Background Clinical assessment of intravascular volume status is challenging. In humans, ultrasonographic assessment of the inferior vena cava diameter, directly or as a ratio to the aortic diameter is used to estimate intravascular volume status. Objectives To ultrasonographically obtain reference values (RV) for caudal vena cava diameter (CVC_D), area (CVC_a) and aortic ratios using 3 views in awake healthy dogs. Animals One hundred and twenty‐six healthy adult dogs from clients, students, faculty, or staff. Methods Prospective, multicenter, observational study. Two observer pairs evaluated CVC_D by a longitudinal subxiphoid view (SV), a transverse 11th‐13th right hepatic intercostal view (HV), and a longitudinal right paralumbar view (PV). Inter‐rater agreements were estimated using concordance correlation coefficients (CCC). For body weight (BW)‐dependent variables, RVs were calculated using allometric scaling for variables with a CCC ≥ 0.7. Results The CCC was ≤0.43 for the CVC/aorta ratio at the PV and ≤0.43 in both inspiration and expiration for CVC at the SV. The RVs using allometric scaling for CVC_a at the HV for inspiration, expiration, and for CVC_D at the PV were 6.16 × BW^0.762, 7.24 × BW^0.787, 2.79 × BW^0.390, respectively. Conclusions and Clinical Importance The CVC_D, measured at the HV and PV in healthy awake dogs of various breeds has good inter‐rater agreement suggesting these sites are reliable in measuring CVC_D. Established RVs for CVC_D for these sites need further comparison to results obtained in hypovolemic and hypervolemic dogs to determine their usefulness to evaluate volume status in dogs.

Perinatal infections with feline panleukopenia virus (FPV) have long been known to be associated with cerebellar hypoplasia in kittens due to productive infection of dividing neuroblasts. FPV, like other parvoviruses, requires dividing cells to replicate which explains the usual tropism of the virus for the digestive tract, lymphoid tissues and bone marrow in older animals. In this study, the necropsy and histopathological analyses of a series of 28 cats which died from parvovirus infection in 2013 were performed. Infections were confirmed by real time PCR and immunohistochemistry in several organs. Strikingly, while none of these cats showed cerebellar atrophy or cerebellar positive immunostaining, some of them, including one adult, showed a bright positive immunostaining for viral antigens in cerebral neurons (diencephalon). Furthermore, infected neurons were negative by immunostaining for p27Kip1, a cell cycle regulatory protein, while neighboring, uninfected, neurons were positive, suggesting a possible re-entry of infected neurons into the mitotic cycle. Next-Generation Sequencing and PCR analyses showed that the virus infecting cat brains was FPV and presented a unique substitution in NS1 protein sequence. Given the role played by this protein in the control of cell cycle and apoptosis in other parvoviral species, it is tempting to hypothesize that a cause-to-effect between this NS1 mutation and the capacity of this FPV strain to infect neurons in adult cats might exist. This study provides the first evidence of infection of cerebral neurons by feline panleukopenia virus in cats, including an adult. A possible re-entry into the cell cycle by infected neurons has been observed. A mutation in the NS1 protein sequence of the FPV strain involved could be related to its unusual cellular tropism. Further research is needed to clarify this point.