Nematodes and trematodes associated with terrestrial gastropods in Nottingham, England.

A parasitological survey of terrestrial slugs and snails was conducted at popular dog walking locations across the city of Nottingham, with the intensions of finding gastropods infected with parasites of medical (or veterinary) importance such as lungworm (metastrongyloid nematodes) and trematodes. A total of 800 gastropods were collected from 16 sites over a 225 km2 area. The extracted nematodes and trematodes were identified by molecular barcoding. Of the 800 gastropods collected, 227 were infected (172 had nematode infections, 37 had trematode infections and 18 had both nematode and trematode infections). Of the nematode infected gastropods genotyped, seven species were identified, Agfa flexilis, Angiostoma gandavense, Angiostoma margaretae, Cosmocerca longicauda, Phasmarhabditis hermaphrodita, Phasmarhabditis neopapillosa and an unknown Cosmocercidae species. Of the trematode infected gastropods genotyped, four species were identified, Brachylaima arcuate, Brachylaima fuscata, Brachylaima mesostoma and an unknown Plagiorchioidea species. No lungworm species were found within the city of Nottingham. To our knowledge, this study represents the first survey of gastropod-associated nematodes and trematodes in the East midlands of the United Kingdom.

De-novo and genome-wide meta-analyses identify a risk haplotype for congenital sensorineural deafness in Dalmatian dogs.

Congenital sensorineural deafness (CSD) has been reported to affect up to 30% of Dalmatian dogs world-wide and while unilaterally deaf dogs can live a close to normal life, dogs suffering bilateral deafness are frequently euthanized. Extreme-white coat patterning as encoded by the gene Melanocyte Inducing Transcription Factor (MITF) has long been postulated as the major risk factor for CSD in the Dalmatian breed. While attempts to identify causative risk variants associated with CSD have been numerous, no genome-wide association study has positively identified MITF as a risk locus for either bilateral or unilateral deafness in the Dalmatian breed to date. In this study, we identified an association with CSD on CFA20 in the vicinity of MITF within Australian Dalmatian dogs. Although not genome-wide significant, the association signal was validated by reanalysing publicly available data and merging the wider data resource with the local data to improve statistical power. The merged data, representing three major global populations of Dalmatian dogs, enabled us to identify a single, well-defined genome-wide significant risk haplotype for CSD. The haplotype was formed by three genome-wide significant associated markers (BICF2G630233852T>C, BICF2G630233861T>C, BICF2G630233888G>A) on CFA20 with 62% of bilaterally deaf dogs homozygous for the risk haplotype (CCA), while 30% of bilaterally deaf and 45% of hearing dogs carried one copy of the risk haplotype. Animals homozygous or heterozygous for the low-risk haplotype were less likely to be unilaterally deaf. While the association between the risk haplotype and deafness is incomplete, animals homozygous for the risk haplotype were 10-times more likely to be bilaterally deaf. Although the underlying causative variants are yet to be discovered, results from this study can now assist with reducing deafness in Dalmatian dogs.

Canine coat pigmentation genetics: a review.

Our understanding of canine coat colour genetics and the associated health implications is developing rapidly. To date, there are 15 genes with known roles in canine coat colour phenotypes. Many coat phenotypes result from complex and/or epistatic genetic interactions among variants within and between loci, some of which remain unidentified. Some genes involved in canine pigmentation have been linked to aural, visual and neurological impairments. Consequently, coat pigmentation in the domestic dog retains considerable ethical and economic interest. In this paper we discuss coat colour phenotypes in the domestic dog, the genes and variants responsible for these phenotypes and any proven coat colour-associated health effects.

Genetics of canine myxomatous mitral valve disease.

Myxomatous mitral valve disease (MMVD) is the most common heart disease and cause of cardiac death in domestic dogs. MMVD is characterised by slow progressive myxomatous degeneration from the tips of the mitral valves onwards with subsequent mitral valve regurgitation, and left atrial and ventricular dilatation. Although the disease usually has a long asymptomatic period, in dogs with severe disease, mortality is typically secondary to left-sided congestive heart failure. Although it is not uncommon for dogs to survive long enough in the asymptomatic period to die from unrelated causes; a proportion of dogs rapidly advance into congestive heart failure. Heightened prevalence in certain breeds, such as the Cavalier King Charles Spaniel, has indicated that MMVD is under a genetic influence. The genetic characterisation of the factors that underlie the difference in progression of disease is of strong interest to those concerned with dog longevity and welfare. Advanced genomic technologies have the potential to provide information that may impact treatment, prevalence, or severity of MMVD through the elucidation of pathogenic mechanisms and the detection of predisposing genetic loci of major effect. Here we describe briefly the clinical nature of the disorder and consider the physiological mechanisms that might impact its occurrence in the domestic dog. Using results from comparative genomics we suggest possible genetic approaches for identifying genetic risk factors within breeds. The Cavalier King Charles Spaniel breed represents a robust resource for uncovering the genetic basis of MMVD.

