About

Paul J. Planet, Ph.D, M.D., is an Assistant Professor of Pediatrics at the Children’s Hospital of Philadelphia and the Perelman School of Medicine at the University of Pennsylvania. He specializes in pediatric infectious diseases with particular interests in antibiotic resistant infections such as MRSA, respiratory infections, and chronic infections in patients with cystic fibrosis. His research program focuses on the evolution and ecology of infectious diseases, utilizing whole genome phylogenetics, high-throughput sequencing, and bioinformatics to generate hypotheses tested through bench-based microbiology and molecular techniques. Dr. Planet also investigates the evolution and spread of antibiotic-resistant strains and the impact of the pulmonary microbiome in cystic fibrosis. He is a senior researcher at the American Museum of Natural History and has contributed to understanding the evolution of SARS-CoV-2.

Research topics

• Biology
• Microbiology
• Medicine
• Genetics
• Virology

Selected publications

• Stewarding the hospital sink drain: a narrative review of practical approaches for controlling gram negative pathogens in low- and middle-income countries

  Antimicrobial Resistance and Infection Control · 2026-01-24 · 1 citations

  articleOpen access

  In low- and middle-income countries (LMICs), gram-negative bacteria cause over half of intensive care unit (ICU) infections, with up to 50% mortality associated with multidrug-resistant (MDR) strains. Hospital sink drains are increasingly recognized as reservoirs for MDR organisms and are well-documented sources for nosocomial infections, yet effective and sustainable decontamination strategies-particularly for resource-limited facilities-remain elusive. This narrative review synthesizes evidence on sinks as pathogen reservoirs, evaluates limitations of existing remediation approaches, presents pilot data from our tertiary hospital in Botswana, and outlines research priorities for LMICs. We identify five dimensions that complicate control of gram-negative pathogens in sink drains: (1) poor visibility of drain interiors limiting awareness of biofilm growth extent; (2) nutrient inputs from non-hand-hygiene uses that can encourage microbial growth; (3) design barriers to cleaning and disinfection; (4) inconsistent pathogen detection methods; and (5) uncertainty about optimal regimens for cleaning and disinfection. We share data from pilot studies assessing treatment interventions for neonatal ICU sinks with high baseline contamination-including periodic addition of boiling water, sodium hypochlorite, and a commercial probiotic cleaner. Carbapenem-resistant Enterobacterales growth was suppressed by treatment with boiling water and sodium hypochlorite, but the highest prevalence of extended-spectrum beta-lactamase-producing Enterobacterales (ESBL-E) and Acinetobacter spp. was observed for sinks treated with sodium hypochlorite; probiotic cleaning was associated with the lowest ESBL-E prevalence. Findings from our literature review and pilot studies collectively support the need for a framework for hospital sink-drain stewardship that shifts away from routine chemical disinfectants and toward effective thermal or microbial strategies (e.g., probiotics, bacteriophages) that could reduce pathogen burden without selecting for more virulent or drug-resistant strains. Future work should define concentrations/regimens, safety precautions, and pathogen monitoring strategies for these approaches and embed them within sink-drain stewardship frameworks suitable to LMIC settings.

  PublisherDOI

• Empowering global disease surveillance with CURED: a tool for rapid identification of unique genomic biomarkers

  mSystems · 2026-03-19

  articleOpen access

  ABSTRACT Rapid tracking of emerging pathogenic microorganisms is crucial for designing effective treatment, infection control, and prevention strategies. While whole-genome sequencing (WGS) offers the necessary granularity to track emerging clones, it remains prohibitively expensive at the scales needed to monitor with high resolution in real time. We present CURED (Classification Using Restriction Enzyme Diagnostics), which uses a training set of sequenced genomes to identify unique k-mers with restriction sites specific to a clonal lineage. CURED enables fast and inexpensive PCR-based diagnostic tests for surveillance or outbreak investigations with minimal use of WGS. Benchmarking against existing tools, CURED compares favorably and scales more efficiently than other k-mer search strategies. We validated and tested CURED in five distinct data sets: (i) previously identified biomarkers described for a methicillin-resistant Staphylococcus aureus (MRSA) clone in Rio de Janeiro, (ii) diagnostic alleles for different lineages in the USA300 MRSA clone, (ii) the extensively drug-resistant Acinetobacter baumannii Global Clone 1 lineage, (iv) toxigenic versus non-toxigenic Clostridioides difficile , and (v) circulating S. aureus clones in a neonatal intensive care unit (NICU). We implemented CURED as part of NICU infection prevention efforts and report the test’s speed, sensitivity, and specificity in a real-world setting. CURED is a scalable, multithreaded, memory-, and cost-efficient pipeline tailored for rapid clone detection and restriction site analysis. While particularly impactful for localized outbreak investigations and targeted surveillance, our preliminary work at the global scale suggests broader implementation is feasible. CURED is freely available at https://github.com/microbialARC/CURED . IMPORTANCE Timely and cost-effective detection of emerging microbial clones is essential for infection prevention and public health surveillance. While whole-genome sequencing remains the gold standard for tracking microbial evolution and transmission, its cost, infrastructure requirements, and turnaround time limit its scalability, especially in resource-limited settings. CURED addresses this gap by enabling the development of inexpensive, PCR-based diagnostic assays informed by genomic data, without requiring further sequencing. By identifying lineage-specific restriction sites through a scalable and memory-efficient k-mer pipeline, CURED enables the translation of genome-scale insights into actionable diagnostics. This tool supports broader implementation of genomic-informed diagnostics in both local and global pathogen surveillance efforts.

