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There are increasing concerns about the effects of disease on wild turkeys (Meleagris gallopavo). Yet, many management agencies lack adequate data on wild turkey diseases and pathogens to address this concern. Toward that end, the Pennsylvania Game Commission increased surveillance efforts on wild turkeys beginning in 2013 (referred to hereafter as the enhanced surveillance period). From 2008–2018, 121 wild turkeys from Pennsylvania were submitted for necropsy, with 102/121 (84.3%) submitted during the enhanced surveillance period (2013–2018). We examined cases to determine causes of morbidity/mortality through gross and microscopic examinations and ancillary tests. The most common causes of morbidity/mortality in the examined wild turkeys were avian pox (66/121; 54.5%), chronic dermatitis (15/121; 12.4%), and trauma (10/121; 8.3%). We diagnosed additional diseases for the first time or more frequently during the enhanced surveillance period, including histomoniasis (7/121; 5.7%) and infectious sinusitis (1/121; 0.8%). Skin lesions were the most common cause of submission (94/121; 77.7%) and were most often attributed to avian pox (66/94, 70.2%), chronic dermatitis (15/94; 16.0%), or lymphoproliferative disease (3/94; 3.2%). During 2013–2018, tissues and sera were collected from any diagnostic cases and hunter-harvested turkeys to create a tissue repository. We used these samples to test for infection or exposure to specific pathogens. We found that 75.3% (61/81) of wild turkeys were positive for lymphoproliferative disease virus, 61.9% (52/84) for Heterakis gallinarum, 28.6% (10/35) for Toxoplasma gondii, and 15.6% (15/32) for Borrelia burgdorferi. We detected antibodies (indicating exposure) to avian paramyxovirus-1 in 34.9% (22/63) of the wild turkeys and West Nile virus in 21% (13/62), but none were seropositive to influenza A viruses (0/62; 0%). The presence of diseases and pathogens in wild turkeys in Pennsylvania are being defined through active and passive surveillance approaches. Such data can begin to address the broader questions of disease impacts on wild turkey populations.

Lymphoproliferative disease virus (LPDV) is a highly prevalent pathogen first described from wild turkeys (Meleagris gallopavo) in 2009, with uncertain implications for wild turkey populations. To establish a baseline of its prevalence and geographic distribution, we gathered LPDV samples across North Carolina, USA, from 2 age classes of wild turkeys in 2013 and 2015. We collected 829 tissue samples, primarily from hunter harvests, and tested for presence of LPDV via polymerase chain reaction (PCR). The overall prevalence of LPDV was 46.1% (382 of 829 turkeys). Prevalence was significantly lower in juveniles than adults (29.7% and 48.4% respectively [χ² = 13.52, df = 1, P < 0.001]). Prevalence of LPDV in adult turkeys was greater in the mountain region than in either the piedmont or coastal regions. Prevalence of LPDV did not vary between years (χ² = 1.47, df = 1, P = 0.26) or sexes (χ² = 0.06, df = 1, P = 0.81). Mean weights of LPDV-positive adult male turkeys (8.9 kg) and LPDV-negative adult male turkeys (8.9 kg) were not different. We observed no correlation between LPDV prevalence and reported turkey harvest, nor between LPDV prevalence and productivity estimates from our annual summer brood survey. Our work is consistent with previous reports that LPDV is a widespread virus in wild turkeys that differs in prevalence across ages and regions. Further investigation of LPDV's effect on turkey poults and transmission of the pathogen among juvenile and adult turkeys is needed.

This study describes the first recognized clinical case of lymphoproliferative disease virus (LPDV) in Canada and extends the range of LPDV in Canada through its detection in Manitoba and Quebec. We assessed the prevalence of LPDV in eastern wild turkeys (Meleagris gallopavo silvestris) with the use of whole, clotted blood from live birds in Manitoba (n = 65) and tissue samples collected postmortem in Quebec (n = 4). We tested for LPDV proviral DNA through PCR amplification and sequencing of a portion of the gag (p31) gene. Samples were also tested for reticuloendotheliosis virus (REV) by PCR. Twenty-four birds (34.8%) were positive for LPDV, including all diagnostic cases. One bird (1.4%) from Quebec had gross and microscopic lesions consistent with LPDV. Two turkeys (2.9%) were REV positive, one (1.4%) of which was co-infected with LPDV. Phylogenetic analysis of LPDV strains from Quebec and Manitoba grouped with previously sequenced samples from Ontario and publicly available sequences from a North American lineage. This study contributes valuable information toward ongoing surveillance and monitoring of LPDV in North America.