Roan, ticked and clear coat patterns in the canine are associated with three haplotypes near usherin on CFA38.

White coat patterning is a feature of many dog breeds and is known to be coded primarily by the gene micropthalmia-associated transcription factor (MITF). This patterning in the coat can be modified by other factors to produce the attractive phenotypes termed 'ticked' and 'roan' that describe the presence of flecks of color that vary in distribution and intensity within otherwise 'clear' white markings. The appearance of the pigment in the white patterning caused by ticking and roaning intensifies in the weeks after birth. We applied genome-wide association to compare English Cocker Spaniels of roan phenotype (N = 34) with parti-color (non-roan) English Cocker Spaniels (N = 9) and identified an associated locus on CFA 38, CFA38:11 057 040 (Praw  = 8.9 × 10-10 , Pgenome  = 2.7 × 10-5 ). A local case-control association in English Springer Spaniels comparing 11 ticked and six clear dogs identified indicative association with a different haplotype, CFA38:11 122 467G>T (Praw  = 1.7 × 10-5 ) and CFA38:11 124 294A>C (Praw  = 1.7 × 10-5 ). We characterize three haplotypes in Spaniels according to their putative functional variant profiles at CFA38:11 111 286C>T (missense), CFA38:11 131 841-11 143 239DUP.insTTAA (using strongly linked marker CFA38:11 143 243C>T) and CFA38:11 156 425T>C (splice site). In Spaniels, the haplotypes work as an allelic series including alleles (t, recessive clear; T, dominant ticked/parti-color; and TR , incomplete dominant roan) to control the appearance of pigmented spots or flecks in otherwise white areas of the canine coat. In Spaniels the associated haplotypes are t (CCT), T (TCC) and TR (TTT) for SNP markers on CFA38 at 11 111 286C>T, 11 143 243C>T and 11 156 425T>C respectively. It is likely that other alleles exist in this series and together the haplotypes result in a complex range of patterning that is only visible when dogs have white patterning resulting from the epistatic gene Micropthalmia-associated transcription factor (the S-locus).

The economic costs of planting, preserving, and managing the world's forests to mitigate climate change.

Forests are critical for stabilizing our climate, but costs of mitigation over space, time, and stakeholder group remain uncertain. Using the Global Timber Model, we project mitigation potential and costs for four abatement activities across 16 regions for carbon price scenarios of $5-$100/tCO2. We project 0.6-6.0 GtCO2 yr-1 in global mitigation by 2055 at costs of 2-393 billion USD yr-1, with avoided tropical deforestation comprising 30-54% of total mitigation. Higher prices incentivize larger mitigation proportions via rotation and forest management activities in temperate and boreal biomes. Forest area increases 415-875 Mha relative to the baseline by 2055 at prices $35-$100/tCO2, with intensive plantations comprising <7% of this increase. Mitigation costs borne by private land managers comprise less than one-quarter of total costs. For forests to contribute ~10% of mitigation needed to limit global warming to 1.5 °C, carbon prices will need to reach $281/tCO2 in 2055.

Association of missense variants in GDF9 with litter size in Entlebucher Mountain dogs.

