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Host-virus associations have co-evolved under ecological and evolutionary selection pressures that shape cross-species transmission and spillover to humans. Observed virus-host associations provide relevant context for newly discovered wildlife viruses to assess knowledge gaps in host-range and estimate pathways for potential human infection. Using models to predict virus-host networks, we predicted the likelihood of humans as hosts for 513 newly discovered viruses detected by large-scale wildlife surveillance at high-risk animal-human interfaces in Africa, Asia, and Latin America. Predictions indicated that novel coronaviruses are likely to infect a greater number of host species than viruses from other families. Our models further characterize novel viruses through prioritization scores and directly inform surveillance targets to identify host ranges for newly discovered viruses.

Emerging infectious diseases in humans are frequently caused by pathogens originating from animal hosts, and zoonotic disease outbreaks present a major challenge to global health. To investigate drivers of virus spillover, we evaluated the number of viruses mammalian species have shared with humans. We discovered that the number of zoonotic viruses detected in mammalian species scales positively with global species abundance, suggesting that virus transmission risk has been highest from animal species that have increased in abundance and even expanded their range by adapting to human-dominated landscapes. Domesticated species, primates and bats were identified as having more zoonotic viruses than other species. Among threatened wildlife species, those with population reductions owing to exploitation and loss of habitat shared more viruses with humans. Exploitation of wildlife through hunting and trade facilitates close contact between wildlife and humans, and our findings provide further evidence that exploitation, as well as anthropogenic activities that have caused losses in wildlife habitat quality, have increased opportunities for animal-human interactions and facilitated zoonotic disease transmission. Our study provides new evidence for assessing spillover risk from mammalian species and highlights convergent processes whereby the causes of wildlife population declines have facilitated the transmission of animal viruses to humans.

Background: The rate of catastrophic musculoskeletal injuries (CMI) in racehorses is high in the United States compared to other countries. Few modifiable risk factors related to lameness, medication, and surgery history have been identified. Objective: To detect management factors that increase risk of CMI by comparing medical histories between horses that sustained, and horses that did not sustain, a CMI. Study design: Case-control. Methods: Racehorse necropsy data (May 2012-June 2013) were obtained through the California Horse Racing Board Postmortem Program. Attending veterinarians of Thoroughbreds (TB) and Quarter Horses (QH) that experienced CMI, and of three matched control horses, were invited to complete an online veterinary medical history survey. We investigated associations between CMI and lameness, medication, surgery, and exercise history using multivariable logistic regression. Results: There were 146 TB (45 cases, 101 controls) and 17 QH (11 cases, 6 controls) surveys completed. TB cases were more likely to show signs of lameness within the 3 months prior to death compared to controls. A high proportion of both cases (64.3%) and controls (76.8%) were administered medications, but unraced TB case horses were more likely to have been administered systemic medications compared to those that previously raced. TB cases were more likely to have raced with greater intensity during their career, but had eased off in the month preceding CMI. For QHs, there was insufficient power to detect significant differences between cases and controls that showed signs of lameness, or that were administered medications. Surgery history was not associated with CMI. Main limitation: Insufficient power to detect small effect sizes. Conclusions: The study provides information that can be used to aid in identification of horses at high risk for catastrophic injury, and management factors that can be modified to reduce the risk for all horses.

