About

Arturo Casadevall, MD, PhD, is a Johns Hopkins Bloomberg School of Public Health faculty member serving as the Chair of Molecular Microbiology & Immunology and holding the titles of Bloomberg Distinguished Professor and Alfred & Jill Sommer Professor. His research focuses on host defense mechanisms, how fungi cause disease, and the development of antibody-based therapies for infectious diseases. His laboratory studies fundamental questions such as how microbes cause disease and how hosts, including humans, protect themselves against microbes. A major focus of his work is on Cryptococcus neoformans, a ubiquitous environmental fungus that causes disease primarily in immunocompromised individuals, including lung infections and fungal meningitis. His research investigates the virulence factors of C. neoformans, such as melanin production, and explores antibody-based treatments, including an antibody to fungal melanin being evaluated for melanoma treatment. Additionally, his lab works with other microorganisms like Bacillus anthracis, aiming to develop countermeasures against biological threats. Dr. Casadevall's extensive background includes education at New York University, where he earned his MD, PhD, and MS, and a distinguished career marked by numerous awards and honors in microbiology and immunology.

Research topics

• Biology
• Virology
• Medicine
• Immunology
• Pathology
• Genetics
• Biochemistry
• Political Science
• Cell biology
• Botany
• Internal medicine
• Geography
• Microbiology
• Environmental planning
• Biotechnology
• Ecology
• Intensive care medicine
• Environmental ethics

Selected publications

• The heat-ramp method to study regulated cell death in a pathogenic yeast <i>Cryptococcus neoformans</i>

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-19

  articleOpen access

  Abstract Human fungal pathogens cause a significant public health burden. While no reliable surveilence data are available, estimations suggest that 1 billion infections and over 2 million deaths are attributable to fungal infections annually worldwide. This drove the World Health Organization to generate a priority list of fungal pathogens for reearch, which includes the yeast Cryptococcus neoformans in a top critical priority. With the rise of drug-resistance and emerging fungal pathogens, new conceptual strategies for antifungal therapies are needed in addition to existing antibiotic development pipelines to meet clinical needs. Intrinsic cell death pathways encoded by pathogenic fungi are largely unstudied but could be leveraged for antifungal therapy analogous to anti-cancer therapeutics that activate apoptosis or other cell death mechanisms. Thus far, molecularly defined fungal cell death mechanisms are best characterized for only a few, predominantly model filamentous species. To extend these studies to pathogenic yeast, here we describe and demonstrate a tunable heat-ramp stimulus that when applied to small volumes of yeast cell suspensions reveals a protracted cell death process in the pathogenic yeast Cryptococcus neoformans . This low cost protocol induces robust and reproducible phenotypes to study gene-dependent mechanisms in laboratory strains and clinical isolates.

  PublisherOA PDFDOI

• Pathophysiology of intracranial hypertension in cryptococcal meningoencephalitis

  mBio · 2026-04-13

  articleOpen accessSenior author

  Cryptococcal meningoencephalitis (CME) is a major cause of death and disability, and intracranial hypertension is a leading, treatable contributor to mortality and neurologic sequelae. Across CME cohorts, markedly elevated cerebrospinal fluid (CSF) opening pressure is common and often occurs despite minimal ventriculomegaly or diffuse edema on neuroimaging. This review synthesizes clinical, microbiological, imaging, pathological, and experimental evidence to define priorities for mechanistic research. Intracranial pressure (ICP) physiology predicts that once intracranial compliance is exhausted, small volume changes can produce rapid pressure increases, making CSF dynamics central to many intracranial hypertension syndromes. In CME, the frequent, rapid improvement after therapeutic CSF drainage, followed by pressure re-accumulation, supports a CSF outflow-limited mechanism for ICP. Convergent observations, including correlations between opening pressure and fungal/capsular polysaccharide burden and postmortem localization of organisms and polysaccharide at candidate CSF efflux sites, support a model of increased CSF outflow resistance. Potential modifiers include cryptococcal phenotypes (e.g., capsule size/architecture, aggregation), host immune and osmotic states, and disruption of perivascular ("glymphatic") transport that may alter clearance and compliance. Alternative dominant mechanisms (e.g., mass effect, obstructive hydrocephalus, venous sinus thrombosis, or inflammatory edema in immune reconstitution inflammatory syndrome/post-infectious inflammatory response syndrome) likely account for a minority of cases but remain clinically important. Current ICP control relies on invasive CSF drainage, and empiric pharmacologic approaches have not translated well, meaning progress will depend on both clinical and basic science research that link fungal and host factors to ICP trajectories, quantify efflux-site burden, directly measure outflow resistance, and explore adjunctive therapeutics that address CSF efflux and fungal clearance.

