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Pathogen Page
Coccidioides spp.
I. General Information
1. NCBI Taxonomy ID:
5500
2. Disease:
Coccidioidomycosis (California disease, Desert rheumatism, San Joaquin valley fever, and Valley fev
3. Introduction
Coccidioidomycosis is a human respiratory disease caused by inhalation of airborne spores produced by Coccidioides spp (Coccidioides immitis and C. posadasii). The pathogen is an anamorphic (asexual) ascomycetous fungus which resides in alkaline desert and semidesert soil in regions of the southwestern United States. The major areas where this disease is endemic include some of the most rapidly growing communities of Arizona and southern California. People who are frequently exposed to dust from the soil in these regions have a high chance of infection with Coccidioides. Recurrent epidemics of coccidioidomycosis appear to be correlated with climatic conditions. Periods of rain in the spring enhance growth of the soilborne saprobic phase of Coccidioides, which results in “blooms” of spores that are air dispersed during the late fall and winter seasons. Risk factors known to contribute to symptomatic coccidioidal infection include pregnancy (third trimester), immunosuppression, age (>65 years), and racial or geographic origin. Antifungal drug therapy for coccidioidomycosis (e.g., amphotericin B, fluconazole, or intraconazole) is typically continued for many months to years. Persons who contract coccidioidal meningitis require lifelong therapy. Coccidioides infection can be life threatening and, at the very least, is responsible for high medical costs incurred by patients as a result of hospitalization, clinic visits, lost wages, and long-term drug therapy (Tarcha et al., 2006).
4. Microbial Pathogenesis
The tiny spores (2 × 4 μm) convert into multinucleate round cells (spherules) within the lungs of the host and undergo isotropic growth to produce large parasitic cells (60 to > 100 μm in diameter). The latter undergo an elaborate process of wall growth and cytoplasmic compartmentalization to form and release a multitude of endospores (4–10 μm in diameter). Each endospore grows and differentiates into a second-generation spherule, which is again able to yield an average of 200 to 300 endospores. Mature spherules most likely escape phagocytosis simply because they are too large to be ingested by neutrophils, macrophages, and dendritic cells (Hung et al., 2007).
5. Host Ranges and Animal Models
Coccidiomycosis is mainly a disease of immunocompromised in humans, but mice and monkeys have been used as animal models of disease (Ivey et al., 2003).
6. Host Protective Immunity
Both clinical and experimental evidence have demonstrated that T-cell immunity is pivotal for defense against this respiratory disease. The ability of the host to elicit a strong delayed-type hypersensitivity response to the pathogen is essential (Tarcha et al., 2006).
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