Bio


Katherine Konvinse, MD, PhD is a resident physician in the Stanford Pediatric Residency Research Track Program. She completed her MD and PhD training at Vanderbilt University School of Medicine. Her current research focuses on characterizing the serum antibody responses in pediatric patients exposed to viral infections including COVID-19 and respiratory syncytial virus (RSV) under the mentorship of Professor PJ Utz.

Clinical Focus


  • Residency

Academic Appointments


Honors & Awards


  • Glasgow-Rubin Certificate of Commendation for Academic Achievement, American Medical Women’s Association (2020)
  • Richard B. Johnston Award, Department of Pediatrics, Vanderbilt University Medical Center (2020)
  • Award for Excellence in Infectious Diseases, Departments of Medicine and Pediatrics, Vanderbilt University Medical Center (2020)
  • Dean’s Award for Exceptional Achievement in Graduate Studies, Vanderbilt University (2018 - 2019)
  • Best Trainee Abstract Award Winner, Pharmacogenomics Research Network – American Society of Human Genetics Joint Symposium (2018)
  • Second Best Poster Award, Personalized Medicine Day, Vanderbilt University (2018)
  • Best Poster Award in the Category of Immunopathogenesis, Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis 2017 (2017)

Boards, Advisory Committees, Professional Organizations


  • Member, American Academy of Pediatrics (2019 - Present)
  • Member, Alpha Omega Alpha Honor Medical Society (2019 - Present)
  • Member, American Physician Scientists Association (2016 - Present)
  • Member, Federation of Clinical Immunology Societies (2016 - Present)
  • Member, Pharmacogenomics Research Network (2016 - Present)
  • Member, American Association of Immunologists (2016 - 2019)

Professional Education


  • Doctor of Philosophy, Vanderbilt University (2019)
  • Master of Science, Vanderbilt University (2017)
  • Doctor of Medicine, Vanderbilt University (2020)
  • Bachelor of Arts, Cornell University (2013)
  • Residency, Stanford University, Pediatrics
  • MD, Vanderbilt University (2020)
  • PhD, Vanderbilt University, Microbiology and Immunology (2019)
  • BA, Cornell University (2013)

Patents


  • Elizabeth Phillips, Simon Mallal, Katherine Konvinse, Abha Chopra. "United States Patent US62/805,717 Detection of Human Leukocyte Antigen-A*32:01 in Connection with Determining Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) and Methods of Treating Bacterial Infection in a Subject with Vancomycin-Induced DRESS.", Vanderbilt University, Feb 14, 2020

All Publications


  • Cross-reactivity between vancomycin, teicoplanin, and telavancin in patients with HLA-A∗32:01-positive vancomycin-induced DRESS sharing an HLA class II haplotype. The Journal of allergy and clinical immunology Nakkam, N., Gibson, A., Mouhtouris, E., Konvinse, K. C., Holmes, N. E., Chua, K. Y., Deshpande, P., Li, D., Ostrov, D. A., Trubiano, J., Phillips, E. J. 2021; 147 (1): 403-405

    View details for DOI 10.1016/j.jaci.2020.04.056

    View details for PubMedID 32439433

    View details for PubMedCentralID PMC7674263

  • Human Herpesvirus 6 Detection during the Evaluation of Sepsis in Infants Using the FilmArray Meningitis/Encephalitis Panel. The Journal of pediatrics Dantuluri, K. L., Konvinse, K. C., Crook, J., Thomsen, I. P., Banerjee, R. 2020; 223: 204-206.e1

    Abstract

    We used the FilmArray meningitis/encephalitis panel for evaluation of sepsis in febrile neonates. We detected human herpesvirus 6, a virus we did not routinely test for previously, in the cerebrospinal fluid of 7 neonates. In all 7 cases, detection of the virus did not warrant antiviral treatment.

