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Sporotrichosis is a deep fungal infection that follows accidental
inoculation of the skin and is characterized by ulceration and/or
nodule formation at the inoculation site, followed by subcutaneous
nodule formation along the course of lymphatic drainage.
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1. Lymphocutaneous sporotrichosis: most common, seen
in 25% of cases. Proximal to local cutaneous lesion, intervening
lymphatics become indurated, nodular, thickened, with occasional
ulcer formation.
2. Fixed cutaneous sporotrichosis: 20% of cases, subcutaneous
papule at inoculation. The patient is previously sensitized to sporotrichosis;
no lymphatic spread.
3. Chancriform form of sporotrichosis: rare, < 8% of
cases with associated lymphadenopathy proximally.
4. Disseminated sporotrichosis: < 1% of cases. Hematogenous
spread to lungs, liver, spleen, pancreas, thyroid, myocardium, or
CNS in immunocompromised host.
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Synonyms Sporotrichum infection,
rose gardener’s disease
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Age Any age. More common in adults.
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Etiology Sporothrix schenckii,
a dimorphic fungus commonly found in soil, rose and barberry thorns, wood
splinters, sphagnum moss, straw, and marsh hay.
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Geography Ubiquitous, worldwide.
More common in temperate and tropical zones.
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Commonly, sporotrichosis begins with a subcutaneous inoculation
by a contaminated thorn, rock, glass, barb, splinter, cat scratch,
or other sharp item. Following subcutaneous inoculation, S. schenckii
grows locally and slowly spreads along the draining lymphatics.
Secondary skin lesions develop along the lymphatic chain. Rarely
inhalation, aspiration, or ingestion causes systemic infection.
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Three days to 12 weeks after inoculation of the fungal organism,
an asymptomatic or slightly painful nodule will appear at the inoculation
site followed by erythematous nodule formation extended proximally
along the path of lymphatic drainage.
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Type Papules, nodules, ulcers (Fig.
21-19).
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Arrangement Linear described as “sporotrichoid” spread
(Fig. 21-20).
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Distribution Upper extremity >
face, trunk.
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Differential
Diagnosis
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The differential diagnosis for sporotrichosis includes tuberculosis,
atypical mycobacterial infection (particularly M. marinum), anthrax,
tularemia, cat-scratch disease, primary syphilis, leishmaniasis,
herpes simplex virus infection, staphylococcal lymphangitis, histoplasmosis, coccidioidomycosis,
blastomycosis, and cryptococcosis.
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Laboratory Examinations
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Dermatopathology Granulomatous,
Langerhans’-type giant cells, pyogenic microabscesses.
Organisms rare, difficult to visualize. Yeast, if visible, appear
as 1 to 3 μm by 3 to 10 μm cigar-shaped forms and will stain with
PAS or silver stains. Fluorescent antibody or PCR can help detect
the S. schenckii organism in vitro.
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Culture Organism isolated few days
after culture of aspirate of skin lesion.
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Sporotrichosis shows little tendency to resolve spontaneously.
The deep fungal infections respond well to systemic therapy, but
relapses are possible.
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Topical therapy for sporotrichosis is not effective. Oral antifungal
agents (fluconazole, ketoconazole, itraconazole) work, but should
be taken 4 to 6 weeks beyond resolution of the lesions. Side effects
include nausea, vomiting, and LFT abnormalities. There has also
been reported success with saturated solution of potassium iodide
(oral SSKI), which enhances the host’s immune system. It
should also given for 4 to 6 weeks beyond clinical resolution of
cutaneous lesions. Side effects include iododerma, GI upset, and
thyroids suppression.
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For severe or systemic disease, especially in immunocompromised
hosts, IV amphotericin B may be needed for 2 to 3 weeks. Side effects
include renal tubular acidosis, hypokalemia, hypomagnesemia, fever,
chills, delirium, phlebitis, nausea, vomiting, hypotension, hypertension,
renal failure, and bone marrow depression.
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Cryptococcosis is a deep fungal infection acquired by the inhalation
of Cryptococcus neoformans, causing a primary pulmonary infection
that can lead to hematogenous dissemination, and spread of infectionges,
kidneys, and/or skin.
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Synonyms Torulosis, European blastomycosis.
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Age All ages. Mort commonly: 30
to 60 years.
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Etiology C. neoformans, a yeast.
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Geography Worldwide, ubiquitous.
Europe, South America > United States.
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C. neoformans, is an opportunistic pathogen that is accidentally
inhaled from infected dust of avian feces (pigeons, parakeets, and
canaries). Serotypes A, B, C, and D can cause disease in humans.
After inhalation, Cryptococcus causes a pulmonary infection. Immunodeficient
hosts may have a subsequent hematogenous dissemination of the organism
to meninges, kidneys, and skin. Transplacental transmission is possible
and Cryptococcus may also inhabit the female genital tract leading
to inoculation of the infant as it passes through the birth canal.
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Often, cryptococcal disease remains localized to the lungs with
absent or minimal symptoms. In immunosuppressed individuals, hematogenous
dissemination leads to CNS infection with headache (80%),
mental confusion, and visual disturbances for months. Thirty percent
of disseminated cases are associated with malignancy (usually Hodgkin’s
disease).