The monitoring of infectious diseases in wildlife is crucial for assessing animal health, pathogen range expansion, and the risk of spillover to naive species, but may be resource and labor intensive. Lymphoproliferative disease virus (LPDV) is an avian oncogenic retrovirus that was first identified in wild turkeys (Meleagris gallopavo) in 2009, though it historically caused mortality in domestic turkeys in Europe and Israel. Subsequent surveys detected a high prevalence and broad distribution throughout the eastern United States, warranting further research on LPDV in wild turkey populations. Current LPDV diagnostics require the collection of tissues, such as bone marrow from dead birds or blood during live capture. In our study, we assessed the sensitivity (true positive) and specificity (true negative) of cloacal swab samples as an alternative LPDV detection method. We compared results from cloacal swab samples with both postmortem detection from bone marrow and antemortem detection from blood, using a multi-tube PCR approach with 3 replicates. Swab samples collected from livecaptured turkeys had a greater sensitivity (88%) than swabs collected from hunter-harvested turkeys (31%), whereas specificity was similar for both collection approaches (livecapture swabs = 75%, n = 85; hunter-harvest swabs = 80%, n = 54). In live-captured turkeys, the estimated LPDV prevalence using cloacal swab samples (73%) was not significantly different from the true prevalence determined using coupled blood samples (76%). However, in hunter-harvested turkeys, the estimated prevalence using cloacal swab samples (28%) was different from the true prevalence estimated using coupled bone marrow samples (72%). In summary, cloacal swab samples can be used to reliably detect LPDV infection in live-captured wild turkeys but should not be used for LPDV detection in hunter-harvested wild turkeys.

Lymphoproliferative disease virus (LPDV) is a retrovirus that infects wild and domestic turkeys (Meleagris gallopavo). The first cases of LPDV in the United States were diagnosed in 2009, and subsequent surveillance has revealed the virus to be widespread in wild turkey populations throughout the eastern half of the country. More research is needed to determine whether LPDV is having a negative effect on turkey populations, but progress has been impeded by the lack of a simple method for diagnosing the virus in living birds. Infected animals may appear asymptomatic, and diagnostics currently rely on tissue or bone marrow, which can be difficult to obtain. This study investigated the reliability of polymerase chain reaction (PCR) to detect LPDV in whole blood, compared with previous methods using buffy coat (concentrated white blood cells) and bone marrow. Paired samples of whole blood and buffy coat were collected from 137 live turkeys and paired samples of whole blood and bone marrow were collected from 32 turkeys postmortem. Compared with buffy coat, whole blood had 97% sensitivity and 100% specificity. When compared with bone marrow, whole blood had 100% sensitivity and 89% specificity. Both comparisons had a high degree of agreement using Cohen's kappa statistic. Based on these results, PCR of whole blood provides detection of LPDV in living birds that is on par with both buffy coat and bone marrow.

We report a case of a 41-year-old male with human immunodeficiency virus (HIV)-associated lymphoproliferative disease (LPD) who was successfully treated with highly active antiretroviral therapy (HAART). He presented with epigastralgia, and an upper endoscopic examination revealed submucosal tumors and ulcerations in his stomach. Histopathologic examination of a biopsy specimen resulted in a diagnosis of diffuse large B-cell lymphoma. He also showed systemic lymphadenopathy; whereas, a concurrent inguinal lymph node biopsy produced a diagnosis of follicular hyperplasia. He was treated with CHOP chemotherapy but the response was poor. He demonstrated several immunological abnormalities, such as eosinophilia and bone marrow insufficiency, and was suspected to be in an immunocompromised state. He was examined for HIV infection and turned out to be positive. The gastric and inguinal lymph node specimens were re-evaluated and diagnoses of HIV-LPD and HIV lymphadenitis were made, respectively. He was treated with HAART and achieved complete remission and has remained tumor-free for 20 months. To the best of our knowledge, there is no previous report in which HIV-LPD was successfully treated with antiretroviral therapy alone. It is assumed that HAART resulted in the restoration of anti-tumor immunity in this case, which led to the eradication of LPD cells.