    View details for DOI 10.1016/j.jpeds.2020.03.023

    View details for PubMedID 32417077

  • Analysis of Skin-Resident Memory T Cells Following Drug Hypersensitivity Reactions. The Journal of investigative dermatology Trubiano, J. A., Gordon, C. L., Castellucci, C., Christo, S. N., Park, S. L., Mouhtouris, E., Konvinse, K., Rose, M., Goh, M., Boyd, A. S., Phillips, E. J., Mackay, L. K. 2020; 140 (7): 1442-1445.e4

    View details for DOI 10.1016/j.jid.2019.11.020

    View details for PubMedID 31883960

    View details for PubMedCentralID PMC7369252

  • Single-cell transcriptomics reveal polyclonal memory T-cell responses in skin with positive abacavir patch test results. The Journal of allergy and clinical immunology Redwood, A. J., Rwandamuriye, F., Chopra, A., Leary, S., Ram, R., McDonnell, W., Konvinse, K., White, K., Pavlos, R., Koelle, D. M., Mallal, S., Phillips, E. J. 2019; 144 (5): 1413-1416.e7

    View details for DOI 10.1016/j.jaci.2019.09.013

    View details for PubMedID 31574267

    View details for PubMedCentralID PMC7051072

  • A Rapid Allele-Specific Assay for HLA-A*32:01 to Identify Patients at Risk for Vancomycin-Induced Drug Reaction with Eosinophilia and Systemic Symptoms. The Journal of molecular diagnostics : JMD Rwandamuriye, F. X., Chopra, A., Konvinse, K. C., Choo, L., Trubiano, J. A., Shaffer, C. M., Watson, M., Mallal, S. A., Phillips, E. J. 2019; 21 (5): 782-789

    Abstract

    Human leukocyte antigen (HLA) alleles have been implicated as risk factors for immune-mediated adverse drug reactions. The authors recently reported a strong association between HLA-A*32:01 and vancomycin-induced drug reaction with eosinophilia and systemic symptoms. Identification of individuals with the risk allele before or shortly after the initiation of vancomycin therapy is of great clinical importance to prevent morbidity and mortality, and improve drug safety and antibiotic treatment options. A prerequisite to the success of pharmacogenetic screening tests is the development of simple, robust, cost-effective single HLA allele test that can be implemented in routine diagnostic laboratories. In this study, the authors developed a simple, real-time allele-specific PCR for typing the HLA-A*32:01 allele. Four-hundred and fifty-eight DNA samples including 30 HLA-A*32:01-positive samples were typed by allele-specific PCR. Compared with American Society for Histocompatibility and Immunogenetics-accredited, sequence-based, high-resolution, full-allelic HLA typing, this assay demonstrates 100% accuracy, 100% sensitivity (95% CI, 88.43% to 100%), and 100% specificity (95% CI, 99.14% to 100%). The lowest limit of detection of this assay using PowerUp SYBR Green is 10 ng of template DNA. The assay demonstrates a sensitivity and specificity to differentiate the HLA-A*32:01 allele from closely related non-HLA-A*32 alleles and may be used in clinical settings to identify individuals with the risk allele before or during the course of vancomycin therapy.

    View details for DOI 10.1016/j.jmoldx.2019.04.006

    View details for PubMedID 31158526

    View details for PubMedCentralID PMC6734857

  • HLA-A*32:01 is strongly associated with vancomycin-induced drug reaction with eosinophilia and systemic symptoms. The Journal of allergy and clinical immunology Konvinse, K. C., Trubiano, J. A., Pavlos, R., James, I., Shaffer, C. M., Bejan, C. A., Schutte, R. J., Ostrov, D. A., Pilkinton, M. A., Rosenbach, M., Zwerner, J. P., Williams, K. B., Bourke, J., Martinez, P., Rwandamuriye, F., Chopra, A., Watson, M., Redwood, A. J., White, K. D., Mallal, S. A., Phillips, E. J. 2019; 144 (1): 183-192

    Abstract

    Vancomycin is a prevalent cause of the severe hypersensitivity syndrome drug reaction with eosinophilia and systemic symptoms (DRESS), which leads to significant morbidity and mortality and commonly occurs in the setting of combination antibiotic therapy, affecting future treatment choices. Variations in HLA class I in particular have been associated with serious T cell-mediated adverse drug reactions, which has led to preventive screening strategies for some drugs.We sought to determine whether variation in the HLA region is associated with vancomycin-induced DRESS.Probable vancomycin-induced DRESS cases were matched 1:2 with tolerant control subjects based on sex, race, and age by using BioVU, Vanderbilt's deidentified electronic health record database. Associations between DRESS and carriage of HLA class I and II alleles were assessed by means of conditional logistic regression. An extended sample set from BioVU was used to conduct a time-to-event analysis of those exposed to vancomycin with and without the identified HLA risk allele.Twenty-three subjects met the inclusion criteria for vancomycin-associated DRESS. Nineteen (82.6%) of 23 cases carried HLA-A*32:01 compared with 0 (0%) of 46 of the matched vancomycin-tolerant control subjects (P = 1 × 10-8) and 6.3% of the BioVU population (n = 54,249, P = 2 × 10-16). Time-to-event analysis of DRESS development during vancomycin treatment among the HLA-A*32:01-positive group indicated that 19.2% had DRESS and did so within 4 weeks.HLA-A*32:01 is strongly associated with vancomycin-induced DRESS in a population of predominantly European ancestry. HLA-A*32:01 testing could improve antibiotic safety, help implicate vancomycin as the causal drug, and preserve future treatment options with coadministered antibiotics.

