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Tanya LeRoith

· Director, Veterinary Teaching HospitalVerified

Virginia Tech · Department of Large Animal Clinical Sciences

Active 1994–2026

h-index34
Citations3.6k
Papers17066 last 5y
Funding$233k
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About

Tanya LeRoith, DVM, PhD, MBA, DACVP, is a clinical professor and director at the Virginia-Maryland College of Veterinary Medicine at Virginia Tech. She serves as the Director of the Veterinary Teaching Hospital and the Director of Virginia Tech Animal Laboratory Services (ViTALS). Her research interests include animal models of infectious disease, viral immunology, and comparative pathology. Dr. LeRoith has a comprehensive background in microbiology, pathology, and veterinary medicine, with her education including a BS in Animal Science from the University of Maryland, a DVM from Virginia-Maryland College of Veterinary Medicine, a PhD in Microbiology/Pathology from Washington State University, and an MBA from Radford University. She is board-certified by the American College of Veterinary Pathologists in Anatomic Pathology. Her professional experience spans from graduate training to faculty roles, culminating in her current leadership positions. Her contributions include advancing veterinary clinical services and research at Virginia Tech, with a focus on infectious diseases and pathology.

Research topics

  • Biology
  • Virology
  • Medicine
  • Immunology
  • Internal medicine

Selected publications

  • Persistence of Sarcocystis neurona and histopathology in horses with equine protozoal myeloencephalitis

    Frontiers in Veterinary Science · 2026-04-15

    articleOpen access

    Currently, little is known about the exact role of Sarcocystis neurona immunopathology in equine protozoal myeloencephalitis (EPM), including the ability to persist after anti-protozoal treatment. The main objectives of this study were to determine whether S. neurona is present in the CNS in horses with EPM, including previously treated cases, and to evaluate the associated histopathology and immune response. For this study, control ( n = 10) and horses with EPM ( n = 9) were confirmed based on our inclusion criteria. Based on our preliminary data, we classified horses with EPM and clinical signs for >6 months as chronically affected ( n = 5) while horses with clinical signs for <6 months were classified as acutely affected ( n = 3). Histopathology changes between acute and chronic horses were identified. Identification of S. neurona was performed postmortem using PCR and IHC. Histopathology analysis with IHC identified S. neurona presence significantly more than PCR ( p < 0.03) when directly compared. Histopathology analysis revealed that horses chronically affected with EPM had increased degenerative changes in their CNS compared to acutely affected horses when necropsy reports were compared. Our study indicates potential important histopathology differences between horses of varying clinical sign duration and the potential persistence of S. neurona after anti-protozoal treatment. Additional studies are warranted to further elucidate the role of S. neurona in disease, including the use of “acute” and “chronic” as clinical definitions for EPM.

  • Case Report: Primary intracranial lymphoma and meningioma manifesting as a composite tumor in a cat

