In Loving Memory of a little Angora AngelGoat, named Black Pearl.

Ten fingers, ten toes, two eyes and a nose..
These are things new moms and dads look for in their newborn children. A popular adage through the decades. So what do you look for in your newborn baby goats? Do things go wrong and if so, why?

I am list owner of 2 goat care Yahoo Groups and kidding season seems to run in cycles- This has been a year for odd neonatal defects among list members across the nation. I thought this would be a good time to share some of them with you. Most of the time your goat babies are born without a thing wrong with them.. then there are those unusual times when normalcy doesn't seem to be in order.

Unfortunately things "can" go wrong, some brought on by medications given during pregnancy, plants eaten, some are vitamin and mineral deficiencies and some are genetic. Sometimes, despite our best efforts things may still go wrong at kidding time. As upsetting as it can be for us to have a problematic birth- I guess this is nature's way of keeping the breed strong. Some of these more common defects will be discussed in this article- this is by no means a complete list, but some of the abnormalities you may be faced with.

Fetus Mummification

If no bacteria are present, the fetus is maintained in the uterus where it undergoes slow decomposition and dehydration (mummification). The cervix usually remains closed. The fetus appears as a brown, dry, leathery structure. Many times it is presented at the normal parturition time. Some things that can cause a mummified kid- Border Disease(Hairy Shaker), Viral agent, closely related to the bovine virus diarrhea virus (BVDV). Affects goats and sheep worldwide.

Toxoplasmosis

Akabane,

Contracted tendons

Most of the time this is caused by lack of room in the uterus, some feel the dam lacking in selenium may cause this but no research has this view supported. This is seen as a genetic defect in Angoras in Australasia. This may not show for 5-6 generations when the affected buck has been a carrier.. Due to recessive autosomal allele (half a gene) [Autosomal recessive (AR) diseases are those in which only individuals who are homozygous for the mutant allele develop the disease] that must reach a certain level before affected animals appear; the time between purchase of a carrier buck and appearance of affected kids may be 5-6 generations.

Anglo-Nubians in the USA, Canada, Australia, and New Zealand can have a genetic condition called mannosidosis. At birth, affected kids have varying degrees of fixed flex ion of the forelimbs and fixed extension of the hind limbs. They can see and bleat and suckle if held up to the teat. Their withdrawal reflexes are normal or depressed, and there is intention tremor, especially of the head. There may be nystagmus, deafness, and facial abnormalities. (Merck Veterinary Manuel)

Rickets

is a metabolic bone disease of young growing animals resulting from a dietary deficiency of calcium, phosphorus, vitamin D, or some combination of these nutrients causing enlarged joints and bowed legs. Neonatal rickets can be caused from the pregnant dam not having enough Vitamin D in her diet- often times found in intensive management where the animals are kept in a covered pen.

Enzootic Ataxia

(Swayback) is caused by copper deficiency of the pregnant dam. Congenital swayback is characterized by stillbirths and the birth of small and weak lambs or goats, which may show fine tremors of the head. Less severely affected kids are bright, but uncoordinated with characteristic weakness of the hind limbs, which results in a swaying or stumbling gait. These lambs are often fine boned and dull coated.

Atresia ani & Atresia recti

Atresia ani simplex occurs when the anal membrane fails to perforate or disappear. The exterior opening of the intestinal tract is then closed. This can be surgically corrected and if not the animal will die within 7 days or so. The feces builds up in the intestine and will eventually burst.

Atresia ani et recti refers to congenital closure of both the anus and rectum. This takes place during fetal development when the rectum and anus openings fail to develop.

Atresia recti simplex refers to the condition in which the lumen of the rectum failed to develop, but the anal opening is normal. There may be malformation of the genito-urinary tract associated with abnormalities of the colon and rectum causing the intestine to empty into the vagina or bladder. Atresia of the gut, particularly the colon, may result from external pressure on the amniotic sac during rectal palpation between days 35 and 40 of gestation.

When an eyelid turns inward, this is a problem that typically affects the lower eyelid. This is a common congenital defect of the eyelids. Vitamin D deficiency may also attribute to this.

Cleft Palate

When the roof of the mouth fails to close leaving an open ridge inside, which in itself would not be an issue except that this opens into the nasal/sinus cavity allowing feedstuffs to aspirate into the sinus and lungs. Ingestion of Lupines, Poison hemlock, Nicotiana, in the first trimester of pregnancy is thought to be one of the major causes of Cleft Palate. It can also be a congenital defect.

Locoweed poisoning in all types of range livestock (most commonly cattle, sheep, and horses) resulted in various clinical signs such as emaciation, visual impairment, neurological ssigns, habituation, abortion, and congenital defects. Locoweed produces musculoskeletal defects in calves and lambs, and hypo plastic testicles and enlarged seminal vesicles in rams. (Merck Veterinary Manuel) *Lupine ingestion during the 40th to 70th days of gestation. The most common signs seen in "crooked calves" are arthrogryposis (immovable joints, pronounced arthro-grip-osis), cleft palate, scoliosis (twisted spine) and shortened maxilla (upper jaw) that looks like an "undershot" jaw.(Environmental Toxicology and Veterinary Extension UCDavis)