About

Derek John Bays, M.D., is an Assistant Clinical Professor in the Department of Internal Medicine at UC Davis Health, specializing in Infectious Diseases. His clinical interests include fungal infections and clinical mycology, with a focus on patients with hematologic malignancies. Dr. Bays's research concentrates on identifying novel methods to prevent invasive fungal infections, exploring how fungal pathogens interact with the patient microbiome, and studying fungal infections such as Valley Fever. He has received recognition for his academic excellence, including Fellow of the Year, Senior Resident of the Year, and Intern of the Year at UC Davis Internal Medicine. Dr. Bays believes in involving patients in their treatment plans through shared decision-making to enhance treatment success.

Research topics

• Medicine
• Internal medicine
• Immunology
• Computer Science
• Dermatology
• Telecommunications
• Intensive care medicine
• Computational biology
• Virology
• Biology

Selected publications

• Liposomal amphotericin B and complement activation-related pseudoallergy (CARPA)

  Antimicrobial Agents and Chemotherapy · 2025-01-30 · 6 citations

  articleOpen access

  Infusion reactions (tachycardia, hypertension, fever, etc.) associated with liposomal amphotericin B are common. Animal models have found complement activation responsible, yet the pathophysiology has not been evaluated in human patients. We performed a prospective observational study and found complement activation-related pseudoallergy (CARPA) responsible in those with infusion reactions.

  PublisherDOI

• Hidden Histoplasmosis: Adrenal and Central Nervous System Mycosis in an Immunocompetent Patient

  Cureus · 2025-08-23 · 2 citations

  articleOpen access

  Macroconidia released from hyphae growing in the soil are inhaled into the lungs, where there is a morphologic change to the pathogenic yeast form. While most infections are either asymptomatic or subclinical, histoplasmosis can present with a wide variety of clinical syndromes ranging from pneumonia to disseminated disease in virtually any organ system. Disseminated disease is typically associated with immunosuppression, specifically T-cell-mediated immunity. Here, we present a case of disseminated histoplasmosis to the central nervous system and adrenal glands complicated by adrenal crisis mimicking metastatic cancer. This occurred without traditional risk factors for disseminated histoplasmosis or travel to classically endemic areas of histoplasmosis, stressing the importance of consideration of invasive fungal infections in light of shifting endemic regions due to climate change.

  PublisherOA PDFDOI

• 840 Limb Salvage After Lomentospora Osteomyelitis in a Burn-Injured Patient Treated with Fosmanogepix

  Journal of Burn Care & Research · 2025-03-01

  articleOpen access

  Abstract Introduction Burn patients are highly susceptible to infections due to factors like loss of the protective skin barrier, immunosuppression, prolonged open wounds, mechanical ventilation and invasive lines. Fungal infections are a significant cause of late-onset morbidity and mortality. Lomentospora prolificans is a virulent fungus with intrinsic resistance to many antifungal agents. Fosmanogepix, a novel antifungal prodrug of manogepix, targets glycosylphosphatidylinositol (GPI)-anchored proteins essential for fungal cell survival. It has demonstrated efficacy against fungi resistant to other antifungal agents, such as Lomentospora prolificans. This case highlights the use of fosmanogepix for a resistant Lomentospora prolificans infection in a burn patient. Methods A 47-year-old male with 40% total body surface area third- and fourth-degree burns was admitted to the burn unit. He required initial escharotomies and fasciotomies followed by serial wound excision and debridement operations including a right lower extremity above the knee amputation. His course was complicated by multiple episodes of acute respiratory distress syndrome, septic shock and progressive tissue ischemia. On hospital day 88, there was clinical suspicion for mold for which tissue cultures and bone biopsies were obtained from his left lower extremity which identified Lomentospora. Combination therapy of voriconazole and terbinafine was initiated, followed by compassionate use of fosmanogepix. Results The Lomentospora prolificans culture was resistant to common antifungals such as amphotericin B, itraconazole, and voriconazole. Given his above the knee amputation on the contralateral extremity, limb salvage was endeavored with combination therapy of voriconazole and terbinafine as well as serial excisions to stabilize the wound until fosmanogepix was procured. Fosmanogepix was initiated on hospital day 124, and no mold growth was observed in subsequent cultures. He was ultimately able to be skin grafted and did not require a left lower extremity amputation. The patient was transitioned to oral fosmanogepix and discharged to a rehabilitation facility on hospital day 158. Conclusions Fosmanogepix, an investigational antifungal, was successfully used to treat Lomentospora prolificans infection in a burn patient resistant to standard antifungal therapies. This case demonstrates the potential of fosmanogepix as an alternative therapy for resistant fungal infections, offering hope for future management of similar cases. Applicability of Research to Practice Burn patients are at increased risk for fungal infections. When infections by resistant organisms such as Lomentospora prolificans occur, early recognition and timely use of novel antifungals like fosmanogepix may be critical for improving outcomes. This case underscores the importance of considering investigational therapies in the management of difficult-to-treat infections. Funding for the Study N/A