    Frontiers in Veterinary Science · 2025-08-07

    articleOpen access

    A 13-year-old, male neutered, Domestic Shorthair cat presented to the Virginia Tech Veterinary Teaching Hospital Neurology service for evaluation of episodes of altered mental status. On initial evaluation, the patient was noted to be alert and responsive, with a vestibular ataxia characterized by falling to the left and circling to the right. The neuroanatomic localization was consistent with multifocal intracranial disease affecting both brainstem and forebrain structures. A brain MRI revealed an extra-axial T2/FLAIR hyperintense, T1 isointense, strongly, homogenously, contrast-enhancing, plaque-like lesion affecting the meninges of the olfactory, frontal, parietal, and temporal areas of both cerebral hemispheres with extension into the falx cerebri and third ventricle. In the left temporal area, the plaque-like lesion was contiguous with a solitary, round, extra-axial, T2/FLAIR hypointense, T1 isointense, strongly and homogenously contrast-enhancing mass lesion. Bilateral caudal transtentorial and foramen magnum herniations were present. The cat's neurologic status declined, and a left rostrotentorial craniectomy, regional durectomy, and temporal mass resection were performed. Both the meningeal plaque-like lesion and the temporal mass were sampled during surgery. The meningeal lesion presented two distinct neoplastic populations consistent with meningioma and large cell lymphoma, while the temporal mass cells were consistent with a meningothelial meningioma. The patient's neurologic status improved postoperatively, and the cat was discharged on prednisolone therapy. The cat died 21 days after surgery, and a necropsy was performed. Gross examination revealed a plaque-like meningeal lesion involving the cerebrum. Histopathologically, the dura mater and subarachnoid space were infiltrated by sheets of CD79a-positive large neoplastic round cells, accompanied by numerous non-neoplastic CD3-positive T cells and IBA1-positive histiocytes, consistent with a T-cell-rich large B-cell lymphoma, and whorls of spindle-shaped cells, consistent with a meningioma. This is a rare case of an intracranial composite tumor of meningioma and primary central nervous system (CNS) T-cell-rich large B-cell lymphoma in a cat. Post-treatment survival in this cat was poor, similar to previously reported outcomes in cats with intracranial lymphoma.

  • Antiviral resistance and barrier integrity at the maternal-fetal interface restrict hepatitis E virus from crossing the placental barrier

    Proceedings of the National Academy of Sciences · 2025-05-01 · 5 citations

    articleOpen access

    Hepatitis E virus (HEV) genotype 1 (HEV-1) infection in pregnant women is associated with adverse outcomes of pregnancy including fulminant hepatic failure, fetal loss, premature birth, and neonatal mortality, although the underlying mechanisms remain largely unclear. In this study, we first demonstrated that HEV-1 robustly infects pregnant gerbils and causes pregnancy-associated adverse outcomes, which were recorded in 4/6 HEV-1-infected but only 1/5 in PBS-inoculated pregnant gerbils. However, vertical transmission of HEV-1 from mothers to newborns is not evident, as HEV-1 RNA was not detected in uterus tissues or in newborn pups. To further determine whether HEV-1 can cross the placental barrier, we established an in vitro blood-placental barrier by coculturing human placental trophoblast cells (BeWo) and umbilical vein endothelial cells (HUVEC) in Transwell inserts. By using the placental barrier under the conditions in this study, we showed that quasi-enveloped or nonenveloped HEV-1, HEV-3, or HEV-4 virions do not readily cross the barrier prior to 4 d postinoculation when it has high barrier integrity. Importantly, we demonstrated that the placental barrier induces local antiviral resistance at the maternal-fetal interface, that interactions between maternal- and fetal-derived cocultured cells are important for induction of antiviral resistance, and that anti-HEV resistance can be transferred to nonplacental HepG2 liver cells. We also revealed that the main effectors of antiviral resistance at the placental barrier are type III interferons (IFN-λ1, λ2/3) and the chemokine CXCL10. The findings have important implications in understanding the mechanisms leading to HEV-1-associated maternal and fetal adverse outcomes in pregnant women.

  • Infant Microbiota Communities and Human Milk Oligosaccharide Supplementation Independently and Synergistically Shape Metabolite Production and Immune Responses in Healthy Mice

