Erythrocytosis and fatigue fractures associated with hepatoblastoma in a 3-year-old gelding

Hepatoblastoma was diagnosed in a 3-year-old Thoroughbred gelding presented with forelimb lameness with bilateral fatigue fractures of the proximal third metacarpal bones. An abdominal mass was detected on ultrasound examination of the abdomen. Absolute erythrocytosis was diagnosed after clinical and haematological evaluation. The fractured metacarpal bones were surgically removed but complications after surgery were fatal. The liver mass was diagnosed as a hepatoblastoma based on histology and immunochemical staining. The combination of hepatoblastoma and fatigue fractures has not been described previously in horses. A potential link between the hepatic and orthopaedic pathologies is hypothesised

Experimental induction of proventricular dilatation disease in cockatiels (Nymphicus hollandicus) inoculated with brain homogenates containing avian bornavirus 4

<p>Abstract</p> <p>Background</p> <p>Proventricular dilatation disease (PDD) is a fatal disorder of psittacine birds worldwide. The disease is characterized by lymphoplasmacytic infiltration of the central and peripheral nervous systems, leading to gastrointestinal motility and/or central nervous system dysfunction. Recently, we detected a significant association between avian bornavirus (ABV) infection and clinical signs of PDD in psittacines. However, it remains unclear whether ABV infection actually causes PDD. To address this question, we examined the impact of ABV inoculation on the cockatiel (<it>Nymphicus hollandicus</it>).</p> <p>Results</p> <p>Five cockatiels were inoculated via multiple routes (intramuscular, intraocular, intranasal, and oral) with a brain homogenate derived from either a PDD(+) avian bornavirus 4 (ABV4) (+) case (n = 3 inoculees) or from a PDD(-) ABV(-) control (n = 2 inoculees). The control birds remained free of clinical or pathological signs of PDD, and tested ABV(-) by RT-PCR and immunohistochemistry (IHC). In contrast, all three cockatiels inoculated with ABV4(+) brain homogenate developed gross and microscopic PDD lesions, and two exhibited overt clinical signs. In numerous tissues, ABV RT-PCR and sequence analysis demonstrated the presence of ABV4 RNA nearly identical to that in the inoculum. ABV was detected in the central nervous system of the three ABV-inoculees by IHC. Pyrosequencing to investigate the viral flora in the ABV4(+) inoculum uncovered 7 unique reads sharing 73–100% nucleotide sequence identity with previously identified ABV sequences and 24 reads sharing 40–89% amino acid sequence identity with viruses in the <it>Retroviridae </it>and <it>Astroviridae </it>families. Of these candidate viral species, only ABV RNA was recovered from tissues of the inoculated birds.</p> <p>Conclusion</p> <p>In this study, the clinical and pathological manifestations of PDD were induced by inoculation of cockatiels with brain homogenates containing avian bornavirus 4. By using high throughput pyrosequencing an in-depth view of the viral content of the inoculum was achieved, revealing that of 3 candidate virus families detected, only the presence of ABV RNA correlated with the development of PDD. This study provides evidence of a causal association between ABV4 infection and PDD in cockatiels.</p

Valvular Heart Disease following Anthracycline Therapy&mdash;Is It Time to Look beyond Ejection Fraction?

The association between anthracycline (ANT) and left ventricle (LV) dysfunction is well known; however, data regarding its direct effect on cardiac valve function is limited. We aimed to evaluate how ANT therapy affected valvular function in patients diagnosed with breast cancer. Data were prospectively collected as part of the Israel Cardio-Oncology Registry (ICOR). Patients underwent echocardiography exams at baseline (T1), during ANT therapy (T2), and after completion within 3 months (T3) and 6 months (T4). A total of 141 female patients were included, with a mean age of 51 &plusmn; 12 years. From T1 to T4, we observed a significant deterioration in LV ejection fraction (60.2 &plusmn; 1.5 to 59.2 &plusmn; 2.7%, p = 0.0004) and LV global longitudinal strain (&minus;21.6 (&minus;20.0&ndash;&minus;23.0) to &minus;20.0 (&minus;19.1&ndash;&minus;21.1)%, p &lt; 0.0001)), and an increase in LV end-systolic diameter (25 (22&ndash;27) to 27 (24&ndash;30) mm, p &lt; 0.0001). We observed a significant increase in the incidence of new mitral regurgitation (MR) development (4 to 19%, p &lt; 0.0001), worsening with concomitant trastuzumab therapy (6% to 31%, p = 0.003), and a trend for tricuspid regurgitation development (4% to 8%, p = 0.19). ANT therapy is associated with the development of a new valvular disease, mainly MR, which may imply the need for a valvular focus in the monitoring of cancer patients