A rare association of Epstein-Barr virus-associated T- and B-lymphoproliferative disease (EBV^sup +^ T- and EBV^sup +^ B-LPD) in a patient with WHIM (warts, hypogammaglobulinemia, infections, and myelokathexis) syndrome is reported. A 26-year-old Japanese female, who had been treated for WHIM syndrome since early childhood, developed hemophagocytic syndrome associated with EBV^sup +^ T-LPD at the lymph nodes and spleen. The disease rapidly resolved in response to prednisolone therapy. However, 6 weeks later, fatal EBV^sup +^ B lymphoma unresponsive to chemotherapy occurred in the intestine and other organs. Caution must be exercised that the patient with WHIM syndrome may be at risk for EBV-LPD.[PUBLICATION ABSTRACT]

Background. The objective of this analysis was to investigate prognostic factors that influence the outcome of Epstein-Barr virus (EBV)—related posttransplant lymphoproliferative disorder (PTLD) after a rituximab-based treatment in the allogeneic hematopoietic stem cell transplant (HSCT) setting. Methods. A total of 4466 allogeneic HSCTs performed between 1999 and 2011 in 19 European Group for Blood and Marrow Transplantation centers were retrospectively analyzed for PTLD, either biopsy-proven or probable disease. Results. One hundred forty-four cases of PTLD were identified, indicating an overall EBV-related PTLD frequency of 3.22%, ranging from 1.16% for matched-family donor, 2.86% for mismatched family donor, 3.97% in matched unrelated donors, and 11.24% in mismatched unrelated donor recipients. In total, 69.4% patients survived PTLD. Multivariable analysis showed that a poor response of PTLD to rituximab was associated with an age ≥30 years, involvement of extra-lymphoid tissue, acute GVHD, and a lack of reduction of immunosuppression upon PTLD diagnosis. In the prognostic model, the PTLD mortality increased with the increasing number of factors: 0–1, 2, or 3 factors being associated with mortality of 7%, 37%, and 72%, respectively (P < .0001). Immunosuppression tapering was associated with a lower PTLD mortality (16% vs 39%), and a decrease of EBV DNAemia in peripheral blood during therapy was predictive of better survival. Conclusions. More than two-thirds of patients with EBV-related PTLD survived after rituximab-based treatment. Reduction of immunosuppression was associated with improved outcome, whereas older age, extranodal disease, and acute graft-vs-host disease predicted poor outcome.

Immunocompromised individuals are at risk for developing lymphocryptovirus-associated lymphoproliferative diseases, such as Epstein Barr virus (EBV)-associated B cell lymphomas and post-transplant lymphoproliferative disorder (PTLD). We previously reported development of cynomolgus lymphocryptovirus (CyLCV)-associated PTLD in Mauritian cynomolgus macaques (MCMs) undergoing hematopoietic stem cell transplantation (HSCT), which mirrored EBV-PTLD in transplant patients. Here, we sought to develop a MCM model of lymphocryptovirus-associated lymphoproliferative disease in immunosuppressed MCMs without HSCT. Five simian immunodeficiency virus (SIV)-infected, CD8α+ cell-depleted MCMs received an infusion of autologous B-lymphoblastoid cells transformed with CyLCV, followed by varying degrees of immunosuppression. Four of five infused macaques developed masses coincident with increasing CyLCV plasma viremia, and necropsies confirmed the presence of multicentric lymphomas, which most commonly manifested in lymph nodes, gastrointestinal tract, adrenal glands, and pancreas. Affected tissues harbored neoplastic lymphocytes double-positive for CD20 and CyLCV EBNA2 antigen, large frequencies of proliferating B cells, and high levels of cell-associated CyLCV DNA. In addition, longitudinal 18F-fluorodeoxyglucose positron-emission tomography (18F-FDG PET) of one MCM successfully detected lymphoproliferative disease in the adrenal glands prior to clinical signs of disease. These data demonstrate successful induction of lymphocryptovirus-associated PTLD-like disease in 4 of 5 MCMs, and thus support the use of MCMs as a preclinical NHP model of EBV-associated lymphoproliferative disease that could be employed to test novel diagnostic and therapeutic modalities.

Epstein–Barr virus (EBV) is strongly associated with the development of post-transplant lymphoproliferative disorder (PTLD) in pediatric liver transplant recipients. PTLD is one of the most common malignancies following liver transplantation and is associated with significant morbidity and mortality. Factors such as EBV–serostatus mismatch and prolonged or high levels of immunosuppression impact a patient’s risk of developing PTLD. While pre-transplant EBV serological screening and post-transplant monitoring of EBV-DNA levels are strongly recommended, universal guidelines for its prevention and management are lacking. Due to a lack of robust prospective studies, current clinical practices vary widely. The treatment of PTLD typically involves reducing immunosuppression and using targeted therapies such as rituximab, or chemotherapy for refractory cases. This review aims to address our current understanding of EBV’s relationship with PTLD, evaluate the available treatment modalities, and highlight evolving strategies for using EBV as a biomarker for PTLD screening and prevention.