- Assistant Professor, Medicine
- Assistant Professor, BIO5 Institute
- Member of the Graduate Faculty
INSTITUTION AND LOCATION
FIELD OF STUDY
Shiraz University School of Medicine, Iran
Resident, Tehran University Hospital, Iran
Graduate school, Gifu University School of Medicine, Gifu, Japan
Post Doctoral fellow, Department of Microbiology & Immunology, Medical College of Ohio,Toledo, Ohio
Microbiology and immunology
Research Associate, Department of Internal Medicine, Division of Infectious Diseases, University of Cincinnati, Cincinnati, Ohio
Intern, Family Practice, Bethesda Family
Practice, Cincinnati, Ohio
Resident, Internal Medicine, Department of Internal Medicine, Good Samaritan Hospital, Cincinnati, Ohio
Fellow, Infectious Diseases, Department
of Internal Medicine, Division of Infectious
Diseases, University of South Florida,
- Ph.D. Dermatology
- Gifu University School of Medicine, Gifu, Japan
- Shiraz University School of Medicine, Shiraz, Iran, Islamic Republic of
- Dept. of Medicine/Valley Fever Center for Excellence, University of Arizona (2017 - Ongoing)
- Florida State University, College of Medicne (2014 - 2017)
- Intercoastal Medical Group (2013 - 2017)
- Infectious Disease Associates (2010 - 2013)
- Dept. of Internal medicine, Div. Infectious Disease, University of Cincinnati (2001 - 2004)
- Dept. of Microbiology & Immunology, Medical College of Ohio (1997 - 2001)
- JSID International Scholarship (Kao Award)
- JSID, Summer 1996 (Award Finalist)
- Graduate Scholarship for Graduate Course, Ministry of Education and Science, Japan
- Ministry of Education and Science, Japan (March 93 -March 97), Spring 1993 (Award Finalist)
- Research Fellowship Scholarship, Ministry of Education and Science, Japan (January 1992 - March 1993)
- Ministry of Education and Science, Japan (January 1992 - March 1993), Winter 1992
- Infectious Diseases Society of America, Summer 2022
- American College of Physicians, Spring 2022
- IDSA leadership Institute
- IDSA, Spring 2022 (Award Finalist)
- Fellow of American College of Physicians
- Winter 2021
Licensure & Certification
- Certification examination in Internal Medicine, American Board of Internal Medicine (2008)
- Arizona State Medical Board, Arizona State Medical Board (2017)
- Certification examination in Infectious Disease, American Board of Internal Medicine (2010)
- Florida State Medical Board, Florida State Medical Board (2015)
We are reminded daily of the critical importance of teachers to the benefit and advancement of civilization. Passing on to others the fruits of one's education, research and experience is an absolute requirement and enduring gift to society. I consider research, clinical duties and teaching as the three most important aspects of my life's work.As an Infectious disease physician, one of my main goals is cultivating the interest in various fields of infectious diseases among the fellows, residents and medical students and general public. In particular I enjoy sharing my expertise in medical mycology especially Coccidioidomycosis and other areas of infectious disease such as virology (HIV and hepatitis).The education of the ID fellows is focused on complicated cases (eg. HIV/AIDS, hepatitis, transplant patients and complicated surgical infections) that they will encounter in near future as they complete their training.In a similar vein with medical residents, I seek to encourage them to be aware of the importance of infectious disease in general medical practice and make them comfortable with various infectious diseases that they will confront in daily practice.With medical students, my goal is to open their minds and have them experience the importance of infectious diseases and all aspects of medicine and perhaps encourage some to consider ID as their future carier.With the general public, it is important to educate everyone about how infectious diseases touch their lives. This might include a broad range of activities such as addressing local groups about Valley Fever, or speaking to the media to raise awareness about the overuse of antibiotics and the ongoing challenges with antibiotic resistance. As important as it is to educate others, It is equally important to continue educate myself. This include reviewing other's research, stay abreast of the latest advancements in antimicrobials and attending conferences to further advance my education.
