John N Galgiani
Director, Valley Fever Center for Excellence
Member of the Graduate Faculty
Professor, BIO5 Institute
Professor, Immunobiology
Professor, Internal Medicine
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

Fridkin, S. K., Pear, S. M., Williamson, T. H., Galgiani, J. N., & Jarvis, W. R. (1996). The role of understaffing in central venous catheter-associated bloodstream infections. INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY, 17(3), 150-158.
Peng, T., Shubitz, L., Simons, J., Perrill, R., Orsborn, K. I., & Galgiani, J. N. (2002). Localization within a proline-rich antigen (Ag2/PRA) of protective antigenicity against infection with Coccidioides immitis in mice. Infection and immunity, 70(7), 3330-5.

Subunits of a proline-rich coccidioidal antigen (Ag2/PRA) of Coccidioides immitis were analyzed by comparison as vaccines in mice. The optimal dose of plasmid vaccine encoding full-length Ag2/PRA was determined to be between 10 and 100 microg. Mice vaccinated with plasmids encoding amino acids (aa) 1 to 106 were as protective as full-length Ag2/PRA (aa 1 to 194). The subunit from aa 27 to 106 was significantly but less protective. Plasmids encoding aa 90 to 151 or aa 90 to 194 were not protective. Analogous results were obtained with recombinant vaccines of the same amino acid sequences. In addition, mixtures of aa 90 to 194 with either aa 1 to 106 or aa 27 to 106 did not enhance protection compared to the active single-recombinant subunits alone. Humoral response of total immunoglobulin G (IgG) and subclasses IgG1 and IgG2a were detectable in subunit vaccinations but at significantly (100-fold) lower concentrations than after vaccination with plasmids encoding full-length Ag2/PRA. Since virtually all protection by vaccination with full-length Ag2/PRA can be accounted for in the first half of the protein (aa 1 to 106), this subunit could make a multicomponent vaccine more feasible by reducing the quantity of protein per dose and the possibility of an untoward reactions to a foreign protein.

Galgiani, J. N. (2008). Vaccines to prevent systemic mycoses: holy grails meet translational realities. The Journal of infectious diseases, 197(7), 938-40.
Park, B. J., Sigel, K., Vaz, V., Komatsu, K., McRill, C., Phelan, M., Colman, T., Comrie, A. C., Warnock, D. W., Galgiani, J. N., & Hajjeh, R. A. (2005). An epidemic of coccidioidomycosis in Arizona associated with climatic changes, 1998-2001. The Journal of infectious diseases, 191(11), 1981-7.

Reports of coccidioidomycosis cases in Arizona have increased substantially. We investigated factors associated with the increase.

REX, J. H., COOPER, C. R., MERZ, W. G., GALGIANI, J. N., & ANAISSIE, E. J. (1995). DETECTION OF AMPHOTERICIN B-RESISTANT CANDIDA ISOLATES IN A BROTH-BASED SYSTEM. ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 39(4), 906-909.