    Journal of Nutrition · 2024-07-26 · 10 citations

    articleOpen access

    BACKGROUND: Multiple studies have demonstrated associations between the early-life gut microbiome and incidence of inflammatory and autoimmune disease in childhood. Although microbial colonization is necessary for proper immune education, it is not well understood at a mechanistic level how specific communities of bacteria promote immune maturation or drive immune dysfunction in infancy. OBJECTIVES: In this study, we aimed to assess whether infant microbial communities with different overall structures differentially influence immune and gastrointestinal development in healthy mice. METHODS: Germ-free mice were inoculated with fecal slurries from Bifidobacterium longum subspecies infantis positive (BIP) or B. longum subspecies infantis negative (BIN) breastfed infants; half of the mice in each group were also supplemented with a pool of human milk oligosaccharides (HMOs) for 14 d. Cecal microbiome composition and metabolite production, systemic and mucosal immune outcomes, and intestinal morphology were assessed at the end of the study. RESULTS: The results showed that inoculation with a BIP microbiome results in a remarkably distinct microbial community characterized by higher relative abundances of cecal Clostridium senu stricto, Ruminococcus gnavus, Cellulosilyticum sp., and Erysipelatoclostridium sp. The BIP microbiome produced 2-fold higher concentrations of cecal butyrate, promoted branched short-chain fatty acid (SCFA) production, and further modulated serotonin, kynurenine, and indole metabolism relative to BIN mice. Further, the BIP microbiome increased the proportions of innate and adaptive immune cells in spleen, while HMO supplementation increased proliferation of mesenteric lymph node cells to phorbol myristate acetate and lipopolysaccharide and increased serum IgA and IgG concentrations. CONCLUSIONS: Different microbiome compositions and HMO supplementation can modulate SCFA and tryptophan metabolism and innate and adaptive immunity in young, healthy mice, with potentially important implications for early childhood health.

  • Dietary prevention of antibiotic‐induced dysbiosis and mortality upon aging in mice

    The FASEB Journal · 2024-12-10 · 2 citations

    articleOpen access

    Oral antibiotic use is both widespread and frequent in older adults and has been linked to dysbiosis of the gut microbiota, enteric infection, and chronic diseases. Diet and nutrients, particularly prebiotics, may modify the susceptibility of the gut microbiome to antibiotic-induced dysbiosis. We fed 12-month-old mice a high glycemic (HG) or low glycemic (LG) diet with or without antibiotics (ampicillin and neomycin) for an additional 11 months. The glycemic index was modulated by the ratio of rapidly digested amylopectin starch to slowly digested amylose, a type-2-resistant starch. We observed a significant decrease in survival of mice fed a HG diet containing antibiotics (HGAbx) relative to those fed a LG diet containing antibiotics (LGAbx). HGAbx mice died with an enlarged and hemorrhagic cecum, which is associated with colonic hyperplasia and goblet cell depletion. Gut microbiome analysis revealed a pronounced expansion of Proteobacteria and a near-complete loss of Bacteroidota and Firmicutes commensal bacteria in HGAbx, whereas the LGAbx group maintained a population of Bacteroides and more closely resembled the LG microbiome. The predicted functional capacity for bile salt hydrolase activity was lost in HGAbx mice but retained in LGAbx mice. An LG diet containing amylose may therefore be a potential therapeutic to prevent antibiotic-induced dysbiosis and morbidity.

  • Microbiota from human infants consuming secretors or non-secretors mothers’ milk impacts the gut and immune system in mice