As both a research scientist and practicing infectious disease clinician I remain keenly aware of the importance of the practical application of basic research, to the broader problems we face treating patients with both invasive and opportunistic fungal infections. Over the last five years, while seeing patients in the Valley fever clinic as well as in our hospital along with an exponential increase in the use of biological response modifiers in patients with autoimmune disorders I have seen the need for more study and a better understanding of the risk and benefits of these medications in a Coccidioidomycosis endemic region. My background is well suited for this task. Post medical residency training in my native Iran, I was able to obtain a Ph.D. at Gifu University in Japan. My research focused on candida albicans and its interaction with the human host. I developed specific expertise in protein purification, molecular biology, and gene manipulation techniques to further identify C. albicans virulence factors. During my post-doctoral work in the US, I started my research on Coccidioides species, and I was able to specifically purify the urease protein, construct a urease knockout strain, and demonstrate lesser virulence in the animal model. The knockout strain showed promise as a potential vaccine candidate, and this work remains an active area of Valley fever research. After moving to Cincinnati, I was able to broaden my research to the genetic manipulation of histoplasma capsulatum and the immune interaction in the animal model. In retrospect, my completion of an internal medicine residency and infectious disease fellowship was a natural extension of my desire to put into practice my research interest and findings. In 2017 I was recruited to the University of Arizona at the Valley Fever Center for Excellence, which has allowed me to continue my Valley fever research and improve the prevention, diagnosis, and treatment of Valley fever. My initial project focused on Coccidioidomycosis diagnostic delays with an emphasis to reduce both unnecessary testing, and treatments and thereby reduce morbidity and mortality. Additional benefits included improving antibiotic stewardship, developing population management programs, and serving as a model to address other opportunistic infections. My emphasis on early events in Coccidioidomycosis allowed me to focus on identifying clinical cues that lead to earlier diagnosis of Valley fever and to assess the impact of clinical practice training on the diagnosis and management of this disease. I completed a prospective study at the Banner University Medical Center to evaluate a rapid lateral flow assay for rapid diagnosis of coccidioidomycosis and the results have been published. Additionally, I am developing plans to study the host’s innate immune response to Coccidioides with a focus on the early events in coccidioidomycosis. I have recently completed a retrospective study and quantified the risk biological response modifiers (BRMs) play in patients with autoimmune disorders such as rheumatoid arthritis, inflammatory bowel disease, or psoriasis. Our ability in the former study to prospectively enroll a large cohort of patients makes us confident that we can contribute to the success of our ongoing projects, which ultimately will allow us to develop a highly sensitive, rapid, portable, and user-friendly detection device for early diagnosis of coccidioidomycosis.
No activities entered.
- Archer, E. (2022). Endemic Mycoses: Better Diagnosis and Reporting Needed . Medscape.
- Bedrick, E. J., Shadarevian, M. D., Ramadan, F. A., Lim, J. R., Khan, R. N., Kaveti, A., Galgiani, J. N., Donovan, F. M., Dequillfeldt, N. P., Davis, N. M., & Buchfuhrer, J. E. (2022). Contribution of Biologic Response Modifiers to the Risk of Coccidioidomycosis Severity.. Open forum infectious diseases, 9(3), ofac032. doi:10.1093/ofid/ofac032More infoThe risk of coccidioidomycosis (CM) as a life-threatening respiratory illness or disseminated CM (DCM) increases as much as 150-fold in immunosuppressed patients. The safety of biologic response modifiers (BRMs) as treatment for patients with autoimmune disease (AI) in CM-endemic regions is not well defined. We sought to determine that risk in the Tucson and Phoenix areas..We conducted a retrospective study reviewing demographics, Arizona residency length, clinical presentations, specific AI diagnoses, CM test results, and BRM treatments in electronic medical records of patients ≥18 years old with International Classification of Diseases (ICD-10) codes for CM and AI from 1 October 2017 to 31 December 2019..We reviewed 944 charts with overlapping ICD-10 codes for CM and AI, of which 138 were confirmed to have both diagnoses. Male sex was associated with more CM (P = .003), and patients with African ancestry were 3 times more likely than those with European ancestry to develop DCM (P
- Donovan, F. (2022). Immunogenetics associated with severe coccidioidomycosis. JCI.Insight.
- Donovan, F. (2022). Clinical Predictors of Coccidioidomycosis from a Cross-Sectional Study. Emerging Infectious Disease.
- Thompson, G. R., Ampel, N. M., Blair, J. E., Donovan, F., Fierer, J., Galgiani, J. N., Heidari, A., Johnson, R., Shatsky, S. A., Uchiyama, C. M., & Stevens, D. A. (2022). Controversies in the Management of Central Nervous System Coccidioidomycosis. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 75(4), 555-559.More infoCentral nervous system infection with Coccidioides spp. is fatal if untreated and complications occur even when therapy is directed by experienced clinicians. We convened a panel of clinicians experienced in the management of coccidioidal meningitis to summarize current controversies and provide consensus for the management of this difficult infection.
