About

Olivia Kates, MD, MA, is an Associate Professor of Medicine in the Division of Infectious Diseases at the Johns Hopkins School of Medicine. Her medical practice focuses on the diagnosis, treatment, and prevention of infections in patients who are immunosuppressed due to solid organ transplantation, cancer, or chemotherapy. Her research involves ethical challenges in infectious diseases and solid organ transplantation, seeking approaches that center interconnectedness, shared resource allocation, and justice. Areas of particular interest include vaccination requirements for organ transplant candidates and antimicrobial stewardship in fraught clinical and social contexts. Dr. Kates completed medical school at Tufts University School of Medicine, internal medicine residency at Columbia University's New York Presbyterian Hospital, and infectious diseases fellowship at the University of Washington, where she also completed a Master of Arts in Bioethics and Humanities, before joining Johns Hopkins in 2021.

Research topics

• Medicine
• Internal medicine
• Intensive care medicine
• Pathology
• Immunology

Selected publications

• Invasive Fungal Infections Following Bruton Tyrosine Kinase Inhibitor Treatment: A Systematic Review and Meta-analysis

  Blood Advances · 2026-04-09

  articleOpen access

  The epidemiology of invasive fungal infections (IFIs) among patients receiving Bruton tyrosine kinase inhibitors (BTKIs) remains incompletely characterized. We conducted a systematic review and meta-analysis of 88 studies including 23,737 patients to evaluate the prevalence and risk factors for IFIs in this population. Among 16 studies that applied the European Organization for Research and Treatment of Cancer and the Mycoses Study Group Education and Research Consortium consensus definitions of IFIs, the pooled prevalence of proven/probable IFIs was 2.83% (95% CI, 1.97-4.06%), with the highest prevalence observed in patients with central nervous system lymphoma (9.02%). Aspergillosis was the most frequently reported IFI (1.76%), followed by pneumocystosis, candidiasis, and cryptococcosis. The only risk factor significantly associated with proven/probable IFIs was concurrent corticosteroid use (OR 5.03, 95% CI, 2.31-10.92) and prior lines of therapy ≥ 3 (OR 3.26, 95% CI, 1.54-6.88). Across clinical trials, the prevalence of fungal infections varied across BTKI agents, ranging from 2.50% with tirabrutinib to 0.62% with pirtobrutinib. Data on antifungal and Pneumocystis jirovecii pneumonia prophylaxis were limited and inconclusive. Among clinical trials that reported fungal infections as adverse events, the prevalence of IFI was the highest in patients treated with tirabrutinib (2.50%), followed by zanubrutinib (2.13%), ibrutinib (1.75%), acalabrutinib (1.31%), orelabrutinib (1.08%), and pirtobrutinib (0.62%). While some findings suggest a potential benefit in selected patients, current evidence remains insufficient to support broad prophylaxis recommendations. These results underscore the need for individualized risk assessment and further research to inform prevention strategies.

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• It Takes Two to Transplant

  Clinical Infectious Diseases · 2026-03-27

  article
  PublisherDOI

• P-2128. First-in-human 18F-Fluorodeoxysorbitol PET for Noninvasive Diagnosis of Invasive Fungal Infections

