PORK INDUSTRY INFORMATION
Congenital defects as a general category occur in pigs across a broad percentage estimated to be between 0.11% and 4.96% (Straw et al., 2008). Inguinal and scrotal hernias are among the most common of these defects in pigs. Umbilical and inguinal hernias have been reported by one source as occurring in 0.4% to 1.5% of all pigs (Keenliside, 2006). Various countries have reported prevalence for scrotal hernias with ranges from 0.22% to 5% (Ontario Canada, Germany, Netherlands and Thailand). Breed differences have been reported from 0.6%, 1.0% and 1.5% for Duroc, Landrace and Yorkshire breeds, respectively (Vogt and Ellersieck, 1990).
Inguinal hernia appears as a bulge over the external inguinal ring. Scrotal hernia appears when intestinal contents are located in the scrotum. Inguinal/scrotal hernias develop when there is an abnormally large opening in the inguinal orifice (Warwick, 1926) (comprised of internal and external inguinal rings) through the abdominal wall which allows the abdominal contents to be forced into the inguinal canal in response to increased intra-abdominal pressure at or after birth. An inguinal hernia might not be apparent at birth but can develop some weeks later.
Economic impact from hernia problems is evidenced through negative impact of poor growth, and high mortality and condemnation rates. The major economic consequence is death due to evisceration (expulsion of intestines or omentum) after castration, although intestinal strangulation may also occasionally cause death. The condition is of less significance where male pigs are not castrated and are slaughtered under 6 months of age so that boar odor or taint is not a problem.
Inguinal and scrotal hernia rates can be significantly affected by genetic (Edwards and Mulley, 1999; St. Jean and Anderson, 2006) and environmental (handling) factors. Studies of the genetic affects have been documented back to 1926 (Warwick). Based on the data, it is believed that multiple genes are involved. Environmental or animal handling factors can also create a predisposition to increased prevalence of inguinal hernias. This includes sudden severe abdominal pressure that may increase the incidence of ruptures. Other examples are improper castration procedures such as handling pigs aggressively, extremely long and deep incisions in castration or pulling the testicle cords or induction of farrowing (which may disrupt the closure of the inguinal ring). For more information on proper castration technique, refer to Choice guidelines for Castration of Pigs.
BRIEF REVIEW OF THE GENETICS OF SCROTAL (INGUINAL) HERNIA
There is pressure on the swine breeding stock suppliers to provide a remedy for reduction of the frequency of hernia problems. A great deal of effort has been applied to try to identify and describe genetic causes. However, geneticists have yet to find a genetic explanation that accounts for the changing frequency of this trait. Selection has been aggressively practiced to reduce the frequency of any genes that may be associated with the trait; boar and gilt pigs are not retained to enter the nucleus population if they come from a litter with a male pig expressing the trait. Obviously, the individual boar that expresses the trait is also culled. These culling practices have had little apparent impact on the frequency of scrotal hernias over time in the whole industry.
There are three primary methods to determine if a trait has a genetic component; the first is to look at the differences between populations, the second is to look at the differences that exist within populations and associate variation that exists within a population between families, and the third is to practice selection on the trait and observe if the value changes. All three of these methods have been used to demonstrate that there is a genetic component that is influencing the expression of scrotal hernia, but without providing any clear solutions.
In 1951, a study was published by WT Magee that demonstrated different frequencies of scrotal hernia occurrence in 13 different lines of pigs. The lines ranged from over 15% to 0.6% occurrence in boar pigs produced. In 1979 (Mikami and Fredeen), the percent incidence of scrotal hernia for Middle Yorkshire and Landrace showed that the two populations differed by 4.2%. Other papers exist in the literature showing differences in populations, which may indicate of some type of genetic influence.
Variation within populations is often presented in the form of a heritability estimate. There are a number of published heritability estimates for the incidence of scrotal hernia. These estimates range from nearly zero to 0.84 (Magee, 1951; Mikami and Fredeen, 1979; Knap, 1986). An interesting result from the work presented by Magee (1951) is evidence of a “maternal” effect
that is in the same magnitude as the additive genetic effect. This suggests that the sow may create a uterine environment that is more or less favorable to the expression of scrotal hernias. BLUP analysis’ do not appear to have been very successful in identifying these animals and reducing the incidence.
A selection study was conducted by Warwick (1926) where boars with a scrotal hernia were bred to sows with littermates that expressed a scrotal hernia and the number of individuals that expressed a scrotal hernia was observed. Warwick describes a rapid increase in observed frequency of scrotal hernias during the study. In only three generations of selection, the frequency of males produced expressing scrotal hernias increased from under 2% to over 40%.
It is evident that there is a genetic component that may influence the expression of scrotal hernias; it can be shown that populations differ, that families within a population vary in their expression of the trait, and that the trait can be selected for and the frequency of occurrence increased. Concurrent with the work that was started in the early 1920’s to study scrotal hernias, a variety of genetic mechanisms have been postulated that explain the control of the trait. Early studies suggested a double recessive genetic model where two independent genes work together to determine the expression of the phenotype. This model was proposed in 1926 by Warwick, but recently studies using both genome wide scan techniques and candidate gene analysis have failed to identify major genes that would account for a major component of variation in the trait. It has long been thought that improved methods of genomic analysis may give better results, but it still is a wish.
