Although intrauterine or transmammary transmission of Mycobacterium avium subsp paratuberculosis may occur frequently in clinically affected sheep, these are less common in subclinically infected ewes. Therefore these modes of transmission are unlikely to compromise existing control programs for ovine Johne's disease on most farms, especially if programs include the immediate culling of clinically affected sheep.

Macroscopic pharyngeal anatomical abnormalities are thought to contribute to the pathogenesis of upper airway (UA) obstruction in obstructive sleep apnea (OSA). Microscopic changes in the UA mucosal lining of OSA subjects are reported; however, the impact of these changes on UA mucosal surface topography is unknown. This study aimed to ) develop methodology to measure UA mucosal surface topography, and) compare findings from healthy and OSA subjects. Ten healthy and eleven OSA subjects were studied. Awake, gated (end expiration), head and neck position controlled magnetic resonance images (MRIs) of the velopharynx (VP) were obtained. VP mucosal surfaces were segmented from axial images, and three-dimensional VP mucosal surface models were constructed. Curvature analysis of the models was used to study the VP mucosal surface topography. Principal, mean, and Gaussian curvatures were used to define surface shape composition and surface roughness of the VP mucosal surface models. Significant differences were found in the surface shape composition, with more saddle/spherical and less flat/cylindrical shapes in OSA than healthy VP mucosal surface models ( < 0.01). OSA VP mucosal surface models were also found to have more mucosal surface roughness ( < 0.0001) than healthy VP mucosal surface models. Our novel methodology was utilized to model the VP mucosal surface of OSA and healthy subjects. OSA subjects were found to have different VP mucosal surface topography, composed of increased irregular shapes and increased roughness. We speculate increased irregularity in VP mucosal surface may increase pharyngeal collapsibility as a consequence of friction-related pressure loss. A new methodology was used to model the upper airway mucosal surface topography from magnetic resonance images of patients with obstructive sleep apnea and healthy adults. Curvature analysis was used to analyze the topography of the models, and a new metric was derived to describe the mucosal surface roughness. Increased roughness was found in the obstructive sleep apnea vs. healthy group, but further research is required to determine the functional effects of the measured difference on upper airway airflow mechanics.

Negative effort dependence (NED), decreased airflow despite increased driving pressure, has been proposed as a specific obstructive sleep apnea (OSA) phenotypic characteristic. We examined conditions under which NED occurs in a collapsible tube, pharyngeal airway bench model with the chamber enclosed, focusing on relationships with surrounding pressure levels and longitudinal strain. Using a vacuum source, graded airflows (V̇; 0-5 l/s) were generated through a thin-walled latex tube enclosed within a rigid, cylindrical chamber, sealed with initial chamber pressures (Pci) of 0-5 cmHO (separate runs), or opened to the atmosphere. Upstream minus downstream pressure (Pu - Pd), maximum airflow (V̇), and chamber pressure (Pc) were measured at 0-50% longitudinal strain. NED occurred across the range of Pci and strains studied but was most pronounced for the chamber open condition. With a sealed chamber, V̇ increased and Pc decreased with increasing Pu - Pd until the onset of NED at V̇ and a Pc value that was designated as critical (Pcc). Pcc was lowest (-17 cmH0) and V̇ was highest (~5 l/s) with chamber sealed: Pci = 0 cmHO and 12.5 to 25% strain. We conclude that for our collapsible tube model, the achievable V̇ before the onset of NED depends on both the initial conditions (Pci and strain) and the dynamics of feedback between driving pressure and chamber pressure (chamber sealed vs. open). NED-based phenotypic analyses for OSA may need to focus on potential feedback control mechanisms (eg lung volume change, muscle activity) that may link peripharyngeal tissue pressure levels to driving pressures for airflow. A collapsible tube, pharyngeal airway bench model was used to study the role of surrounding pressure and longitudinal wall strain at the onset of negative effort dependence (NED). NED occurred to varying degrees across all conditions tested, but maximum airflow was achieved with ) low initial surrounding pressure,) a feedback mechanism between surrounding pressure and driving pressure; and ) a moderate amount of strain applied. Potential impacts on OSA phenotypic analyses are discussed.

Introduction The impact of sleep disordered breathing (SDB) on arterial intima-media thickness (IMT), a surrogate measure for cardiovascular disease, remains uncertain, in part because of the potential for non-SDB vascular risk factor interactions. In the present study, we determined predictors for common carotid (CCA) and femoral (CFA) artery IMT in an adult, sleep clinic cohort where non-SDB vascular risk factors (particularly diabetes) were eliminated or controlled. Methods We recruited 296 participants for polysomnography (standard SDB severity metrics) and CCA/CFA ultrasound examinations, followed by a 12 month vascular risk factor minimisation (RFM) and continuous positive pressure (CPAP) intervention for participants with a range of SDB severity (RFM Sub-Group, n = 157; apnea hyponea index [AHI]: 14.7 (7.2–33.2), median [IQR]). Univariable and multivariable linear regression models determined independent predictors for IMT. Linear mixed effects modelling determined independent predictors for IMT change across the intervention study. P<0.05 was considered significant. Results Age, systolic blood pressure and waist:hip ratio were identified as non-SDB predictive factors for CCA IMT and age, weight and total cholesterol:HDL ratio for CFA IMT. No SDB severity metric emerged as an independent predictor for either CCA or CFA IMT, except in the RFM Sub-Group, where a 2-fold increase in AHI predicted a 2.4% increase in CFA IMT. Across the intervention study, CCA IMT decreased in those who lost weight, but there was no CPAP use interaction. CFA IMT, however, decreased by 12.9% (95%CI 6.8, 18.7%, p = 0.001) in those participants who both lost weight and used CPAP > = 4hours/night. Conclusion We conclude that SDB severity has little impact on CCA IMT values when non-SDB vascular risk factors are minimised or not present. This is the first study, however, to suggest a potential linkage between SDB severity and CFA IMT values. Trial registration Australian New Zealand Clinical Trials Registry, ACTRN12611000250932 and ACTRN12620000694910.