  Open Forum Infectious Diseases · 2025-01-29

  articleOpen access

  Abstract Background Invasive mold infections are increasingly prevalent in immunosuppressed patients and associated with high mortality. Definitive diagnosis is challenging and may require invasive procedures (bronchoalveolar lavage, biopsy) or rely on biomarkers, e.g., galactomannan, which has limited sensitivity for Aspergillus and does not detect other mold species. There is need for sensitive, noninvasive tools to diagnose invasive mold infections. Molds, but not mammalian cells, metabolize sorbitol; recent studies suggest that 18F-fluorodeoxysorbitol (18F-FDS), a fluoro-analog of sorbitol, could be developed as a diagnostic tool for invasive mold infections.Figure 1.18F-FDS uptake in molds. 18F-FDS and 18F-FDG uptake in Aspergillus (panels a-b), Rhizopus (panels c-d), and Mucor (panels e-f) performed at least in triplicate, demonstrating substantial and rapid uptake by the laboratory as well as all clinical isolates (120 min), suggesting that this is a conserved process across molds. No uptake is noted in heat killed organisms or mammalian cells, demonstrating that the uptake is not due to nonspecific binding. (g) Schematic representation of the tissue mass occupied by a bacterial versus fungal infection. Representative tissue histology from mice (panel h) and human tissues (eight unique patients with pulmonary, cerebral or rhinosinusal invasive aspergillosis) demonstrating that fungi constitute a significantly higher mass (15.6%-25.9%) of the infected lesions versus E. coli infections (1.5%) (panel i) and therefore can be visualized well in vivo even though they have lower uptake than E. coli. Data are expressed as median and interquartile range (IQR). Statistical analyses were performed using a two-tailed Mann-Whitney U test. Histology staining: GMS-Grocott Methenamine Silver for fungi and Gram stain for bacteria. Abbreviations: Bq/mg= Becquerel per milligram of protein; HK: Heat-killed; ATCC: American Type Culture Collection. Methods We tested 18F-FDS uptake by clinical isolates of relevant mold pathogens; evaluated 18F-FDS positron emission tomography (PET) to detect invasive infections with Aspergillus, Rhizopus, and Mucor in clinically relevant mouse models; and performed first-in-human 18F-FDS PET in patients with invasive aspergillosis (NCT05611892).Figure 2.PET/CT in mouse models of pulmonary aspergillosis. 18F-FDS PET/CT can detect and localize infectious lesions due to pulmonary aspergillosis in immunosuppressed mice which colocalize well with the lesions noted on CT (panel a). However, even though lung disease is noted on the CT in LPS-induced sterile inflammation in mice, no 18F-FDS PET signal is noted (panel b). (c) 18F-FDS PET signal quantified as SUVmean shows significantly higher activity at fungal infection sites (n = 5 mice) versus sterile inflammation (n = 7 mice) (P = 0.003). Similar experiments were performed with 18F-fluorodeoxyglucose (18F-FDG) (n = 5 mice per group). As shown in panels d-f, 18F-FDG PET cannot distinguish fungal lesions (P > 0.999) from sterile inflammation as 18F-FDG is a nonspecific marker of inflammation. (g) GMS staining in lung samples from mice infected with Aspergillus at different magnification levels (Sidebars: 5 mm, 2 mm, and 200µm). Lesions are highlighted with arrows and outlined in yellow. Data are expressed as median and interquartile range (IQR). Statistical analyses were performed using a two-tailed Mann-Whitney U test. Abbreviations: SUVmean: Standardized uptake value mean. LPS: Lipopolysaccharide. B: bladder. Br: brain. F: fat tissue. G: gastrointestinal tract. H: heart. K: kidneys. Results 18F-FDS was rapidly accumulated by laboratory and all clinical strains of molds tested, with no uptake in heat-killed fungi or mammalian cells (Fig. 1). 18F-FDS PET was able to detect and localize infectious lesions due to pulmonary aspergillosis in immunosuppressed mice and differentiate them from LPS-induced sterile inflammation (Fig. 2); and to detect and localize rhinosinusal infections due to Aspergillus, Rhizopus, and Mucor; as well as cerebral aspergillosis (Fig. 3). Finally, first-in-human 18F-FDS PET in three patients with invasive pulmonary or cerebral aspergillosis was safe and detected infectious lesions (target-to-nontarget ratio > 3), including in a patient with an azole-resistant infection (Fig. 4).Figure 3.Extrapulmonary mouse models of invasive fungal infections. 18F-FDS PET/CT can detect and localize invasive rhinosinusal infections in immunosuppressed mice due to Aspergillus (panel a), Rhizopus (panel b) and Mucor (panel c) and cerebral aspergillosis (panel d). 18F-FDS PET signal quantified as SUVmean shows significantly higher activity at fungal rhinosinusal and brain infection sites respectively (panels e and g) versus sterile inflammation, which is confirmed using postmortem ex vivo gamma counting (panels f and h). GMS staining for fungi in mice with rhinosinusal infection by Aspergillus (panel i), Rhizopus (panel j), Mucor (panel k) and cerebral aspergillosis (panel l) at different magnification levels (Sidebars: 500 µm, and 100µm). At least four mice were used for each group for all experiments. Lesions are highlighted with arrows and outlined in yellow. Data are expressed as median and interquartile range (IQR). Statistical analyses were performed using a two-tailed Mann-Whitney U test. Abbreviations: SUV mean: Standardized uptake value mean; %ID/g: Percentage of Injected Dose per gram of tissue. LPS: Lipopolysaccharide. Conclusion 18F-FDS PET is a promising, noninvasive diagnostic tool for detection and localization of invasive mold infections in several sites. Notably, Gram-negative, Enterobacterales bacteria also metabolize sorbitol, however, patient characteristics, and response to empiric antibiotics can help distinguish bacterial versus mold infections. 18F-FDS PET represents an innovative approach to a growing diagnostic challenge in vulnerable patients, with potential to improve diagnosis and treatment, monitor responses, and enable individualized care.Figure 4.First-in-human 18F-FDS PET in patients with invasive aspergillosis. 18F-FDS PET was performed in three patients with invasive aspergillosis in accordance with U.S. FDA guidelines recruited from an ongoing study approved by the Johns Hopkins Hospitals IRB (clincialtrials.gov NCT05611892). The PET signal is clearly visualized (and quantifiable) in a 35-year-old male with refractory Hodgkin lymphoma and cerebral aspergillosis (panel a-c), a 67-year-old female with nodular pulmonary aspergillosis (panels d-f) and in a 55-year-old male with long term corticosteroid and immunosuppressive treatment with invasive pulmonary aspergillosis due to an azole-resistant Aspergillus calidoustus (panels g-i). 18F-FDS accumulates substantially at the infection sites with a target to non-target ratio of > 3 in all patients. Lesions are pointed with yellow arrows. Data are expressed as median and interquartile range (IQR). Statistical analyses were performed using a two-tailed Mann-Whitney U test. Abbreviations: SUV mean: Standardized uptake value mean. H: heart. L: liver. V: vessels. Disclosures Sanjay K. Jain, MD, Fujirebio Diagnostics, Inc. (Malvern PA): Grant/Research Support|Novobiotics, LLC: Advisor/Consultant|Novobiotics, LLC: Grant/Research Support|T3 Pharmaceuticals (Basel, Switzerland): Grant/Research Support