In the past two decades, average litter size (ALS) in Entlebucher Mountain dogs decreased by approximately 0.8 puppies. We conducted a GWAS for ALS using the single-step methodology to take advantage of 1632 pedigree records, 892 phenotypes and 372 genotypes (173 662 markers) for which only 12% of the dogs had both phenotypes and genotypes available. Our analysis revealed associations towards the growth differentiation factor 9 gene (GDF9), which is known to regulate oocyte maturation. The trait heritability was estimated at 43.1%, from which approximately 15% was accountable by the GDF9 locus alone. Therefore, markers flanking GDF9 explained approximately 6.5% of the variance in ALS. Analysis of WGSs revealed two missense substitutions in GDF9, one of which (g.11:21147009G>A) affected a highly conserved nucleotide in vertebrates. The derived allele A was validated in 111 dogs and shown to be associated with decreased ALS (-0.75 ± 0.22 puppies per litter). The variant was further predicted to cause a proline to serine substitution. The affected residue was immediately followed by a six-residue deletion that is fixed in the canine species but absent in non-canids. We further confirmed that the deletion is prevalent in the Canidae family by sequencing three species of wild canids. Since canids uniquely ovulate oocytes at the prophase stage of the first meiotic division, requiring maturation in the oviduct, we conjecture that the amino acid substitution and the six-residue deletion of GDF9 may serve as a model for insights into the dynamics of oocyte maturation in canids.

The Burmese cat as a genetic model of type 2 diabetes in humans.

The recent extension of genetic tools to the domestic cat, together with the serendipitous consequences of selective breeding, have been essential to the study of the genetic diseases that affect them. Cats are increasingly presented for veterinary surveillance and share many of human's heritable diseases, allowing them to serve as natural models of these conditions. Feline diabetes mellitus is a common condition in domestic cats that bears close pathological and clinical resemblance to type 2 diabetes in humans, including pancreatic ß-cell dysfunction and peripheral insulin resistance. In Australia, New Zealand and Europe, diabetes mellitus is almost four times more common in cats of the Burmese breed than in other breeds. This geographically based breed predisposition parallels familial and population clustering of type 2 diabetes in humans. As a genetically isolated population, the Australian Burmese breed provides a spontaneous, naturally occurring genetic model of type 2 diabetes. Genetically isolated populations typically exhibit extended linkage disequilibrium and increased opportunity for deleterious variants to reach high frequencies over many generations due to genetic drift. Studying complex diseases in such populations allows for tighter control of confounding factors including environmental heterogeneity, allelic frequencies and population stratification. The homogeneous genetic background of Australian Burmese cats may provide a unique opportunity to either refine genetic signals previously associated with type 2 diabetes or identify new risk factors for this disease.

Potential complementarity between forest carbon sequestration incentives and biomass energy expansion.

There is a growing literature on the potential contributions the global forest sector could make toward long-term climate action goals through increased carbon sequestration and the provision of biomass for energy generation. However, little work to date has explored possible interactions between carbon sequestration incentives and bioenergy expansion policies in forestry. This study develops a simple conceptual model for evaluating whether carbon sequestration and biomass energy policies are carbon complements or substitutes. Then, we apply a dynamic structural model of the global forest sector to assess terrestrial carbon changes under different combinations of carbon sequestration price incentives and forest bioenergy expansion. Our results show that forest bioenergy expansion can complement carbon sequestration policies in the near- and medium-term, reducing marginal abatement costs and increasing mitigation potential. By the end of the century these policies become substitutes, with forest bioenergy expansion increasing the costs of carbon sequestration. This switch is driven by relatively high demand and price growth for pulpwood under scenarios with forest bioenergy expansion, which incentivizes management changes in the near- and medium-term that are carbon beneficial (e.g., afforestation and intensive margin shifts), but requires sustained increases in pulpwood harvest levels over the long-term.

Relationship between transitional lumbosacral vertebrae and eight lumbar vertebrae in a breeding colony of Labrador Retrievers and Labrador Crosses.

OBJECTIVE: Transitional lumbosacral vertebrae (TLSV) is a hereditary malformation of the spinal column diagnosed in various dog breeds. The aim of this study was to explore whether different lumbosacral phenotypes have an inherited basis. METHODS: Radiographs of all dogs within a breeding colony were performed and assessed. A comparison of the incidence of TLSV, eight lumbar vertebrae (8LV), and fusion of the first caudal vertebrae to the sacrum or near fusion of this area was made between litters of normal parentage and litters where one or both of the parents had an anomaly. RESULTS: Of the 119 puppies included in the study, 69 had normal conformation, 9 had 8LV, 9 had TLSV and 32 had fusion of the first caudal vertebra (Ca1) to the caudal sacral segment or a reduced joint space in this area. Results indicated that all the abnormal types likely had common underlying genetic causes. Compared with the population as a whole, significantly more progeny were observed to have abnormalities of the sacral region when both parents were affected by either fusion of Ca1 to the third sacral vertebra (S3) and/or had 8LV. Significantly more progeny were normal compared with the entire study population when both parents were normal. Strong similarity between parental and progeny phenotypes suggested that the characteristics were heritable and likely influenced by major gene effects. CONCLUSION: When performing screening radiographs for TLSV, assessment for 8LV and fusion of Ca1 to S3 should be included.

