John N Galgiani
Director, Valley Fever Center for Excellence
Professor, BIO5 Institute
Professor, Medicine
Primary Department
Department Affiliations
(520) 626-4968
Work Summary
Valley Fever (coccidioidomycosis) occurs more in Arizona than anywhere else. My research and others at the Valley Fever Center for Excellence involve understanding how disease is caused by infection, how the immune system stops or prevents illness, and how we can better diagnose, treat, or prevent this public health problem.
Research Interest
Dr. Galgiani has focused his career on Arizona’s special problems with Valley Fever. His work has included studies of the impact of Valley Fever on the general population and on special groups such as organ transplant recipients and patients with AIDS. For 19 years, as part of the NIH-sponsored Mycoses Study Group, Dr. Galgiani has been the project director of a coccidioidomycosis clinical trials group. Through collaboration, this group has evaluated new therapies for Valley Fever more rapidly and with greater clarity than might otherwise have been possible by investigators working in isolation. Dr. Galgiani has also been involved with efforts to prevent Valley Fever through vaccination. His group discovered and patented a recombinant antigen which is the basis for a vaccine candidate suitable for further development and clinical trials. Most recently, he has become the project leader for developing a new drug, nikkomycin Z, for treating Valley Fever. With recent NIH and FDA grant awards, clinical trials with this drug were resumed in 2007. Dr. Galgiani is also Chief Medical Officer of Valley Fever Solutions, Inc, a start-up company founded to assist in the drug’s development. In 1996, the Arizona Board of Regents accepted Dr. Galgiani’s proposal to establish the Valley Fever Center for Excellence for the Arizona universities. Based at the University of Arizona, the Center is pledged to spread information about Valley Fever, help patients with the severest complications of this disease, and to encourage research into the biology and diseases of its etiologic agent. The Center maintains a website (www.VFCE.Arizona.edu) and answers inquiries from health care professionals located in Arizona, other parts of the United States, and even from other countries. The Valley Fever Corridor Project, begun in 2009, intends to facilitate communication among Arizona clinicians to also improve patient care. In 2011, The Valley Fever Center in Phoenix was announced as a partnership between St. Joseph’s Hospital and the UA College of Medicine in Phoenix. It began operation in June, 2012. Research is increasing into the environmental biology of the fungus within its desert soil habitat as well as how the fungus caused disease and the body’s immunity controls it. Since Arizona has the only medical schools situated directly within the endemic region for Valley Fever, it is quite appropriate that Arizona lead in solving this problem. As Director of the Center, Dr. Galgiani is working for its full implementation as a means of ensuring an institutional commitment to accomplish this goal. Keywords: Coccidioidomycosis, Valley Fever, antifungal drugs, vaccines, serologic tests,

Publications

Ganley, K. J., Bosch, P. R., Blair, J. E., Rischard, F., & Galgiani, J. N. (2017). Oxygen Consumption Deficits in Patients With Residual Fatigue After Primary Coccidioidomycosis. Open Forum Infectious Diseases, 4(3). doi:https://doi.org/10.1093/ofid/ofx136
Vinh, D. C., Schwartz, B., Hsu, A. P., Miranda, D. J., Valdez, P. A., Fink, D., Lau, K. P., Long-Priel, D., Kuhns, D. B., Uzel, G., Pittaluga, S., Hoover, S., Galgiani, J. N., & Holland, S. M. (2011). Interleukin-12 receptor β1 deficiency predisposing to disseminated Coccidioidomycosis. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 52(4), e99-e102.
Catanzaro, A., Cloud, G. A., Stevens, D. A., Levine, B. E., Williams, P. L., Johnson, R. H., Rendon, A., Mirels, L. F., Lutz, J. E., Holloway, M., & Galgiani, J. N. (2007). Safety, tolerance, and efficacy of posaconazole therapy in patients with nonmeningeal disseminated or chronic pulmonary coccidioidomycosis. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 45(5), 562-8.

Coccidioidomycosis can be difficult to treat with available therapies, particularly in patients with progressive or disseminated disease. Posaconazole is a new azole antifungal with potent activity against Coccidioides species, the causative agent of coccidioidomycosis.

Ampel, N. M., Giblin, A., Mourani, J. P., & Galgiani, J. N. (2009). Factors and outcomes associated with the decision to treat primary pulmonary coccidioidomycosis. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 48(2), 172-8.

Studies that assess the value of initiating oral antifungal therapy to treat primary pulmonary coccidioidomycosis have not been published previously.

Shubitz, L. F., Dial, S. M., & Galgiani, J. N. (2011). T-lymphocyte predominance in lesions of canine coccidioidomycosis. Veterinary pathology, 48(5), 1008-11.

Coccidioidomycosis is a systemic fungal infection endemic to the southwestern United States. Although cell-mediated immunity is considered critical in control of the infection, little is known of the cellular population in naturally occurring lesions. To characterize the lymphocytic infiltration, archived formalin-fixed, paraffin-embedded tissues (subcutis, pericardium/heart, lung, bone, and synovium) from 18 dogs with coccidioidomycosis were studied with immunohistochemistry for CD3 and CD79a. In nearly all lesions, T lymphocytes were more numerous than B lymphocytes and were distributed throughout the lesion with concentration in the periphery of granulomas, whereas B lymphocytes were mostly confined to the periphery of granulomas. The predominance of T lymphocytes in lesions of canine coccidioidomycosis was independent of the tissue evaluated, the number of intralesional organisms, and the nature or severity of the inflammatory response.