Metaphyseal osteopathy (MO) (hypertrophic osteodystrophy) is a developmental disorder of unexplained etiology affecting dogs during rapid growth. Affected dogs experience relapsing episodes of lytic/sclerotic metaphyseal lesions and systemic inflammation. MO is rare in the general dog population; however, some breeds (Weimaraner, Great Dane and Irish Setter) have a much higher incidence, supporting a hereditary etiology. Autoinflammatory childhood disorders of parallel presentation such as chronic recurrent multifocal osteomyelitis (CRMO), and deficiency of interleukin-1 receptor antagonist (DIRA), involve impaired innate immunity pathways and aberrant cytokine production. Given the similarities between these diseases, we hypothesize that MO is an autoinflammatory disease mediated by cytokines involved in innate immunity. To characterize immune dysregulation in MO dogs we measured serum levels of inflammatory markers in 26 MO and 102 control dogs. MO dogs had significantly higher levels (pg/ml) of serum Interleukin-1beta (IL-1β), IL-18, IL-6, Granulocyte-macrophage colony stimulating factor (GM-CSF), C-X-C motif chemokine 10 (CXCL10), tumor necrosis factor (TNF), and IL-10. Notably, recovered MO dogs were not different from dogs during active MO disease, providing a suggestive mechanism for disease predisposition. This is the first documentation of elevated immune markers in MO dogs, uncovering an immune profile similar to comparable autoinflammatory disorders in children.

Most human infectious diseases, especially recently emerging pathogens, originate from animals, and ongoing disease transmission from animals to people presents a significant global health burden. Recognition of the epidemiologic circumstances involved in zoonotic spillover, amplification, and spread of diseases is essential for prioritizing surveillance and predicting future disease emergence risk. We examine the animal hosts and transmission mechanisms involved in spillover of zoonotic viruses to date, and discover that viruses with high host plasticity (i.e. taxonomically and ecologically diverse host range) were more likely to amplify viral spillover by secondary human-to-human transmission and have broader geographic spread. Viruses transmitted to humans during practices that facilitate mixing of diverse animal species had significantly higher host plasticity. Our findings suggest that animal-to-human spillover of new viruses that are capable of infecting diverse host species signal emerging disease events with higher pandemic potential in that these viruses are more likely to amplify by human-to-human transmission with spread on a global scale.

It is currently unclear whether changes in viral communities will ever be predictable. Here we investigate whether viral communities in wildlife are inherently structured (inferring predictability) by looking at whether communities are assembled through deterministic (often predictable) or stochastic (not predictable) processes. We sample macaque faeces across nine sites in Bangladesh and use consensus PCR and sequencing to discover 184 viruses from 14 viral families. We then use network modelling and statistical null-hypothesis testing to show the presence of non-random deterministic patterns at different scales, between sites and within individuals. We show that the effects of determinism are not absolute however, as stochastic patterns are also observed. In showing that determinism is an important process in viral community assembly we conclude that it should be possible to forecast changes to some portion of a viral community, however there will always be some portion for which prediction will be unlikely.

BackgroundDespite the popularity of the horse racing industry in the United States and the wide recognition that horse racing is one of the most hazardous occupations, little focused research into the prevention of falls by and injuries to jockeys has been conducted.PurposeTo describe the incidence rates and characteristics of falls and injuries to Thoroughbred and Quarter Horse racing jockeys in the state of California.Study designDescriptive epidemiology study.MethodsData on race-day falls and injuries were extracted from jockey accident reports submitted to the California Horse Racing Board from January 2007 to December 2011. Denominator data, number of jockey race rides, were obtained from commercial and industry databases. Jockey fall, injury, and fatality incidence rates and ratios in Thoroughbred and Quarter Horse flat races were estimated using Poisson regression. Characteristics of falls and injuries are described and compared.ResultsIn Thoroughbred races, 184 jockey injuries occurred from 360 reported jockey falls, 180,646 race rides, 23,500 races, and 3350 race meetings. In Quarter Horse races, 85 jockey injuries occurred from 145 jockey falls, 46,106 race rides, 6320 races, and 1053 race meetings. Jockey falls occurred at a rate of 1.99 falls per 1000 rides in Thoroughbred races, with 51% of falls resulting in jockey injury, and 3.14 falls per 1000 rides in Quarter Horse races, with 59% of falls resulting in jockey injury. The majority of falls occurred during a race, with catastrophic injury or sudden death of the horse reported as the most common cause in both Thoroughbred (29%) and Quarter Horse (44%) races. During the period studied, 1 jockey fatality resulted from a fall. Jockey fall rates were lower but injury rates were comparable to those reported internationally.ConclusionOn average, a licensed jockey in California can expect to have a fall every 502 rides in Thoroughbred races and every 318 rides in Quarter Horse races. While jockey fall rates were lower, injury rates were similar to those in other racing jurisdictions. The high proportion of jockey falls caused by horse fatalities should be further investigated.

