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Drugs & Diseases > Pulmonology

BLASTOMYCOSIS

Updated: Jan 09, 2019
* Author: Chidinma Chima-Melton, MD; Chief Editor: Zab Mosenifar, MD, FACP,
FCCP more...

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Sections
Blastomycosis

* Sections Blastomycosis
* Overview

* Practice Essentials
* Background
* Pathophysiology
* Etiology
* Epidemiology
* Prognosis
* Patient Education
* Show All
* Presentation

* History
* Physical Examination
* Show All
* DDx
* Workup

* Approach Considerations
* Sputum Examination
* Culture
* Skin Tests and Serodiagnosis
* Chest Radiography
* Computed Tomography Scanning
* Bronchoscopy
* Immune Deficiency Workup
* Histologic Findings
* Show All
* Treatment

* Approach Considerations
* Antifungal Treatment
* Consultations
* Deterrence/Prevention
* Show All
* Medication

* Medication Summary
* Antifungals, Systemic
* Show All
* Media Gallery
* References

Overview

PRACTICE ESSENTIALS

Blastomycosis is a systemic pyogranulomatous infection usually caused by the
inhalation of (spores) conidia of Blastomyces dermatitidis. Clinical
presentations vary widely, ranging from an asymptomatic, self-limited pulmonary
infection to acute respiratory distress syndrome (ARDS), a life-threatening
disease. [1]

Composite photomicrograph of a tissue specimen from a patient with blastomycosis
infection shows an abundance of large budding cells that had been configured in
chains. Courtesy of CDC/Dr. Lucille K. George.
View Media Gallery

SIGNS AND SYMPTOMS

Blastomycosis is usually localized to the lungs and may present with:

* A self-limited flulike illness with fever, chills, myalgia, headache, and a
nonproductive cough

* An acute illness resembling bacterial pneumonia, with high fever, chills, a
productive cough, and pleuritic chest pain; mucopurulent or purulent sputum

* Chronic illness, with low-grade fever, a productive cough, fatigue, night
sweats, and weight loss

* Rapidly progressive, and severe disease (eg, multilobar pneumonia or ARDS),
with fever, shortness of breath, tachypnea, hypoxemia and, finally,
hemodynamic collapse

Extrapulmonary manifestations are present in 25-40% of patients, who may present
with:

* Cutaneous lesions - Usually either verrucous or ulcerative and may be
asymptomatic

* Osteoarticular lesions - Cause bone or joint pain; possible soft-tissue
swelling; possible involvement of any bone, but the vertebrae and pelvis are
common sites

* Genitourinary manifestations including prostatitis and epididymitis - May be
asymptomatic or may cause pain on urination

* Other sites - B dermatitidis has been reported to involve almost all organs,
including the eye, liver, spleen, breast, thyroid, and adrenal gland.

* Central nervous system involvement - Intracranial or epidural abscesses and
meningitis

See Presentation for more detail.

DIAGNOSIS

Culture and cytopathology are the gold standard for the diagnosis of
blastomycosis. The fastest way to diagnose blastomycosis is direct
identification of the broad based budding yeast forms under microscopy.
Identification from culture may not be evident for 2 to 4 weeks, and it often
requires invasive procedures such as bronchoscopy or tissue biopsy to obtain
specimens. [1]

More recently, molecular DNA probes have been developed to facilitate the rapid
identification of B dermatitidis from clinical specimens. A commercially
available chemiluminescent DNA probe assay (AccuProbe) is commonly used and
produces results from culture within hours once there is adequate growth. [2]

In addition, tests targeting virulence factors BAD1 and DRK1 through real-time
polymerase chain reaction (RT-PCR) and serologic antibody-based assays have been
developed but are as yet not commercially available. [3, 4, 5]

Chest imaging findings are nonspecific and may range from scattered
centrilobular nodules to areas of dense consolidation. Computed tomography (CT)
scanning is not always necessary, but it can provide better definition of the
character and distribution of abnormalities observed on a chest radiograph.