  PublisherDOI

• Distribution of capsule and O types in Klebsiella pneumoniae causing neonatal sepsis in Africa and South Asia: A meta-analysis of genome-predicted serotype prevalence to inform potential vaccine coverage

  PLoS Medicine · 2026-01-12 · 3 citations

  articleOpen access

  BACKGROUND: Klebsiella pneumoniae causes ~20% of sepsis in neonates, with ~40% crude mortality. A vaccine administered to pregnant women, protecting against ≥70% of K. pneumoniae infections, could avert ~400,000 cases and ~80,000 deaths annually, mostly in Africa and South Asia. Vaccine formulations targeting the capsular polysaccharide (K) or lipopolysaccharide (O) antigens are in development. Global K. pneumoniae populations display extensive K and O diversity, necessitating a polyvalent vaccine targeted to the serotypes associated with neonatal disease in relevant geographical regions. We investigated the prevalence of K and O types associated with neonatal sepsis in Africa and South Asia to inform maternal vaccine design. METHODS AND FINDINGS: We analysed 1,930 K. pneumoniae neonate blood isolates from 13 surveillance studies across 35 sites in 13 countries. We used pathogen whole-genome sequencing to predict K and O serotypes and adjust for local transmission clusters, and Bayesian hierarchical meta-analysis to estimate K and O prevalence overall and per region, treating site as a random effect. Eighty-seven K loci were identified. KL2, KL102, KL25, KL15, and KL62 accounted for 49% of isolates. We estimate that 20 K loci, combining the eight most prevalent per region, could cover 72.9% of all infections (95% credible interval: [69.4%, 76.5%]) and ≥70% in each of Eastern, Western, and Southern Africa and South Asia. Preliminary findings from three sites suggested sufficient temporal stability of K loci to maintain 20-valent K vaccine coverage over 5-10 years, but more longitudinal data are needed to support this prediction. O types were far less diverse (n = 14 types). We estimate the top-5 (O1⍺β,2⍺, O1⍺β,2β, O2⍺, O2β, and O4) would cover 86.2% [82.6, 89.9%] of total infections (76%-92% per region), while the top-10 would cover ~99% of infections in all four regions. The main limitations of our study are the reliance on genome sequences to predict K and O serotypes (as serological typing is not available) and a lack of longitudinal data to explore stability of antigen prevalence over time. CONCLUSIONS: Neonatal sepsis is associated with diverse K and O types, with substantial geographic and temporal variation even after adjusting for localised transmission clusters. Despite this, a single 20-valent K vaccine could theoretically cover ≥70% of infections in all target regions. Locally-targeted vaccines could achieve higher coverage with lower valency, but are less feasible. In principle, very high coverage could be achieved with lower valency O-based vaccines, however, the protective efficacy against disease of antibodies targeting the O antigen remains uncertain. Further research is needed on cross-reactivity, antigen exposure, and stability of antigens over time, to better inform vaccine development.