Exploring the shell-based taxonomy of the Sri Lankan land snail Corilla H. and A. Adams, 1855 (Pulmonata: Corillidae) using mitochondrial DNA.

The land-snail genus Corilla is endemic to Sri Lanka and India's Western Ghats. The ten extant Sri Lankan species belong to two distinct shell forms that are associated respectively with lowland and montane rainforest. We here present the first molecular phylogenetic analysis for Corilla. Our dataset includes nine nominal Sri Lankan species and is based on three mitochondrial genes (CO1, ND1 and 16S). Although the deeper nodes in the trees are not fully resolved, the results do suggest speciation in Corilla has involved repeated, ecologically-driven convergence in shell form. The mtDNA data agree with the current shell-based taxonomy for C. adamsi, C. beddomeae, C. carabinata, C. humberti and C. colletti, consistently supporting the first four as monophyletic, and supporting the last also as monophyletic in nearly all analyses. Corilla adamsi, C. beddomeae and C. colletti may each contain at least one additional, previously undescribed species. The relationship between northern and eastern C. odontophora couldn't be reliably resolved, but our results suggest that they are distinct species and that there is further species-level or intraspecific (geographical) differentiation within eastern C. odontophora. The current, morphologically-defined species limits of the three remaining nominal species, C. gudei, C. erronea and C. fryae, are inconsistent with the mtDNA sequence data. Northern and southern C. gudei appear to be distinct species: the sister taxon of southern C. gudei is C. humberti, and most analyses showed that the sister taxon of northern C. gudei is the lowland C. carabinata. Corilla erronea and C. fryae constitute a well supported clade in which both nominal species are paraphyletic. While most intra-clade CO1 p-distances are moderate to relatively large, the phylogenetic structuring within the clade does not seem to correspond to any obvious morphological, elevational or geographical patterns. These results are difficult to interpret, and further detailed study is needed before the taxonomic status of C. erronea and C. fryae can be resolved.

A dominant TRPV4 variant underlies osteochondrodysplasia in Scottish fold cats.

OBJECTIVE: Scottish fold cats, named for their unique ear shape, have a dominantly inherited osteochondrodysplasia involving malformation in the distal forelimbs, distal hindlimbs and tail, and progressive joint destruction. This study aimed to identify the gene and the underlying variant responsible for the osteochondrodysplasia. DESIGN: DNA samples from 44 Scottish fold and 54 control cats were genotyped using a feline DNA array and a case-control genome-wide association analysis conducted. The gene encoding a calcium permeable ion channel, transient receptor potential cation channel, subfamily V, member 4 (TRPV4) was identified as a candidate within the associated region and sequenced. Stably transfected HEK293 cells were used to compare wild-type and mutant TRPV4 expression, cell surface localisation and responses to activation with a synthetic agonist GSK1016709A, hypo-osmolarity, and protease-activated receptor 2 stimulation. RESULTS: The dominantly inherited folded ear and osteochondrodysplasia in Scottish fold cats is associated with a p.V342F substitution (c.1024G>T) in TRPV4. The change was not found in 648 unaffected cats. Functional analysis in HEK293 cells showed V342F mutant TRPV4 was poorly expressed at the cell surface compared to wild-type TRPV4 and as a consequence the maximum response to a synthetic agonist was reduced. Mutant TRPV4 channels had a higher basal activity and an increased response to hypotonic conditions. CONCLUSIONS: Access to a naturally-occurring TRPV4 mutation in the Scottish fold cat will allow further functional studies to identify how and why the mutations affect cartilage and bone development.

Heritability of racing durability traits in the Australian and Hong Kong Thoroughbred racing populations.