Safety and efficacy in geese of a PER.C6-based inactivated West Nile virus vaccine

Studies were performed with an inactivated vaccine against the mosquito-borne flavivirus, West Nile virus (WNV). The mammalian cell line, PER.C6, was selected as the platform for WNV growth since both the neurovirulent strains NY99 and ISR98 that cause epidemics in humans and high mortality in geese, respectively, could be propagated to high titers (10(9) to 10(10)TCID(50)/ml) on these cells. Based on the high DNA homology of the WNV envelope (E) protein and non-structural protein 5 (NS5), and identical neurovirulence in mice and geese, we concluded that NY99 and ISR98 viruses are closely related and therefore vaccine studies were performed with ISR98 as a model for NY99. A robust challenge model in domestic geese was set up resulting in 100% mortality within 7 days of intracranial challenge with 500 TCID(50) WNV. Geese were used to assess the efficacy and safety of an inactivated WNV vaccine produced on PER.C6 cells. Efficacy studies demonstrated 91.4% (53/58) protection of geese compared to no protection (0/13) in geese receiving a sham vaccine. A follow-up study in 1800 geese showed that the vaccine was safe with a survival rate of 96.6% (95% lower CL 95.7%). Initial studies on the correlates of protection induced by the vaccine indicate an important role for antibodies since geese were protected when injected intra-cranial with a mixture of serum from vaccinated, non-challenged geese and WNV. In all, these results provide a scientific basis for the development of an inactivated WNV vaccine based on NY99 produced on PER.C6 cells for human and equine us

Immune Checkpoint Inhibitor-Induced Myocarditis vs. COVID-19 Vaccine-Induced Myocarditis—Same or Different?

Immune checkpoint inhibitor (ICI) and coronavirus disease 2019 (COVID-19) vaccine-induced myocarditis possibly share common mechanisms secondary to overactivation of the immune system. We aimed to compare the presenting characteristics of ICIs and COVID-19 vaccine-induced myocarditis. We performed a retrospective analysis of characteristics of patients diagnosed with either ICIs or COVID-19 vaccine-induced myocarditis and compared the results to a control group of patients diagnosed with acute viral myocarditis. Eighteen patients diagnosed with ICIs (ICI group) or COVID-19 vaccine (COVID-19 vaccine group)-induced myocarditis, and 20 patients with acute viral myocarditis (Viral group) were included. The ICI group presented mainly with dyspnea vs. chest pain and fever among the COVID-19 vaccine and Viral groups. Peak median high sensitivity Troponin I was markedly lower in the ICI group (median 619 vs. 15,527 and 7388 ng/L, p = 0.004). While the median left ventricular (LV) ejection fraction was 60% among all groups, the ICI group had a lower absolute mean LV global longitudinal strain (13%) and left atrial conduit strain (17%), compared to the COVID-19 vaccine (17% and 30%) and Viral groups (18% and 37%), p = 0.016 and p = 0.001, respectively. Despite a probable similar mechanism, ICI-induced myocarditis’s presenting characteristics differed from COVID-19 vaccine-induced myocarditis

The Mechanism of Effort Intolerance in Patients with Peripheral Arterial Disease: A Combined Stress Echocardiography and Cardiopulmonary Exercise Test

Aim: We used a combined stress echocardiography and cardiopulmonary exercise test (CPET) to explore effort intolerance in peripheral arterial disease (PAD) patients. Methods: Twenty-three patients who had both PAD and coronary artery disease (CAD) were compared with twenty-four sex- and age-matched CAD patients and fifteen normal controls using a symptom-limited ramp bicycle CPET on a tilting dedicated ergometer. Echocardiographic images were obtained concurrently with gas exchange measurements along predefined stages of exercise. Oxygen extraction was calculated using the Fick equation at each activity level. Results: Along the stages of exercise (unloaded; anaerobic threshold; peak), in PAD + CAD patients compared with CAD or controls, diastolic function worsened (p = 0.051 and p = 0.013, respectively), and oxygen consumption (p p p = 0.0024 and p = 0.0027, respectively) were reduced. Notably, oxygen pulse was blunted due to an insufficient increase in both stroke volume (p = 0.025 and p = 0.028, respectively) and peripheral oxygen extraction (p = 0.031 and p = 0.038, respectively). Chronotropic incompetence was more prevalent in PAD patients and persisted after correction for beta-blocker use (62% vs. 42% and 11%, respectively). Conclusions: In PAD patients, exercise limitation is associated with diastolic dysfunction, chronotropic incompetence and peripheral factors