See Workup for more detail.

MANAGEMENT

Antifungal treatment is as follows:

* Patients with mild to moderate pulmonary disease - Oral azole (eg,
itraconazole)

* Patients with moderate-to-severe disseminated disease or immune compromise:
Initially, amphotericin B with step-down to an oral azole after clinical
improvement

* Patients with central nervous system (CNS) disease as well as pregnant women:
Always be treat initially with amphotericin B

See Treatment and Medication for more detail.

Next: Background

BACKGROUND

Oral azoles, usually itraconazole or amphotericin B, are first-line treatment
for blastomycosis depending on the severity of the disease, its clinical form,
and the host's immune status. In general, mild to moderate disease is typically
treated with oral itraconazole—except in pregnant women and those with CNS
disease, all of whom should always receive amphotericin B. Patients with
moderately severe to severe disseminated disease should receive amphotericin B
followed by a long-term oral azole when they clinically improve. [6]

Blastomycosis requires prolonged treatment. Patients with mild to moderate
disseminated blastomycosis without central nervous system involvement should be
treated for 6 months. In patients with bone involvement, the treatment period
should be extended to 12 months. Individuals with severe disease occasionally
require even longer treatment. See Treatment and Medication.

Previous
Next: Background

PATHOPHYSIOLOGY

Blastomycosis is a systemic pyogranulomatous infection caused by the inhalation
of conidia (spores) of B dermatitidis, the asexual (imperfect) form of
Ajellomyces dermatitidis, a dimorphic fungus. The mycelial form grows as a
fluffy white mold at 25°C (77°F) and a brown folded yeast at 37°C (98.6°F). The
conidia are round, ranging from 2 to 10 μm in diameter, and become aerosolized
when the fungus in the mycelia phase in the soil is disturbed. These can be
inhaled, passing into the lower respiratory tract and resulting in pulmonary
infection.

The inhaled conidia are phagocytized by bronchopulmonary mononuclear cells. The
organism’s susceptibility to phagocytosis and killing by neutrophils, monocytes,
and alveolar macrophages explain why some individuals remain asymptomatic
despite exposure to environments that would cause clinical infection in others.
At 37°C (98.6°F), B dermatitidis converts from the mycelial form to the yeast
form.

This transformation provides a survival advantage to the infecting fungus, as
the yeast form is larger, at 8-10 μm in diameter, and possesses a thick cell
wall that provides greater resistance to phagocytosis and killing. The histidine
kinase DRK1 regulates dimorphism from mold to yeast and virulence gene
expression in B dermatitidis. DRK1 knockout strain grown at 37°C (98.6°F) is
locked in the mold morphology. [7] Another virulence factor is BAD-1, an
immune-modulating glycoprotein that is expressed on the cell surface and
released into the extracellular matrix. [8] BAD-1 facilitates the binding of B
dermatitidis to macrophages. The yeast forms multiply and may disseminate
through the blood and lymphatics to other organs. The evoked pyogranulomatous
inflammatory response is a distinctive feature of blastomycosis characterized by
an initial influx of neutrophils, followed by macrophage and granuloma
formation.

Blastomycosis may be asymptomatic in nearly 50% of infected persons. In the
remainder, the median incubation period from inhalation of the fungus to
manifestations of symptoms is 45 days (range: 21-106 days). Symptoms of
blastomycosis are similar to influenza, with most patients presenting with
cough, fever, sputum production, chest pain, and dyspnea. Cellular immunity is a
major protective factor in preventing progressive disease secondary to B
dermatitidis.

The lungs are the usual point of entry. In one study, pulmonary involvement was
present in 91% of all cases. [9] Pulmonary symptoms range from acute and chronic
pneumonias to acute respiratory distress syndrome (ARDS). Evidence of
dissemination to other organs may be present.

Rarely, an extrapulmonary site (eg, skin, bone) may be the only presenting
clinical manifestation.