Neural tube defects (NTDs) is a general term for central nervous system malformations secondary to a failure of closure or development of the neural tube. The resulting pathologies may involve the brain, spinal cord and/or vertebral column, in addition to associated structures such as soft tissue or skin. The condition is reported among the more common birth defects in humans, leading to significant infant morbidity and mortality. The etiology remains poorly understood but genetic, nutritional, environmental factors, or a combination of these, are known to play a role in the development of NTDs. The variable conditions associated with NTDs occur naturally in dogs, and have been previously reported in the Weimaraner breed. Taking advantage of the strong linkage-disequilibrium within dog breeds we performed genome-wide association analysis and mapped a genomic region for spinal dysraphism, a presumed NTD, using 4 affected and 96 unaffected Weimaraners. The associated region on canine chromosome 8 (pgenome  =3.0 × 10(-5)), after 100,000 permutations, encodes 18 genes, including NKX2-8, a homeobox gene which is expressed in the developing neural tube. Sequencing NKX2-8 in affected Weimaraners revealed a G to AA frameshift mutation within exon 2 of the gene, resulting in a premature stop codon that is predicted to produce a truncated protein. The exons of NKX2-8 were sequenced in human patients with spina bifida and rare variants (rs61755040 and rs10135525) were found to be significantly over-represented (p=0.036). This is the first documentation of a potential role for NKX2-8 in the etiology of NTDs, made possible by investigating the molecular basis of naturally occurring mutations in dogs.

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Background: Certain stride characteristics have been shown to affect changes in biomechanical factors that are associated with injuries in human athletes. Determining the relationship between stride characteristics and musculoskeletal injury (MSI) may be key in limiting injury occurrence in the racehorse. Objectives: This study aimed to determine whether changes in race day speed and stride characteristics over career race starts are associated with an increased risk of MSI in racehorses. Study design: Case–control study. Methods: Speed, stride length, and stride frequency data were obtained from the final 200 m sectional of n = 5660 race starts by n = 584 horses (case n = 146, control n = 438). Multivariable joint models, combining longitudinal and survival (time to injury) analysis, were generated. Hazard ratios and their 95% confidence intervals (CI) are presented. Results: The risk of MSI increased by 1.18 (95% CI 1.09, 1.28; P < 0.001) for each 0.1 m/s decrease in speed and by 1.11 (95% CI 1.02, 1.21; P = 0.01) for each 10 cm decrease in stride length over time (career race starts). A more marked rate of decline in speed and stride length was observed approximately 6 races prior to injury. Risk of MSI was highest early in the horse's racing career. Main limitations: Only final sectional stride characteristics were assessed in the model. The model did not account for time between race starts. Conclusions: Decreasing speed and stride length over multiple races is associated with MSI in racehorses. Monitoring stride characteristics over time may be beneficial for the early detection of MSI. [ABSTRACT FROM AUTHOR]