- Donovan, F. (2021). Cutaneous Leishmaniasis Caused by an Unknown Leishmania Strain, Arizona, USA. Emerging Infectious Diseases, 1714-1717.
- Messina, J. A., Maziarz, E. K., Galgiani, J., Truong, J. T., Htoo, A. K., Heidari, A., Johnson, R. H., Narang, A. T., Donovan, F. M., Ewell, M., Catanzaro, A., Thompson, G. R., Ampel, N. M., Perfect, J. R., Naggie, S., & Walter, E. B. (2021). A randomized, double-blind, placebo-controlled clinical trial of fluconazole as early empiric treatment of coccidioidomycosis pneumonia (Valley Fever) in adults presenting with community-acquired pneumonia in endemic areas (FLEET-Valley Fever). Contemporary clinical trials communications, 24, 100851.More infoCoccidioidomycosis is a fungal infection endemic in the southwestern United States (US). Primary pulmonary coccidioidomycosis (PPC) is a leading cause of community-acquired pneumonia (CAP) in this region, although its diagnosis is often delayed, leading to lag in antifungal treatment and subsequent morbidity. The impact of early empiric antifungal therapy as part of treatment for CAP in endemic areas on clinical outcomes is unknown.
- Bardwell, J., August, J., Farran, S., Florita, C., Donovan, F., & Zangeneh, T. T. (2020). Infection of Aortic Endograft Caused by Coccidioidomycosis. The American journal of medicine, 133(1), e1-e2. doi:10.1016/j.amjmed.2019.07.013
- Donovan, F. M., Ramadan, F. A., Khan, S. A., Bhaskara, A., Lainhart, W. D., Narang, A. T., Mosier, J. M., Ellingson, K. D., Bedrick, E. J., Saubolle, M. A., & Galgiani, J. N. (2020). Comparison of a Novel Rapid Lateral Flow Assay to Enzyme Immunoassay Results for Early Diagnosis of Coccidioidomycosis. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America.More infoCoccidioidomycosis (CM) is a common cause of community acquired pneumonia (CAP) where CM is endemic. Manifestations include self-limited pulmonary infection, chronic fibrocavitary pulmonary disease, and disseminated coccidioidomycosis (DCM). Most infections are identified by serological assays including enzyme-linked immunoassay (EIA), complement fixation (CF) and immunodiffusion (IMDF). These are time-consuming and take days to result, impeding early diagnosis. A new lateral flow assay (LFA, Sōna, IMMY, Norman OK) improves time-to-result to one hour.
- Pu, J., Donovan, F. M., Ellingson, K., Leroy, G., Stone, J., Bedrick, E., & Galgiani, J. N. (2020). Clinician Practice Patterns that Result in the Diagnosis of Coccidioidomycosis Before or During Hospitalization. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America, 73(7), e1587-e1593. doi:10.1093/cid/ciaa739More infoCoccidioidomycosis (CM) is common and important within endemic regions, requiring specific testing for diagnosis. Long delays in diagnosis have been ascribed to ambulatory clinicians, but how their testing practices have impacted patient care have not been systematically unexplored.
- Donovan, F. (2019). Delays in Coccidioidomycosis Diagnosis and Associated Healthcare Utilization in Tucson, Arizona. Emerging Infectious Diseases, 25 (9), 1745-1747.
- Donovan, F. M., Shubitz, L., Powell, D., Orbach, M., Frelinger, J., & Galgiani, J. N. (2019). Early Events in Coccidioidomycosis. Clinical Microbiology Reviews, 33(1).More infoSUMMARYSince its description nearly 130 years ago, hundreds of studies have deepened our understanding of coccidioidomycosis, also known as valley fever (VF), and provided useful diagnostic tests and treatments for the disease caused by the dimorphic fungi spp. In general, most of the literature has addressed well-established infections and has described patients who have experienced major complications. In contrast, little attention has been given to the earliest consequences of the pathogen-host interaction and its implications for disease manifestation, progression, and resolution. The purpose of this review is to highlight published studies on early coccidioidomycosis, identify gaps in our knowledge, and suggest new or former research areas that might be or remain fertile ground for insight into the early stages of this invasive fungal disease.
