BackgroundThree flaviviruses (equine pegivirus [EPgV]; Theiler's disease–associated virus [TDAV]; non‐primate hepacivirus [NPHV]) and equine parvovirus (EqPV‐H) are present in equine blood products; the TDAV, NPHV, and EqPV‐H have been suggested as potential causes of serum hepatitis.ObjectiveTo determine the prevalence of these viruses in horses with equine serum hepatitis.AnimalsEighteen horses diagnosed with serum hepatitis, enrolled from US referral hospitals.MethodsIn the prospective case study, liver, serum, or both samples were tested for EPgV, TDAV, NPHV, and EqPV‐H by PCR.ResultsBoth liver tissue and serum were tested for 6 cases, serum only for 8 cases, and liver only for 4 cases. Twelve horses received tetanus antitoxin (TAT) 4‐12.7 weeks (median = 8 weeks), 3 horses received commercial equine plasma 6‐8.6 weeks, and 3 horses received allogenic stem cells 6.4‐7.6 weeks before the onset of hepatic failure. All samples were TDAV negative. Two of 14 serum samples were NPHV‐positive. Six of 14 serum samples were EPgV‐positive. All liver samples were NPHV‐negative and EPgV‐negative. EqPV‐H was detected in the serum (N = 8), liver (N = 4), or both samples (N = 6) of all 18 cases. The TAT of the same lot number was available for virologic testing in 10 of 12 TAT‐associated cases, and all 10 samples were EqPV‐H positive.Conclusions and Clinical ImportanceWe demonstrated EqPV‐H in 18 consecutive cases of serum hepatitis. EPgV, TDAV, and NPHV were not consistently present. This information should encourage blood product manufacturers to test for EqPV‐H and eliminate EqPV‐H–infected horses from their donor herds.

In several species, there is a strong correlation between indicators of red cell mass (RCM) and thromboelastometry results. The horse has a reliable, temporary, polycythemia in response to phenylephrine infusion. Our objective was to evaluate the effects of an in-vivo increase in circulating RCM on thromboelastometry results in an equine model of transient polycythemia. Six healthy research horses had whole blood thromboelastometry with contact activator and tissue factor initiation after recalcification of citrated samples. Additional samples were frozen for thrombin-antithrombin (TAT). Complete blood count biochemical analysis, fibrinogen, activated partial thromboplastin time (aPTT), and prothrombin time (PT) were performed. Additional samples were taken at 5 min and 2 h after phenylephrine infusion. Thromboelastometry was performed separately on four horses not receiving phenylephrine with the samples divided and spiked with phenylephrine ex vivo. Red cell count (P<0.001) and hematocrit (P<0.001) were significantly higher at 5 min after phenylephrine compared with baseline and 2 h. There was no change in platelet count, fibrinogen, PT, aPTT, or TAT at any time point. Both ex-tem and in-tem parameters were hypocoagulable at 5 min after phenylephrine compared to baseline and 2 h. There was no effect of phenylephrine in the ex-vivo spiking studies on any of the thromboelastometry parameters. Whole blood thromboelastometry results were hypocoagulable in this equine model of in-vivo transient polycythemia only during the polycythemic phase. All other coagulation parameters were unchanged. In the absence of other indicators of hypocoagulability, this may point to an artifact of thromboelastometry. Alternatively, the data may reflect true in-vivo hypocoagulability in patients with increased circulating RCM.

Mechanical stress is an important modulator of lung morphogenesis, postnatal lung development, and compensatory lung regrowth. The effect of mechanical stress on stem or progenitor cells is unclear. We examined whether proliferative responses of epithelial progenitor cells, including dually immunoreactive (CCSP and proSP-C) progenitor cells (CCSP+/SP-C+) and type II alveolar epithelial cells (ATII), are affected by physical factors found in the lung of emphysematics, including loss of elastic recoil, reduced elastin content, and alveolar destruction. Mice underwent single lung pneumonectomy (PNY) to modulate transpulmonary pressure (mechanical stress) and to stimulate lung regeneration. Control mice underwent sham thoracotomy. Plombage of different levels was employed to partially or completely abolish this mechanical stress. Responses to graded changes in transpulmonary pressure were assessed in elastin-insufficient mice (elastin +/-, ELN+/-) and elastase-treated mice with elastase-induced emphysema. Physiological regrowth, morphometry (linear mean intercept; Lmi), and the proliferative responses of CCSP+/SP-C+, Clara cells, and ATII were evaluated. Plombage following PNY significantly reduced transpulmonary pressure, regrowth, and CCSP+/SP-C+, Clara cell, and ATII proliferation following PNY. In the ELN+/- group, CCSP+/SP-C+ and ATII proliferation responses were completely abolished, although compensatory lung regrowth was not significantly altered. In contrast, in elastase-injured mice, compensatory lung regrowth was significantly reduced, and ATII but not CCSP+/SP-C+ proliferation responses were impaired. Elastase injury also reduced the baseline abundance of CCSP+/SP-C+, and CCSP+/SP-C+ were found to be displaced from the bronchioalveolar duct junction. These data suggest that qualities of the extracellular matrix including elastin content, mechanical stress, and alveolar integrity strongly influence the regenerative capacity of the lung, and the patterns of cell proliferation in the lungs of adult mice.

