Everyone has heard the phrase, "Don’t
throw out the baby with the bath water." But do dog breeders ever
stop to consider how this admonition applies to them? Certainly not
the novice who righteously declares that he will never, ever, keep
anything that has even the possibility of producing the smallest
genetic defect. Not even the experienced breeder who refuses to
consider an otherwise excellent line because it sometimes throws
cataracts. This tendency toward genetic over-kill not only culls
dogs that might have something to offer, it can exacerbate the very
problems breeders are trying to avoid. The following is a real life
example of what can happen when breeders exercise short-sighted
culling in the name of genetic disease control.
About twenty years ago, breeders of Basenjis launched a campaign to
wipe out a fatal genetic disease called pyruvate kinase deficient
hemolytic anemia (HA). HA is caused by a recessive gene. Dogs with a
single copy of the gene are healthy, but those with two copies die.
A screening test was developed that would indicate carriers as well
as affected animals. Breeders zealously screened their dogs,
eliminating not only affected animals but the healthy carriers from
the breeding population.
Today HA is rare in Basenjis, but the incidence of Progressive
Retinal Atrophy is significantly higher. As is yet another fatal
disorder, a kidney problem called Fanconi’s Disease. Neither of
these diseases has a screening test that will indicate carriers. Had
breeders been less fanatical in their pursuit of HA, they might have
retained the healthy carriers in the breeding population, breeding
them only to non-carriers so they could avoid producing HA-affected
puppies. By such a method they could have retained the good aspects
of those carriers, including freedom from genes for PRA or Fanconi,
while gradually lowering the incidence of the HA gene.
Fortunately for the Basenji, there is still a native population of
the breed in Africa. The Basenji club prevailed upon the AKC to
allow them to re-open the stud book to admit some African-born
Basenjis. This badly needed source of new genetic material comes at
great trouble and expense for those breeders who make the effort to
acquire one of these imports. This option isn't even possible in
some breeds, and even where it is, convincing a large registry like
AKC to accept undocumented foreign imports is itself a daunting
task.
In spite of what happened with the Basenji, this should not be
viewed as an indictment of screening tests. The problem wasn’t the
HA test, but the drastic culling process that breeders undertook
when using it. If there is a test which can identify carriers, make
use of it. Breeders need to know as much as possible about the
genetic potential of their breeding stock. Ideally, they should be
willing to share the results, whether good or bad, with other
breeders.
Knowledgeable dog people know there is no perfect dog. Even the best
of them have faults. The faults are not only those conformation or
behavioral problems you can readily observe, but also bad genes.
Dogs have at least 80,000 genes. No matter how high the standards
for selection of breeding stock or how strict the culling of
offspring, every dog will have genes for unwanted traits. Experts
agree that every individual--be he dog, human or
cauliflower--probably carries, three "lethal equivalents." This may
leave you wondering why we aren't seeing dogs and cauliflowers, not
to mention each other, dropping like flies all around us.
Under normal circumstances, lethal genes remain rare. Natural
populations breed randomly, maintaining a varied mix of alleles, or
forms, of genes. Only occasionally will the right combination of bad
alleles match up to produce an affected individual. In addition, the
lethal nature of these diseases limits the ability of affected
animals to pass them on to their offspring because affected
individuals often don’t live long enough to reproduce. But the
breeding of purebred livestock, including dogs, is not natural or
random. It is selective based on the wants and needs of breeders. As
a result, the number of lethal equivalents in most breeds exceeds
the average of three, the problem genes having been inadvertently
concentrated through the standard inbreeding practices used to
maximize production of desired traits. Two examples in Australian
Shepherds are Pelger-Huet Anomaly and merle. Genes with lethal
effects are only the tip of the iceberg. There are dozens, if not
hundreds, of genes whose effects are anywhere from minor to
extremely bad.
Breeders routinely evaluate breeding stock by studying conformation
and/or performance attributes in minute detail. Virtues are weighed
against faults, then compared to the virtues and faults of
prospective mates. If the overall analysis is positive, the breeder
will proceed. Hereditary diseases and defects need to be given the
same kind of consideration, in and of themselves and in combination
with all the dog’s other traits.
Some faults are severe enough to eliminate a dog from breeding
consideration entirely, but even genetic defects and disease may not
necessarily fall into this category, in some circumstances. Remember
the case of the Basenjis and HA. Dogs proven to be carriers of
traits in which only homozygotes (those with two copies of the gene)
are affected, can be used if care is taken never to mate one carrier
to another and not to use them extensively.
If the mode of inheritance for a trait is unknown or polygenic,
identifying carriers can be difficult. Individuals which repeatedly
produce traits like hip dysplasia, epilepsy or thyroid disease
should be pulled from further breeding because of the serious and
debilitating nature of those diseases. But their relatives may be
used if care is taken to select mates unlikely to carry the same
defect. If at any point an individual proved to be a repeat producer
of the defect, it could then be removed from the breeding program.
Many faults are variable in expression. This includes such genetic
defects as hip dysplasia (HD) and missing teeth. In Clumber
Spaniels, where HD was once almost universal, elimination of all
affected animals was not an option if the breed was to be preserved.
By selecting away from the most severely affected dogs, Clumber
breeders have managed to improve their overall situation, producing
more non-dysplastic dogs and fewer which are severely affected, even
though HD is still common. A similar situation has occurred with
Collies and Collie Eye Anomaly.
In the case of missing teeth, a fault common to show line Australian
Shepherds, something similar could be done. There are sufficient
quality dogs available with full dentition that dogs missing
multiple teeth ought not to be bred. However, those missing one or
two teeth could be bred to mates with full dentition which are out
of families with full dentition. Twenty years ago, missing teeth in
Aussies were almost unheard of. Twenty years from now the situation
could be to nearly its starting point if breeders were conscientious
about screening and mate selection--and none of the good traits
those dogs have need be lost along the way.
The overall size of a breeding population must be taken into account
before making final decisions on whether a dog exhibiting or
carrying a defects ought to be bred. Australian Shepherds are
numerous, but certain sub-sets of the breed are not. In North
America there are thousands of Aussies, but in other parts of the
world populations typically number only a few hundred breeding
animals at best. Opportunities to add new stock are infrequent,
especially in those countries with strict quarantine laws and import
restrictions. Even in North America a breeder's selection of
potential mates may be limited if his breeding goals are very
specific, such as producing a particular type of stock dog.
In small populations, breeders may have no choice but to use some
defective animals. The only alternative is to resort to increased
inbreeding which will narrow the available gene pool even further
and bring other, possibly worse, defects to the fore. If defective
dogs are to be used, breeders should take special care to avoid
subsequently in-breeding on those dogs. Neither should such a dog be
bred extensively. Among its offspring, only those which do not
exhibit the defective trait should be considered for further
breeding.
If breeders approach genetic disease with an objective eye and if
they are honest with themselves and each other about the potential
for producing genetic diseases and defects in any given cross, they
can obtain healthy babies while the bath water full of bad genes
drains slowly away.