    View details for DOI 10.1016/j.jaci.2019.01.045

    View details for PubMedID 30776417

    View details for PubMedCentralID PMC6612297

  • Applications of Immunopharmacogenomics: Predicting, Preventing, and Understanding Immune-Mediated Adverse Drug Reactions. Annual review of pharmacology and toxicology Karnes, J. H., Miller, M. A., White, K. D., Konvinse, K. C., Pavlos, R. K., Redwood, A. J., Peter, J. G., Lehloenya, R., Mallal, S. A., Phillips, E. J. 2019; 59: 463-486

    Abstract

    Adverse drug reactions (ADRs) are a significant health care burden. Immune-mediated adverse drug reactions (IM-ADRs) are responsible for one-fifth of ADRs but contribute a disproportionately high amount of that burden due to their severity. Variation in human leukocyte antigen ( HLA) genes has emerged as a potential preprescription screening strategy for the prevention of previously unpredictable IM-ADRs. Immunopharmacogenomics combines the disciplines of immunogenomics and pharmacogenomics and focuses on the effects of immune-specific variation on drug disposition and IM-ADRs. In this review, we present the latest evidence for HLA associations with IM-ADRs, ongoing research into biological mechanisms of IM-ADRs, and the translation of clinical actionable biomarkers for IM-ADRs, with a focus on T cell-mediated ADRs.

    View details for DOI 10.1146/annurev-pharmtox-010818-021818

    View details for PubMedID 30134124

    View details for PubMedCentralID PMC6409210

  • Antibiotic Allergy in Pediatrics. Pediatrics Norton, A. E., Konvinse, K., Phillips, E. J., Broyles, A. D. 2018; 141 (5)

    Abstract

    The overlabeling of pediatric antibiotic allergy represents a huge burden in society. Given that up to 10% of the US population is labeled as penicillin allergic, it can be estimated that at least 5 million children in this country are labeled with penicillin allergy. We now understand that most of the cutaneous symptoms that are interpreted as drug allergy are likely viral induced or due to a drug-virus interaction, and they usually do not represent a long-lasting, drug-specific, adaptive immune response to the antibiotic that a child received. Because most antibiotic allergy labels acquired in childhood are carried into adulthood, the overlabeling of antibiotic allergy is a liability that leads to unnecessary long-term health care risks, costs, and antibiotic resistance. Fortunately, awareness of this growing burden is increasing and leading to more emphasis on antibiotic allergy delabeling strategies in the adult population. There is growing literature that is used to support the safe and efficacious use of tools such as skin testing and drug challenge to evaluate and manage children with antibiotic allergy labels. In addition, there is an increasing understanding of antibiotic reactivity within classes and side-chain reactions. In summary, a better overall understanding of the current tools available for the diagnosis and management of adverse drug reactions is likely to change how pediatric primary care providers evaluate and treat patients with such diagnoses and prevent the unnecessary avoidance of antibiotics, particularly penicillins.

    View details for DOI 10.1542/peds.2017-2497

    View details for PubMedID 29700201

    View details for PubMedCentralID PMC5914499

  • The Combined Utility of Ex Vivo IFN-γ Release Enzyme-Linked ImmunoSpot Assay and In Vivo Skin Testing in Patients with Antibiotic-Associated Severe Cutaneous Adverse Reactions. The journal of allergy and clinical immunology. In practice Trubiano, J. A., Strautins, K., Redwood, A. J., Pavlos, R., Konvinse, K. C., Aung, A. K., Slavin, M. A., Thursky, K. A., Grayson, M. L., Phillips, E. J. 2017; 6 (4): 1287-1296.e1

