AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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Background

Coccidioidomycosis is an infection caused by the soil-inhabiting fungus Coccidioides immitis. This fungus is endemic to certain regions of North and South America. The endemic areas in the United States include Arizona, south central California, Nevada, New Mexico, and the western half of Texas. Other endemic areas are the regions of Mexico that border the western United States. The fungus also is endemic to some Central American countries, including Guatemala, Honduras, and Nicaragua. Other areas, such as desert regions of South America (Argentina, Paraguay, Venezuela), also are endemic.

Historical perspectives

Wenicke and Posadas first described a case of coccidioidomycosis in 1892 in South America. Two years later in the United States, a patient with disseminated coccidioidomycosis was first reported in California in 1894. In 1896, Rixford and Gilchrist reported 2 cases in which they identified the infecting agent as a protozoanlike organism and named it Coccidioides immitis. Ophuls further described the life cycle and pathology of C immitis in 1905. The epidemiology of coccidioidomycosis was studied by Charles E. Smith in the Joaquin Valley after he and his colleagues developed serologic testing for coccidioidomycosis. The first effective therapy for coccidioidomycosis, intravenous amphotericin B was first used in 1957. Since the 1980s, various oral antifungal agents, including ketoconazole and itraconazole, have lead to further advances in treatment of coccidioidomycosis.

Life cycle of C immitis

C immitis is a fungus that thrives in soil and grows in either of 2 phases—the mycelial arthrospore phase in the soil or the spherule endospore phase in infected tissues. Mycelia are most prolific during the rainy season, but, at this stage, they are the least infectious. As the soil becomes dryer, the branching septated hyphae develop into arthrospores, which readily disarticulate as single fungal cells and become airborne when disturbed by wind or soil excavation. An arthrospore measures 3-5 microns, and it remains viable for long periods of time. Once inhaled, an arthrospore develops into a thick-walled spherule filled with endospores. Once released, each endospore can start the development of a new spherule and extend the infection, repeating its growth phase and continuing the cycle.

Coccidioidomycosis is not transmitted from person to person. Risk of infection is highest in dry summer months. A second period of risk usually occurs in the late fall, terminating with winter rains. Dust exposure is a critical factor for acquiring an infection. Individuals who dig in the soil or who are exposed to disrupted earth are at the greatest risk.

Pathophysiology

Following inhalation and maturity of the fungi, humoral immunity predictably begins with immunoglobulin M (IgM) antibodies, and immunoglobulin G (IgG) antibodies follow. Cell-mediated immunity, particularly T cells, becomes a key factor in determining recovery from coccidioidomycosis. A pyogenic infection develops, and, eventually, a granulomatous respiratory infection ensues. Caseation without calcification may occur. Respiratory infection usually results in endobronchiolitis. A spectrum of signs may be observed on chest x-ray films. These include (1) a nonspecific increase in pulmonary markings, (2) patchy bronchopneumonia, and (3) pleural effusion (hilar adenopathy is common).

Depending on the host's immune response, infection with C immitis may evolve into one of the clinical syndromes described below.

Primary coccidioidal pneumonia

Most patients with primary pulmonary coccidioidomycosis are asymptomatic, and the infection resolves spontaneously. In approximately 5% of patients, a persistent pulmonary focus of coccidioidomycosis may develop, manifested as a nodule, cavity, or chronic progressive pneumonia. In addition, C immitis can disseminate from the lungs and thoracic cavity to infect other areas of the body, such as bone, joints, skin, and meninges.

Nodules

In approximately 5-7% of patients with coccidioidal pneumonia, the infection evolves to form a sharply circumscribed, usually noncalcified, pulmonary nodule. Malignancy is a major concern while evaluating these nodules. In a review of 200 solitary pulmonary nodules surgically resected from patients within endemic areas, 33.5% were found to be malignant (Read, 1972).

Cavities

Another common manifestation of persistent pulmonary coccidioidomycosis is cavity formation. This occurs in approximately 5% of patients. The typical coccidioidal cavity is thin-walled, solitary, and peripheral in location. Coccidioidal cavities commonly are asymptomatic, and approximately 50% disappear within 2 years of their occurrence. The cavities may wax and wane over the years.