  PublisherDOI

• An approach to Candidozyma auris surveillance in a low prevalence setting

  American Journal of Infection Control · 2025-11-28

  articleOpen access

  OBJECTIVES: Candidozyma auris (C auris) is a multidrug-resistant fungal pathogen of increasing global concern. We describe the development and validation of an active surveillance program for patients at high risk of C auris colonization in the setting of regionally reported cases of invasive infection. METHODS: From 2021 to 2024, 1,146 surveillance tests were obtained using the BD ESwab collection system. Surveillance testing was performed on the BD MAX PCR platform. RESULTS: Of 1,146 specimens tested over a 3-year period, only four surveillance tests were positive. Individuals with positive surveillance tests were isolated, and contact tracing of potentially exposures revealed no secondary cases. CONCLUSIONS: This report demonstrates the importance of establishing hyperlocal epidemiology and robust infection prevention practices when determining the prevalence of and responding to emerging pathogens.

  PublisherDOI

• <i>Candida albicans</i> gastrointestinal colonization resistance: a host-microbiome balancing act

  Infection and Immunity · 2025-08-11 · 2 citations

  reviewOpen access1st authorCorresponding

  ABSTRACT While Candida albicans is a common, commensal yeast colonizing 50%–60% of humans, it has the potential to expand in the gastrointestinal tract and enter the blood stream resulting in invasive candidiasis. Invasive candidiasis carries a mortality approaching 50%, especially in the most vulnerable, immunocompromised population. Antibacterial use causes an increase in C. albicans gastrointestinal colonization, indicating that the colonic microbiota plays a major role in preventing an uncontrolled expansion, a phenomenon known as colonization resistance. Antibacterials, medications, diet, and co-morbid conditions can all alter the microbiome, creating an altered environment known as dysbiosis. Our understanding of the microbiome continues to advance, and there is increasing evidence that the interactions that the microbiome has on the host are vital in maintaining colonization resistance to pathogens including C. albicans . This review will focus on colonization resistance to C. albicans within the gastrointestinal tract. The scope includes the benefits and consequences of C. albicans colonization, interkingdom interactions of the microbiome on C. albicans , microbiome-host interactions and how these modulate C. albicans colonization, and the impact of medications and diet on colonization resistance.

  PublisherDOI

• P-2211. 5-Aminosalicylic Acid Prevents Antibiotic Induced Expansion of <i>Candida albicans</i> in the Gastrointestinal Tract