Background: Proximal sesamoid bone fractures are common catastrophic injuries in racehorses. Understanding the response of proximal sesamoid bones to race training can inform fracture prevention strategies. Objectives: To describe proximal sesamoid bone microstructure of racehorses and to investigate the associations between microstructure and racing histories. Study design: Cross‐sectional. Methods: Proximal sesamoid bones from 63 Thoroughbred racehorses were imaged using micro‐computed tomography. Bone volume fraction (BVTV) and bone material density (BMD) of the whole bone and four regions (apical, midbody dorsal, midbody palmar and basilar) were determined. Generalised linear regression models were used to identify the associations between bone parameters and race histories of the horses. Results: The mean sesamoid BVTV was 0.79 ± 0.08 and BMD was 806.02 ± 24.66 mg HA/ccm. BVTV was greater in medial sesamoids compared with lateral sesamoids (0.80 ± 0.07 vs 0.79 ± 0.08; P <.001) predominantly due to differences in the apical region (medial—0.76 ± 0.08 vs lateral—0.72 ± 0.07; P <.001). BVTV in the midbody dorsal region (0.86 ± 0.06) was greater than other regions (midbody palmar—0.79 ± 0.07, basilar—0.78 ± 0.06 and apical—0.74 ± 0.08; P <.001). BVTV was greater in sesamoids with more microcracks on their articular surface (Coef. 0.005; 95% CI 0.001, 0.009; P =.01), greater extent of bone resorption on their abaxial surface (Grade 2—0.82 ± 0.05 vs Grade 1—0.80 ± 0.05 or Grade 0—0.79 ± 0.06; P =.006), in horses with a low (0.82 ± 0.07) or mid handicap rating (0.78 ± 0.08) compared with high rating (0.76 ± 0.07; P <.001), in 2‐ to 5‐year‐old horses (0.81 ± 0.07) compared with younger (0.68 ± 0.08) or older horses (0.77 ± 0.08; P <.001) and in horses that commenced their racing career at less than 4 years of age (0.79 ± 0.08 vs 0.77 ± 0.77; P <.001). BMD was greater in the midbody dorsal (828.6 ± 19.6 mg HA/ccm) compared with other regions (apical—805.8 ± 21.8, midbody palmar—804.7 ± 18.4 and basilar—785.0 ± 17.1; P <.001), in horses with a handicap rating (low—812.1 ± 20.0, mid—821.8 ± 21.3 and high—814.6 ± 19.4) compared with those with no rating (791.08 ± 24.4, P <.001), in females (806.7 ± 22.0) and geldings (812.2 ± 22.4) compared with entires (792.7 ± 26.2; P =.02) and in older horses (<2‐year‐old—763.7 ± 24.8 vs 2‐ to 5‐year‐old—802.7 ± 23.4, and 6‐ to 12‐year‐old—817.8 ± 20.0; P =.002). Main limitations: Data were cross‐sectional. Conclusions: Densification of the proximal sesamoid bones is associated with the commencement of racing in younger horses and the presence of bone fatigue‐related pathology. Lower sesamoid BVTV was associated with longevity and better performance. [ABSTRACT FROM AUTHOR]

Background: With each stride, galloping horses generate large skeletal loads which influence bone physiology, and may contribute to musculoskeletal injury. Horse speed and stride characteristics are related, but the usefulness of using horse speed and distance travelled as a proxy for stride characteristics is unknown. Objectives: We aimed to determine stride characteristics, their variance and their relationship with speed in horses performing maximally. Study design: Retrospective cross‐sectional analysis of archived data. Methods: Stride characteristics obtained using GPS and inertial sensors in Thoroughbred horses were retrieved. Data per 200 m race segment ('sectionals') for horses competing in races (N = 25,259 race starts) were analysed to determine if speed predicted stride parameters. Multivariable mixed‐effects linear regression models were fitted. Results: Mean (±SD) stride length, stride count (number of strides per 200 m), duration and speed were 7.08 ± 0.39 m, 28.32 ± 1.56 strides/200 m, 0.43 ± 0.02 s/stride and 16.63 ± 1.04 m/s across all sectionals and starts. Speed and stride length decreased, and stride count increased with race progression (P < 0.001). Male sex, greater race distance, better finishing position and firmer track surfaces were associated with less strides per 200 m and longer stride durations. Main limitations: Lack of an independent party validation of the measurement system used in this study. Conclusions: There was a substantial inter‐horse variation in stride parameters, with speed predicting half or less of this variation. Speed alone does not fully explain stride characteristics in horses. Future studies aimed at investigating the impact of gait on bone biology and pathology would benefit from accounting for stride characteristics (eg length and duration). [ABSTRACT FROM AUTHOR]