- Donovan, F. M., Zangeneh, T. T., Malo, J., & Galgiani, J. N. (2017). Top Questions in the Diagnosis and Treatment of Coccidioidomycosis. Open forum infectious diseases, 4(4), ofx197.More infoRevised and greatly expanded treatment guidelines for coccidioidomycosis were published last year by the Infectious Diseases Society of America. We have selected 4 questions that commonly arise in the management of patients suspected of this disease and for which there remain divided opinions.
- Donovan, F., Blatt, S., & Gonzales, Y. (2006). Cat Scratch Disease Presenting as Severe Thrombocytopenia. Resident and Staff Physician.
- Mirbod, F., Nakashima, S., Kitajima, Y., Ghannoum, M. A., Cannon, R. D., & Nozawa, Y. (2016). Molecular cloning of a gene encoding translation initiation factor (TIF) from Candida albicans. Journal of medical and veterinary mycology : bi-monthly publication of the International Society for Human and Animal Mycology, 34(6), 393-400.More infoThe differential display technique was applied to compare mRNAs from two clinical isolates of Candida albicans with different virulence; high (potent strain, 16240) and low (weak strain, 18084) extracellular phospholipase activities. Complementary DNA fragments corresponding to several apparently differentially expressed mRNAs were recovered and sequenced. A complementary DNA fragment seen distinctly in the potent phospholipase producing strain was highly homologous to the yeast translation initiation factor (TIF). The selected DNA fragment was then used as a probe to isolate its corresponding complementary DNA clone from a library of C. albicans genomic DNA. The sequence of isolated gene revealed an open reading frame of 1194 nucleotides with the potential to encode a protein of 397 amino acids with a predicted molecular weight of 43 kDa. Over its entire length, the amino acid sequence showed strong homology (78-89%) to Saccharomyces cerevisiae TIF and (63-80%) to mouse eIF-4A proteins. Therefore, our C. albicans gene was identified to be TIF (Ca TIF). Northern blot analysis in the two strains of C. albicans revealed that Ca TIF expression is 1.5-fold higher in the potent phospholipase producing strain. The restriction endonuclease digestion of genomic DNA from this potent strain revealed at least two hybridized bands in Southern blot analysis, suggesting two or more closely related sequences in the C. albicans genome.
- Donovan, F., Somboonbwit, C., Soliman, E., Gotuzzo, E., & Perez, N. (2009). St. Louis Encephalitis. Web Med.
- Donovan, F., Somboonwit, C., Tash, K., & Houston, S. H. (2009). Immunosuppression and infection risk in SOT receipients. Infections in Medicine, 26(2), 41-46.
- Mirbod-Donovan, F., Schaller, R., Hung, C. Y., Xue, J. M., Reichard, U., & Cole, G. T. (2006). Urease produced by Coccidioides posadasii contributes to the virulence of this respiratory pathogen. INFECTION AND IMMUNITY, 74(1), 504-515.
- Mirbod, F., Schaller, R. A., & Cole, G. T. (2002). Purification and characterization of urease isolated from the pathogenic fungus Coccidioides immitis. Medical mycology, 40(1), 35-44.More infoCoccidioides immitis, the causative agent of San Joaquin Valley fever (coccidioidomycosis), produces a urease which has been suggested to contribute to the virulence of this fungal pathogen. Urease catalyzes the hydrolysis of urea and has been proposed to at least partly account for alkalinity of the microenvironment in which C. immitis grows due to the release of ammonia and ammonium ions. The C. immitis urease was purified to homogeneity (1048-fold) from the mycelial cytosol by chromatographic fractionation. The sequence of 12 N-terminal amino-acid residues of the purified, native polypeptide was identical to that predicted by the translated urease gene sequence which has been reported. The isolated enzyme exhibited a specific activity in the presence of urea of 1750 micromol min(-1) mg(-1) protein, has a native molecular mass of 450 kDa, revealed a Km for urea of 4.1 mM, had a pH optimum of 8.0 and is heat stable. Hydroxyurea, acetohydroxamic acid (AHA) and boric acid each inhibited activity of the purified enzyme. Urease activity was enhanced by the presence of 5-10 mM concentrations of Mg2+ or Mn2+, but inhibited by Li+, Ni2+, Cu2+ or Zn2+. The reversible urease inhibitor, AHA, blocked enzyme activity in the crude mycelial cytosolic fraction when added at a concentration of 10 mM. On the other hand, 10 mM AHA added to 4-day-old mycelial cultures only partially decreased the amount of ammonium detected in the culture medium. It is evident, therefore, that C. immitis urease activity does not account for the total amount of ammonia secreted during in vitro growth of the pathogen. Other metabolic sources of ammonia, which may also contribute to the virulence of C. immitis, are under investigation.