In earlier reported case series, extrapulmonary involvement was noted in 50% of
chronic blastomycosis cases. However, in present times, with earlier recognition
and effective treatment, the extrapulmonary manifestations are seen in only
about 20% of cases. Extrapulmonary dissemination occurs more commonly in
patients with chronic pulmonary illness or immunocompromise.

Skin is the most common site of extrapulmonary blastomycosis and is involved in
about 20% of cases. Other areas affected, and the approximate frequency of such
involvement, are as follows [9] :

* Bone - 5%

* Prostate and other genitourinary organs - 2%

* Meninges and brain - 1%

* Other (lymph nodes, adrenal, eye, liver, spleen, trachea, breast, and
thyroid) - 3%

Reactivation of blastomycosis may occur after a pulmonary infection that
resolved, with or without treatment. An extrapulmonary site (eg, skin, bone,
brain) is rarely a site of reactivation.

Previous
Next: Background

ETIOLOGY

Relatively recent advances in genotyping of Blastomyces by microsatellite typing
and ITS2 sequencing have demonstrated that there are two unique clades, or
species, of Blastomyces: B dermatitidis infection is more prevalent in patients
with comorbidities and more likely to cause disseminated infection, and B
gilchristii is more likely to cause isolated pulmonary disease. In a
retropective review of children with blastomycosis confirmed by culture or
cytopathology, the majority of the children had isolated pulmonary disease with
systemic findings. [10] Those with extrapulmonary disease were less likely to
have systemic symptoms or additional laboratory evidence of infection, which
made delays in diagnosis more common. More than 90% of the pediatric cases were
caused by B gilchristii. [11]

B dermatitidis is the asexual (imperfect) form of Ajellomyces dermatitidis,
which is a thermal dimorphic fungus. The mycelial form grows as a fluffy white
mold at 25°C (77°F) and a brown folded yeast at 37°C (98.6°F) body temperature.
The fungus is usually isolated in the soil in its mycelial form in wet earth
that has been enriched with animal droppings, rotting wood, and other decaying
vegetable matter.

The conidia are round, ranging from 2 to 10 μm in diameter, and become
aerosolized when the fungus in the mycelia phase is disturbed. The conidia are
inhaled, passing into the lower respiratory tract and resulting in pulmonary
infection. In infected tissue specimens, B dermatitidis appears as a
characteristic thick-walled yeast, 8-10 μm in diameter, which provides greater
resistance to phagocytosis and killing.

As dogs are infected with blastomycosis in a similar way and often in the same
place as humans, an early clue to the diagnosis in humans is a history of a
fungal infection in a pet dog. Blastomycosis is not transferred from animals to
humans other than from bite wounds. [12] This condition has also been reported
in other animals, including horses, cows, cats, bats, foxes, and lions.

Previous
Next: Background

EPIDEMIOLOGY

UNITED STATES STATISTICS

Blastomycosis can be endemic or sporadic. Most cases of blastomycosis occur in
the United States and Canada, although occasional cases have been reported in
Central and South America, Africa, the United Kingdom, India, and the Middle
East. [13] The disease is endemic in the central and southeastern parts of the
United States, near the Mississippi River, Ohio River, and Great Lakes. Thus,
Arkansas, Kentucky, Mississippi, North Carolina, Tennessee, Louisiana, Illinois,
and Wisconsin are commonly affected. [14] However, blastomycosis is reportable
only in five states: Arkansas, Louisiana, Michigan, Minnesota, and Wisconsin.
[15]

The true incidence and prevalence of blastomycosis are unknown, because there
are no reliable antigen markers for skin testing. Its incidence in Northern
Ontario has been reported as 117.2 cases per 100,000 population, the highest
incidence in North America. [16] Based on confirmed cases, the annual US
incidence is 1-2 cases per 100,000 people in Arkansas, Louisiana, Michigan,
Minnesota, and Wisconsin. [6] Wisconsin may have the highest incidence of
blastomycosis of any state, with yearly rates ranging from 10 to 40 cases per
100,000 persons in some northern counties, [17] and 2.9 hospitalizations per
100,000 person-years. [18] 2012 data from Illinois and Wisconsin found an
annual incidence of 0.4-2.6 cases per 100,000 population; in contrast, 2007-2017
data from New York revealed an average annual incidence of 0.1-0.2 cases per
100,000. [15]

