Congenital defects in llamas
"Congenital" means "present at birth."
Some congenital defects are hereditary, some are not. Some are actually both — having a hereditary component, but they must also have an environmental influence (trigger) before they can manifest.
Very few formal scientific studies have investigated congenital defects in llamas, and none to date have reached a full conclusion about the origin of any of these defects. Observation of occurance in related and unrelated individuals makes it clear that some defects are certainly genetic.
At least one private (unpublished) study has shown strong evidence exists for DNA damage (mutation) in a llama parent with subsequent eqpigenetic heritabiity: Progeny inherit the defect from the parent alone, but that parent's ancestors are unaffected and cannot produce defective offspring unless exposure to the mutagenic agent is ongoing.
Serious congenital defects (lethal, no surgical correction possible):
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Patellar luxation (congenital form)
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Megaesophagus (juvenile onset form)
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Choanal atresia accompanied by additional defects — the normal airway between nose and throat is blocked by bone; additional defects may be both external and internal
Serious congenital defects (lethal if not surgically corrected)
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Choanal atresia in isolation (no additional defects) — the normal airway between nose and throat is blocked by bone (NOTE: corrective surgery, although possible, seldom results in adequate quality of life)
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Anal atresia — no anal opening at all, or an anal sphincter but without a patent (open) anus.
Nonlethal congenital defects (surgical correction not required for survival)
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Polydactyly — extra toes (most common) or limbs
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Syndactyly — fused toes
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Absence of tail and minimized tail — both hereditary and dominant; unaffected relatives can be bred without risk
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Gross incisor misalignment — hereditary, but variable expression and unknown mechanism
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Malconformed and "gopher" ears — some forms are both hereditary and dominant; unaffected relatives can be bred without risk. Other forms have a recessive component, and can be produced from some unaffected relatives.
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Cleft palate — Note: surgical correction adviseable (when possible) for quality of life
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Wry face — Note: ongoing dental care required for quality of life
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Reproductive system defects such as incomplete reproductive tract, cervical malformation, imperforate hymen (female); missing (or internal) testicle(s), abnormally large, small, or significantly mismatched testes (male)— Note: Some reproductive system defects show heritability (from the opposite sex parent or from both parents) or occur in related animals such that heritability is virtually certain; others appear to have a clear environmental or teratogenic component
Congenital defects that appear to have an environmental or teratogenic cause, perhaps with a hereditary component
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Choanal atresia (in isolation, without other defects present)— the normal airway between nose and throat fails to develop normally and is blocked by a variable range of bone and/or soft tissue at birth
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Umbilical hernia — Large hernias present at birth and larger hernias acquired postpartum that do not resolve on their own require intervention, sometimes surgical. These are believed to have a hereditar component by some. Hernias requiring intervention have also been demonstrated to occur at a markedly higher rate whenever the dam has experienced significant inflammation during late pregnancy.Note: More commonly, a small hernia can develop a week or so after birth (thus not congenital in the strictest sense of the word) and resolves without intervention. Self-resolving hernias are only noted by smaller breeders who make a point to handle crias and inspect them for hernias, and this may be a normal developmental variant.
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Carpus valgus ("knock knees") — malnutrition in utero is a definitive cause (major mineral imbalance involving the interplay among calcium, phosphorus, magnesium, vitamin D and vitamin K), but genetic makeup of the individual ("genetic predisposition") may determine how seriously (or even if) it will be affected.
Congenital defects with cause as yet undetermined in llamas
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Heart defects
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Immunodeficiency
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Cataracts present at birth
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Abnormally small size
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Contracted tendons
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Monobrachia (single front leg)
Congenital differences that are hereditary and are NOT defects
Most of these differences are listed as serious and unacceptable defects by the show association and/or the lama registry. In reality, they do no harm to the llama nor do they significantly change a llama's ability to perform functions for humans. The reason for blacklisting these variations is clearly political. Most breeders would not want these traits their breeding herds for one reason only -- to improve sales potential.
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Blue eyes — Note — light blue eyes have been anecdotally associated with deafness in alpaca; dark blue eyes have not. Deafness is certainly a defect.
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Pink toenails
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Extra upper canines
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Extra teats
Frequency of congenital defects in llamas
When llamas' popularity as an "investment" surged, it was widely stated that llamas had no hereditary defects. Once it became obvious this was not true, the PR line changed to llamas have fewer defects than other livestock. In actual fact, some defects are more common than in other livestock, some occur at a similar rate, and others occur rarely.
In general, duplication errors are more common in llamas (ie, extra digits, extra canines, double cervix) than in other species. Because all lamas (as a genus) all have double upper canines, this prediliction may have originally been a hereditary advantage.
Choanal atresia occurs only in llamas and in humans. Choanal atresia is the most common lethal congenital defect in lamas.
Heritable dominant defects (such as malconformed and gopher ears) and inherited undesirable traits (such as blue eyes) are largely found in the unregistered, "cria mill" and "backyard breeder" portions of the gene pool, where the parental selection bar is low or nonexistant. It does pay to screen breeding stock for known hereditary defects, and to purchase registered stock (with known ancestry) from responsible breeders whose goals include the overall health of the gene pool.
Farms that don't provide good nutrition based on the specific needs dictated by their own locale eventually see increasing rates of birth defects associated with malnutrition, such as rickets, carpus valgus, poor vigor at birth, low birth weights, decreasing adult size, and low fertility.
Farms that limit or eliminate environmental, ingested, and injected exposure to chemical, drug, and feed additives during pregnancy statistically experience far fewer congenital defects of certain types.