  PublisherDOI

• Rapid dissemination of Staphylococcus aureus in the neonatal intensive care unit is associated with invasive infection

  Nature Communications · 2026-02-09 · 2 citations

  articleOpen accessSenior author

  Staphylococcus aureus is a leading cause of severe infections in neonatal intensive care units (NICUs). We present results of precision surveillance of S. aureus carriage and invasive infection in a cohort study of high-risk infants in the NICU with the goal of identifying novel strategies for prevention and control. Using whole genome sequence guided epidemiology over a 3-year timeframe, we identify spatial and temporal links for transmission between babies, suggesting shared spaces, caregivers, and physical proximity as major risks for transmission in the NICU. Moreover, environmental surveillance reveals potential environmental reservoirs of S. aureus. Remarkably, specific clusters of S. aureus strains that are associated with invasive infection are also detected in more infants over time during routine surveillance, suggesting a strong link between the rate of dissemination and disease in this vulnerable population. Overall, our findings demonstrate a strong association amongst colonization, transmission, persistence, and the development of invasive infections, underscoring the importance of targeted measures to prevent S. aureus infections in the NICU setting. In this work, authors use whole genome tracking in a neonatal intensive care unit to reveal a strong link between Staphylococcus aureus colonization and invasive infection, pinpointing critical new targets for infection prevention in high-risk infants.

  PublisherOA PDFDOI

• The Guild Model of CF Airway Microbial Ecology

  mBio · 2026-04-30

  articleOpen access

  Ecological guilds are groups of organisms that utilize the same class of resources and occupy similar niches, regardless of their taxonomic identities. Here we propose the Guild Model for Cystic Fibrosis Airway Microbial Ecology, which considers the ecological function and wider role of each microbe in the ecosystem. This model consists of four functional guilds: (i) "Brewers" metabolize host-derived substrates (e.g., mucins) and produce fermentation products; (ii) "Drunkards" exploit the metabolic niche built by Brewers, consuming fermentation products and secreting exopolysaccharides to build biofilms; (iii) "Putrifiers" produce toxic compounds causing inflammation and tissue necrosis; and (iv) "Nihilists" are specialist pathogens characterized by intracellular or lytic life cycles and cytotoxin production. By focusing on microbial function and the broader community context, this model offers a refined framework for interpreting cystic fibrosis airway ecology. Although developed for CF, the Guild Model is adaptable to other diseases influenced by microbial ecology.

  PublisherDOI

• Functional CFTR may be required for Prevotella melaninogenica regulation of epithelial cell defense against Staphylococcus aureus

  Journal of Cystic Fibrosis · 2025-11-05

  articleOpen access

  BACKGROUND: Prevotella melaninogenica is enriched in the lungs of people with cystic fibrosis (pwCF), yet its functional impact on respiratory tract homeostasis remains incompletely understood. Prior studies identified immune modulatory effects following lung exposure to Prevotella, but the relevance of these findings for CF infections is unknown. METHODS: The impact of P. melaninogenica on infection with the CF pathogen Staphylococcus aureus was evaluated using a mouse lung infection model and by measuring S. aureus adherence to human respiratory tract cystic fibrosis transmembrane conductance regulator (CFTR) mutant and isogenic wild-type (WT)-corrected CFBE41o- epithelial cells. Epithelial cytokine/chemokine secretion and RNA-sequencing were performed to compare P. melaninogenica-induced signaling programs in WT-corrected versus CFTR mutant cells. RESULTS: P. melaninogenica significantly reduced S. aureus lung infection, associated with elevated S. aureus killing by lung neutrophils and impaired S. aureus adherence to epithelial cells. Live or killed P. melaninogenica were sufficient to mediate these effects, which were dependent on TLR2. P. melaninogenica impairment of S. aureus adherence required functional CFTR, as this effect was lost in CFTR mutant cells but restored by CFTR modulators. RNA-sequencing identified several antibacterial defense pathways selectively upregulated by P. melaninogenica in WT corrected epithelial cells, correlating with higher IL-8 and IL-6 cytokine production. CONCLUSIONS: P. melaninogenica enhanced neutrophil and epithelial defense against S. aureus, but the benefits of epithelial cell regulation by P. melaninogenica were lost with CFTR dysfunction. CFTR modulators rescued P. melaninogenica responsiveness in epithelial cells, highlighting the potential for synergistic effects of host-microbiome interactions and CFTR targeted therapies.

