eMedicine Specialties > Pulmonology > Infectious Lung Diseases
Coccidioidomycosis
Updated: Sep 17, 2009
Introduction
Background
Coccidioidomycosis is an infection caused by the soil-inhabiting fungi Coccidioides immitis and Coccidioides posadasii. These fungi are endemic to certain regions of North and South America. The endemic areas in the United States include Arizona, south central California (San Joaquin Valley), Nevada, New Mexico, and the western half of Texas. Other endemic areas are the regions of Mexico that border the western United States. The fungi also are 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.
A Coccidioides immitis spherule containing daughter cysts. Courtesy of Thomas Matthew.
Historical perspectives
Wernicke 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 a few cases in which they identified the infecting agent as a protozoanlike organism and named it Coccidioides immitis. Ophuls further described the fungal life cycle and pathology of C immitis in 1905. The case of Harold Chope, a Stanford University medical student, is instructive. He inhaled a culture of Coccidioides in 1929 and went on to develop erythema nodosum and respiratory symptoms. The epidemiology of coccidioidomycosis was studied by Charles E. Smith in the Joaquin Valley after he and his colleagues developed coccidioidin skin test and serologic testing for coccidioidomycosis.
Two species of Coccidioides have been isolated: C immitis, geographically located and limited to the San Joaquin Valley, and C posadasii, located in all other endemic regions. Few clinical and immunologic differences are noted between the 2 species of Coccidioides. For all intents and purposes, all subsequent references to C immitis also apply to C posadasii.
The first effective therapy for coccidioidomycosis, intravenous amphotericin B, was first used in 1957. Since the 1980s, various oral antifungal agents, including ketoconazole, itraconazole, and fluconazole, have led to further advances in the treatment of coccidioidomycosis.
Life cycle of C immitis (and C posadasii)
C immitis and C posadasii are fungi that thrive in soil and exist in either of 2 phases—the mycelial arthrospore phase in the soil or the spherule endospore phase in infected tissues. These are hardy endemic fungi that can exist in the dry desert for months to years. During the rainy season, the mycelia grow rapidly, but they are also the least infectious. As the soil becomes dryer, the branching, septated hyphae develop into arthrospores, which readily disarticulate as single arthroconidia and become airborne when disturbed by wind or soil excavation. An arthrospore measures 3-5 µm, and it remains viable for long periods. Of note, the fungus does not grow at elevations higher than 3700 feet.
Once inhaled, an arthrospore develops into a thick-walled spherule filled with endospores. The spherules eventually open and release the hundreds of endospores. Each endospore leads to the development of a new spherule and further proliferation of the infection. These aspects of the life cycle provide further insight in the acquisition of infection and disease caused by Coccidioides.
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.
Acquisition of infection
Coccidioidomycosis is not transmitted from person to person. Infection is usually confined to subjects in the endemic regions of North and South America as defined in Background, with most cases seen in the southwestern United States. A travel history is important because cases can be imported. The incidence of infection is highest in the dry summer months, extending into the late fall. The infection rate has been noted to increase following periods of increased rainfall (winter or summer), corresponding to increased mycelial growth.
Dust exposure is integral in acquiring infection. This risk is highlighted by circumstances in which more exposure to soil and dust occurs, such as with new construction, archeological excavation, and, most notably, following the Northridge, California earthquake of 1994. An increased incidence in infections has been noted over the past decade, attributable to a variety of factors. In addition to new construction, the population in the southwestern United States has also increased, increasing the number of susceptible hosts. Additionally, an increased awareness of the infection has also led to increased diagnosis. Noted that laboratory personnel can become infected when opening and inhaling microbiologic cultures growing Coccidioides; therefore, proper precautions are necessary whenever Coccidioides is suspected.
Pathophysiology
Inhalation of arthrospores is the portal of entry for the vast majority of coccidioidal infections. Once in the respiratory tract, spherules proliferate, and host cell–mediated immunity is crucial for controlling the infection. This is lymphocyte mediated (CD4+ CD8+ and CD20+), and the development of cell-mediated immunity, as measured by skin test reactivity to coccidioidin, can predict control of the infection. The lack of skin test reactivity has been associated with an increased risk of disseminated disease. Defects in antigen-presenting dendritic cells has been suggested as a possible explanation for failure of host containment.
