What is the pathophysiology of coccidioidomycosis?

Updated: Aug 27, 2019
  • Author: Duane R Hospenthal, MD, PhD, FACP, FIDSA, FASTMH; Chief Editor: Michael Stuart Bronze, MD  more...
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The vast majority of coccidioidal infections result from airborne transmission. Pulmonary infection can result from inhalation of a single spore in humans, but high inoculum exposures are more likely to result in symptomatic disease. Inhaled C immitis or C posadasii arthroconidia (ie, spores; see the image below) are deposited into the terminal bronchiole.

Arthroconidia become airborne and infect the human 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.

In the bronchioles, the arthroconidia enlarge to form spherules, which are round double-walled structures measuring approximately 20-100 μm in diameter. The spherules undergo internal division within 48-72 hours and become filled with hundreds to thousands of offspring (ie, endospores). Rupture of the spherules leads to the release of endospores, which mature to form more spherules. [4]  

As an arthroconidium transforms into a spherule, the resulting inflammation results in a local pulmonary lesion. Extracts of C immitis organisms react with complement, leading to the release of mediators of chemotaxis for neutrophils.

Some of the endospores are engulfed by macrophages, initiating the acute inflammation phase. If the infection is not cleared during this process, a new set of lymphocytes and histiocytes descend on the infection site, leading to granuloma formation with the presence of giant cells. This is the chronic inflammation phase. People with severe disease may have both acute and chronic forms of inflammation.

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