The mouse is the most extensively studied animal species in respiratory research, yet the technologies available to assess airway function in conscious mice are not universally accepted. We hypothesized that whole body plethysmography employing noninvasive restraint (RWBP) could be used to quantify specific airway resistance (sRaw-RWBP) and airway responsiveness in conscious mice. Methacholine responses were compared using sRaw-RWBP vs. airway resistance by the forced oscillation technique (Raw-FOT) in groups of C57, A/J, and BALB/c mice. sRaw-RWBP was also compared with sRaw derived from double chamber plethysmography (sRaw-DCP) in BALB/c. Finally, airway responsiveness following allergen challenge in BALB/c was measured using RWBP. sRaw-RWBP in C57, A/J, and BALB/c mice was 0.51 +/- 0.03, 0.68 +/- 0.03, and 0.63 +/- 0.05 cm/s, respectively. sRaw derived from Raw-FOT and functional residual capacity (Raw*functional residual capacity) was 0.095 cm/s, approximately one-fifth of sRaw-RWBP in C57 mice. The intra- and interanimal coefficients of variations were similar between sRaw-RWBP (6.8 and 20.1%) and Raw-FOT (3.4 and 20.1%, respectively). The order of airway responsiveness employing sRaw-RWBP was AJ > BALBc > C57 and for Raw-FOT was AJ > BALB/c = C57. There was no difference between the airway responsiveness assessed by RWBP vs. DCP; however, baseline sRaw-RWBP was significantly lower than sRaw-DCP. Allergen challenge caused a progressive decrease in the provocative concentration of methacholine that increased sRaw to 175% postsaline values based on sRaw-RWBP. In conclusion, the technique of RWBP was rapid, reproducible, and easy to perform. Airway responsiveness measured using RWBP, DCP, and FOT was equivalent. Allergen responses could be followed longitudinally, which may provide greater insight into the pathogenesis of chronic airway disease.

Objective To develop a perceived exertion scale for dogs exercising on a treadmill and to assess intra‐ and inter‐observer variability. Materials and Methods Fifteen healthy client‐owned dogs participated in paired exercise trials. Measurements of lactate, glucose, heart rate, temperature, respiratory rate and regional tissue oximetry were obtained before, during and after exercise. Perceived exertion scale scores were recorded during exercise and using video recordings to evaluate inter‐observer variability. Correlations were evaluated using the Spearman's non‐parametric method. Results Thirteen dogs completed both trials. Dogs walked or trotted on the treadmill with an average perceived exertion score of 2 in both trials. Holter heart rate was positively correlated with perceived exertion scale scores from all observers for both trials. In trial 1, plasma glucose decreased in association with increase in perceived exertion and, in trial 2, cutaneous oximetry decreased, respiratory rate increased and temperature increased with increases on the perceived exertion scale. Inter‐observer perceived exertion scale scores were positively correlated in both trials. There was no intra‐observer variability between trials. Clinical Significance The perceived exertion scale correlated with the measured physiologic parameters in dogs exercising at mild to moderate intensity. The perceived exertion scale was consistent and repeatable but larger study numbers and further validation are needed before it can be widely applied.

Qualitative evidence of an increase in lung attenuation and patchy alveolar patterns in the ventral lung region were more pronounced in foals ≤ 7 days of age than in older foals. Quantitative analysis revealed that mean ± SD lung attenuation was greater in foals ≤ 7 days of age (-442 ± 28 HU) than in foals > 7 days of age (-521 ± 24 HU). Lung aeration and gas volumes were lower than in other regions ventrally and in the mid lung region caudal to the heart. CONCLUSIONS AND CLINICAL RELEVANCE-Identified radiographic patterns and changes in attenuation were most consistent with atelectasis and appeared more severe in foals ≤ 7 days of age than in older neonatal foals. Recognition of these changes may have implications for accurate CT interpretation in sedated neonatal foals with pulmonary disease.

Acute, moderate hyperglycemia in healthy adult horses does not have a detectable effect on coagulation based on evaluated parameters. Jugular catheter placement results in a transient increase in thrombin generation as determined by increased TAT concentrations.

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