  PublisherDOI

• Fungal proliferation before and after the Cretaceous–Paleogene mass extinction event in North America

  Proceedings of the National Academy of Sciences · 2026-05-12

  articleOpen accessSenior authorCorresponding

  Palynological evidence of postcatastrophe fungal proliferation after global calamities has been found for the Permian-Triassic and Cretaceous-Paleogene (K/Pg) extinction events. However, unlike the globally documented post-Permian fungal bloom, evidence of a post-Cretaceous event has previously been limited to a single site in New Zealand. Our analysis of a K/Pg boundary section from the Denver Basin in Colorado revealed a fungal proliferative spike occurring immediately after the Chicxulub meteorite impact. The discovery of a postimpact fungal bloom in North America corroborates the New Zealand finding and supports the interpretation that this was a global phenomenon. We also identified a prolonged interval of elevated fungal abundance in the Late Cretaceous, dating to approximately 30,000 to 10,000 y before the impact, temporally correlated to a period of climatic cooling at the site and intriguingly coincident with the high-volume Poladpur phase of the Deccan Traps volcanic eruptions. Taken together with reports of fungal expansion following prior global calamities, these findings indicate that fungi can often flourish in the aftermath of ecosystem-level collapse. Given the capacity of fungi to cause disease in both plants and animals, the occurrence of fungal proliferative events has potential implications for the recovery of species surviving global cataclysms.

  PublisherDOI

• Transforming the American Academy of Microbiology for social good through scientific portfolios

  mBio · 2026-05-05

  articleOpen access

  As the research landscape evolves, scientific societies must adapt their programs to meet changing community needs. The American Academy of Microbiology (Academy or AAM) has recently developed a new model centered around scientific portfolios aimed at advancing its vision of becoming an effective scientific think tank. Here, we describe this transition and the process used to develop and implement a portfolio-based approach. We highlight the Climate Change and Microbes Scientific Portfolio as a case study, demonstrating its successes and its ability to guide the design of future portfolios.

  PublisherDOI

• Communicable episode 31: Climate change and fungal spread

  CMI Communications · 2025-08-05

  articleOpen access
  PublisherDOI

• Antibody-Fab and -Fc features promote Mycobacterium tuberculosis restriction

  Immunity · 2025-05-30 · 9 citations

  articleOpen access

  Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), a leading cause of death by an infectious disease globally, has no efficacious vaccine. Antibodies are implicated in M. tuberculosis control, but the mechanisms of action remain poorly understood. We assembled a library of monoclonal antibodies (mAb) and screened for M. tuberculosis-restrictive activity in mice, identifying protective antibodies targeting diverse antigens. To dissect the mechanism of mAb-mediated M. tuberculosis restriction, we optimized a protective lipoarabinomannan-specific mAb, generating Fc variants. In vivo analysis of these Fc variants revealed a role for Fc-effector function in M. tuberculosis restriction. Restrictive Fc variants altered distribution of M. tuberculosis across innate immune cells. Single-cell transcriptomics highlighted distinctly activated pathways within innate immune cell subpopulations, identifying early activation of neutrophils as a key signature of mAb-mediated M. tuberculosis restriction. Therefore, antibody-mediated restriction of M. tuberculosis is associated with reorganization of the tissue-level immune response to infection and depends on the collaboration of antibody Fab and Fc.

  PublisherDOI

• Fungal proliferation before and after the Cretaceous-Paleogene mass extinction in North America

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-12

  articleOpen accessSenior author

  Palynological evidence of post-catastrophe fungal proliferation after global calamities has been found for the Permian-Triassic and Cretaceous-Paleogene (K/Pg) extinction events. However, unlike the globally documented post-Permian fungal bloom, evidence of a post-Cretaceous event has previously been limited to a single site in New Zealand. Our analysis of a K/Pg boundary section from the Denver Basin in Colorado revealed a fungal proliferative spike occurring immediately after the Chicxulub impact. The discovery of a post-impact fungal bloom in North America corroborates the New Zealand finding and supports the interpretation that this was a global phenomenon. We also identified a prolonged interval of elevated fungal abundance in the Late Cretaceous, dating to approximately 30,000-10,000 years before the impact, temporally correlated to a period of climatic cooling at the site and intriguingly coincident with the Poladpur phase of the Deccan Traps. Taken together with reports of fungal expansion following prior global calamities, these findings indicate that fungi can often flourish in the aftermath of ecosystem-level collapse. Given the capacity of fungi to cause disease in both plants and animals, the occurrence of fungal proliferative events has major potential implications for the recovery of surviving species after global cataclysms.