Chronic progressive coccidioidal pneumonia

Patients with this manifestation present with chronic systemic symptoms such as low-grade fever, weight loss, cough, chest pain, and hemoptysis. These symptoms often are indolent and simulate tuberculosis when coupled with radiographic findings of bilateral apical cavitation and fibrosis.

Dissemination

Disseminated coccidioidomycosis usually occurs within weeks to months of the primary pneumonia. In some patients with disseminated disease, no radiographic evidence of previous pulmonary disease and no history of a preceding respiratory illness may be present. Males and certain ethnic groups, such as African Americans and Filipinos, are more likely to develop disseminated disease. Patients with depressed cellular immunity, such as those with lymphoma, HIV infection, organ transplants, or those receiving high-dose corticosteroids, also are more likely to develop dissemination. Skin, bones, joints, and meninges are the most frequent sites of dissemination. The infection also may spread to bone marrow, myocardium, and kidneys.

Frequency

United States

Coccidioidomycosis affects an estimated 100,000 people each year in the United States. Coccidioidomycosis is endemic in the western hemisphere from California to Argentina. Although it usually affects only those individuals in endemic areas, coccidioidomycosis is being recognized increasingly outside of these areas, as travelers pass through endemic areas.

International

Affected areas are in the lower Sonoran areas, characterized by a semiarid climate with hot summers and alkaline soils. These areas include northern Mexico and Central and South America.

Mortality/Morbidity

• Infection is directly related to the degree of exposure to airborne arthrospores. Therefore, those exposed to large amounts of dust in endemic areas (eg, farmers, archeologists) have higher rates of infection.
• Infection rates usually are calculated from cocci skin testing, and approximately 40% of those infected develop symptomatic disease, usually pulmonary.
• The pulmonary infection in the vast majority of individuals (approximately 90%) resolves without sequelae. Approximately 10% of patients progress to harbor pulmonary sequelae of cavitary lesions and nodules. In approximately 1%, infection extends to dissemination.

Race

• Filipinos have the highest risk of dissemination, approximately 10-175 times the risk of whites. Filipinos have 10 times the risk of developing meningitis compared to whites.
• Blacks and individuals of Hispanic descent also have a higher risk of dissemination. Blacks have 5 times the risk of developing meningitis and a 5-times greater risk of death.

CLINICAL

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History

Approximately 30-40% of individuals develop clinical symptoms after infection. The disease spectrum ranges from a mild flulike illness to subacute pneumonia.

• Most symptomatic patients have a febrile respiratory illness beginning 7-21 days after exposure (mean incubation period = 10-16 d).
• Most patients complain of cough, chest pain, fever, and fatigue.
• A study by Johnson and colleagues (1996) reported the following symptoms:
• • Cough (73%)
  • Chest pain (44%)
  • Shortness of breath (32%)
  • Fever (76%)
  • Fatigue (39%)
  • Chills (29%)
  • Erythema nodosum (26%)

Physical

More than half of the cases are subclinical. Consider coccidioidomycosis in those individuals who are at risk for infection and who develop a constellation of nonspecific signs or unusual rashes, such as erythema nodosum, erythema multiforme, toxic erythema, or arthralgias.

Signs of synovitis, bony tenderness, osteomyelitis, meningitis, hydrocephalus, lymphadenopathy, and abdominal masses or tenderness all may indicate the presence of a coccidioidal infection.

• Skin
• • A wide variety of rashes, including maculopapular lesions, erythema multiforme, and erythema nodosum, may develop.
  • Interestingly, the development of erythema nodosum is an indicator of a good prognosis.
• Pulmonary
• • Bronchitis, bronchiolitis, reactive airways disease, pneumonia, and pleural effusions may develop.
  • Frank empyemas and bronchiole pleural fistulas are possible.
  • Pleural friction rub is possible.
• Musculoskeletal
• • Nonspecific tenderness in myalgic and arthralgic areas develops.
  • One third of patients with dissemination have musculoskeletal involvement.
  • Bone lesions are unifocal in 60% of cases, and joint lesions are unifocal in 90% of cases.
  • Multiple lesions or vertebral lesions are associated with a poor prognosis.
• Hepatomegaly
• Splenomegaly
• Tachycardia
• Central nervous system
• • Acute or chronic meningitis is possible.
  • Acute hydrocephalus may be the first sign of disseminated coccidioidomycosis.
  • Hyperreflexia is possible.
  • Headache may be noted.

