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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, wartlike 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
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Superficial
Cutaneous
Subcutaneous
Systemic
Opportunistic
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Sporotrichosis
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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.
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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.
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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.
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Prevention
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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
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Treatment
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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.
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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, planatedividing, 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.
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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
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Management:
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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.
Lobomycosis
Description:
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.
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Rhinosporidiosis:
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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
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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.
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Clinical Presentation
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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.
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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.
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 (
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Agent
The causative agent of the disease is Rhinosporidium seeberi
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Treatment:
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Rhinosporidiosis cannot be treated with antibiotics, although there have been
reports of three patients being treated with dapsone over the course of a year
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Antimicrobial treatments have proven ineffective,