There is little doubt that the incidence of scrotal hernias has a genetic component. Choice assumes that the underlying genetic mechanism influencing hernias is that of a quantitative threshold trait with incomplete penetrance. Or, more simply, the trait expresses itself in a binary fashion, the boar pig either expresses a hernia or it does not. When it expresses the trait, we assume that it has exceeded some threshold level. We cannot differentiate the degree of severity that the scrotal hernia — the boar is either normal (no observed scrotal hernia) or it is abnormal (expression of a scrotal hernia). The incomplete penetrance also suggests that there may be environmental factors that influence the expression, so that two individuals with the exact same genetic value may or may not express the trait depending on their environment. This is how animals from similar genetic lines, or even the same fathers, raised in different environments can have different average expression values.
Not allowing siblings from a litter with abnormalities to be used for breeding and the culling of the dam places a considerable degree of selection pressure against the increased frequency of the trait in monitored populations.Selection to reduce the frequency of scrotal hernias has been practiced to some degree in all breeding stock since the early 1920s.
The incidence of scrotal hernias has a genetic component that influences the expression of the trait.
Genetic models proposed to describe the inheritance have not been effective in optimizing selection practices that effectively reduce the incidence of the trait.
The trait has been a problem since the scientific community began looking at the genetic component. It continues to be problematic and, in spite of efforts to select against it, will continue to be a commercial production issue.
The industry traditionally places blame on the sire(s) as the primary cause of an increase in the incidence of scrotal hernias in a herd. This is contrary to most genetic models since the dam contributes 50% of the offspring’s genes and a maternal environment that may also influence the expression of the trait.
CHOICE – REDUCING GENETIC RISK FOR SCROTAL HERNIA
Research by Choice and others has confirmed that incidence of scrotal hernia in pigs has a genetic component. Our strategy and procedures for reducing genetic risk are summarized in the bullet point below:
- At the base of this approach in all lines is a process of rigorous culling of immediate family in which a scrotal hernia occurs. When a scrotal hernia piglet is observed in any line, that piglet, its full sibs are culled from the breeding herd. Culling of sires of affected piglets is not included in this base protocol because the sires have already left the herd due to rapid turnover of generations.
Berge, S. 1941. Three hereditary anomalies in pigs. Hereditas, 27:176-192.
Ding N.S., H.R. Mao, Y.M. Guo, J. Ren, S.J. Xiao, G.Z. Wu, H.Q. Shen, L.H. Wu, G.F. Ruan, B. Brenig and L.S. Huang. 2009. A genome-wide scan reveals candidate susceptibility loci for pig hernias in an intercross between White Duroc and Erhualian. J Anim Sci 87:2469-2474.
Du, F.-X., N. Mathialagan, C.J. Dyer, M.D. Grosz, L.A. Messer, A.C. Clutter, T. Wang, M.M. Lohuis and J.C. Byatt. 2004a. Mapping Genes affecting scrotal hernia condition in domestic pigs. J Anim Sci 82(Suppl. 1):897.
Du, F.-X., N. Mathialagan, C.J. Dyer, M.D. Grosz, L.A. Messer, A.C. Clutter, M.M. Lohuis and J.C. Byatt. 2004b. Discovery and mapping of a QTL affecting scrotal hernia incidence on SSC2 in domestic pigs. Proceedings of the meeting of the International Society of Animal Genetics.
Du Z., X. Zhoa, N. Vukasinovic, F. Rodriguez, A.C. Clutter and M.F. Rothschild. 2009. Association and haplotype analyses of positional candidate genes in five genomic regions linked to scrotal hernia in commercial pig lines. PLoS ONE 4(3): e4837. doi:10.1371/journal.pone.0004837.
Edwards, M.J. and R.C. Mulley. 1999. Genetic, Developmental, and Neoplastic Diseases, in Diseases of Swine, B.E. Straw, S. D’Allaire, W.L. Mengling, D.J. Taylor, Editors. Iowa State University Press: Ames, IA. p. 704-705.
Keenliside, J. Belly and scrotal ruptures (aka. umbilical and inguinal hernias), in 8th Ann Red Deer Swine Technology Workshop. 2006: Red Deer, Alberta, CA. p. 127-130.
Knap, P. W. 1986. Congenital defects inheritance of AI Boars: Genetic parameters and breeding value estimation procedures. Livestock Prod Sci 15:337-352.
Magee, W. T. 1951. Inheritance of scrotal hernia in swine. J Anim Sci 10:516-522.
Mikami, H. and H.T. Fredeen. 1979. A genetic study of cryptorchidism and scrotal hernia in pigs. Can J Genet Cytol 21:9-19.
St. Jean, G. and D.E. Anderson. 2006. Anesthesia and Surgical Procedures in Swine, in Diseases of Swine, B.E. Straw, J.J. Zimmerman, S. D’Allaire, D.J. Taylor, Editors. Blackwell Publishing: Ames, IA. p. 1123-1124.
Straw, B., R. Bates and G. May. 2008. Anatomical abnormalities in a group of finishing pigs: prevalence and pig performance, Journal of Swine Health and Production, January 2009.
Vogt, D.W. and M.R. Ellersieck. 1990. Heritability of susceptibility to scrotal herniation in swine. Am J Vet Res 51:1501-1503.
Warwick, B.L. 1926. A study of hernia in swine. Wisc Agr Exp Sta Res Bul 69:1-27.
Zhao, X., Zhi-Qiang Du, N. Vukasinovic, F. Rodriguez, A.C. Clutter and M.F. Rothschild. 2009. Biological candidate gene analyses identify that HOXA10 and MMP2 are associated with scrotal hernia in pigs. Am J Vet Res 2009;70:1006–1012.