Causes

C immitis is a fungus present in the soil in certain endemic regions, which, when inhaled, causes coccidioidomycosis. The infection is acquired during the dry summer months or the late fall.

• Following inhalation, an initial pyogenic infection develops, followed by a granulomatous respiratory infection. In most patients, the asymptomatic pulmonary infection resolves spontaneously. However, in approximately 5% of patients, a persistent pulmonary focus or dissemination to other parts of the body (eg, bone, joints, skin, meninges) occurs. The infection also may spread to bone marrow, myocardium, and kidneys.
• Disseminated coccidioidomycosis may occur in an otherwise healthy individual, but several risk factors have been identified, as follows:
• • Male sex
  • Ethnicity (eg, African American, Filipino)
  • Pregnancy
  • Diabetes
  • Depressed cellular immunity, as in patients with lymphoma, HIV infection, organ transplants, or patients receiving high-dose corticosteroids

DIFFERENTIALS

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Other Problems to be Considered

Other fungal infections
Lymphoma
Other causes of cough, fever, and fatigue
Old granuloma

Tuberculosis and other granulomatous infections are in the differential diagnosis of coccidioidomycosis. Thin- or thick-walled cavities in an asymptomatic patient are suggestive of coccidioidomycosis.

The differential diagnosis of coccidioidomycosis cystic lesions include the following:

Blebs
Bullae
Pneumatoceles
Congenital cystic lesions
Traumatic lesions
Pneumocystis carinii pneumonia
Hydatid disease

The differential diagnosis of coccidioidomycosis for focal or multifocal cavitary lesions include the following:

Neoplasms such as bronchogenic carcinomas and lymphomas,
infections, or abscesses
Immunologic disorders such as Wegener granulomatosis and rheumatoid nodule
Pulmonary infarct
Septic embolism
Lymphocytic interstitial pneumonia
Localized bronchiectasis

The differential diagnosis of coccidioidomycosis for diffuse involvement with cystic or cavitary lesions include the following:

Pulmonary lymphangioleiomyomatosis
Pulmonary Langerhans cell histiocytosis
Honeycomb lung associated with advanced fibrosis
Diffuse bronchiectasis
Metastatic disease

WORKUP

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Lab Studies

• Once coccidioidomycosis is considered in the differential diagnosis, performing special laboratory tests to detect the infection is necessary. The 2 tests to diagnosis a patient with pulmonary coccidioidomycosis are sputum cultures and serum coccidioidal antibodies.
• Sputum culture
• • Isolating C immitis from a clinical specimen definitely establishes a diagnosis.
  • The identification of spherules in direct examination of sputum also is diagnostic but is less sensitive than cultures.
  • The organism usually grows within 5 days on most routine microbiologic media.
  • A culture that is negative for C immitis does not rule out coccidioidomycosis.
• Coccidioidal antibodies
• • Two types of serologic tests are available to detect IgG antibodies—a precipitin test (TP) and a complement fixation (CF) test. Two immunodiffusion procedures are also available to detect these antibodies.
  • Serologic diagnosis of coccidioidomycosis is detecting IgM and IgG antibodies directed against the organism. CF was the original established method used to measure anticoccidioidal antibodies but is generally reserved for specimen other than serum, especially cerebrospinal fluid. Enzyme-linked immunoassays (EIA) are highly sensitive but false-positive results can be seen. The latex tests are easy to perform but have a higher rate of false positives than EIA.
  • An immunodiffusion TP with positive results is observed more frequently in patients with primary coccidioidomycosis, and it becomes negative several months later.
  • The immunodiffusion CF antibody appears later in the course of the illness and is measured as a quantitative titer. It may be prognostically significant.
  • A test result that is negative for antibodies does not rule out the disease.
  • The new techniques of molecular diagnosis have been applied to identifying coccidioidomycosis from tissue samples. Chemiluminescent DNA probes and PCR assays that target multicopy genes (18S rDNA) have been used. However, the value of gene amplification from the native specimens in cases of suspected coccidioidomycosis has not been established (Bialek, 2005).