  Open Forum Infectious Diseases · 2025-01-29

  articleOpen access1st authorCorresponding

  Abstract Background Antibiotic treatment sets the stage for intestinal domination by Candida albicans which is necessary for development of invasive disease, but the resources driving this bloom remain poorly defined. We sought to determine these factors in order to design novel prophylaxis strategies for reducing gastrointestinal (GI) colonization. Figure 1 C. albicans colonization (CFU/g feces). All mice were treated with 10^6 of C. albicans (ATCC 28367) and randomized to receive mock treatment, 0.25% 5-ASA in mouse chow, streptomycin 20mg via oral gavage, and 0.25% 5-ASA in mouse chow with streptomycin 20mg via oral gavage. Feces was collected to enumerate C. albicans colonization. Methods We initially developed a generalizable framework, termed metabolic footprinting to determine the metabolites C. albicans preferentially uses in the mouse GI tract. After identifying the metabolites C. albicans utilizes, we used in vitro growth assays in the presence and absence of oxygen to validate out metabolomics findings. We next determined if a probiotic E. coli that utilizes oxygen would reduce C. albicans colonization compared to a mutant E. coli that could not respire oxygen. Finding that oxygen was a necessary resource, we utilized germ-free mice to determine if Clostridia spp. known to reduce GI oxygen would prevent C. albicans colonization. Lastly, we sought to see if 5-aminosalicylic acid (5-ASA) could prevent C. albicans colonization. Figure 2 Germ-free Swiss Webster mice received a cecal microbiota transplant from streptomycin-treated C57BL/6J mice (Strep) or from mock-treated C57BL/6J mice (Mock). Seven days later, some mice were inoculated with a community of human Clostridia isolates (C17), received a second cecal microbiota transplant from mock-treated C57BL/6J mice (Mock), or were switched to chow supplemented with 5-aminosalicylic acid (5-ASA: +). Seven days later, all mice were challenged with 105 C. albicans CFU (strain ATCC28367) and cecal contents were collected 1 week later to enumerate C. albicans CFU/g cecal contents Results We found that C. albicans preferentially utilizes simple carbohydrates including fructo-oligosaccharides (e.g., 1-kestose), disaccharides (e.g., β-gentiobiose), and alcoholic sugars (e.g., sorbitol) and is able to grow in vitro on minimal media supplemented with either of these nutrients. However, in the hypoxic environment that is found in the "healthy" colon, C. albicans cannot utilize these nutrients. We next found that pre-colonization in a mouse model with a probiotic E. coli significantly reduced C. albicans colonization, but the mutant E. coli had no effect on colonization. We next showed that Clostridia supplementation restored GI hypoxia and reduced C. albicans colonization. Remarkably, we found that 5-ASA significantly reduced GI colonization of C. albicans. Conclusion We have shown that C. albicans requires oxygen to colonize the GI tract. Importantly, we found that 5-ASA can prevent an antibiotic mediated bloom of C. albicans by restoring GI hypoxia, which warrants additional studies to determine if 5-ASA can be used as an adjunctive prophylactic treatment in high-risk patients. Disclosures George R. Thompson, III, MD, Astellas: Advisor/Consultant|Cidara: Advisor/Consultant|Cidara: Grant/Research Support|F2G: Advisor/Consultant|F2G: Grant/Research Support|Melinta: Advisor/Consultant|Melinta: Grant/Research Support|Mundipharma: Advisor/Consultant|Mundipharma: Grant/Research Support|Pfizer: Advisor/Consultant

  PublisherOA PDFDOI

• Immunogenetics associated with severe coccidioidomycosis

  UNC Libraries · 2025-07-31

  articleOpen access

  Disseminated coccidioidomycosis (DCM) is caused by Coccidioides, pathogenic fungi endemic to the southwestern United States and Mexico. Illness occurs in approximately 30% of those infected, less than 1% of whom develop disseminated disease. To address why some individuals allow dissemination, we enrolled patients with DCM and performed whole-exome sequencing. In an exploratory set of 67 patients with DCM, 2 had haploinsufficient STAT3 mutations, and defects in &beta;-glucan sensing and response were seen in 34 of 67 cases. Damaging CLEC7A and PLCG2 variants were associated with impaired production of &beta;-glucan-stimulated TNF-&alpha; from PBMCs compared with healthy controls. Using ancestry-matched controls, damaging CLEC7A and PLCG2 variants were overrepresented in DCM, including CLEC7A Y238* and PLCG2 R268W. A validation cohort of 111 patients with DCM confirmed the PLCG2 R268W, CLEC7A I223S, and CLEC7A Y238* variants. Stimulation with a DECTIN-1 agonist induced DUOX1/DUOXA1-derived hydrogen peroxide [H2O2] in transfected cells. Heterozygous DUOX1 or DUOXA1 variants that impaired H2O2 production were overrepresented in discovery and validation cohorts. Patients with DCM have impaired &beta;-glucan sensing or response affecting TNF-&alpha; and H2O2 production. Impaired Coccidioides recognition and decreased cellular response are associated with disseminated coccidioidomycosis.

  PublisherDOI

• Isavuconazole therapeutic drug monitoring and association with adverse events

  Journal of Antimicrobial Chemotherapy · 2025-04-28 · 15 citations

  articleOpen access

  OBJECTIVES: Isavuconazole is efficacious in the treatment of aspergillosis, mucormycosis, and other invasive fungal infections. Therapeutic drug monitoring is generally not assessed during treatment with isavuconazole due to its high oral bioavailability, modest drug-drug interactions, and linear pharmacokinetics. This study aimed to determine whether an exposure-toxicity relationship exists for isavuconazole in those experiencing potential adverse drug events. METHODS: This retrospective study analysed adult outpatients receiving isavuconazole and the occurrence of adverse events. Patients with and without adverse events were compared to identify serum drug concentrations predictive of potential drug-related toxicity. RESULTS: Ninety-five patients, corresponding to 219 serum levels total, were analysed. Thirty-seven (38.9%) developed adverse events, most commonly transaminitis (29.7%), diarrhoea (24.3%), and nausea (18.9%). Using Youden's index, a serum level of 5.86 µg/mL corresponded to a threshold balancing sensitivity (41.0%) and specificity (87.1%) in the determination of toxicity risk. All 24 patients undergoing isavuconazole dose reduction demonstrated resolution of symptoms. CONCLUSIONS: Our findings identified an exposure-toxicity relationship for isavuconazole. Therapeutic drug monitoring may be beneficial for those on isavuconazole therapy who develop signs or symptoms of potential toxicity. Additionally, in patients with adverse events attributed to isavuconazole, dose reduction often led to resolution.