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Seen in 15% of
systemic cases.
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Type Papules, pustules, plaques,
nodules, ulcers (Fig. 21-21).
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Site of Predilection Face (especially
around nose and mouth), scalp.
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CNS Headache, behavioral disturbance,
seizures.
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Pulmonary Cough, pneumonia, pleural
effusions.
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Other Hepatomegaly, splenomegaly,
lymphadenopathy.
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Differential
Diagnosis
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The differential diagnosis for Cryptococcus includes blastomycosis,
histoplasmosis, molluscum contagiosum, HSV, and other bacterial
or systemic fungal infections.
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Laboratory Examinations
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Dermatopathology Thick-walled organisms
5 by 20 μm in the skin biopsy. Methylene blue, alcian blue, or mucicarmine
will brightly stain the polysaccharide capsule.
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Indirect Immunofluorescence Anitbodies
available to detect cryptococcal organism in body fluids of tissue
specimens.
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Culture Cryptococcus from body
fluids or tissues can be grown on Sabouraud’s agar.
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CXR Pneumonia, infiltrates, nodules,
abscesses, or pleural effusions may be present.
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Untreated, secondary cutaneous cryptococcosis is fatal in 80% of
cases. Appropriate antifungal treatment leads to an 80% cure
rate. And a dramatic decrease in the incidence of Cryptococcal infection
in the HIV population has been seen with the use of fluconazole
and highly active antiretroviral therapy.
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Prevention of Cryptococcus in high-risk patients (on chemotherapy,
high-dose steroids, neutropenia) and antifungal prophylaxis (fluconazole,
voriconazole, moconazole, ketoconazole, itraconazole) is recommended.
The treatment of choice for Cryptococcus used to be amphotericin
B for 2 months. Side effects include renal tubular acidosis, hypokalemia,
hypomagnesemia, fever, chills, delirium, phlebitis, nausea, vomiting,
hypotension, hypertension, renal failure, and bone marrow depression.
It is now recommended to use voriconazole or one of the echinocandins
(caspofungin).
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Histoplasmosis is a common, highly infectious systemic fungal
infection caused by Histoplasma capsulatum and characterized by
an asymptomatic pulmonary infection that occasionally disseminates.
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Synonyms Darling’s disease,
cave disease, Ohio Valley disease, reticuloendotheliosis.
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Etiology H. capsulatum exists in
the soil in warm moist climates
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Geography Endemic in SE and central
US.
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Birds, fowl, or bats are reservoirs for histoplasmosis. The feces
of these animals contain the organism, thus their habitats (caves,
chicken coops, construction sites) are high-risk areas for contracting
the disease.
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Humans acquire H. capsulatum by inhaling the aerosolized spores
from contaminated soil. Histoplasmosis exists as self-limited pulmonary
infection in 75% of cases, which are asymptomatic. Flu-like
pulmonary symptoms (fever, malaise, cough, and chest pain) develop
in 25% of cases and < 1% of patients progress
to disseminated histoplasmosis (fever, hepatosplenomegaly, anemia, and
weight loss), especially in the setting of immunosuppression.
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Type Papules, plaques, pustules
(Fig. 21-22), nodules, abscesses, or ulcers.
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Distribution Any site, mucosa surface.
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Pulmonary Cough, dyspnea, chest
pain
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Other Hepatosplenomegaly, and weight
loss.
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Differential
Diagnosis
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The differential diagnosis of histoplasmosis includes miliary
tuberculosis, coccidioidomycosis, paracoccidioidomycosis, cryptococcosis,
leishmaniasis, and lymphoma.
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Laboratory Examinations
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Dermatopathology Skin biopsy may
show small intracellular yeast-like forms with a rim of clearing
within histiocytes and giant cells. PAS or Gomori methenamine silver
stains will make yeast more visible.
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Touch Preparation Lesional skin
touched to glass slide and stained with Giemsa stain will show H.
capsulatum.
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Culture Tissue or blood inoculated
on Sabouraud’s agar may grow H. capsulatum.
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Histoplasmosis Skin Test In infants,
a positive reaction 2 to 3 weeks after infection indicates active,
current infection; but in endemic populations, up to 90% of
children and adults react positively, signifying past or present
infection.
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Serology Immunodiffusion, agar
gel precipitin, yeast phase complement fixation, collodion, or latex
particle agglutination can be performed on blood samples. Titers
greater than 1:32 are highly suggestive of active histoplasmosis
disease.
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CXR Interstitial infiltrates and/or
hilar adenopathy.
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In 99% of cases, asymptomatic pulmonary histoplasmosis
is a benign and self-limited disease, and treatment is not necessary.
In symptomatic or disseminated form, untreated histoplasmosis has
a high mortality rate.
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If bird or bat droppings are to be cleared in an endemic area
for H. capsulatum, protective equipment (respirators, goggles, and
so forth) should be worn. Most cases of histoplasmosis do not require
therapy. In severe systemic cases or disseminated disease, systemic
antifungals (amphotericin B, itraconazole, voriconazole) may be
necessary. Side effects include renal tubular acidosis, hypokalemia,
hypomagnesemia, fever, chills, delirium, phlebitis, nausea, vomiting,
hypotension, hypertension, renal failure, and bone marrow depression.