Imaging Studies

• Chest radiograph findings may include pulmonary parenchymal lesions, hilar or mediastinal adenopathy, pleural disease, and pulmonary nodules.
• • Primary pulmonary coccidioidomycosis
    • Asymptomatic patients may have normal findings on chest radiograph, a small calcified granuloma, hilar lymph node calcification, minor areas of lung scaring, or pleural thickening.
    • In symptomatic patients, the pulmonary lesions can be parenchymal, pleural, or mediastinal. Well-defined patchy densities or segmental/lobar consolidation that is central rather than peripheral is observed in 75% of patients. These may resolve spontaneously within 1-2 weeks. Scattered patchy infiltrates termed persistent coccidioidal pneumonia is a less common presentation and may take as long as 1-2 months to resolve. Hilar lymphadenopathy is present in about 20% of primary infections. Pleural thickening or small pleural effusion may be observed in 20% of patients with coccidioidomycosis. Pleural effusion may occur without parenchymal or lymph node involvement.
• Persistent pulmonary coccidioidomycosis: Although primary coccidioidal infection resolves spontaneously in most cases, approximately 5% may develop a persistent pulmonary disease that consists of persistent pneumonia, a lung nodule, a cavity, bronchiectasis, empyema, or pneumothorax. These manifestations commonly occur in immunosuppressed patients or other populations at high risk of developing coccidioidomycosis. The pattern of persistent pneumonia is segmental and lobar consolidation, which may be multifocal or bilateral.
• Pulmonary nodules
  • Pulmonary nodules from coccidioidomycosis are the most common radiographic findings in persistent pulmonary infection. The nodules may be solitary or multiple. They may persist for years and resolve or may break down and spread locally or disseminate. The nodules commonly are present in the upper lobes, the size may vary from 1.5-6 cm, and calcification is less common.
  • Pulmonary nodules may be better defined on CT scan of the lungs rather than standard chest radiography.
• Cavitary pulmonary coccidioidomycosis: Cavitary pulmonary coccidioidomycosis is another radiographic presentation. The cavities develop as a result of central necrosis in the granulomas or areas of consolidation. The cavities may be thin walled or thick walled and may develop in the lung apex similar to tuberculosis. A single asymptomatic thin-walled cavity probably is more common than others. Rarely. these cavities may be colonized by aspergillus and develop mycetoma. Cavities also may break down into the pleural cavity, causing pneumothorax, empyema, and bronchopleural fistula.
• Chest radiography and chest computed tomography in coccidioidomycosis commonly reveal cysts and cavities. Differentiating cystic and cavitary lung lesions is not always an easy task. Evaluating wall thickness is quite helpful; cysts have wall thickness less than or equal to 4 mm and cavities have a wall thickness greater than 4 mm. Other features of coccidioidomycosis include a surrounding infiltrate or mass and focal or multifocal disease from diffuse involvement.
• Another pulmonary manifestation is bronchiectasis, which may occur in 1-2% of patients. Endobronchial coccidioidal infection can be present rarely, or bronchial stenosis from scarring may be evident.
• Hilar or mediastinal adenopathy: Hilar adenopathy occurs in approximately 20% of cases, with or without parenchymal infiltrates. This usually is unilateral and may persist for months. It may mimic lymphoma or bronchogenic cancer.
  • Pleural space: Pleural involvement in pulmonary coccidioidomycosis may manifest as a pleural effusion or a pneumothorax. Small effusions are observed in approximately 20% of cases of primary pulmonary coccidioidomycosis. These usually resolve spontaneously. Pneumothorax may be observed secondary to the rupture of a subpleural coccidioidal cavity into the pleural space, with the development of pyopneumothorax or bronchopleural fistula. This presentation is rare.
  • Disseminated pulmonary coccidioidomycosis: Dissemination of coccidioidomycosis may occur to other regions of the lung or to extrathoracic organs. The radiographic manifestations of dissemination include a miliary pattern resembling miliary tuberculosis because of hematogenous spread or a reticular nodular pattern resembling lymphangitic spread of cancer because of transbronchial spread. The infection also may spread to the pericardium, upper respiratory tract, and paratracheal and mediastinal lymph nodes. The hilar lymph node involvement is secondary to primary infection, whereas paratracheal or mediastinal lymphadenopathy occurs secondary to dissemination. Pericardial involvement may lead to pericardial effusion, cardiac tamponade, or constrictive pericarditis.