The immune response to coccidioidal infection is used in the diagnosis and assessment of the severity of infection. Immunoglobin M (IgM) can be detected in 50% of primary coccidioidal infections within the first week and in 90% of infections by the third week. Immunoglobulin G (IgG) is used to gauge the intensity of the immune response and provides information on the host control of the infection and risk for disseminated (extrathoracic) disease. IgG may not be detected for several months, but it can persist for years. Note that most (60%) of coccidioidal infections are subclinical and never come to medical attention.
Clinical syndromes
Because the respiratory tract is the portal of entry, the manifestations of the initial infection are often detected after plain chest radiography. Findings include (1) unilateral infiltrate, (2) consolidation, (3) hilar adenopathy, (4) pleural effusion, (5) nodules, and (6) thin walled cavities. Depending on the host's immune response, infection with C immitis may evolve into one of the clinical syndromes described below.
Primary pulmonary coccidioidomycosis/acute pneumonia
Up to 60% of patients with primary pulmonary coccidioidomycosis are asymptomatic or have subclinical disease that never comes to medical attention, and the infection resolves spontaneously. Those who become symptomatic manifest a respiratory syndrome approximately 1-3 weeks following inhalation of arthrospores. The symptoms are indistinguishable from other respiratory illnesses, with fever, sore throat, cough, headache, fatigue, and pleuritic chest pain. The symptoms are often attributed to a virus or community-acquired pneumonia. Resolution occurs over several weeks, and 95% or more of patients recover without any further sequelae.
If chest radiography is performed, common findings include segmental or lobar infiltrates, consolidation, and hilar adenopathy. In endemic regions, infiltrates and adenopathy are highly suggestive of coccidioidal pneumonia. Pleural effusions may be seen in up to 15% of patients and are exudative; pleural fluid eosinophilia is a common finding. Approximately 20% of these effusions may eventually be determined to be an empyema. In addition, cutaneous manifestations such as erythema multiforme or erythema nodosum are associated with the acute infection and predict a favorable outcome. Also see Coccidioidomycosis.
More extensive pneumonia, respiratory failure, and the acute respiratory distress syndrome can also be seen, often associated with inhalation of a large number of arthrospores or related to an underlying immunocompromised state (eg, HIV infection, immunosuppressant therapy, immune-modulating therapy).
In approximately 5% of patients, a pulmonary focus of coccidioidomycosis may persist and manifest as a nodule, cavity, or chronic progressive pneumonia. Coccidioides can also disseminate to involve extrathoracic sites, including bone, joints, skin, and meninges.
Chronic progressive coccidioidal pneumonia
Patients with symptoms that persist beyond 3 months define patients with chronic progressive coccidioidal pneumonia. Symptoms may include a low-grade fever, chronic cough, chest pain, hemoptysis, and weight loss. Cavitary lesions with associated infiltrates or fibrosis are typical findings and may resemble pulmonary tuberculosis. However, cocci serologies are uniformly positive. Persistent disease warrants extended antifungal therapy, ranging from years to life long.
Pulmonary nodules
In approximately 5-7% of patients with coccidioidal pneumonia, the infection evolves to form a sharply circumscribed, usually noncalcified, pulmonary nodule. This is often the initial finding on the chest radiograph, and nodules usually measure 1-2 cm. Serologic testing is positive in 30-60% of nodules. The nodules may cavitate or may persist for years. Malignancy is a major concern while evaluating these nodules. Fluorodeoxyglucose positron-emission tomography (FDG-PET) scanning cannot be used to distinguish between malignant and coccidioidomas in an endemic area. If a noninvasive diagnosis cannot be made, surgical resection may be required. In a review of 200 solitary pulmonary nodules surgically resected from patients within endemic areas, 33.5% were found to be malignant.1
Pulmonary cavities
Another 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, but thick-walled cavities have also been reported. Coccidioidal cavities are usually asymptomatic, but they can be subject to hemorrhage, rupture (pneumothorax), and secondary infection. Cavities smaller than 2.5 cm typically resolve spontaneously over 1-2 years. However, cavities larger than 5 cm often persist and can be associated with hemoptysis, with the development of an aspergilloma or mycetoma in the cavity. In the past, these cavities often were surgically resected, but this has diminished since the advent of effective antifungal therapy.