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• New stories, same Stigma: Framing analysis of news articles about people with alcohol-related conditions needing liver transplants

  SSM - Qualitative Research in Health · 2025-05-05 · 2 citations

  articleOpen accessSenior authorCorresponding

  Background: Public stigma surrounding alcohol use disorder (AUD) negatively impacts people with alcohol-related liver disease (ALD) in need of liver transplants (LT). Representations of LT for ALD are socially constructed in part through media, but media on this topic has been underexplored in current research. Methods: Research team members conducted systematic searches during 7/2022-5/2024 for online, publicly available articles about LT for ALD within leading English-language news sites in the US by monthly visits (n = 24). Using inductive framing analysis, we coded and identified patterns in news articles (n = 42) from 1990 to 2021 to generate frames. Findings: Our inductive analysis generated 4 main frames: (a) making individual exceptions: good people in a bad group, (b) appealing to societal costs: individual actions putting a strain on society, (c) questioning professionals' judgements: doctors' discretionary power, and (d) portraying healthcare as a competition: unfair play in a zero-sum game. Media characterized people with ALD as less deserving of liver transplant, but with individual exceptions. Articles described people with "self-induced" illnesses as irresponsible towards themselves, other LT candidates, and society; doctors as "gatekeepers" with discretionary power over how to apply criteria or rules; and the liver transplant waitlist as a competitive zero-sum game in which people with ALD are or should be deprioritized. Discussion: News articles reflect our society's stigmatization of alcohol-related conditions as well as misconceptions about transplant listing and allocation. Such mischaracterizations can further marginalize stigmatized patients with alcohol-related conditions in need of LTs. We offer recommendations for public communications, including avoiding representations of patients with ALD as exceptions to the norm and contextualizing LT for ALD within the context of public health and social and systemic factors.

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• P-2286. Invasive Fungal Infections in Patients Treated with Bruton Tyrosine Kinase Inhibitors: a Systematic Review and Meta-Analysis