    mSystems · 2024-03-26 · 11 citations

    articleOpen access

    ABSTRACT Maternal secretor status is one of the determinants of human milk oligosaccharides (HMOs) composition, which, in turn, influences the gut microbiota composition of infants. To understand if this change in gut microbiota impacts immune cell composition, intestinal morphology, and gene expression, 21-day-old germ-free C57BL/6 mice were transplanted with fecal microbiota from infants whose mothers were either secretors (SMM) or non-secretors (NSM) or from infants consuming dairy-based formula (MFM). For each group, one set of mice was supplemented with HMOs. HMO supplementation did not significantly impact the microbiota diversity; however, SMM mice had a higher abundance of genus Bacteroides , Bifidobacterium , and Blautia , whereas, in the NSM group, there was a higher abundance of Akkermansia , Enterocloster , and Klebsiella . In MFM, gut microbiota was represented mainly by Parabacteroides , Ruminococcaceae_unclassified , and Clostrodium_sensu_stricto . In mesenteric lymph node, Foxp3+ T cells and innate lymphoid cells type 2 were increased in MFM mice supplemented with HMOs, while in the spleen, they were increased in SMM + HMOs mice. Similarly, serum immunoglobulin A was also elevated in MFM + HMOs group. Distinct global gene expression of the gut was observed in each microbiota group, which was enhanced with HMOs supplementation. Overall, our data show that distinct infant gut microbiota due to maternal secretor status or consumption of dairy-based formula and HMO supplementation impacts immune cell composition, antibody response, and intestinal gene expression in a mouse model. IMPORTANCE Early life factors like neonatal diet modulate gut microbiota, which is important for the optimal gut and immune function. One such factor, human milk oligosaccharides (HMOs), the composition of which is determined by maternal secretor status, has a profound effect on infant gut microbiota. However, how the infant gut microbiota composition determined by maternal secretor status or consumption of infant formula devoid of HMOs impacts infant intestinal ammorphology, gene expression, and immune signature is not well explored. This study provides insights into the differential establishment of infant microbiota derived from infants fed by secretor or non-secretor mothers milk or those consuming infant formula and demonstrates that the secretor status of mothers promotes Bifidobacteria and Bacteroides sps. establishment. This study also shows that supplementation of pooled HMOs in mice changed immune cell composition in the spleen and mesenteric lymph nodes and immunoglobulins in circulation. Hence, this study highlights that maternal secretor status has a role in infant gut microbiota composition, and this, in turn, can impact host gut and immune system.

  • Colonic epithelial hypoxia remains constant during the progression of diabetes in male UC Davis type 2 diabetes mellitus rats

    BMJ Open Diabetes Research & Care · 2024-03-01 · 4 citations

    articleOpen access

    INTRODUCTION: Colonocyte oxidation of bacterial-derived butyrate has been reported to maintain synergistic obligate anaerobe populations by reducing colonocyte oxygen levels; however, it is not known whether this process is disrupted during the progression of type 2 diabetes. Our aim was to determine whether diabetes influences colonocyte oxygen levels in the University of California Davis type 2 diabetes mellitus (UCD-T2DM) rat model. RESEARCH DESIGN AND METHODS: Age-matched male UCD-T2DM rats (174±4 days) prior to the onset of diabetes (PD, n=15), within 1 month post-onset (RD, n=12), and 3 months post-onset (D3M, n=12) were included in this study. Rats were administered an intraperitoneal injection of pimonidazole (60 mg/kg body weight) 1 hour prior to euthanasia and tissue collection to estimate colonic oxygen levels. Colon tissue was fixed in 10% formalin, embedded in paraffin, and processed for immunohistochemical detection of pimonidazole. The colonic microbiome was assessed by 16S gene rRNA amplicon sequencing and content of short-chain fatty acids was measured by liquid chromatography-mass spectrometry. RESULTS: (false discovery rate <0.05) genera in colon contents. The intensity of pimonidazole staining of colonic epithelia did not differ across groups (p=0.37). Colon content concentrations of acetate and propionate also did not differ across UCD-T2DM groups; however, colonic butyric acid levels were higher in D3M rats relative to PD rats (p<0.01). CONCLUSIONS: The advancement of diabetes in UCD-T2DM rats was associated with an increase in facultative anaerobes; however, this was not explained by changes in colonocyte oxygen levels. The mechanisms underlying shifts in gut microbe populations associated with the progression of diabetes in the UCD-T2DM rat model remain to be identified.

  • Persistence of Sarcocystis Neurona and Histologic Lesions in Horses with Equine Protozoal Myeloencephalitis (Epm)

    SSRN Electronic Journal · 2024-01-01 · 1 citations

    preprintOpen access
  • A hepatitis B virus core antigen‐based virus‐like particle vaccine expressing SARS‐CoV‐2 B and T cell epitopes induces epitope‐specific humoral and cell‐mediated immune responses but confers limited protection against SARS‐CoV‐2 infection