There were 1,216 blastomycosis-related deaths in the United States during
1990–2010. [19] Among those 1,216 deaths, blastomycosis was reported as the
underlying cause of death for 741 (60.9%) and as a contributing cause of death
for 475 (39.1%). The overall age-adjusted mortality rate for the period was 0.21
per 1 million person-years. [19]

Significant construction, such as interstate road expansion, can release
Blastomyces spores from the soil. [20] One such urban outbreak comprised 34
confirmed cases of blastomycosis in Indianapolis from 2005 to 2008, which
coincided with a period of major highway construction in the same area. [20]
Residence near rivers and waterways is also associated with an increased risk of
blastomycosis, particularly major freshwater drainage basins such as those of
the Nelson River, St Lawrence River and northeast Atlantic Ocean Seaboard,
Mississippi River System, and Gulf of Mexico Seaboard and southeast Atlantic
Ocean Seaboard. [21] In Vilas County, north-central Wisconsin, 73 patients with
laboratory-confirmed blastomycosis were identified over an 11-year period, in
which 82% of these patients lived or had visited within 500 m of rivers or
associated waterways. [22]

As noted under Etiology, canine blastomycosis can be an early warning sign for
concomitant blastomycosis in humans. One case series of five households in which
six patients were diagnosed with blastomycosis, one or more pet dogs were
diagnosed with blastomycosis an average of 6 months before the patients
themselves became symptomatic. [12]

INTERNATIONAL STATISTICS

Blastomycosis can be seen outside of the United States. Internationally, most
reported cases stem from Canada (Ontario, Manitoba) and Africa. Most African
cases originate from South Africa [23] and Zimbabwe, [24] although cases have
also been seen in Nigeria [25] and Tunisia. [26, 27] The disease is often
mistaken for pulmonary tuberculosis or malignancy, and only after lack of
response to standard treatment is the diagnosis made. [24, 25, 28] Cases have
also been reported from disparate regions, including China, [16] Mexico, South
America, the Middle East, and India. [13]

Because of the erroneous belief that the disease is limited to the United
States, blastomycosis is often referred to as North American blastomycosis,
which is an obsolete term. The term European blastomycosis is a confusing
synonym of cryptococcosis, a systemic infection caused by the yeastlike fungus
Cryptococcus neoformans. Likewise, South American blastomycosis (ie, Brazilian
blastomycosis) is an older name for paracoccidioidomycosis, a chronic, often
fatal, mycosis caused by a large dimorphic fungus, Paracoccidioides
brasiliensis.

RACIAL, SEXUAL, AND AGE-RELATED DIFFERENCES IN INCIDENCE

Most studies of blastomycosis have shown no racial disparity in susceptibility.
Rather, the distribution tends to mirror the ethnic and racial makeup of the
area affected. However, in a few case series, certain races show a higher
incidence of the disease. Some examples include an outbreak in Wisconsin, where
20 of the 55 patients affected were Hmong, [29] and an analysis of Missouri
cases in which 57% of those affected were black although black individuals
account for only 13% of the population. [30] One possible explanation for these
findings is that these groups have greater exposure to environments containing
wet soil or organic matter where B dermatitidis thrives.