- Sugiyama, Y., Nakashima, S., Mirbod, F., Kanoh, H., Kitajima, Y., Ghannoum, M. A., & Nozawa, Y. (1999). Molecular cloning of a second phospholipase B gene, caPLB2 from Candida albicans. MEDICAL MYCOLOGY, 37(1), 61-67.
- Leidich, S. D., Ibrahim, A. S., Fu, Y., Koul, A., Jessup, C., Vitullo, J., Fonzi, W., Mirbod, F., Nakashima, S., Nozawa, Y., & Ghannoum, M. A. (1998). Cloning and disruption of caPLB1, a phospholipase B gene involved in the pathogenicity of Candida albicans. JOURNAL OF BIOLOGICAL CHEMISTRY, 273(40), 26078-26086.
- Mirbod, F., Nakashima, S., Kitajima, Y., Cannon, R. D., & Nozawa, Y. (1997). Molecular cloning of a Rho family, CDC42Ca gene from Candida albicans and its mRNA expression changes during morphogenesis. JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY, 35(3), 173-179.
- Mirbod, F., Nakashima, S., Kitajima, Y., Ghannoum, M. A., Cannon, R. D., & Nozawa, Y. (1996). Molecular cloning of a gene encoding translation initiation factor (TIF) from Candida albicans. Journal of medical and veterinary mycology : bi-monthly publication of the International Society for Human and Animal Mycology, 34(6), 393-400.More infoThe differential display technique was applied to compare mRNAs from two clinical isolates of Candida albicans with different virulence; high (potent strain, 16240) and low (weak strain, 18084) extracellular phospholipase activities. Complementary DNA fragments corresponding to several apparently differentially expressed mRNAs were recovered and sequenced. A complementary DNA fragment seen distinctly in the potent phospholipase producing strain was highly homologous to the yeast translation initiation factor (TIF). The selected DNA fragment was then used as a probe to isolate its corresponding complementary DNA clone from a library of C. albicans genomic DNA. The sequence of isolated gene revealed an open reading frame of 1194 nucleotides with the potential to encode a protein of 397 amino acids with a predicted molecular weight of 43 kDa. Over its entire length, the amino acid sequence showed strong homology (78-89%) to Saccharomyces cerevisiae TIF and (63-80%) to mouse eIF-4A proteins. Therefore, our C. albicans gene was identified to be TIF (Ca TIF). Northern blot analysis in the two strains of C. albicans revealed that Ca TIF expression is 1.5-fold higher in the potent phospholipase producing strain. The restriction endonuclease digestion of genomic DNA from this potent strain revealed at least two hybridized bands in Southern blot analysis, suggesting two or more closely related sequences in the C. albicans genome.
- Donovan, F., Nakashima, S., Mori, S., Kitajima, Y., & Nosawa, Y. (1995). Phospholipid biosynthesis in growing and non -growing conditions in Candida albicans. Jpn. J. Med. Mycol, 36, 53-59.
- IBRAHIM, A. S., MIRBOD, F., FILLER, S. G., BANNO, Y., COLE, G. T., KITAJIMA, Y., EDWARDS, J. E., NOZAWA, Y., & GHANNOUM, M. A. (1995). EVIDENCE IMPLICATING PHOSPHOLIPASE AS A VIRULENCE FACTOR OF CANDIDA-ALBICANS. INFECTION AND IMMUNITY, 63(5), 1993-1998.
- MIRBOD, F., BANNO, Y., GHANNOUM, M. A., IBRAHIM, A. S., NAKASHIMA, S., KITAJIMA, Y., COLE, G. T., & NOZAWA, Y. (1995). PURIFICATION AND CHARACTERIZATION OF LYSOPHOSPHOLIPASE-TRANSACYLASE (H-LPTA) FROM A HIGHLY VIRULENT-STRAIN OF CANDIDA-ALBICANS. BIOCHIMICA ET BIOPHYSICA ACTA-LIPIDS AND LIPID METABOLISM, 1257(2), 181-188.