  PublisherDOI

• A conserved enzymatic toolkit targeting host cell metabolism is associated with Cryptococcus neoformans intracellular survival in protozoal and mammalian phagocytic cells

  PLoS Pathogens · 2025-12-26

  articleOpen accessSenior author

  The outcome of the interaction between Cryptococcus neoformans and infected hosts can be determined by whether the fungal cell survives ingestion by phagocytic cells. This applies to both unicellular and multicellular hosts such as amoeba and animals, respectively. Ingestion by phagocytic cells results in the formation of the cryptococcal phagosome but this structure has proved difficult to isolate. In this study, we report the successful isolation of cryptococcal phagosomes from murine and human phagocytes, followed by their characterization using proteomic and transcriptional analysis. Comparison of cryptococcal proteins from Acanthamoeba castellanii, Mus musculus, and Homo sapiens phagocytes revealed the existence of a shared set suggesting a conserved fungal response to ingestion by phagocytic cells. Given that the cryptococcal intracellular pathogenic strategy is ancient, dating to at least to the cretaceous epoch, these results are consistent with the notion that the fungal response to ingestion reflects the result of selection pressures by environmental ameboid predators over eons of evolutionary time. We propose the existence of a conserved cryptococcal toolkit for intracellular survival that includes metabolic enzymes, which disrupt host cell metabolic function, thus providing a common strategy for cryptococcal survival after ingestion by phylogenetically distant phagocytic hosts.

  PublisherDOI

• A Rapid Systematic Review of U.S. Food and Drug Administration–authorized COVID-19 Treatments

  Open Forum Infectious Diseases · 2025-10-04 · 1 citations

  letterOpen access
  PublisherDOI

• Pathogenicity and virulence of Cryptococcus neoformans from an environmental perspective

  Virulence · 2025-08-14 · 8 citations

  articleOpen access1st authorCorresponding

  is common in the environment resulting in widespread human exposure but disease in immunocompetent hosts is rare. The fungus is endowed with powerful virulence factors that allow it to resist immunological mechanisms for clearance. Despite this, the fungus does not appear to have any need for an animal host in its life cycle and consequently these virulence factors are traits selected for environmental survival that function accidentally as enablers of virulence in susceptible hosts. Considerable progress has been made in understanding its life cycle, ecology, pathogenicity mechanisms, and antigenic composition for vaccine design. In this essay, the problem of cryptococcal pathogenesis and virulence is approached from the viewpoint of considering these processes in the context of its environment and ecology.

  PublisherDOI

Recent grants

• Molecular Characterization of C. neoformans Antibodies

  NIH · $3.9M · 2015–2018

• Biology of Fungal Melanin

  NIH · $533k · 2003–2020

• NIH Grant R21GM071421

  NIH · $251k · 2006

• NIH Grant R01AI033774

  NIH · $7.2M · 2015

• The Molecular and Cellular Basis of Infectious Diseases (MCBID) Program

  NIH · $12.2M · 1994–2026

Frequent coauthors

• John R. Perfect

  Duke University

  153 shared

• Ekaterina Dadachova

  University of Saskatchewan

  148 shared

• Joshua D. Nosanchuk

  Albert Einstein College of Medicine

  141 shared

• Ruth E. Stark

  City College of New York

  136 shared

• Shmuel Shoham

  Johns Hopkins Medicine

  126 shared

• Rafael Prados‐Rosales

  Universidad Autónoma de Madrid

  115 shared

• Aaron A.R. Tobian

  109 shared

• Evan M. Bloch

  Johns Hopkins University

  107 shared

Awards & honors

• Stanley Konkol Memorial Award (1979)
• Chemistry Department Service Award (1979)
• Salk Scholarship (1979-1983)
• Medical Scientist Training Program Fellowship (1979-1985)
• Montefiore Fellow of the Year Award (1989)