EuroTier 2008
Congenital defects
Occurrence: Worldwide
Age affected: Newborn
Effects: Inguinal or umbilical hernia ("rupture"), hermaphrodite, cryptorchidism, atresia ani, pityriasis rosea, cysts.
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Congenital defects are usually present at birth or become obvious shortly after birth. They may occur spontaneously during the development of an individual piglet, they may be hereditary, caused by infection during pregnancy, be of nutritional or toxic origin or the cause may be unknown. Examples of spontaneous abnormalities include cleft palate, Siamese twins and some heart defects and they are relatively uncommon. Hereditary causes of congenital abnormalities may be dominant or recessive and include umbilical and inguinal hernias, hermaphrodites, inverted nipples, cryptorchids (retained testicles), atresia ani (blind anus) cleft palate (some), pityriasis rosea (a skin condition of growers), splay leg, porcine stress syndrome and the associated conditions, congenital tremor type AIII* in Landrace pigs and thrombocytopaenic purpura. The major infectious conditions are congenital tremors Ai* and AII*, although weak piglets may be born as a result of a number of infections including leptospirosis. *) See Congenital tremor (myoclonia congenita).
Nutritional conditions with conglenital effects include deficiencies of iodine, riboflavin, vitamin A and Vitamin E and poisoning by the Fusarium mycotoxin zearalenone which causes weakness, splay let and vulval enlargement. Some congenital conditions are of unknown cause. Most types of congenital tremor Type B are of unknown cause, as is naval bleeding (failure of the umbilical cord to contract) where Vitamin C deficiency may be involved.
Clinical signs of many congenial conditions are visible at birth. Defects such as Siamese twins, congenital tremors and splay let will be obvious immediately, and other conditions such as cleft palate are detectable by inspection at birth. Where inspection is not rigorous, some may not be detected until the clinical signs have developed fully. Piglets with cleft palate may not suck successfully and become hypoglycaemic, those with atresia ani may not be detected until 2 or 3 weeks of age when the males become swollen with retained faeces. Females may not be detected until selection for breeding or even service, when the presence of a common vagina and rectum is found. The condition can remain undetected unless defecation through the vulva is noted. The porcine stress syndrome may not be noted at all, but in certain circumstances (heat stress, transport, anaesthesia with halothane) the condition may be triggered and the typical clinical signs of blanching, muscular tremors, air hunger and death then develop. Some congenital conditions result in death (cleft palate, congenital tremor AI*, atresia ani in males), others remain throughout life (hermaphrodites, hernias) and others disappear (splay leg in days, pitryriasis rosea and congenital tremor in weeks).
*) See Congenital tremor (myoclonia congenita)
Inspection alone can lead to the recognition of congenital conditions soon after birth and to their identification as cases of a particular condition, by the clinical signs or anatomical abnormalities present. Post-mortem examination may be necessary. The cause can then be determined from the literature. Where the condition is new, the following should be recorded: anatomical abnormalities and clinical signs present; number of piglets affected: their sex, occurrence in more than one litter, identity of the sow and the boar; presence in successive litters from related parents and any association with diet or infection. Where nutrition or intoxication is involved, the condition appears in the litters of sows of all ages, when genetic mechanisms are involved the condition occurs in successive litters from the same or related parents and where infection is the cause, the condition occurs once only in the litters of non-immune sows of all ages. Statistical analysis of records of breeding studies may be required to confirm dominant or recessive inherited traits. Laboratory examination can be used to confirm the presence of microscopical abnormalities, the presence of nutritional deficiency and the presence or past presence of infection and the presence or absence of particular genes.
Physical conditions such as umbilical and inguinal hernias may be treated by surgical repair where herniated pigs are to be castrated. Piglets with potentially fatal conditions, such as cleft palate or atresia ani, should be killed humanely. Piglets may be supported until natural recovery occurs as in splay leg or congenital tremor AIII* (sex linked in male Landrace). Where thrombocytopaenic purpura is expected in a litter, cross suckling can be used to prevent the intake of damaging colostrum. Nutritional and toxic conditions can be corrected and prevented, but affected pigs may still be born for a while. The same may occur with infections. Congenital tremor AI tends to be rapidly fatal, but is caused by swine fever, so consultation with official veterinarians should take place over all congenital tremors. Vaccination will eventually prevent leptospirosis. Conditions of hereditary original can be easily identified and eliminated if dominant. Recessive conditions may not justify control, especially in large outbred herds but become more important in small, specialist or pure bred herds. The Porcine stress syndrome is a recessive genetic condition cause by mutation in a single gene and carriers have been identified in the laboratory and eliminated from the breeding pool in many countries.
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