Hernias in Growing Pigs
Two of the more common anatomical defects that occur on pig farms are
- scrotal hernias
These hernias typically occur at frequencies of 1.7 to 6.7%, but in some instances can increase or “spike” for a variety of reasons (Thailer et al., 1996). The difficulty with these types of physical defects is that they often render the pig less valuable as a market pig and can cause morbidity and possibly mortality.
Umbilical hernias occur due to weakened supportive muscles around the umbilical stump or navel area of the pig. This causes the umbilical opening not to close properly and intestines protrude through the intestinal wall to form the “ball-like” structure often seen on the pig. The frequency ranges from 0.4 to 1.2% (Searcy et al., 1994).
Hernias are classified as direct or indirect depending on whether intestinal loops outside the abdomen are covered by peritoneum or vaginal tunic (indirect), or whether intestines directly contact skin (direct) (Grindflek et al., 2006).
Intestines in direct contact with skin stimulate formation of adhesions. Umbilical hernias, of any size, are usually direct and therefore complicated by adhesions that can interfere with normal digestion. A moderate amount of adhesion should only somewhat reduce the pigs’ performance and their carcasses should be of similar value to pigs that do not have this condition.
However, problems arise if the intestines are ruptured during the slaughter process and the intestinal contents contaminate the carcass. Often these pigs are sent to specialty harvest facilities that can accommodate them and slaughter them with minimal risk of carcass condemnation. This re-sorting in the market chain causes the reduction in value.
The genetic control of umbilical hernias is not entirely clear. A “familial” cause has been suggested and a few specific genes have been recently shown to associate with this condition (Zhao et al., 2008). However, in general this condition is not due to simple inheritance of a few genes. Environmental conditions definitely play a role in the incidence of this defect. It is thought that environmental compromises such as navel infections early in life may be linked to the incidence of this condition. Proper sanitation and hygiene may have a greater chance of reducing the incidence of this condition than trying to eliminate certain boars or dams.
If there is a genetic influence to this condition, it may be related to poor environmental conditions. This indicates there may be genetic variability controlling the musculature of the navel and those with a propensity with weaker navel muscles in a poor environment could trigger this belly rupture condition.
Environmental factors such as abnormal stretching of the umbilical cord (during farrowing or placing naval clips too close to the skin) or infection of the umbilical stump could contribute to failure of the umbilical cord opening to close. Investigation of a hereditary component is complicated by the nature of the defect. While there may be a range in the ability of the umbilical stump to close, the characteristic is not easily measured except in the extreme (categorical measure – affected vs not affected).
Scrotal hernias obviously occur only in males although the more encompassing category of inguinal hernia includes both genders. Inguinal herniation in females is rare and usually associated with intersexuality (Tianti et al., 2002). Occurrence of scrotal hernia has been reported as 2% (Germany Gat), 5% (Iowa, Magee), 1-5% (Gat 2005), 1.35 and 0.22-0.54% (Dutch, Charasu) and 0.6, 1.0 and 1.5% (Duroc, Landrace, York, Vogt et al 1990). It is thought that scrotal hernias are caused by failed obliteration of the process vaginalis after descent of the testis (Clarnette et al., 1998), or from failed involution at the internal inguinal ring (Clarnette & Hudson, 1997) such that it does not close off properly after the testes descend into the scrotum. This usually allows the distal jejunum and ileum to drop into the scrotum. If the intestines are present in the scrotum at the time of castration, the intestines are either ruptured or “fall out” of the pig. Intestines may migrate to the scrotum after castration. It is difficult to repair either rupture condition surgically. It is typically advised not to try to repair umbilical hernias. Scrotal hernias can sometimes be repaired if found in early stages. However, in both cases, advanced hernia cases are extremely difficult, if not impossible, to surgically repair on a practical basis. Scrotal hernias more frequently involve the left side with an occurrence on the left about 5 times that of on the right (Magee, 1951).
For years, the appearance of scrotal hernias has been linked to certain boar lines and based on differences among sires within lines estimates of heritability of scrotal hernia has been estimated as 0.15 (Magee, 1951) and 0.2- 0.6 (Gatphayak et al., 2005). It has been shown that there are several genes that associate with this condition but do not have absolute control (Zhao et al., 2008). Likely Quantitative Trait Loci (QTL) have been detected on SSC1, SSC2, SSC5, SSC15, SSC17 and SSCX (Grindflek et al., 2006). If this condition is prevalent to either a single boar, or boar family (close relatives of a boar), the incidence of scrotal hernias may be primarily due to genetics. The elimination of the boar, boar family and other close relatives should reduce further incidence. However, since this condition is due to multiple genes, it is fair to say that there is a genetic contribution from the sow herd. Another unusual occurrence with this physical defect is that often the incidence may be small or not observed within the pure lines that make up the crossbred pig, but the incidence within the crossbred pig can by higher than in the pure lines that comprise it. This suggests that there may be a detrimental heterosis cause to this condition but this has not been fully substantiated. It also happens, within commercial herds, that two herds using the same dam and boar lines can have dramatically different incidences of this condition with one herd having little or no incidence and the other seeing a high incidence. This suggests there is a genotype by environmental interaction. When this occurs, there is something within the environment that is stimulating a particular genotype to allow for this condition to occur. It can be very difficult to determine the genetic cause when the underlying environmental factor or factors triggering this malady are unknown.
The occurrence of scrotal and umbilical hernias is often a frustrating concern for commercial farms. One can conclude that both environmental and genetic causes can stimulate the incidence of these physical defects. Neither trait is controlled through simple genetic inheritance, thus there are no simple procedures to reduce their incidence. If the incidence of either of these defects occurs through the introduction of a new boar or female line, farms should work with their genetic suppliers in a systematic approach to develop a plan to reduce the incidence of these maladies. In addition, farms should evaluate their own management and hygiene procedures to minimize environmental causes.
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