Procedures

• Bronchoscopy
• • Fiberoptic bronchoscopy is a valuable tool when noninvasive measures do not yield a diagnosis.
  • Bronchoscopy is very useful in patients with parenchymal infiltrates, cavitary lesions, or bronchopleural fistulas.
  • In a recent study, bronchoscopy specimens led to a diagnosis of coccidioidomycosis in 42% of individuals infected with HIV and in 31% of individuals without HIV infection (DiTomasso, 1994).
  • Bronchoscopy usually is not helpful in patients with a solitary pulmonary nodule secondary to coccidioidomycosis.
• Transthoracic needle biopsy
• • In patients with a solitary pulmonary nodule secondary to coccidioidomycosis, in whom bronchoscopy is not helpful, a percutaneous transthoracic needle biopsy may be performed.
  • The specimen should be sent for cytology to rule out a malignant lesion; fungal stains may identify spherules, and culture for C immitis should be performed.
• Obtaining lung tissue by transbronchial bronchoscopy, percutaneous aspiration, video-assisted thoracoscopic surgery, or open thoracotomy usually is unnecessary because other noninvasive investigations are diagnostic.

Histologic Findings

If the noninvasive investigations are not diagnostic, examination of lung tissue using periodic acid-Schiff stain (PAS) or methenamine silver stain allows the spherule to be visualized easily.

TREATMENT

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Medical Care

Most patients exposed to Coccidioides species acquire primary coccidioidomycosis, which is an asymptomatic infection or has self-limited symptoms. The uncommon pulmonary sequelae of coccidioidomycosis include residual pulmonary nodules, coccidioidal cavities, and diffuse reticulonodular pneumonia.

• Residual pulmonary nodules, if confirmed to be a consequence of an initial coccidioidal infection, pose no clinical consequences and require no treatment. An old chest radiograph should be retrieved to look for a previous abnormality and to assess stability. A positive serology test and an old lesion on the chest is likely to be coccidioidal in origin. Further diagnostic studies depend on suspicion of malignancy. Other factors, such as patient age, smoking history, and nodule size, should be taken into account. If suspicion of malignancy is strong, the nodule should be aspirated percutaneously or surgically resected for cytology and culture. Antifungal therapy is not recommended.
• Residual thin-walled coccidioidal cavities are commonly solitary and peripheral and in the absence of symptoms, treatment is not recommended. Follow-up chest radiographs are recommended at 6-month intervals for 2 years to establish stability.

  Treatment is recommended if symptoms such as local pleural discomfort and hemoptysis occur. Such symptoms often improve when treated with oral antifungal agents. The usual dose for ketoconazole or fluconazole is 400 mg daily; itraconazole is given 200 mg bid. The duration of treatment is typically between 6 months and 1 year, or sometimes longer. Improvement in respiratory symptoms and chest radiographs indicate a clinical response to treatment.

  If symptoms persist, an alternative approach is to surgically resect the cavity. This approach should only be used if medical therapy has failed since the surgery is technically difficult and associated with potential for residual postoperative discomfort.

  If cavities rupture, a bronchopleural fistula results and a chest radiograph shows an air-fluid level. An early diagnosis should be followed by the surgical resection. For the delayed diagnosis (1 or more wk), a conservative approach with chest tube placement and oral antifungal treatment should be instituted. However, surgery is indicated in patients who are unresponsive.

• Treatment for chronic fibrocavitary pneumonia is oral antifungal azoles for at least a year. Fluconazole 400 mg per day and itraconazole 200 mg bid appear to be equivalent in efficacy. Amphotericin B can be used for refractory infections unresponsive to oral therapy.
• In diffuse reticulonodular pneumonia, particularly in patients who are immunosuppressed, treatment with amphotericin B is the best option. After improvement is observed, treatment can be switched to an oral azole for at least 1 year. In patients who have persistent immunodeficiency state, indefinite treatment may be required.

Surgical Care

Currently, indications for surgical resection of chronic pulmonary coccidioidal infection are severe hemoptysis, bronchopleural fistula, or a failure of antifungal therapy to control symptoms.

Surgery in patients with chronic pulmonary coccidioidal infection is not uniformly curative and may result in serious complications. The potential complications of surgery include the development of postoperative bronchopleural fistula and postoperative cavity formation.

Consultations

Pulmonary and infectious disease consultations are mandatory.