    Abstract

    For severe cutaneous adverse reactions (SCARs) associated with multiple antibiotics dosed concurrently, clinical causality is challenging and diagnostic approaches are limited, leading to constricted future antibiotic choices.To examine the combined utility of in vivo and ex vivo diagnostic approaches at assigning drug causality in a cohort of patients with antibiotic-associated (AA)-SCARs.Patients with AA-SCARs were prospectively recruited between April 2015 and February 2017. In vivo testing (patch testing or delayed intradermal testing) was performed to the implicated antibiotic(s) at the highest nonirritating concentration and read at 24 hours through 1 week. Ex vivo testing used patient peripheral blood mononuclear cells (PBMCs) stimulated with a range of pharmacologically relevant concentrations of implicated antibiotics to measure dose-dependent IFN-γ release from CD4+ and CD8+ T cells via an enzyme-linked immunoSpot assay.In 19 patients with AA-SCARs, combined in vivo and ex vivo testing assigned antibiotic causality in 15 (79%) patients. Ten patients (53%) with AA-SCARs were positive on IFN-γ release enzyme-linked immunoSpot assay, with an overall reported sensitivity of 52% (95% CI, 29-76) and specificity of 100% (95% CI, 79-100), with improved sensitivity noted in acute (within 1 day to 6 weeks after SCAR onset) testing (75%) and in patients with higher phenotypic scores (59%). There was increased use of narrow-spectrum beta-lactams and antibiotics from within the implicated class following testing in patients with a positive ex vivo or in vivo test result.We demonstrate the potential utility of combined in vivo and ex vivo testing in patients with AA-SCARs to assign drug causality with high specificity.

    View details for DOI 10.1016/j.jaip.2017.09.004

    View details for PubMedID 29100867

    View details for PubMedCentralID PMC5930120

  • Severe Delayed Cutaneous and Systemic Reactions to Drugs: A Global Perspective on the Science and Art of Current Practice. The journal of allergy and clinical immunology. In practice Peter, J. G., Lehloenya, R., Dlamini, S., Risma, K., White, K. D., Konvinse, K. C., Phillips, E. J. 2017; 5 (3): 547-563

    Abstract

    Most immune-mediated adverse drug reactions (IM-ADRs) involve the skin, and many have additional systemic features. Severe cutaneous adverse drug reactions (SCARs) are an uncommon, potentially life-threatening, and challenging subgroup of IM-ADRs with diverse clinical phenotypes, mechanisms, and offending drugs. T-cell-mediated immunopathology is central to these severe delayed reactions, but effector cells and cytokines differ by clinical phenotype. Strong HLA-gene associations have been elucidated for specific drug-SCAR IM-ADRs such as Stevens-Johnson syndrome/toxic epidermal necrolysis, although the mechanisms by which carriage of a specific HLA allele is necessary but not sufficient for the development of many IM-ADRs is still being defined. SCAR management is complicated by substantial short- and long-term morbidity/mortality and the potential need to treat ongoing comorbid disease with related medications. Multidisciplinary specialist teams at experienced units should care for patients. In the setting of SCAR, patient outcomes as well as preventive, diagnostic, treatment, and management approaches are often not generalizable, but rather context specific, driven by population HLA-genetics, the pharmacology and genetic risk factors of the implicated drug, severity of underlying comorbid disease necessitating ongoing treatments, and cost considerations. In this review, we update the basic and clinical science of SCAR diagnosis and management.

    View details for DOI 10.1016/j.jaip.2017.01.025

    View details for PubMedID 28483310

    View details for PubMedCentralID PMC5424615

  • Old dog begging for new tricks: current practices and future directions in the diagnosis of delayed antimicrobial hypersensitivity. Current opinion in infectious diseases Konvinse, K. C., Phillips, E. J., White, K. D., Trubiano, J. A. 2016; 29 (6): 561-576

    Abstract

    Antimicrobials are a leading cause of severe T cell-mediated adverse drug reactions (ADRs). The purpose of this review is to address the current understanding of antimicrobial cross-reactivity and the ready availability of and evidence for in-vitro, in-vivo, and ex-vivo diagnostics for T cell-mediated ADRs.Recent literature has evaluated the efficacy of traditional antibiotic allergy management, including patch testing, skin prick testing, intradermal testing, and oral challenge. Although patch and intradermal testing are specific for the diagnosis of immune-mediated ADRs, they suffer from drug-specific limitations in sensitivity. The use of ex-vivo diagnostics, especially enzyme-linked immunospot, has been highlighted as a promising new approach to assigning causality. Knowledge of true rates of antimicrobial cross-reactivity aids empirical antibiotic choice in the setting of previous immune-mediated ADRs.In an era of increasing antimicrobial resistance and use of broad-spectrum antimicrobial therapy, ensuring patients are assigned the correct 'allergy label' is essential. Re-exposure to implicated antimicrobials, especially in the setting of severe adverse cutaneous reaction, is associated with significant morbidity and mortality. The process through which an antibiotic label gets assigned, acted on and maintained is still imprecise. Predicting T cell-mediated ADRs via personalized approaches, including human leukocyte antigen-typing, may pave future pathways to safer antimicrobial prescribing guidelines.