Disseminated coccidioidomycosis (nonmeningeal and meningeal)
Disseminated coccidioidomycosis usually occurs within weeks to months of the primary pneumonia. Some patients may have no radiographic evidence of previous pulmonary disease, and no history of a preceding respiratory illness may be present. Certain ethnic groups, such as African Americans and Filipinos, are more likely to develop disseminated disease. Women in their third trimester of pregnancy and infants younger than 1 year are also at risk for dissemination. Any condition that compromises cellular immunity also increases the risk of dissemination; this includes patients with HIV infection, organ transplants, or hematologic malignancies and patients on immunosuppressant agents such as high-dose corticosteroids or tumor necrosis factor inhibitors.
Disseminated coccidioidomycosis usually results from hematogenous spread and can involve nearly any body site. Common meningeal sites include skin, soft tissue, bones, and joints. Other reported sites of involvement include the upper airway, myocardium, pericardium, liver, spleen, kidneys, prostate, male and female genital tracts, and lymph nodes. Dissemination is typically associated with complement fixation titers greater than or equal to 1:16. Often, combined medical and surgical therapy is required for disease control.
Meningeal involvement is a particularly severe form of disseminated coccidioidomycosis. Prior to effective therapy, meningeal coccidioidomycosis was uniformly fatal and, even with therapy, is associated with significant morbidity. Headache is the most common presenting symptom, and other neurologic symptoms include alterations in sensorium, cranial nerve defects, and obstructing hydrocephalus. Diagnosis requires analysis of cerebrospinal fluid, and typical findings include positive cerebrospinal fluid serology, elevated white blood cell count, elevated total protein values, and decreased glucose levels. Meningeal enhancement can be seen on computed tomography (CT) or magnetic resonance imaging (MRI) scans. Patients usually require life-long antifungal therapy.
Frequency
United States
Coccidioidomycosis is endemic in the western hemisphere from California to Argentina. Although residents of endemic areas are at highest risk for acquiring infection, coccidioidomycosis is being recognized increasingly outside of these areas, as travelers pass through endemic areas.
The exact incidence of coccidioidal infections can only be inferred because approximately 60% of those infected are asymptomatic, have subclinical disease, and never come to medical attention. An estimated 150,000 infections occur annually in the United States. Based on skin test data, 80% or more of residents living in endemic areas for 5 years or longer will have a positive coccidioidin skin test result. The prevalence of positive skin test results ranges from 50-70% in the southwestern United States and increases with age.
Arizona, where coccidioidomycosis is a reportable condition, has the greatest number of cases. This likely only represents symptomatic cases. More than 5,000 cases are reported annually in Arizona, and the state has noted a steady increase in cases, with 7 cases per 100,000 persons in 1990, increasing to 15 cases per 100,000 persons in 1995, and an estimated 75 cases per 100,000 persons in 2007. The incidence in Kern County, California from 2000-2007 was 150 cases per 100,000 persons.
International
The incidence of coccidioidal infections in other endemic areas of North and South America is unknown. The infection risk remains highest in the endemic areas of northern Mexico and Central and South America. However, the incidence over time may not mirror the increase seen in the southwestern United States, because the latter increase has been driven by construction and immigration of uninfected individuals into the area.
Mortality/Morbidity
Infection is related to exposure and inhalation of airborne arthrospores in endemic areas. Proximity to dust and soil increases the risk of infection (eg, construction workers, farm workers, archeologists), which can be further exacerbated by an underlying compromised immune system. Morbidity is substantial in coccidioidomycosis, but mortality is very low.
- Initial infection virtually always involves the lungs (see Pathophysiology).
- Most patients are asymptomatic or have subclinical disease.
- Approximately 40% of patients develop symptomatic disease, usually involving the respiratory tract.
- Approximately a quarter of patients develop a constellation of symptoms referred to as Valley fever, characterized by erythema nodosum or erythema multiforme, febrile arthralgias, and chest pain, which is often pleuritic.
- The pulmonary infection resolves in greater than 90-95% of patients, without sequelae.
- Approximately 5% of patients develop more severe pulmonary disease (cavities or chronic progressive coccidioidal pneumonia). Respiratory symptoms are related to the severity of lung involvement and destruction, and they ranges from cough to respiratory failure and acute respiratory distress syndrome.
- Less than 1% of all patients (symptomatic and asymptomatic) develop disseminated disease, but the number with symptomatic disease who disseminate may be in the 5% range.
- The most common sites of dissemination are the skin, musculoskeletal system, and meninges. Bone involvement occurs in approximately 40% of patients with disseminated disease, and the most commonly involved joints are the knees, wrists, and ankles.
- Other areas of involvement include the genitourinary tract and peritoneum (peritonitis). Ocular coccidioidomycosis is rare.