MEDICATION

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Amphotericin B, fluconazole, and itraconazole are the antifungal agents currently available that have anticoccidioidal activity. Most authorities recommend prolonged oral therapy with either fluconazole (400 mg/d) or itraconazole (200 mg bid). Therapy generally is continued for at least 6 months after resolution of symptoms and maximal regression of radiographic abnormalities. Relapses have been reported in 7-39% of patients. Amphotericin B should be considered as initial therapy in patients with life-threatening disease.

Drug Category: Antifungals

Their mechanism of action may involve increasing the permeability of the cell membrane, which in turn causes intracellular components to leak.

FOLLOW-UP

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Further Inpatient Care

• Patients with coccidioidomycosis who have progressive pneumonia or disseminated disease require hospitalization, intravenous antifungal therapy, and other supportive therapy.

Further Outpatient Care

• Patients on oral antifungal therapy should be monitored closely to monitor the adverse effects of medications and to assess for disease progression or resolution.

Deterrence/Prevention

• Advise high-risk populations (individuals who are immunocompromised, pregnant woman, African Americans, Filipinos, individuals with diabetes) to avoid high-risk activities or use protective measures when exposure to C immitis is possible (eg, when working in construction and archeological digs).

Complications

• Chronic progressive coccidioidal pneumonia
• Skin manifestations (eg, erythema nodosum, erythema multiforme)
• Osteomyelitis and septic arthritis
• Acute and chronic meningitis
• Bone marrow involvement resulting in pancytopenia

Prognosis

• Most cases are self-limited and resolve within a few months.
• Prognosis is poor if the patient has weak cell-mediated immunity or high IgG levels.
• Relapse of extrapulmonary or disseminated disease is common.

Patient Education

• People living or traveling in endemic areas should be educated to minimize high-risk outdoor exposure and to seek prompt medical attention if they develop a persistent fever or respiratory symptoms.
• A travel history always should be obtained from a patient presenting with any pulmonary symptoms.
• For excellent patient education resources, visit eMedicine's Procedures Center. Also, see eMedicine's patient education article Bronchoscopy.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Failure to consider coccidioidomycosis or other fungal infections in patients with a chronic illness who have not responded to other therapies or who are residents of or travelers to endemic regions

MULTIMEDIA

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Media file 1:  A Coccidioides immitis spherule containing daughter cysts. Courtesy of Thomas Matthew.
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Media file 2:  A Coccidioides immitis spherule without the daughter cysts. Courtesy of Thomas Matthew.
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Media file 3:  Arthroconidia become airborne and infect the human host to begin the parasitic phase of its life cycle. The Arthroconidia develop into spherules containing endospores, which propagate infection in human tissues. Courtesy of Thomas Matthew.
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Media file 4:  Erythema nodosum can be observed in coccidioidomycosis, tuberculosis, histoplasmosis, drug reactions, and streptococcal infections.
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Media file 5:  A rapid growth of Coccidioides immitis on culture medium is characteristic.
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Media file 6:  Lung involvement from Coccidioides immitis. The preoperative chest radiograph had shown lung suggestive of malignancy.
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Media file 7:  A right lower lobe nodule was observed in a patient who winters in Arizona. The percutaneous needle biopsy confirmed this to be coccidioidoma.
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Media file 8:  The CT scan on a patient who winters in Arizona shows a nodular lesion on CT scan, which is enhanced on contrast infusion. Diagnosis was later confirmed to be coccidioidoma.
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Media file 9:  A case of a right lower lobe nodule was followed for 2 years after the percutaneous needle biopsy confirmed this to be coccidioidoma. No antifungal treatment was required.
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Media file 10:  A patient developed cough, low-grade fever, and dyspnea following a visit to Palm Springs, Calif. He has a history of diabetes. The immunofixation test showed immunoglobulin M (IgM) antibodies against Coccidioides immitis. On bronchoscopy, C immitis was cultured. This is chronic progressive coccidioidal pneumonia and requires antifungal therapy.
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REFERENCES

