Subcutaneous Infection:

Sporotrichosis, Chromoblastomycosis

Lobomycosis, Rhinosporidiosis Description:

Sporotrichosis is an infection caused by, a fungus that occurs naturally in temperate and tropical locations. Of the two clinical syndromes of sporotrichosis, the subcutaneous variety is the most common form. The organism is introduced into the skin through a local injury, such as a thorn prick.

Chromoblastomycosis A mycotic infection of the cutaneous and subcutaneous tissues characterised by the development in tissue of dematiaceous (brown-pigmented), planate-dividing, rounded sclerotic bodies. Infections are caused by the traumatic implantation of fungal elements into the skin and are chronic, slowly progressive and localised. Tissue proliferation usually occurs around the area of inoculation producing crusted, verrucose, wart-like lesions. World-wide distribution but more common in bare footed populations living in tropical regions.

Aetiological agents include various dematiaceous hyphomycetes associated with decaying vegetation or soil, especially Phialophora verrucosa, Fonsecaea pedrosoi, F. compacta and Cladophialophora carrionii. Sporothrix schenckii , Loboa loboi ,Rhinosporidium seeberi

Mycoses: diseases cause by fungi

• Superficial • Cutaneous• Subcutaneous • Systemic • Opportunistic

• Sporotrichosis

• clinical syndromes of sporotrichosis, the subcutaneous and the systemic, the subcutaneous variety is the most common form. The organism is introduced into the skin through a local injury, such as a thorn prick.

• Subcutaneous sporotrichosis can present as a lymphatic infection or a fixed infection. The lymphatic form is more common and usually develops on exposed skin sites such as the hands or feet. Days to weeks after dermal inoculation, the infection begins as a nodule that may break down to form a small ulcer. The draining lymphatics become inflamed and swollen and a chain of secondary nodules develops along the course of the lymphatics. These may also break down and ulcerate. The nodules are mildly painful, and systemic symptoms are mild or absent.

• Symptoms• Symptoms include a small, painless, red lump that develops at the site of infection

and eventually turns into an ulcer. The lump may develop up to 3 months after an injury.

• Sores are often on the hands and forearm, because these areas are common injury sites.

• The fungus follows lymphatic channels in the body. Small ulcers appear in lines on the skin as the infection goes up an arm or leg. These sores do not heal unless they are treated and may remain for years. The nodules may drain small amounts of pus from time to time.

• Body-wide (systemic) sporotrichosis can cause lung and breathing problems, bone infection, arthritis, and infection of the nervous system.

• In the fixed variety syndrome, the infection remains localized to the one site. A granuloma develops that may ulcerate. Satellite nodules may form around the primary lesion. This form is most common in tropical and subtropical areas.

• Prevention• The most important step in preventing sporotrichosis is

preventing mold spores from entering the skin. • People who work with roses, hay, or sphagnum moss

should cover any scratches or breaks in their skin.• They should wear heavy boots and gloves to prevent

puncture wounds

• Treatment• The skin infection is usually treated with an antifungal

medicine called itraconazole. It is taken by mouth and continued for 2 to 4 weeks after the skin lesions have cleared. You may have to take the medicine for 3 to 6 months.

• Fluconazole is used in patients who do not respond to itraconazole. Systemic or disseminated infection is often treated with amphotericin B, or sometimes itraconazole. Therapy for systemic disease can last up to 12 months.

Chromoblastomycosis:Clinical manifestations:Lesions of chromoblastomycosis are most often found on exposed parts of the body and usually start a small scaly papules or nodules which are painless but may be itchy. Satellite lesions may gradually arise and as the disease develops rash-like areas enlarge and become raised irregular plaques that are often scaly or verrucose. In long standing infections, lesions may become tumorous and even cauliflower-like in appearance. Other prominent features include epithelial hyperplasia, fibrosis and microabscess formation in the epidermis. Chromoblastomycosis must be distinguished from other cutaneous fungal infections such as blastomycosis, lobomycosis, paracoccidioidomycosis and sporotrichosis. It may also mimic protothecosis, leishmaniasis, verrucose tuberculosis, certain leprous lesions and syphilis. Mycological and histopathological investigations are essential to confirm the diagnosis.

Chronic verrucous chromoblastomycosis of the hand due to Cladophialophora carrionii. Note: tissue hyperplasia forming a white verrucoid cutaneous lesion. In Australia, chromoblastomycosis due to C. carrionii occurs mostly on the hands and arms of timber and cattle workers in humid tropical forests.

Laboratory diagnosis:

1. Clinical Material: Skin scrapings and/or biopsy.

2. Direct Microscopy: (a) Skin scrapings should be examined using 10% KOH and Parker ink or calcofluor white mounts; (b) Tissue sections should be stained using H&E, PAS digest, and Grocott's methenamine silver (GMS).

Interpretation: The presence in tissue of brown pigmented, planate-dividing, rounded sclerotic bodies from a patient with supporting clinical symptoms should be considered significant. Remember direct microscopy or histopathology does not offer a specific identification of the causative agent. Note: direct microscopy of tissue is necessary to differentiate between chromoblastomycosis and phaeohyphomycosis where the tissue morphology of the causative organism is mycelial.

Skin scrapings from a patient with chromoblastomycosis mounted in 10% KOH and Parker ink solution showing characteristic brown pigmented, planate-dividing, rounded sclerotic bodies.

H&E stained section showing characteristic dark brown sclerotic cells which divide by binary fission and not by budding. Note all agents of chromoblastomycosis form these sclerotic bodies in tissue.