REASONS FOR PERFORMING STUDY: Many attempts have been made to improve the well-being of racing Thoroughbreds through improvements in management and veterinary care. However, these attempts are often limited by the industry's ability to regulate a large number of environmental variables and as a result have arguably had limited success in providing long-lasting change for the breed. OBJECTIVES: To identify heritable durability traits for Thoroughbred horses racing in Australia and Hong Kong. STUDY DESIGN: Heritability analysis of a longitudinal dataset. METHODS: Performance data on the Thoroughbred populations racing in Australia and Hong Kong between 2000 and 2011 (n = 168,993) were used to estimate the heritabilities and probability values of fixed effects and covariates for a range of racing durability traits. Heritabilities for all durability traits were estimated using a single trait animal model. Each model included, as a minimum, the effects of sex and trainer. RESULTS: Racing longevity (0.12 ± 0.01), racing persistence (0.10 ± 0.01), racing frequency (0.03 ± 0.01), spells (a time period between consecutive races, official trials and/or jump-outs greater than 90 days in length) per year (0.05 ± 0.01), spells per 10 starts (0.03 ± 0.01) and variation of days between races (0.08 ± 0.03) were all significantly heritable for horses racing in Australia. Racing longevity (0.08 ± 0.02), racing persistence (0.04 ± 0.02), spells per year (0.06 ± 0.02) and spells per 10 starts (0.11 ± 0.04) were significantly heritable for horses racing in Hong Kong. CONCLUSIONS: The heritabilities estimated for durability traits in this study provide support for the successful and practical application of genetic selection methodologies to improving the well-being of racing Thoroughbreds.

Progressive retinal atrophy in Shetland sheepdog is associated with a mutation in the CNGA1 gene.

Progressive retinal atrophy (PRA) is the collective name of a class of hereditary retinal dystrophies in the dog and is often described as the equivalent of retinitis pigmentosa in humans. PRA is characterized by visual impairment due to degeneration of the photoreceptors in the retina, usually leading to blindness. PRA has been reported in dogs from more than 100 breeds and can be genetically heterogeneous both between and within breeds. The disease can be subdivided by age at onset and rate of progression. Using genome-wide association with 15 Shetland Sheepdog (Sheltie) cases and 14 controls, we identified a novel PRA locus on CFA13 (Praw  = 8.55 × 10(-7) , Pgenome  = 1.7 × 10(-4) ). CNGA1, which is known to be involved in human cases of retinitis pigmentosa, was located within the associated region and was considered a likely candidate gene. Sequencing of this gene identified a 4-bp deletion in exon 9 (c.1752_1755delAACT), leading to a frameshift and a premature stop codon. The study indicated genetic heterogeneity as the mutation was present in all PRA-affected individuals in one large family of Shelties, whereas some other cases in the studied Sheltie population were not associated with this CNGA1 mutation. To our knowledge, this is the first report of a mutation in CNGA1 causing PRA in dogs.

Heritability of racing performance in the Australian Thoroughbred racing population.

Performance data for 164,046 Thoroughbreds entered in a race or official barrier trial in Australia were provided by Racing Information Services Australia. Analyses estimating the heritability for a range of racing performance traits using a single-trait animal model were performed using ASREML-R. Log of cumulative earnings (LCE; 0.19 ± 0.01), log of earnings per race start (0.23 ± 0.02) and best race distance (0.61 ± 0.03) were all significantly heritable. Fixed effects for sex were significant (P < 0.001) for all performance traits aside from LCE (P = 0.382). With the exception of annual earnings, trainer was also significant for all performance traits. As the application of modern genetic selection methodologies continues to gain popularity in the racing industry, contemporary heritability estimates from the current population of Thoroughbreds will play a vital role in identifying which traits are better suited to selection and in the development of more accurate genomic evaluations for racing performance.

Performance selection for Thoroughbreds racing in Hong Kong.

REASONS FOR PERFORMING STUDY: Different indicators of racing performance are commonly used in the racing industry to assess the genetic superiority of racing Thoroughbreds. However, how well these indicators predict the performance of future progeny or siblings varies depending on the population and circumstances in which the indicators were recorded or achieved. OBJECTIVES: To identify heritable indicators of racing performance for horses racing in Hong Kong. STUDY DESIGN: Heritability analysis of racing performance traits. METHODS: Performance data on the population of Thoroughbreds racing in Hong Kong between 3 September 2000 and 12 March 2011 (n = 4947) were acquired and used to estimate the heritabilities and probability values of fixed effects and covariates for a range of racing performance traits. Heritabilities for all performance traits were estimated using a single trait animal model. Each model included, as a minimum, the effects of sex, region of origin and trainer. RESULTS: Heritability estimates for traits relating to finish position ranged from 0.01 to 0.06. Average handicap weight had a heritability of 0.07 ± 0.03. The effects of sex (fixed) and trainer (random) were significant (P<0.05) for all performance traits relating to earnings measures, handicap weights and finish positions. The heritability of win time at 1600 m was 0.52 ± 0.06 and was the only significant estimate of heritability for win time in the current study. CONCLUSIONS: Although significantly affected by multiple environmental factors, certain indicators of Hong Kong racing performance can be reliably used to predict the performance of the individual's progeny or siblings. However, despite Hong Kong's controlled racing environment, these indicators appear to be no more heritable than in other less controlled racing environments.

