It resides in the soil in certain parts of the Southwestern United States, northern Mexico, and some other areas in the Americas, but its evolution was connected to its animal hosts.

[4] The two species can be distinguished by DNA polymorphisms and different rates of growth in the presence of high salt concentrations: C. posadasii grows more slowly.

Also in 1905 Samuel Darling studied a case and, referring to the misnamed organism a protozoan, named it Histoplasma capsulatum, meaning three major endemic fungi in the United States were all initially misidentified as protozoa.

Studies by Cooke on the immunology of the disease, and in 1927 a filtrate of culture specimens, later named coccidioidin, began to be used in skin testing to delineate the epidemiology of infection.

The investigations revealed, among other things, that a majority of the cases described a history of dust exposure, that coccidioidomycosis was common in the area, and that racial differences determined the host's response to the fungus.

Research by Smith resulted in more than a few discoveries that included serologic testing, that chlamydospores of the fungus c. immitis could be wind-blown dispersing the spores when the hot weather converted the soil to dust, scientific results of military personnel testing in the southern San Joaquin Valley before and during WWII, as well as people of Japanese descent (many US citizens) interned in camps, prisoners of war, and agricultural workers.

Smith's research added to the fundamental discoveries of microbiology, epidemiology, clinical findings, and diagnosis that had emerged since Posadas' initial case report in 1892.