  Open Forum Infectious Diseases · 2025-01-29

  reviewOpen access

  Abstract Background Controversy surrounds the true incidence of invasive fungal infections (IFIs) in patients on Bruton tyrosine kinase inhibitors (BTKIs) due to incomplete epidemiological data. This systematic review and meta-analysis evaluated the prevalence and risk factors of IFIs in BTKI-treated patients.Figure 1.Forest plot for the prevalence of invasive fungal infections in patients treated with Bruton tyrosine kinase inhibitors This study was registered under PROSPERO (CRD42024523198). The prevalence was calculated using a generalized linear mixed model random-effects meta-analysis and presented as effect sizes with 95% confidence intervals (CIs). IFIs were defined according to The European Organization for Research and Treatment of Cancer and the Mycoses Study Group Education and Research Consortium (EORTC/MSGERC) consensus definitions. Methods Studies up to April 17, 2024, from Pubmed, Scopus, and Embase, including observational studies reporting prevalence and/or associated risk factors of IFIs with at least 30 BTKI-treated patients, were searched and analyzed. IFIs were defined according to standard definitions. The prevalence of IFIs and odds ratio (ORs) for the risk factors associated with IFIs were reported alongside 95% confidence intervals (CIs).Figure 2.Forest plot for the prevalence of proven/probable invasive fungal infections in patients treated with Bruton tyrosine kinase inhibitors according to the World Health Organization regions Results This study included 14,679 patients across 24 studies (13,981 with hematologic malignancies and 67 with chronic graft-versus-host disease). Of these, 15 studies specifically included only proven/probable IFIs (ppIFIs) (Figure 1 and Table 1). The overall IFI prevalence was 2.23% (95% CI 1.73-2.88%), and for ppIFIs, was 2.64% (95% CI 1.87-3.70%). The median durations from BTKI initiation to ppIFI onset ranged from 24-186 days. The highest prevalence of ppIFIs was in patients with mantle cell lymphoma (7.60%, 95% CI 3.14-17.26%), followed by chronic lymphocytic leukemia (3.01%, 95% CI 1.93-4.66%), and Waldenström's macroglobulinemia (2.18%, 95% CI 0.33-12.96%). Regional ppIFI prevalence was the highest in Western Pacific (7.58%, 95% CI 3.19-16.94%), followed by Europe (2.60%, 95% CI 1.49-4.49%) and America (2.37%, 95% CI 1.59-3.52%) (Figure 2). The most common ppIFIs were invasive aspergillosis (1.78%, 95% CI 1.24-2.57%), followed by pneumocystosis (0.80%, 95% CI 0.16-3.81%), invasive candidiasis (0.40%, 95% CI 0.14-1.16%), and cryptococcosis (0.33%, 95% CI 0.19-0.56%). Corticosteroid use was significantly associated with ppIFIs (OR 5.03, 95% CI 2.31-10.92) (Figure 3).Figure 3.Forest plot for risk factors associated with proven/probable invasive fungal infections in patients treated with Bruton tyrosine kinase inhibitorsGRADE = Grading of Recommendations Assessment, Development and Evaluation certainty of evidence; OR = odds ratio. Odds ratios were directly extracted from regression analysis or manually calculated by comparing associated factors between patients with and without invasive fungal infections. Conclusion In conclusion, the prevalence of IFIs in patients treated with BTKIs (mostly ibrutinib) reaches 2%, and up to 7.6% in those with mantle cell lymphoma, indicating a significant risk. Antifungal prophylaxis should be customized based on individual underlying diseases and steroid use.Table 1.Characteristics of included studies BTKI = Bruton tyrosine kinase inhibitor; cGVHD = chronic graft-versus-host disease; CLL = chronic lymphocytic leukemia; DLBCL = diffuse large B-cell lymphoma; EORTC/MSGERC = the European Organization for Research and Treatment of Cancer and the Mycoses Study Group Education and Research Consortium; FL = follicular lymphoma; HCL = hairy cell leukemia; HM = hematologic malignancies; LPL = lymphoplasmacytic lymphoma; MCL = mantle cell lymphoma; MZL = marginal zone lymphoma; NA = not available; NHL = non-Hodgkin’s lymphoma; PCNSL = primary central nervous system lymphoma; PLL = prolymphocytic leukemia; RS = Richter’s syndrome; SCNSL = secondary central nervous system lymphoma; SLL = small lymphocytic lymphoma; USA = United States of America; WM = Waldenström's macroglobulinemia Disclosures Shmuel Shoham, MD, F2G: Grant/Research Support Veronica Dioverti, MD, AlloVir: Grant/Research Support|Regeneron: Advisor/Consultant|Regeneron: Grant/Research Support Nitipong Permpalung, MD, MPH, CareDx: Grant/Research Support|Cidara Therapeutics: Grant/Research Support|ClearView: Advisor/Consultant|IMMY Diagnostics: Grant/Research Support|Merck: Grant/Research Support|Pearl Diagnostics: Grant/Research Support|Pulmicide: Advisor/Consultant|Scynexis: Grant/Research Support

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• When Infection Control Practices and Democracy Collide: Reply to Paladino and Riva

  The Journal of Infectious Diseases · 2025-03-26

  article1st authorCorresponding
  PublisherDOI

• Welcome to Ethics Rounds

  Clinical Infectious Diseases · 2025-05-06

  articleOpen access1st authorCorresponding

  Ethics is central to one-on-one and population-level infectious diseases care. To give home and voice to the full scope of infectious diseases ethics, from grand to granular, from bedside to global, we hereby inaugurate the Ethics Rounds section of Clinical Infectious Diseases.