Identification of Angiostrongylus cantonensis and other nematodes using the SSU rDNA in Achatina fulica populations of Metro Manila.

Angiostrongylus cantonensis is a parasitic nematode that causes eosinophilic meningitis in humans. Accidental infection occurs by consumption of contaminated intermediates, such as the giant African land snail, Achatina fulica. This study surveyed the presence of A. cantonensis juveniles in A. fulica populations from 12 sites in Metropolitan Manila, Philippines using the SSU rDNA. Fourteen distinct sequences from 226 nematodes were obtained; of these, two matched A. cantonensis and Ancylostoma caninum, respectively, with 100% identity. Exact identities of the remaining twelve sequences could not be determined due to low percent similarities. Of the sequenced nematodes, A. cantonensis occurred with the highest frequency (139 out of 226). Most of these (131 out of 139) were collected in just one area in Quezon City. Nematode infection of A. fulica in this area and two others from Makati and another area in Quezon City, respectively, were highest, combining for 95% of the total infection. Ancylostoma caninum, on the other hand, was detected in four different sites. A. caninum is a canine parasite, and this is the first report of the nematode in A. fulica. These results cause public health concerns as both A. cantonensis and A. caninum are zoonotic to humans.

Heritability of epistaxis in the Australian Thoroughbred racehorse population.

Post exercise epistaxis, the manifestation of a severe form of exercise-induced pulmonary haemorrhage (EIPH), has been observed in many equine racing populations. Although multiple analyses have suggested that non-genetic factors may lead to the development of this condition, relatively little consensus has been reached regarding its genetic aetiology. The objective of this study was to provide insight into both genetic and non-genetic factors that may contribute to the expression of epistaxis in the Australian Thoroughbred racing population. Racing records and reported epistaxis occurrences were acquired for 117,088 horses entered in races and official barrier trials from 1 August 2000 until 22 February 2011. Heritability was estimated using two different logistic generalised linear mixed models (lifetime epistaxis risk h(2) = 0.27 and individual race epistaxis risk h(2) = 0.50). Sex, age, and year of birth were shown to be significant; however, trainer, jockey, race distance, condition of the track (i.e. 'going'), racecourse, track surface, number of race starters, year and month of race were not significant. Evidence suggests genetic and non-genetic links to EIPH expressed as epistaxis.

Profiling the careers of Thoroughbred horses racing in Hong Kong between 2000 and 2010.

REASONS FOR PERFORMING STUDY: Research in Thoroughbred racehorses is often specific to horses from a given racing population or region. In order to investigate trends in racehorse careers across populations accurately, population-specific benchmarks for performance outcomes must be established. OBJECTIVES: To provide summary statistics for performance outcomes for Thoroughbreds racing in Hong Kong between 2000 and 2010 and to document and provide evidence on the current differences in racing careers across sexes and regions of origin for horses racing in Hong Kong. STUDY DESIGN: Performance data on the population of Thoroughbreds racing in Hong Kong between 3 September 2000 and 12 March 2011 (n = 4950) were acquired and used to describe and compare the careers of Thoroughbred racehorses in Hong Kong. METHODS: Career length, number of career starts and number of spells from racing per year were evaluated. Kaplan-Meier survival curves, stratified by sex, age group, country of origin and region of origin were produced for career length. A Cox's proportional hazards model was fitted to assess factors influencing the risk of retirement from racing in Hong Kong. RESULTS: Log-rank tests for equality of career length survivor functions showed significant differences (P<0.001) across sexes, age groups, countries of origin and regions of origin. An increased age at first start in Hong Kong tended to increase the hazard rate for retirement from racing in Hong Kong, whereas greater earnings per race and originating from Europe tended to reduce the hazard rate for racing retirement. CONCLUSIONS AND POTENTIAL RELEVANCE: Differences in career outcomes within a racing population appear to be influenced partly by the region from which a horse originates, with specific effects on each performance outcome also varying between regions. Future research should take into account these potential differences when comparing results across populations.