  PublisherOA PDFDOI

• Contribution of nosocomial transmission to <i>Klebsiella pneumoniae</i> neonatal sepsis in Africa and South Asia: analysis of infection clusters inferred from pathogen genomics and temporal data

  medRxiv · 2025-11-17

  preprintOpen access

  Abstract Background Klebsiella pneumoniae is the leading cause of sepsis among neonates in low- and middle-income countries (LMICs) in Africa and Asia, contributing substantially to the overall burden of antimicrobial resistant (AMR) infections and mortality among neonates globally. Pathogen sequencing has been used to investigate case clusters and confirm nosocomial transmission in a small number of neonatal units. Here we utilise pathogen sequence data to estimate the fraction of K. pneumoniae neonatal sepsis attributable to nosocomial transmission in African and South Asian countries. Methods and Findings We estimated the proportion of invasive K. pneumoniae disease involved in nosocomial transmission clusters in a given neonatal unit, using single-linkage clustering based on pairwise temporal and genetic distances estimated from bacterial whole-genome sequences aggregated from 10 contributing studies. Analysing 1,523 K. pneumoniae isolates from 27 units in 13 countries in Africa and South Asia between 2013 and 2023, we inferred 156 nosocomial transmission clusters, ranging from 2 to 188 neonates each (83 of the clusters comprised ≥3 cases). Overall, we estimated that 1,035 neonatal infections (68.0%) were part of nosocomial transmission clusters. Excluding the first infection in each cluster as a potential index case, we estimate at least 879 (57.7%) infections were acquired via nosocomial transmission. Sensitivity analyses showed that results were robust to the choice of genetic distance estimation methods and thresholds used to define clusters, and cluster estimates were stable over temporal distance thresholds ranging from 2 to 8 weeks. Isolates were mostly extended-spectrum beta-lactamase (ESBL) producers (90.9%) and included 172 multi-locus sequence types (STs). Fourteen STs, including several globally recognised multidrug-resistant lineages, were associated with transmission clusters at multiple units and these were collectively responsible for two-thirds of all infections. Carriage of carbapenemase genes (adjusted odds ratio, aOR = 2.08 [95% confidence interval, CI: 1.04–4.14], p=0.02) and ESBL genes (aOR = 2.48 [95% CI: 1.26–4.90] p=0.006) were significantly positively associated with transmission. Conclusions Nosocomial transmission contributes to a substantial proportion of K. pneumoniae sepsis in neonatal care units in Africa and South Asia. Reducing transmission within these settings through improved infection prevention and control and other measures could substantially reduce the neonatal sepsis burden. A high burden of transmission clusters is associated with the same drug-resistant lineages that are recognised as high-risk clones associated with hospital outbreaks in high-income countries, indicating global connectivity of the AMR pathogen population. Author Summary Why Was This Study Done? Klebsiella pneumoniae is the leading cause of sepsis among neonates in low- and middle-income countries (LMICs) in Africa and Asia, and the infections are difficult to treat due to rising rates of antimicrobial resistance. Invasive bacterial diseases are typically transmitted to neonates from their mothers before, during or soon after birth (vertical transmission) or from the hospital environment and healthcare workers (horizontal transmission). The fraction of K. pneumoniae neonatal sepsis cases attributable to horizontal transmission is unknown, but this information is important to understand the role of infection prevention and control (IPC) measures in lowering disease burden. What Did the Researchers Do and Find? We developed a simple method to detect transmission clusters from genetic and temporal distance data and found the method to be robust to the choice of genetic and temporal distance thresholds. We applied this method to detect transmission clusters among 1,523 K. pneumoniae neonatal sepsis cases from 10 studies and 27 hospitals across Africa and South Asia. We estimate over half of sepsis cases (68.0%) were part of a transmission cluster, and by excluding the hypothetical index case for each cluster we estimate at least 57.7% of infections were acquired via nosocomial transmission. Most of the isolates (90.9%) were extended-spectrum beta-lactamase (ESBL) producers (conferring resistance to third-generation cephalosporin antibiotics), and carriage of ESBL and carbapenemase genes (conferring resistance to carbapenem antibiotics) were positively associated with transmission. Fourteen genetic lineages were associated with clusters in multiple neonatal units, together accounting for two-thirds of all infections. Many of these same lineages are common causes of drug-resistant hospital outbreaks in high-income countries. What Do These Findings Mean? A substantial proportion of K. pneumoniae neonatal sepsis cases are potentially preventable with improvements in IPC in neonatal units. Further work is needed to identify and better understand transmission routes and risk factors for transmission to support the implementation of effective and scalable IPC solutions. Our findings highlight the importance of genomic surveillance to support IPC interventions for K. pneumoniae and other pathogens, and reveal many of the same ‘drug-resistant problem clones’ are responsible for hospital outbreaks across high-and low-income countries. The high rates of ESBL gene carriage among isolates in this study indicates that empirical treatment based on the current WHO guidelines may result in high rates of treatment failure. The limitations of this study include the lack of sufficient clinical data to allow high-resolution investigation of transmission dynamics, as well as facility-level data to investigate contributors to the observed differences in transmission burden across sites.

