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75.4% of French Bulldogs have moderately to severely stenotic nostrils, while prevalence amongst Pugs (65.3%) and English Bulldogs (44.2%) is lower.4
The OFA in the US (ofa.org) has instituted a pilot database for computer-assisted measurement of nares openings from digital photographs in English Bulldog and other bully breeds. They also have an existing database for evaluating hypoplastic trachea from a lateral radiograph.
The Swedish and Finnish Kennel Clubs have developed standardized working (walking and jogging) tests to document labored breathing as a screening test for BOAS. These walking tests have also been evaluated with WBBP. Studies show English Bulldogs with more severe BOAS walked a shorter distance, more slowly and their recovery from exercise took longer than those with only mild signs of BOAS. Increases in body temperature during exercise were significantly higher in English Bulldogs than in controls.5
Continuing research on the phenotypic screening of BOAS is correlating WBBP, standardized walking tests, and nares and body measurements to more accurately define the BOAS phenotype. Some of these test results could in the future be combined into an estimated breeding value (EBV) to compare between prospective breeding dogs.
CONCLUSIONS
While several breeds have a high incidence of BOAS, there is still considerable within-breed variation to enable breeders to breed away from genetically susceptable dogs. Current phenotypic screening tests to select against BOAS liability include standardized walking
tests (usually administered by breed or kennel clubs), nares and trachea measurements, and selecting for a breed-appropriate but longer muzzle. Based on research models, genetic testing panels against BOAS liability should be available in the near future.
Part of changing the culture that has caused the rapid popularity of extreme brachycephalic breeds is to remove the social media fixation on them. In some studies, more than half of all advertising that includes a dog has a Pug, English Bulldog, or French Bulldog. The British Veterinary Association has called for a moratorium on advertisements containing extreme brachycephalic breeds.
Dog show judge’s education is important to select against the breed extremes of short muzzles and
tight nares and to reward moderation of phenotypic morphology. Veterinarians should educate breeders and owners on the morbidity of BOAS. Breeders should use genetic screening in breeding schemes, and prospective owners should seek health-conscious breeders who
use genetic screening. Lastly, as environmental aspects influence approximately 50% of the clinical presentation of BOAS, owners can improve their dogs’ health by keeping them slim and fit.
REFERENCES
1. Ladlow J, Liu NC, Kalmar L, Sargan D. Brachycephalic obstructive airway syndrome. Vet Rec. 2018 Mar 31;182(13):375-378. doi: 10.1136/vr.k1403.
2. Farnworth MJ, Chen R, Packer RM, et. al. Flat Feline Faces: Is Brachycephaly Associated with Respiratory Abnormalities in the Domestic Cat (Felis catus)? PLoS One. 2016 Aug 30;11(8):e0161777. doi: 10.1371/journal.pone.0161777.
3. O’Neill DG, Jackson C, Guy JH, et. al. Epidemiological associations between brachycephaly and upper respiratory tract disorders in dogs attending veterinary practices in England. Canine Genet Epidemiol. 2015 Jul 14;2:10. doi: 10.1186/ s40575-015-0023-8.
4. Liu NC, Troconis EL, Kalmar L, et. al. Conformational risk factors of brachycephalic obstructive airway syndrome (BOAS) in pugs, French bulldogs, and bulldogs. PLoS One. 2017 Aug 1;12(8):e0181928. doi: 10.1371/journal. pone.0181928.
5. Lilja-Maula L, Lappalainen AK, Hyytiäinen HK, et. al. Comparison of submaximal exercise test results and severity of brachycephalic obstructive airway syndrome in English bulldogs. Vet J. 2017 Jan;219:22-26. doi: 10.1016/j. tvjl.2016.11.019.
6. Marchant TW, Johnson EJ, McTeir L, et. al. Canine Brachycephaly Is Associated with a Retrotransposon-Mediated Missplicing of SMOC2. Curr Biol. 2017 Jun 5;27(11):1573-1584.e6. doi: 10.1016/j.cub.2017.04.057.
GENES RELATED TO BOAS
There are several studies into the genes causing BOAS. Groups of BOAS+ and BOAS- dogs can be compared through DNA analysis. Results show that many genes are involved in BOAS making it a polygenic disorder. Therefore the task is to identify if there are single genes that have a major effect on BOAS, or if a panel of genes provides a major difference in the liability to develop clinical BOAS. Such a panel would provide a genomic breeding value (GBV) to compare prospective breeding dogs, and possibly differentiate those with a genetic predisposition to become mildly, moderately, or severely affected with BOAS.
Several genetic studies have been conducted to identify genes associated with skull morphology, brachycephaly and BOAS. Identified genes include IGF1, THSB2, SMOC2, FGF4 and BMP3. However many of these genes are fixed (non-variable) in brachycephalic and BOAS liable breeds. Therefore they do not cause a genetic difference between BOAS+ and BOAS- dogs. Studies from the Cambridge group into a regulatory gene affecting SMOC2 expression show that it affects the facial skeleton in a dose-dependent manner and accounts for 36% of facial length differences.6 This
group has identified a panel of 11-13 genetic markers that account for 35% of the phenotypic variation in Pugs, 47% in French Bulldogs, and 51% in English Bulldogs. Based on this panel they have been able to predict the most severely affected BOAS dogs in each breed. They also find that those less likely to develop BOAS through GBVs have longer muzzles and wider nares openings.
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