Etiology
Coccidioidomycosis is caused by two nearly identical species, Coccidioides immitis and C posadasii.[14] Previously these two agents have been called the Californian and non-Californian species, respectively.[15] In the alkaline soils of the endemic area, the fungus grows as a saprophobic mold, the hyphae of which form arthroconidia (spores). Natural forces such as wind or earthquakes, or disruption of the soil by construction or various activities cause disruption of the hyphae and dispersion of the arthroconidia.[16][17]
Most cases are spread via the respiratory route. The fungus is thermally dimorphic; therefore, once the airborne arthroconidia are inhaled, they settle in lung tissue where they undergo great morphologic change and develop into spherules. Spherules undergo repeated internal divisions until they are filled with hundreds of endospores. When the spherule ruptures‚ endospores are released, and each is then capable of further spherule formation.[16]
Pathophysiology
Once inhaled, the arthrospore traverses the respiratory passages to the lung, where it begins to transform into a spherule. The spherule enlarges, septates, and forms endospores, which are subsequently released. The growth and rupture of the spherule incites an acute inflammatory response, which recruits neutrophils and eosinophils. Later, with further control of the infection, a chronic inflammatory response is elicited, with granuloma formation consisting of lymphocytes, histiocytes, and multinucleated giant cells surrounding unruptured spherules. Pulmonary macrophages, having ingested spherules in the acute infection, may move to hilar or regional lymph nodes. The incubation period is 7 to 21 days. About 40% of people develop symptomatic infection.
Extrathoracic spread occurs in approximately 0.5% of people; it is not fully understood how this happens, but it may be accomplished through a transient fungemia.[2] Meningitis is the most serious form of extrathoracic coccidioidomycosis. Dissemination to bones, joints, and skin also can occur.[8] Host cellular immune mechanisms serve to slow the progress of infection, but control of coccidioidomycosis is critically dependent on intact T-lymphocyte function.[2] People who lack intact T-lymphocyte function, such as those with advanced HIV infection, recipients of organ transplants, or those receiving immunosuppressants such as corticosteroids, are more susceptible to severe and disseminated infection.
The humoral immune system is active in producing antibodies to a variety of coccidioidal antigens, and some of these antibody responses form the basis of diagnostic serology. However, none of the humoral responses has a large role in the control of infection.[2]
Classification
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