- Mirbod, F., Banno, Y., Ghannoum, M. A., Ibrahim, A. S., Ibrahim, A. S., Nakashima, S., Kitajima, Y., Cole, G. T., & Nozawa, Y. (1995). Purification and characterization of lysophospholipase-transacylase (h-LPTA) from a highly virulent strain of Candida albicans.. Biochimica et biophysica acta, 1257(2), 181-8. doi:10.1016/0005-2760(95)00072-kMore infoA lysophospholipase-transacylase (h-LPTA) was purified to homogeneity from a clinical isolate of Candida albicans (C. albicans) that had high extracellular phospholipase activity (strain 16240). The purified enzyme was a glycoprotein with molecular mass of 84 kDa on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The specific activities of the enzyme were 117 mumol/min per mg protein for fatty acid release and 459 mumol/min per mg protein for phosphatidylcholine (PC) formation. An apparent Km of the hydrolase activity of the enzyme for 1-palmitoyl-sn-glycero-3-phosphocholine (1-palmitoyl-lyso-PC) was 60.6 microM. The enzyme had a pH optimum at 6.0. Transacylase activity of the enzyme was partially inhibited by palmitoylcarnitine (35% inhibition) and N-ethylmaleimide. In contrast, the hydrolase activity of the enzyme was stimulated by palmitoylcarnitine but was partially inhibited by N-ethylmaleimide. The enzyme exhibited broad specificity to lyso-phospholipids. The h-LPTA activity was not dependent on divalent cations (Ca2+ and Mg2+) and was not inhibited by addition of EDTA or EGTA. These results show that C. albicans strain 16240 with high extracellular phospholipase activity produced h-LPTA in large amount. This enzyme is biochemically distinct from the LPTA enzyme previously isolated from C. albicans 3125.
- Donovan, F., Inoue, I., Seishima, M., Mori, S., & Nozawa, Y. (1994). Lipid synthesis during cell growth of Cryptococcus neoformans. Jpn. J. Med. Mycol., 35, 421-427.
- Donovan, F., Mori, S., & Nozawa, Y. (1993). Methods for Phospholipid Extraction in Candida albicans: an Extraction Method with High Efficacy. J. Med. Vet. Mycol., 31, 405-409.
- Galgiani, J. N., Donovan, F. M., Song, H., Gu, Y., & Leroy, G. (2021, December). Integrating Automated Biomedical Lexicon Creation for Valley Fever Diagnosis. In 2021 IEEE/ACM Conference on Connected Health: Applications, Systems and Engineering Technologies (CHASE).
- Donovan, F. (2022, Fall). Determining The Impact of Biologic Response Modifiers on Coccidioidomycosis Severity. Biennial Meeting. Albuquerque, New Mexico.
- Donovan, F. (2022, November). Updates in Coccidioidomycosis. Tubac Rotary Club. Tubac, AZ.
- Donovan, F. (2022, November). Valley fever Diagnostics Current Methods and Challenges. National Academies of Science. UC Irvine, CA: National Academies of Science Engineering Medicine.
- Donovan, F., Galgiani, J. N., Ramadan, F., Ellingson, K., Ramadan, F., Ellingson, K., Donovan, F., & Galgiani, J. N. (2020, March). A Clinical Profile of Newly Diagnosed Valley Fever in Hospital Settings. SHEA/CDC Decennial 6th International Conference on Healthcare Associated Infections. Atlanta, GA: SHEA/CDC Decennial 6th International Conference on Healthcare Associated Infections.
- Donovan, F. (2018, April). Delays in Diagnosis of Coccidioidomycosis in Tucson, AZ. Cocci Study Group. Flagstaff, Arizona.
- Donovan, F. (2018, April). Valley Fever is under-recognized even in endemic areas. Cocci study Group. Flagstaff, Arizona: Coocidioidomycosis Symposium.
- Song, H., Gu, Y., Donovan, F., Leroy, G. A., & Galgiani, J. N. (2021, November). Automated Biomedical Lexicon Creation with Graph Search for Word Embeddings. IEEE CHASE. Washington DC.
- Donovan, F. (2017, August). Delays in diagnosing coccidioidomycosis within its endemic region.. 7th International Coccidioidomycosis Symposium. Standford, CA: Stanford Center for Continuing Medical Education.
- Donovan, F. (2017, November). Delays in diagnosing coccidioidomycosis within its endemic region.. Jr Investigator Poster Forum. College of Medicine-Tucson, University of Arizona.