    Journal of Medical Virology · 2023-01-19 · 9 citations

    articleOpen access

    The hepatitis B virus core antigen (HBcAg) tolerates insertion of foreign epitopes and maintains its ability to self-assemble into virus-like particles (VLPs). We constructed a ∆HBcAg-based VLP vaccine expressing three predicted severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) B and T cell epitopes and determined its immunogenicity and protective efficacy. The recombinant ∆HBcAg-SARS-CoV-2 protein was expressed in Escherichia coli, purified, and shown to form VLPs. K18-hACE2 transgenic C57BL/6 mice were immunized intramuscularly with ∆HBcAg VLP control (n = 15) or ∆HBcAg-SARS-CoV-2 VLP vaccine (n = 15). One week after the 2nd booster and before virus challenge, five ∆HBcAg-SARS-CoV-2 vaccinated mice were euthanized to evaluate epitope-specific immune responses. There is a statistically significant increase in epitope-specific Immunoglobulin G (IgG) response, and statistically higher interleukin 6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) expression levels in ∆HBcAg-SARS-CoV-2 VLP-vaccinated mice compared to ∆HBcAg VLP controls. While not statistically significant, the ∆HBcAg-SARS-CoV-2 VLP mice had numerically more memory CD8+ T-cells, and 3/5 mice also had numerically higher levels of interferon gamma (IFN-γ) and tumor necrosis factor (TNF). After challenge with SARS-CoV-2, ∆HBcAg-SARS-CoV-2 immunized mice had numerically lower viral RNA loads in the lung, and slightly higher survival, but the differences are not statistically significant. These results indicate that the ∆HBcAg-SARS-CoV-2 VLP vaccine elicits epitope-specific humoral and cell-mediated immune responses but they were insufficient against SARS-CoV-2 infection.

  • An FcRn-targeted mucosal vaccine against SARS-CoV-2 infection and transmission

    Nature Communications · 2023-11-06 · 26 citations

    articleOpen access

    SARS-CoV-2 is primarily transmitted through droplets and airborne aerosols, and in order to prevent infection and reduce viral spread vaccines should elicit protective immunity in the airways. The neonatal Fc receptor (FcRn) transfers IgG across epithelial barriers and can enhance mucosal delivery of antigens. Here we explore FcRn-mediated respiratory delivery of SARS-CoV-2 spike (S). A monomeric IgG Fc was fused to a stabilized spike; the resulting S-Fc bound to S-specific antibodies and FcRn. Intranasal immunization of mice with S-Fc and CpG significantly induced antibody responses compared to the vaccination with S alone or PBS. Furthermore, we intranasally immunized mice or hamsters with S-Fc. A significant reduction of virus replication in nasal turbinate, lung, and brain was observed following nasal challenges with SARS-CoV-2 and its variants. Intranasal immunization also significantly reduced viral airborne transmission in hamsters. Nasal IgA, neutralizing antibodies, lung-resident memory T cells, and bone-marrow S-specific plasma cells mediated protection. Hence, FcRn delivers an S-Fc antigen effectively into the airway and induces protection against SARS-CoV-2 infection and transmission.

Recent grants

Frequent coauthors

  • Xiang‐Jin Meng

    China Medical University

    81 shared
  • C. Lynn Heffron

    Virginia Tech

    52 shared
  • Debin Tian

    Virginia–Maryland College of Veterinary Medicine

    39 shared
  • James Weger‐Lucarelli

    Virginia Tech

    36 shared
  • Thomas E. Cecere

    Virginia–Maryland College of Veterinary Medicine

    35 shared
  • Harini Sooryanarain

    Virginia–Maryland College of Veterinary Medicine

    32 shared
  • Danielle M. Yugo

    Virginia–Maryland College of Veterinary Medicine

    28 shared
  • F. William Pierson

    Virginia Tech

    27 shared

Awards & honors

  • 2006 — AdvanceVT Seed Grant Recipient
  • 2005 — Harriet B. Rigas Award for Outstanding Woman in Gradu…
  • 2004 — Charles L. Davis Foundation Student Scholarship Award
  • 2002-2005 — NIH Mentored Clinical Scientist Developmental Aw…
  • 2000-2002 — Achievement Rewards for College Scientists (ARCS…
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