    View details for DOI 10.1097/QCO.0000000000000323

    View details for PubMedID 27753687

    View details for PubMedCentralID PMC5113146

  • Altered TGF-α/β signaling drives cooperation between breast cancer cell populations. FASEB journal : official publication of the Federation of American Societies for Experimental Biology Franco, O. E., Tyson, D. R., Konvinse, K. C., Udyavar, A. R., Estrada, L., Quaranta, V., Crawford, S. E., Hayward, S. W. 2016; 30 (10): 3441-3452

    Abstract

    The role of tumor heterogeneity in regulating disease progression is poorly understood. We hypothesized that interactions between subpopulations of cancer cells can affect the progression of tumors selecting for a more aggressive phenotype. We developed an in vivo assay based on the immortalized nontumorigenic breast cell line MCF10A and its Ras-transformed derivatives AT1 (mildly tumorigenic) and CA1d (highly tumorigenic). CA1d cells outcompeted MCF10A, forming invasive tumors. AT1 grafts were approximately 1% the size of CA1d tumors when initiated using identical cell numbers. In contrast, CA1d/AT1 mixed tumors were larger than tumors composed of AT1 alone (100-fold) or CA1d (3-fold), suggesting cooperation in tumor growth. One of the mechanisms whereby CA1d and AT1 were found to cooperate was by modulation of TGF-α and TGF-β signaling. Both of these molecules were sufficient to induce changes in AT1 proliferative potential in vitro. Reisolation of AT1 tumor-derived (AT1-TD) cells from these mixed tumors revealed that AT1-TD cells grew in vivo, forming tumors as large as tumorigenic CA1d cells. Cooperation between subpopulations of cancer epithelium is an understudied mechanism of tumor growth and invasion that may have implications on tumor resistance to current therapies.-Franco, O. E., Tyson, D. R., Konvinse, K. C., Udyavar, A. R., Estrada, L., Quaranta, V., Crawford, S. E., Hayward, S. W. Altered TGF-α/β signaling drives cooperation between breast cancer cell populations.

    View details for DOI 10.1096/fj.201500187RR

    View details for PubMedID 27383183

    View details for PubMedCentralID PMC5024699

  • PPARγ isoforms differentially regulate metabolic networks to mediate mouse prostatic epithelial differentiation. Cell death & disease Strand, D. W., Jiang, M., Murphy, T. A., Yi, Y., Konvinse, K. C., Franco, O. E., Wang, Y., Young, J. D., Hayward, S. W. 2012; 3: e361

    Abstract

    Recent observations indicate prostatic diseases are comorbidities of systemic metabolic dysfunction. These discoveries revealed fundamental questions regarding the nature of prostate metabolism. We previously showed that prostate-specific ablation of PPARγ in mice resulted in tumorigenesis and active autophagy. Here, we demonstrate control of overlapping and distinct aspects of prostate epithelial metabolism by ectopic expression of individual PPARγ isoforms in PPARγ knockout prostate epithelial cells. Expression and activation of either PPARγ 1 or 2 reduced de novo lipogenesis and oxidative stress and mediated a switch from glucose to fatty acid oxidation through regulation of genes including Pdk4, Fabp4, Lpl, Acot1 and Cd36. Differential effects of PPARγ isoforms included decreased basal cell differentiation, Scd1 expression and triglyceride fatty acid desaturation and increased tumorigenicity by PPARγ1. In contrast, PPARγ2 expression significantly increased basal cell differentiation, Scd1 expression and AR expression and responsiveness. Finally, in confirmation of in vitro data, a PPARγ agonist versus high-fat diet (HFD) regimen in vivo confirmed that PPARγ agonization increased prostatic differentiation markers, whereas HFD downregulated PPARγ-regulated genes and decreased prostate differentiation. These data provide a rationale for pursuing a fundamental metabolic understanding of changes to glucose and fatty acid metabolism in benign and malignant prostatic diseases associated with systemic metabolic stress.

    View details for DOI 10.1038/cddis.2012.99

    View details for PubMedID 22874998

    View details for PubMedCentralID PMC3434663