Growth Anomalies
Generally, the incidence of growth anomalies in domestic animals is low. However, developmental abnormalities are due to both genetic and environmental factors that can be single and multiple in nature.
Developmental anomalies in farm animals are the impact of genetic and environmental factors. Congenital abnormalities are abnormalities of structure and function present at birth. Causes of congenital defects are unknown however they may be due to genetic (inherited by autosomal recessive genes) or environmental factors or a combination of both. Genetic defects occur due to genes missing or present in excess or gene mutation or gene translocation. Environmental factors that cause abnormalities are nutritional deficiencies (vitamins and mineral) in dam, teratogenic drugs or chemical exposure, viral infection, radiations, mechanical interference of the fetus, rectal palpation for pregnancy diagnosis, and dam exposure to toxic agents during organogenesis.
Examples: Hypotrichosis, Dwarfism, Osteopetrosis, spider lamb syndrome, split wing, complex vertebral malformation, etc.
Major impact of abnormal development is the loss of the nonviable fetus leads to financial loss and maintenance cost of the dam retained for another year. To control these abnormalities, it is better to avoid animals that carry these genes. A better way for prevention is selective breeding. Use bulls or semen from reputed breeders where bulls are tested for genetic disorders.
26.6.1 Congenital and Inherited Anomalies
Developmental anomalies in farm animals are the impact of genetic and environmental factors. Studying the etiology of the abnormalities will help to overcome and prevent the problem associated.
(a) Congenital malformations or congenital deformities— Structural abnormalities present at birth.
(b) Developmental or congenital abnormalities—Any defects and anomalies, in both the functional and morphological imperfections.
(c) Monsters are generally deformed fetuses.
(d) Teratology is the branch of embryology and prenatal pathology dealing with abnormal development and congenital defects.
26.6.2 Inherited Defects
Inherited defects occur due to mutation in the genes and the impact of which may vary. The occurrence might be due to the impact of single gene or by polygenetic effect as in case of cattle hypertrichosis, where the different genes at two interacting loci control the trait. Breeding of both the horses with Overo color pattern had led to the failure of intestinal tract innervation secondary to ileocolonic aganglionosis due to congenital anomalies. Similarly, breeding of dairy goats with dominant polled traits resulted in polled intersex goats. Such heritable defects have been reported to occur due to different embryonic anomalies like embryonic death, stillbirth, and birth of compromised offspring.
Mating or artificial insemination of monophosphate synthase (DUMPS) deficient Holstein cattle results in lethal autosomal recessive traits, where normal fertilization and embryonic development will occur: however, the fetus will be born dead. Similarly, homozygosity results in arginosuccinate synthetase deficiency thus affecting the urea cycle where the animals are healthy at birth while the ammonia concentration increases in body eventually leading to death after a few days of birth. This condition is known as citrullinemia. Canine X-linked muscular dystrophy is seen in Golden Retrievers, Labrador Retrievers, and other canine breeds, which occurs due to the presence of a single copy of a defective allele on an X chromosome the defect arises due to a defect on the X chromosome.
26.6.2.1 Infectious Agents
Infectious agents esp. viral infection affects fetal or embryonic development. Bovine viral diarrhea virus (BVDV) during prenatal infection causes congenital disorders like cerebellar hypoplasia, alopecia, brachygnathia, internal hydrocephalus, ocular defects, and impaired immunocompetence.
Similarly, infection in pregnant ewes with BVDV infection also resulted in congenital anomalies. Pestivirus infections also cause congenital defects. Pregnant ewes infected with the border disease virus exhibit embryonic and fetus mortality or congenital defects involving the skin, skeletal, nervous, endocrine, and immune systems.26.6.2.2 Environmental Factors
Normal fetal growth is influenced both directly by the placental (amniotic) environment and indirectly by the maternal environment. Maternal health, correct placentation, maternal nutrition, excess concentration of drugs and chemicals, xenobiotics, and physical agents are the factors causing developmental anomalies.
Table 26.1 Vitamin and mineral deficiencies causing development defects in animals
| S. no. | Compound | Defects |
| 1 | Iodine deficiency | Congenital goiter or cretinism |
| 2 | Copper deficiency | Enzootic ataxia |
| 3 | Manganese deficiency | Congenital limb |
| 4 | Vitamin D deficiency | Neonatal rickets |
| 5 | Vitamin A | Eye defects or harelip |
| 6 | Deficiencies of choline, riboflavin, pantothenic acid, cobalamin, and folic acid | Teratogenic effects |
| 7 | Hypervitaminosis A | Teratogenic effects |
26.6.2.3 Nutritional Factors
Both vitamin and micro-mineral deficiencies are implicated in a variety of developmental defects (Table 26.1).
26.6.2.4 Physical Agents
During twinning, large fetal size causes congenital joint contracture due to uterine crowding. Transverse or caudal presentation results in torticollis, scoliosis, and limb abnormalities in foals. Similarly, umbilical cord twisting in foals is associated with urachus. Aggressive transrectal palpation of amnionic vesicle before 42 days of gestation induced atresia coli due to disruption of vascular supply to the intestinal tract in cattle.
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