3. Culture: Clinical specimens should be inoculated onto primary isolation media, like Sabouraud's dextrose agar.

Cultures of the aetiologic agents of chromoblastomycosis are typically olivaceous-black with a suede-like surface.

Interpretation: The dematiaceous hyphomycetes involved are well recognised as environmental fungi, therefore a positive culture from a non-sterile specimen, such as sputum or skin, needs to be supported by clinical history and direct microscopic evidence in order to be considered significant. Culture identification is the only reliable means of distinguishing these fungi.

• 4. Serology: There are currently no commercially available serological procedures for the diagnosis of chromoblastomycosis.

• 5. Identification: Culture characteristics and microscopic morphology are important, especially conidial morphology, the arrangement of conidia on the conidiogenous cell and the morphology of the conidiogenous cell. Cellotape flag and/or slide culture preparations are recommended.

• Causative agents:• Cladophialophora carrionii, Fonsecaea pedrosoi, Phialophora

verrucosa

• Management:• The treatment of chromoblastomycosis has been exceedingly

difficult. Successful surgical excision requires the removal of a margin of uninfected tissue to prevent local dissemination. Flucytosine with or without thiabendazole has been extensively used in the past. However both itraconazole [400 mg/day] and terbinafine [500 mg/ day] for 6 to 12 months have been used successfully for the treatment of chromoblastomycosis.

LobomycosisDescription:Lobomycosis is a chronic, localised, subepidermal infection characterised by the presence of keloidal, verrucoid, nodular lesions or sometimes by vegetating crusty plaques and tumours. The lesions contain masses of spheroidal, yeast-like organisms tentatively referred to as Loboa loboi. There is no systemic spread. The disease has been found in humans and dolphins and is restricted to the Amazon Valley in Brasil.

Clinical manifestations:The initial infection is thought to be caused by traumatic implantation such as an arthropod sting, snake bite, sting-ray sting, or wound acquired while cutting vegetation. The lesions begin as small, hard nodules resembling keloids and may spread slowly in the dermis and continue to develop over a period of many years. Older lesions become verrucoid and may ulcerate. The disease may be transfered to other areas of of the skin by further trauma or autoinoculation. Thus the areas of involvement may become quite extensive. Lesions are found on the arms, legs, face or ears.

Lobomycosis showing extensive verrucoid lesions on the legs.90% of cases are men, mostly in farmers and other high risk groups exposed to various harsh conditions as well as aquatic habitats.

Laboratory diagnosis:1. Clinical material: Tissue sample obtained by curettage or surgical biopsy.2. Direct Microscopy: (a) Tissue can be macerated and mounted in 10% KOH and Parker ink or calcofluor white mounts or (b) Tissue sections should be stained using PAS digest, Grocott's methenamine silver (GMS) or Gram stains.Interpretation: The presence of chains of darkly pigmented, spheroidal, yeast-like organisms tentatively referred to as Loboa loboi is typical for lobomycosis.

GMS stained tissue specimen showing numerous darkly pigmented yeast-like cells, often in chains, 9-12 um in size.3. Culture: The aetiologic agent known as "Loboa loboi" remains to be cultured.4. Serology: There are currently no serological tests available.5. Identification: Clinical features, geographic location and microscopic morphology are important.

Causative agents:Loboa loboi

Management:The most successful treatment is for wide surgical excision of the affected area, however care must be taken to prevent contamination of surgical wounds, as relapse is common. Clofazimine at 100-200 mg/day has been used with varying results but it would appear that antifungal drugs are ineffective. The course of the infection is slow and chronic and the although not life threatening the prognosis is poor.

• Rhinosporidiosis:

• An infectious disease caused by Rhinosporidium seeberi which occurs mainly in the nasal cavity or nearby mucosa-lined structures such as the conjunctiva. On rare occasions other parts of the body may be infected e.g. genital, rectum, ear and skin. The infection tends to persist for long periods of time (sometimes decades) and occasionally secondary bacterial infection can occur. Infection usually occurs through exposure to stagnant water contaminated with the infectious agent

• R seeberi had been considered a water mold. Molecular biological techniques have recently demonstrated that this organism is an aquatic protistan parasite. It is currently included in a new class, the Mesomycetozoea, along with organisms that cause similar infections in amphibians and fish.

• Clinical Presentation

• Rhinosporidiosis manifests primarily with the development of red, swollen polyps in the nasal mucosa or the ocular conjunctivae.

• The polyps are deep red or pink, are sessile or pedunculated, and tend to bleed easily. They are seldom observed outside the nasal cavity in a nasal infection. Gray or yellow spots, which represent the sporangia form of R. seeberi, can also often be observed in the polyps.

• The feeling is most commonly described as foreign body being felt in the nasal passages, while the development of polyps in the ocular conjunctivae is readily visible. The polyps can lead to unilateral nasal obstruction as well as bleeding, although symptoms are variable depending on the location of the polyps. Other symptoms may include local pruritus, coryza with sneezing, rhinorrhea, and nasal discharge . In eye infection, increased tearing can occur as the disease progresses. Photophobia and redness of the eye can also occur.

• Agent• The causative agent of the disease is Rhinosporidium seeberi

Figure :A mature sporangium that is extruding its endospores to the surface of the skin. A watery environment induces the release. A trophocyte can be seen in the lower right corner (bottom half cut off slide). The granular nature of its cytoplasm is observable in the slide

Figure : PAS stain of a biopsied polyp that shows trophocytes. The thick walls of the trophocytes are stained pink (

• Treatment:• Rhinosporidiosis cannot be treated with antibiotics, although there

have been reports of three patients being treated with dapsone over the course of a year

• Antimicrobial treatments have proven ineffective,