- Mortality from coccidioidomycosis is rare, occurring in approximately 0.07% of all infections.
Race
Differently ethnic groups are affected differently with respect to the effects of coccidioidal infection. However, the influence of environmental factors has clouded this association. Certain ethnic groups appear to have a higher risk for developing severe infections, especially dissemination and subsequent mortality.
- 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 with 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.
Sex
- More cases may occur in men, owing to environmental exposures.
- Women in the third trimester of pregnancy are at an increased risk for disseminated disease.
Age
- Patients younger than 1 year are at an increased risk for disseminated disease.
Clinical
History
Most coccidioidal infections are asymptomatic. Approximately 30-40% of individuals develop clinical symptoms after infection. The disease spectrum ranges from a mild influenzalike illness, to subacute pneumonia, to, rarely, respiratory failure.
- Most symptomatic patients have a febrile respiratory illness beginning 7-21 days after exposure (mean incubation period = 10-16 d).
- Most patients report cough, chest pain, fever, and fatigue.
- A study by Johnson and colleagues reported the following symptoms2 :
- Cough (73%)
- Chest pain (44%)
- Shortness of breath (32%)
- Fever (76%)
- Fatigue (39%)
- Chills (29%)
- Erythema nodosum (26%)
- Other symptoms include the following:
- Night sweats
- Weight loss
- Urticaria
- Arthralgias (“desert rheumatism”)
Physical
No physical findings are pathognomonic for coccidioidal infection. However, in endemic areas, coccidioidal infection should be a strong consideration for patients who present with an influenzal illness and a lower extremity rash.
Primary coccidioidal infection
- Skin
- Maculopapular lesions
- Erythema multiforme
- Erythema nodosum (good prognostic indicator for recovery from coccidioidomycosis)
- Toxic erythema
Erythema nodosum can be observed in coccidioidomycosis, tuberculosis, histoplasmosis, drug reactions, and streptococcal infections.
- Musculoskeletal - Nonspecific arthralgias and myalgias (often referred to as "desert rheumatism")
- Pulmonary (most common physical findings)
- Rhonchi and wheezing with bronchitis, bronchiolitis, reactive airways disease
- Crackles, consolidative findings, decreased breath sounds and pleural friction rub associated with pneumonia and pleural effusion/empyema
- Decreased breath sounds associated with a bronchopleural fistulas and pneumothorax
- Skin
- Verrucous granulomas (face), erythematous plaques and nodules.
- Biopsy of the lesions demonstrating spherules
- Musculoskeletal (bones, joints)
- One third of patients with dissemination
- Unifocal bone lesions (lytic or sclerotic, 60% of cases) and unifocal joint lesions (90% of cases, monoarticular arthritis)
- Pain and tenderness with vertebral osteomyelitis or paraspinous abscesses
- Rarely, infected tendon sheaths demonstrating a villonodular synovitis
- Hepatomegaly
- Splenomegaly
- Central nervous system
- Headache, in acute or chronic meningitis
- Acute hydrocephalus - May be the first sign of disseminated coccidioidomycosis
- Hyperreflexia (possibly)
- Cranial nerve abnormalities
Causes
See Pathophysiology. Coccidioidomycosis is caused by inhalation of the fungus C immitis or C posadasii. Infection occurs in endemic areas and is most commonly acquired in the summer or the late fall. Most infections are asymptomatic and self-contained.
Disseminated coccidioidomycosis may occur in an otherwise healthy individual, but it more often occurs in patients with the following underlying risk factors:
- HIV disease/AIDS
- Thymectomy
- Lymphoma
- Taking immunosuppressive medications (transplant patients) and first year of organ transplant
- Chemotherapy for solid tumors
- Corticosteroids (>20 mg prednisone)
- Antitumor necrosis factor therapy
- Diabetes mellitus
- Pregnancy (highest in third trimester)
- Preexisting cardiopulmonary conditions
More on Coccidioidomycosis |
 Overview: Coccidioidomycosis |
| Differential Diagnoses & Workup: Coccidioidomycosis |
| Treatment & Medication: Coccidioidomycosis |
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| Multimedia: Coccidioidomycosis |
| References |
| Next Page » |
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Further Reading
Keywords
coccidioidomycosis, coccidioides infection, coccidioidal infection, cocci infection, coccidioidal pneumonia, coccidioidal lung infection, San Joaquin Valley fever, valley fever,