  PublisherOA PDFDOI

• Hypoxemic Respiratory Failure and Coccidioidomycosis-Associated Acute Respiratory Distress Syndrome

  Open Forum Infectious Diseases · 2024-02-01 · 4 citations

  articleOpen access

  Abstract Background Severe coccidioidomycosis presenting with respiratory failure is an uncommon manifestation of disease. Current knowledge of this condition is limited to case reports and small case series. Methods A retrospective multicenter review of patients with coccidioidomycosis-associated acute respiratory distress syndrome (CA-ARDS) was conducted. It assessed clinical and laboratory variables at the time of presentation, reviewed the treatment course, and compared this cohort with a national database of patients with noncoccidioidomycosis ARDS. Survivors and nonsurvivors of coccidioidomycosis were also compared to determine prognostic factors. Results In this study, CA-ARDS (n = 54) was most common in males, those of Hispanic ethnicity, and those with concurrent diabetes mellitus. As compared with the PETAL network database (Prevention and Early Treatment of Acute Lung Injury; n = 1006), patients with coccidioidomycosis were younger, had fewer comorbid conditions, and were less acidemic. The 90-day mortality was 15.4% for patients with coccidioidomycosis, as opposed to 42.6% (P &amp;lt; .0001) for patients with noncoccidioidomycosis ARDS. Patients with coccidioidomycosis who died, as compared with those who survived, were older, had higher APACHE II scores (Acute Physiology and Chronic Health Evaluation), and did not receive corticosteroid therapy. Conclusions CA-ARDS is an uncommon but morbid manifestation of infection. When compared with a national database, the overall mortality appears favorable vs other causes of ARDS. Patients with CA-ARDS had a low overall mortality but required prolonged antifungal therapy. The utility of corticosteroids in this condition remains unconfirmed.

  PublisherOA PDFDOI

• Salmonella re-engineers the intestinal environment to break colonization resistance in the presence of a compositionally intact microbiota

  Cell Host & Microbe · 2024-08-23 · 40 citations

  articleOpen access

  The gut microbiota prevents harmful microbes from entering the body, a function known as colonization resistance. The enteric pathogen Salmonella enterica serovar (S.) Typhimurium uses its virulence factors to break colonization resistance through unknown mechanisms. Using metabolite profiling and genetic analysis, we show that the initial rise in luminal pathogen abundance was powered by a combination of aerobic respiration and mixed acid fermentation of simple sugars, such as glucose, which resulted in their depletion from the metabolome. The initial rise in the abundance of the pathogen in the feces coincided with a reduction in the cecal concentrations of acetate and butyrate and an increase in epithelial oxygenation. Notably, these changes in the host environment preceded changes in the microbiota composition. We conclude that changes in the host environment can weaken colonization resistance even in the absence of overt compositional changes in the gut microbiota.

  PublisherOA PDFDOI

Frequent coauthors

• George R. Thompson

  University of California Davis Medical Center

  43 shared

• Thaynara Parente de Carvalho

  University of California, Davis

  13 shared

• Hannah P. Savage

  University of California, Davis

  12 shared

• Stuart H. Cohen

  12 shared

• Renato L. Santos

  Universidade Federal de Minas Gerais

  12 shared

• Andreas J. Bäumler

  10 shared

• Ian McHardy

  Scripps Health

  10 shared

• Hugo L. P. Masson

  The Ohio State University

  9 shared

Labs

• Infectious Diseases, UC Davis HealthPI

Awards & honors

• Fellow of the Year, UC Davis Internal Medicine (2020)
• Senior Resident of the Year, UC Davis Internal Medicine (201…
• Intern of the Year, UC Davis Internal Medicine (2016)
• Eli Benjamin Endowed Fund for Biological Science, UC Davis S…
• Golden Goblet Award, UC Davis School of Medicine (2015)