What is Coccidioidomycosis?

Coccidioidomycosis, also known as Valley fever, cocci, or desert rheumatism, is a fungal disease caused by Coccidioides immitis or Coccidioides posadasii. It is endemic in certain parts of the United States and northern Mexico. The fungus grows in the soil and becomes airborne during rainy periods, leading to infections when the spores are inhaled. Coccidioidomycosis is a common cause of pneumonia in the affected areas. The disease is not contagious but can recur or become chronic in some cases.

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Etiology of Coccidioidomycosis

Coccidioides is a genus of dimorphic fungi that can exist as mycelia or spherules. The sexual form of this fungus has not been discovered yet. Molecular analysis indicates its relationship to ascomycetes like Histoplasma capsulated or Blastomyces dermatitidis. Within the genus, there are two recognized species: C. immitis, primarily found in California, and C. posadasii, found in other parts of the US and the world. Clinically, the manifestations and susceptibilities of these species are indistinguishable. Identifying the species requires molecular methods as they are phenotypically identical. Therefore, routine identification to the species level is not done in clinical microbiology laboratories.

Coccidioides thrive in arid, high-salt desert environments and grows as mycelia or filaments in soil and agar. The infectious particles, called arthroconidia, are inhaled and transformed into spherules filled with endospores within the lungs and tissues. The bursting of spherules releases endospores, leading to the spread of infection.

Figure 1. Life cycle of Coccidioides immitis/posadasii.
(Source: DiCaudo, D. J., 2006)

Pathophysiology of Coccidioidomycosis

Coccidioides species exist as mycelia in the environment and laboratory, growing through apical extension and forming septae. After a week, mycelial cells undergo autolysis, resulting in the formation of barrel-shaped arthroconidia. These arthroconidia become airborne and can reach the terminal bronchioles upon inhalation. Once in the lungs, arthroconidia transform into spherical spherules by shedding their outer layer.

Spherules grow to a diameter of 75 microns and internally divide into compartments containing endospores. The rupture of the spherules releases endospores into the alveolar sacs, triggering acute inflammation. Endospores can multiply within tissues and promote mycelial growth when released into the environment. In some susceptible individuals, spherules may leave the lungs and cause extrapulmonary infections, often involving mediastinal lymphadenopathy.

Histopathological examination shows a mix of acute and chronic inflammation in infected tissues. Neutrophils and eosinophils are attracted to the site when spherules rupture. Chronic granulomatous infection is associated with mature unruptured spherules, indicating controlled infection. T-lymphocytes, particularly T-helper 2 cells, play a crucial role in defense against Coccidioides species. Dysfunction or deficiency of T-helper 2 cells is observed in patients with extrapulmonary or disseminated disease. Innate cellular immunity is effective in early infection, but as spherules grow larger, innate immune cells such as neutrophils, monocytes, and natural killer cells become less effective.

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