  PublisherOA PDFDOI

• Microbial succession at weaning is guided by microbial metabolism of host glycans

  Microbiome · 2025-10-28 · 1 citations

  articleOpen access

  BACKGROUND: The weaning transition from a milk-based to a solid-food diet supports critical developmental changes to the intestinal microbiota and immune system. However, the specific microbial and host features that influence microbial succession at weaning are not well understood. RESULTS: Here, we developed a simple approach to investigate the complex dynamics of microbial succession during weaning by co-housing gnotobiotic mice colonized with the defined pre-weaning community PedsCom and the adult-derived consortium Oligo-MM12 (OMM12). Co-housing PedsCom mice with OMM12 recapitulated microbial succession at weaning and induced immune system maturation in PedsCom mice. Unexpectedly, we found that the OMM12 microbes with the highest host glycan utilization profiles were the most adept colonizers of PedsCom mice. Genomic analysis confirmed that PedsCom is deficient in the carbohydrate-active enzymes responsible for degrading host-derived glycans, including mucins, compared to adult-derived consortia. We validated a role for glycan utilization in vivo by demonstrating that the mucus-degrading commensal microbe Akkermansia muciniphila critically depends on the metabolism of mucin glycans for stable colonization of PedsCom mice. CONCLUSIONS: These findings highlight the importance of host-derived glycans in shaping microbial communities during the weaning transition and suggest host glycans as novel targets to modulate intestinal microbial populations, introduce beneficial probiotics, and enhance immune system development during weaning. Video Abstract.

  PublisherOA PDFDOI

• 279 Host-Mediated Bacterial Interference to Prevent Epithelial Colonization by MRSA

  Journal of Investigative Dermatology · 2025-11-01

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Evolution of strain diversity and virulence factor repertoire in pediatric Staphylococcus aureus isolates

  PLoS ONE · 2025-07-31 · 1 citations

  articleOpen accessCorresponding

  BACKGROUND: Invasive Staphylococcus aureus infections cause high morbidity and mortality in children and adults. With rising antimicrobial resistance, optimal prevention strategies and novel therapeutics are needed. As an effective vaccine remains elusive, characterization of invasive isolates over time is required to identify determinants of invasive infection. METHODS: S. aureus isolates recovered from children with invasive infection and those with colonization were obtained. Isolates were examined by whole genome sequencing to evaluate gene repertoire, sequence type, clonal complex, and phylogenetic characterization, and isolate characteristics were correlated to clinical data. RESULTS: 118 children with invasive S. aureus infections were enrolled; 56% of infections were caused by methicillin-susceptible S. aureus (MSSA). Methicillin-resistance (MRSA) was associated with increased inflammation, though clinical outcomes of MRSA vs MSSA did not differ. Colonization isolates exhibited higher sequence type diversity than invasive isolates. Nine distinct clonal complexes (CC) were identified among all isolates; CC8 and CC5 were associated with higher clinical severity scores. Accessory gene regulator locus type 1, Panton-Valentine Leukocidin, and arginine catabolic mobile element declined over time. Staphylokinase and leukocidin ED were associated with invasive infection, while enterotoxin B was more frequent in colonizing isolates. CONCLUSIONS: We observed a significant expansion in sequence type diversity among invasive clinical isolates over 12 years with the emergence of newly invasive clones in recent years. The presence of staphylokinase and LukED were associated with invasive infection over time. These findings provide insights into the pathogenesis of invasive S. aureus and may provide putative targets for immunologic approaches to prevention.

  PublisherDOI

Recent grants

• NIH Grant K08AI101005

  NIH · $405k · 2015

• Bacterial Interference to Prevent Staphylococcus aureus Infection

  NIH · $457k · 2018–2022

• In Host Evolution of Nontuberculous Mycobacteria in Cystic Fibrosis

  NIH · $485k · 2020–2023

• Bacterial Interference to Prevent Staphylococcus aureus Infection

  NIH · $1.3M · 2018–2023

Frequent coauthors

• Ahmed M. Moustafa

  University of Pennsylvania

  220 shared

• Apurva Narechania

  American Museum of Natural History

  119 shared

• Barry N. Kreiswirth

  Hackensack Meridian Health

  105 shared

• Barun Mathema

  Columbia University

  99 shared

• César A. Arias

  Universidad El Bosque

  90 shared

• Chanelle Ryan

  Children's Hospital of Philadelphia

  77 shared

• Liang Chen

  71 shared

• José M. Munita

  Universidad del Desarrollo

  69 shared