Case 01-1
History/Physical Findings:
A 68-year-old man presented with a one-month history of malaise,
poor appetite, weight loss, sinus drainage and a cough. He was an
otherwise healthy non-smoker, retired geologist who spent his winters
in Arizona. A chest radiograph was obtained and followed by a flexible
bronchoscopy and mediastinoscopy with lymph node samples sent for
culture and histology.
Laboratory Findings:
Chest Radiograph:
Chest radiograph revealed an ill-defined right lung opacity and
mediastinal lymphadenopathy.
Surgical Pathology:
The lymph node biopsy showed several thick walled spherules in a
background of granulomatous inflammation.
 
Culture:
A single white mold grew in the Shaedler broth . It was subbed to a
mycological agar (Sabouraud dextrose agar). Growth on day 4 revealed
delicate hyphae with early arthroconidia formation. Growth on day 9
revealed alternately staining barrel-shaped arthroconidia with
disarticulation.
 
Discussion:
Coccidiomycosis was first recognized in 1892 and as a fungal
infection in 1900. It is endemic in the soutwestern United States,
Mexico, Central and South America with an incidence in the United
States of 100,000 infections/yr. Outbreaks are associated with dust
storms, archeological digs, climatic conditions and earthquakes.
C. Immitis is a soil fungus with a biphasic life cycle: the
saprophytic and the parasitic. The saprophytic stage occurs in the
environment with the organism existing in a mycelial state. As the mold
matures, barrel-shaped arthroconidia form and alternate with empty
cells. The arthroconidia fracture from hyphae and are dispersed as an
aerosol. This leads to infection of a new soil site or inhalation by a
susceptible host. In the host the parasitic phase is initiated. The
arthrospore swells into a spherule and the protoplasm divided to form
endospores. The spherule ruptures releasing endospores where in can
returned to the environment via secretion or cause auto-infection
within the host.
60% of acute infections are asymptomatic while 40% develop symptoms of
cough, sputum production, chest pain, fever, sweats, anorexia, weakness
and arthralgias. Chest radiograph may reveal pulmonary infiltrates,
pleural effusion and mediastinal adenopathy. Approximately 1/200
infected develop chronic infection with pulmonary cavities, empyema,
bronchopleural fistulas or extrapulmonary disease with involvement of
the meninges, bones and joints, skin and soft tissue. Wide spread
miliary infection is rare and carries a poor prognosis.
Diagnosis includes culture showing alternately staining, thick walled
arthroconidia with disarticulation. Definitive diagnosis requires
conversion into the parasitic form or confirmation using a
chemiluminescent DNA probe. Tissue biopsy shows spherules with
endospore formation. A skin test may be used to screen for exposure
while serologic testing is helpful to determine active disease.
The differential diagnosis on tissue morphology includes
Histoplasmosis, Cryptococcus and Blastomycosis. The differential on
culture includes other arthroconidia producing organisms such as
Malbranchia, Gymnoascus, Trichosporon and Geotrichum.
Diagnosis:
Based on tissue histology and culture morphology, a diagnosis of
Coccidioides immitis was made.
Treatment:
Most patients with acute primary infection recover without
treatment. Factors indicating treatment include high antibody titers,
circumstances suggesting high innoculum (i.e. laboratory accident),
negative skin test and concurrent disease. Chronic or disseminated
disease is usually treated until disease is inactive with an average of
2-3 months. Chemotherapy includes amphotericin B or an oral azole.
Surgery may be indicated for cavitary lesions, empyemas or fistula
formation.
References:
- Galgiani, JN. Coccidiomycosis: a regional disease of national
importance: rethinking approaches for control. Ann Int Med
1999:130:293-300.
- Stevens, DA. Current Concepts: coccidiomycosis. N Engl J Med
1995;332:1077-1082.
Contributors:
Robin LeGallo, M.D.
Department of Pathology
University of Virginia Health Sciences Center
Donald J. Innes, Jr., M.D.
Department of Pathology
University of Virginia Health Sciences Center
Questions should be addressed to:
dji@Virginia.EDU
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