has been documented in 1983, in a dolphin handler. Human-to-human transmission has not been documented, although the inoculation of a tissue homogenate in a volunteer reproduced the disease. The lesion slowly progressed over 4 years before a small satellite lesion developed.As for clinical symptoms, the name keloidal blastomycosis describes the lesions very well. Lobomycosis often develops at sites of minor trauma, but sometimes, no history of trauma can be recalled. The disease predominately affects exposed areas and extremities. Skin lesions slowly develop over time. Only after the lesions have become large do patients tend to consult a doctor. The lesions often begin as small papules or pustules, mildly pruritic or resulting in a burning sensation. The disease leads to verrucoid or lobulated keloidal nodules and crusty plaques. Lesions are well defined, smooth, painless. They are easily moved around since they lie free over the deeper tissues. Older lesions typically become wart-like and ulcerative with satellite lesions resulting from autoinoculation. The epidermis may be shiny, atrophic, and discolored. The mucosae are spared. The disease does not seem to heal spontaneously. The infection may spread proximally from the extremities, suggesting lymphatic dissemination. Patients lack other systemic symptoms and lobomycosis does not affect the general health of the patient, although squamous cell carcinoma has been described on old scar lesions. Keloids are the most important differential diagnosis and are much more common.
Diagnosis relies on a skin biopsy. The fungus is abundant in lobomycotic skin lesions. It is a spherical intracellular yeast 6-12
mm in diameter. The melanin-containing birefringent 1 mm thick cell wall resists digestion by macrophages. L. loboi is predominantly an intracellular pathogen. Organisms, singly or in chains, reside predominantly in macrophage vacuoles. They seem to reproduce by budding. Linear or radiating chains of 5-10, even 20 organisms linked by tubules are characteristic. Granulomata with foreign-body giant cells and foamy macrophages with abundant round cells are typical. The epidermis is usually atrophic, but in some cases may show pseudoepitheliomatous hyperplasia or ulceration. There is no necrosis, and fibrosis is infrequent. There is no tendency to invade subcutaneous tissue. The organism can be seen with haematoxylin and eosin, but the best stain is Grocott silver-methenamine, which will show the typical yeasts chains. Asteroid bodies in giant cells have been found in about 25% of biopsies.Attempts at medical treatment have failed. Surgery is successful only when the lesion is small and can be fully resected. Repeated cryotherapy appears to be more successful. The present antifungals do not seem promising, but more study is needed. Clofazimine has been tried with limited success.
