Coccidioides immitis

Coccidioides immitis

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.

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Surgical Pathology:

The lymph node biopsy showed several thick walled spherules in a background of granulomatous inflammation.

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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.

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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:

  1. Galgiani, JN. Coccidiomycosis: a regional disease of national importance: rethinking approaches for control. Ann Int Med 1999:130:293-300.

  2. 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