  PublisherOA PDFDOI

• Fatal Donor-Derived KSHV Inflammatory Cytokine Syndrome (KICS) in Lung Transplant

  The Journal of Heart and Lung Transplantation · 2025-04-01 · 1 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• 18F-Fluorodeoxysorbitol PET for noninvasive detection of invasive mold infections: preclinical and first-in-human studies

  Nature Communications · 2025-07-10 · 4 citations

  articleOpen access

  F-FDG), which is widely available, and represents a promising, noninvasive diagnostic tool for detecting, localizing and monitoring of invasive mold infections throughout the body.

  PublisherDOI

• Optimizing IVIg in Xenotransplantation: A Call to Action

  Transplantation · 2025-04-01 · 2 citations

  articleOpen access

  Posttransplant hypogammaglobulinemia is associated with an increased risk for infections, including bacteremia, pneumonia, invasive fungal infections, and end-organ cytomegalovirus disease.1 Infection risk is particularly high in recipients with IgG levels of <400 mg/dL.1 Experimental genetically modified pig-to-human xenotransplantation involves multimodal immunosuppression, including multiple manipulations of the B-cell compartment to suppress antibody production, for the prevention of hyperacute and acute antibody-mediated rejection. The first pig-to-human heart xenotransplant recipient developed severe hypogammaglobulinemia with an IgG level of 185 mg/dL, for which he was treated with 2 doses of IVIg.2 The University of Maryland xenotransplant team hypothesized that IVIg administration may have contributed to the eventual failure of the xenograft. Mohiuddin et al2 reported that the second dose of IVIg was correlated with clinical deterioration and a marked increase in anti-pig xenoantibody concentrations. Postmortem, they found “…strong binding to the donor porcine aortic endothelial cells was observed with three different lots of the same brand and manufacturer of IVIg.”2 However, the investigators did not observe complement-dependent cytotoxicity.2 The authors commented that “The role of anti-pig antibodies in IVIg preparation and their role in endothelial damage might be more important in xenotransplantation than in allotransplantation and should be further investigated,” and in terms of future lessons for xenotransplantation, “…the use of IVIg … might need strong justification.”2 In contrast, Cooper et al3 cast doubt on the role of IVIg in the fate of the xenograft. Based on their previous work on anti-pig antibodies in IVIg and lack of associated cytotoxicity, Cooper et al3 suggested that it was more likely recipient production, rather than exogenous IVIg, that was responsible for the rise in anti-pig antibodies. They concluded that, although IVIg in this setting is likely safe, anti-pig antibody levels in IVIg preparations vary, and screening to select IVIg lots that have low anti-pig antibody levels would be prudent.3 Although opinions may vary, enough questions have been raised that xenotransplant clinicians may be reluctant to administer IVIg, even for severe hypogammaglobulinemia. Given the intensive immunosuppression required in xenotransplantation, severe hypogammaglobulinemia could contribute to a high risk for bacterial, viral, and fungal infections.1 In turn, infections could have an adverse impact on xenograft function and could affect the success of the xenotransplant. We advocate addressing this concern in 2 ways: (1) optimizing methods for screening commercially available IVIg products for anti-pig antibodies, and (2) it would be valuable to have an IVIg product available that has undergone removal of anti-pig antibodies. Advances in antibody screening of xenorecipient serum in a pig-to-baboon model have been described by Hisadome et al4 and might be applicable to the screening of IVIg. Regarding IVIg which has undergone removal of anti-pig antibodies, Liu et al5 reported methodologies for extracorporeal removal of anti-pig antibodies by immunoabsorption. If such methods could be applied to IVIg preparations, “Xenotransplant-modified-IVIg” could become a reality. We encourage the development and further study of IVIg screening methods and modified IVIg products to optimize the safety and outcomes of future xenotransplant recipients.

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Frequent coauthors

• Nitipong Permpalung

  Johns Hopkins University

  38 shared

• Anawin Sanguankeo

  Siriraj Hospital

  24 shared

• Rongpong Plongla

  King Chulalongkorn Memorial Hospital

  24 shared

• Chatphatai Moonla

  Chulalongkorn University

  24 shared

• Pattama Torvorapanit

  King Chulalongkorn Memorial Hospital

  24 shared

• Kasama Manothummetha

  Johns Hopkins Medicine

  18 shared

• Nipat Chuleerarux

  Jackson Memorial Hospital

  18 shared

• Surachai Leksuwankun

  King Chulalongkorn Memorial Hospital

  18 shared