Blastomycosis has been reported to occur more frequently in males, possibly due
to greater occupational and recreational exposure. Men are more likely to
participate in activities associated with B dermatitidis, such as fishing,
hunting, and camping. In Wisconsin from 1986 to 1995, 60% of cases were in
males. [31] However, analysis of outbreak cases from a common source and more
recent reports do not indicate a significant sex difference. [32] Moreoever,
historically, epidemiologic reports were skewed due to the collection of data
from Veterans Administration (VA) hospitals nationwide, which predominantly
serve male patients. [33]

The mean age at diagnosis is approximately 45 years, with most patients aged
30-69 years. However, persons of any age can acquire the disease, including
infants and very elderly persons. [34]

The disease is rare in children and adolescents. A retrospective study at a
children's hospital in Arkansas identified only 10 patients diagnosed with the
disease between 1983 and 1995. [35] In past reviews, however, about 2-10% of
patients reported were younger than 15 years. In children, both sexes are
equally susceptible.

Previous
Next: Background

PROGNOSIS

Immunocompetent patients with blastomycosis generally do not experience
complications and can expect a full recovery. Relapse or recurrence of
blastomycosis is rare, and it varies by the therapeutic agent, treatment length,
and patient's immune capacity. Successful blastomycosis treatment is achieved in
80-95% of cases. [10] In contrast, immunocompromised patients with blastomycosis
have a poor prognosis.

Cellular immunity is the fundamental host defense against B dermatitidis. Loss
or compromise in T-lymphocyte function—for example, in human immunodeficiency
virus infection / acquired immunodeficiency syndrome (HIV/AIDs) or with immune
suppression after solid organ transplant, can predispose to severe disseminated
disease or cavitary lung disease, and it often involves the central nervous
system (CNS). [36, 37, 38]

COMPLICATIONS

Potential complications include progressive pulmonary disease and extrapulmonary
dissemination. Risk of dissemination is increased in immunocompromised
individuals. Severe pulmonary disease complicated by cavitary lesions and acute
respiratory distress syndrome (ARDS) occurs in approximately 20% of compromised
hosts. [39] CNS disease appears to be 3-5 times more common in
immunocompromised patients than in immunocompetent hosts. Meningitis or mass
lesions has/have been reported to occur in approximately 40% of adult patients
with AIDS.

Extrapulmonary disease, frequently to the skin, bones, genitourinary system, and
CNS, can occur in 25-40% of patients with blastomycosis. The skin is the
second-most common site of involvement after the lungs, and cutaneous findings
range from the characteristic verrucous lesions to friable ulcerative lesions.
Complications include abscesses and nodules, and extensive cutaneous lesions may
undergo central healing with scarring and contracture.

Osteomyelitis occurs in approximately 25% of extrapulmonary cases, [14] usually
concomitantly with pulmonary blastomycosis. The infection can spread into nearby
joints, leading to septic arthritis, or contiguous spread from the vertebral
bodies can cause psoas abscesses.

Previous
Next: Background

PATIENT EDUCATION

Although immunocompromised patients (including those with human immunodeficiency
virus infection / acquired immunodeficiency syndrome [HIV/AIDS]) living in or
visiting blastomycosis-endemic areas cannot completely avoid exposure to B
dermatitidis, they should be counseled about reducing the risk of acquiring
blastomycosis by avoidance of occupational and recreational activities known to
be associated with increased risk (eg, wooded areas along waterways).

Clinical Presentation

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Media Gallery

* Cutaneous blastomycosis.

* Lateral chest radiograph reveals the ill-defined lingular opacity and an
absence of pleural effusions.

* Composite photomicrograph of a tissue specimen from a patient with
blastomycosis infection shows an abundance of large budding cells that had
been configured in chains. Courtesy of CDC/Dr. Lucille K. George.

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CONTRIBUTOR INFORMATION AND DISCLOSURES

Author

Chidinma Chima-Melton, MD Assistant Clinical Professor in Pulmonary and Critical
Care Medicine, UCLA Health; Burn Intensivist and Hospitalist, West Hills
Hospital and Medical Center; Pulmonologist and Intensivist, Los Robles Medical
Center and West Hills Hospital and Medical Center

Chidinma Chima-Melton, MD is a member of the following medical societies:
American College of Chest Physicians, American Thoracic Society