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• Ampel NM. Combating opportunistic infections: coccidioidomycosis. Expert Opin Pharmacother. Feb 2004;5(2):255-61.
• Ampel NM. Combating opportunistic infections: coccidioidomycosis. Expert Opin Pharmacother. Feb 2004;5(2):255-61.
• Batra P, Batra RS. Thoracic coccidioidomycosis. Semin Roentgenol. Jan 1996;31(1):28-44. [Medline].
• Bayer AS. Fungal pneumonias: pulmonary coccidioidal syndromes (Part 2). Miliary, nodular, and cavitary pulmonary coccidioidomycosis; chemotherapeutic and surgical considerations. Chest. Jun 1981;79(6):686-91. [Medline].
• Bayer AS. Fungal pneumonias; pulmonary coccidioidal syndromes (Part I). Primary and progressive primary coccidioidal pneumonias -- diagnostic, therapeutic, and prognostic considerations. Chest. May 1981;79(5):575-83. [Medline].
• Bialek R, González GM, Begerow D. Coccidioidomycosis and blastomycosis: advances in molecular diagnosis. FEMS Immunol Med Microbiol. Sep 1 2005;45(3):355-60. [Medline].
• Castellino RA, Blank N. Pulmonary coccidioidomycosis. The wide spectrum of roentgenographic manifestations. Calif Med. Jul 1968;109(1):41-9. [Medline].
• Catanzaro A, Galgiani JN, Levine BE. Fluconazole in the treatment of chronic pulmonary and nonmeningeal disseminated coccidioidomycosis. NIAID Mycoses Study Group. Am J Med. Mar 1995;98(3):249-56. [Medline].
• Como JA, Dismukes WE. Oral azole drugs as systemic antifungal therapy. N Engl J Med. Jan 27 1994;330(4):263-72. [Medline].
• DiTomasso JP, Ampel NM, Sobonya RE. Bronchoscopic diagnosis of pulmonary coccidioidomycosis. Comparison of cytology, culture, and transbronchial biopsy. Diagn Microbiol Infect Dis. Feb 1994;18(2):83-7. [Medline].
• Galgiani JN. Coccidioidomycosis. West J Med. Aug 1993;159(2):153-71. [Medline].
• Hyde L. Coccidioidal pulmonary cavitation. Dis Chest. Oct 1968;54:Suppl 1:273-7. [Medline].
• Johnson RH, Caldwell JW, Welch G. The great Coccidiodomycosis epidemic: Clinical Features. Coccidiodomycosis. Einstein HE, Catanzaro A. Bethesda, MD. 1996;Proceedings of Fifth International Conference:77-87.
• Kim KI, Leung AN, Flint JD. Chronic pulmonary coccidioidomycosis: computed tomographic and pathologic findings in 18 patients. Can Assoc Radiol J. Dec 1998;49(6):401-7. [Medline].
• Martins TB, Jaskowski TD, Mouritsen CL. Comparison of commercially available enzyme immunoassay with traditional serological tests for detection of antibodies to Coccidioides immitis. J Clin Microbiol. Apr 1995;33(4):940-3. [Medline].
• Marty F, Mylonakis E. Antifungal use in HIV infection. Expert Opin Pharmacother. Feb 2002;3(2):91-102. [Medline].
• McGahan JP, Graves DS, Palmer PE. Classic and contemporary imaging of coccidioidomycosis. AJR Am J Roentgenol. Feb 1981;136(2):393-404. [Medline].
• Pappagianis D, Zimmer BL. Serology of coccidioidomycosis. Clin Microbiol Rev. Jul 1990;3(3):247-68. [Medline].
• Read CT. Coin lesion, pulmonary: in the Southwest. (Solitary pulmonary nodules). Ariz Med. Oct 1972;29(10):775-81. [Medline].
• Ryu JH, Swensen SJ. Cystic and cavitary lung diseases: focal and diffuse. Mayo Clin Proc. Jun 2003;78(6):744-52. [Medline].
• Sarosi GA, Parker JD, Doto IL. Chronic pulmonary coccidioidomycosis. N Engl J Med. Aug 13 1970;283(7):325-9. [Medline].
• Tucker RM, Denning DW, Arathoon EG. Itraconazole therapy for nonmeningeal coccidioidomycosis: clinical and laboratory observations. J Am Acad Dermatol. Sep 1990;23(3 Pt 2):593-601. [Medline].
• Yamada H, Kotaki H, Takahashi T. Recommendations for the treatment of fungal pneumonias. Expert Opin Pharmacother. Aug 2003;4(8):1241-58. [Medline].

Article Last Updated: Jun 22, 2006