[note: this first appeared as “Cryptorchidism in the German Shepherd Dog,” but is applicable to all breeds.]
The most common congenital* anomaly of the scrotum and testicles is the apparent absence of one or both gonads. I use the word “apparent” because the missing testicle(s) usually are actually present inside the body cavity of the dog. The Greek kryptos means hidden, secret, or covered, and the Greek orchi- is a combining form referring to the testicles. The condition is therefore called cryptorchidism and the dog so afflicted is called a cryptorchid. If one testicle is retained, he is a unilateral (one-sided) cryptorchid and if both, a bilateral cryptorchid. A word commonly applied to the former is monorchid but this is a misnomer, as monorchidism would mean the presence of only one testicle anywhere in the body, not just in the scrotum. True monorchids are quite rare, as are anorchids (males with no testicles), and either condition can be verified only be extensive surgery.
* Webster’s Dictionary is by necessity succinct and does not always tell the whole story. In the world of Biology/Genetics, the word “congenital” (literally, “with birth”) means that the condition existed some time before and at parturition (delivery, whether Caesarian or natural birth), and a secondary meaning is that even if not detected then, it is considered as dating from parturition. In common usage, congenital defects can include both genetic and environmentally-caused conditions/defects... think of the thalidomide babies of the late 1950s and early 1960s, which phenomenon was a mystery when they first appeared, puzzling medical people who scrambled to figure out why this seemingly “genetic recessive” of missing limbs etc. suddenly became so widespread. Then they tied it to the use of the drug and saw that it was congenital but not genetic. You can consider the slight difference this way: Genetic disorders or traits are congenital (even if unseen at the time, such as eventual pattern baldness or Huntington’s chorea) but not all congenital problems or conditions are genetic (passed from one generation to the next by way of the genes). So, your “Mr. Webster” could improve his definition by adding one word, and re-stating: “Developing during gestation but not necessarily through heredity.”
A dog whose testicles have been removed is commonly but inaccurately referred to as having been “neutered,” but more accurately he is called a castrate. Such a dog generally has no (or greatly reduced) response to sexual stimuli, while a sterile bilateral cryptorchid may have normal sex urge, and a unilateral cryptorchid is usually both virile and fertile.
The AKC and almost every other club require every dog competing in shows to have two normal testicles in the scrotum. Judges are supposed to examine the scrotum, and usually a quick pass of the hand between the thighs will let them know if one is too spongy, hard, or abnormally small, indicating the possibility of disease or chicanery. (Unfortunately the UKC has slipped up on including this as a qualifying trait.) In some countries testicle abnormalities are more severely penalized and in some places less is demanded of the judge than is the case in the United States. I have excused, placed at the end of a class, or disqualified dogs (depending on the Standard and country’s rules) with unequal testes, in spite of the fact that they have been given awards or not penalized by previous judges. But I have also seen the same thing in regard to dentition — I have disqualified dogs for DQ faults listed in their Standard that had already amassed championship points from judges who either did not understand the Standard or gave the typical AKC cursory look at incisors and little else.
Examining the Pups
A tube called the vaginal process runs from the parietal peritoneum (the inner lining of the abdomen) to the scrotum which that lining encloses. Inside this tube are the spermatic cord, artery, vein, nerves, vas deferens, and the cremaster muscle. It is the function of this muscle to pull the testicle closer to the body in cold environs, and to allow the scrotum to hang lower in warmer conditions. In the abdominal wall, there is a ring-like passageway through which the testicles move sometime soon after birth; in cryptorchidism, one or both stay inside that wall while the opening gets too small for later passage. It may be a genetic defect in the length of the spermatic cord that is the most important reason. In puppies under eight weeks of age, the cremaster muscle also may function to keep the testicles in the tubes but still outside that “vaginal ring” of the abdominal wall, instead of allowing them to descend all the way to the scrotum. Perhaps a defect in this muscle is responsible for the fairly common “elevator testicle” in certain family lines: in this phenomenon, one goes up, comes down, and goes back up again. Usually this is outgrown rather early, but I knew of one pup that still exhibited this condition at the age of five months. In some breeds, such as Toy Fox Terriers, it is not uncommon to find testicles absent from any scrotum, but present just outside the vaginal ring, very hard to palpate.
People who can’t find the testicles in young puppies may be holding the little shoelace-tuggers in the wrong position. The testicles should descend before birth, but are so small and mobile they may be nearly impossible to find on a wriggling pup that doesn’t want to be constrained. But if you cradle the pup’s upper body in the bend of your arm and let his bottom half hang, you should be able to feel them, especially if thumb and index finger are run down the prepuce, one on each side of the penile sheath, pushing the tiny gonads toward the scrotum. You can use the middle finger to feel for them while the other two fingers slide downward and push in that direction. It’s a little like squeezing toothpaste from one end toward the opening of the tube. In some pups, they simply will have to be pushed into the scrotum this way in order to be noticed. Some folks panic when only one can be found; they run to the veterinarian for some magic shot of hormone to make the other appear. While the synthetic hormone APL (anterior pituitary-like) has had some success in humans, its efficacy is probably zero in dogs. First, it definitely is of no benefit once the testicle has grown too large to squeeze through the vaginal ring, and therefore the need would have to be discovered at or soon after the time of birth, which is all but impossible even if one has the most sensitive fingers in the world. Then, if the other testicle does appear in the scrotum, it’s probably coincidental and not due to the APL: the testicle was going to drop anyway, or it was in the inguinal canal outside of the abdominal wall and held up by a tight cremaster which loosened as the pup aged. (There is no evidence that APL works as a relaxant on the cremaster.) Even if APL were a successful way to induce testicles to drop, the pup’s genetic makeup would remain the same and he would pass the defect along to many of his offspring. As a responsible breeder you would find a pet (non-breeding) home for him.
In Germany for a short while, unilateral cryptorchids were eligible for showing and breeding, as the fault seemed to have no effect on utility or beauty in the GSD and other working breeds. By 1930, the SV prohibited not only showing, but registration as well. For a long time, one could still show unilateral cryptorchids in many countries... I remember it was allowed in Canada during my early years as a handler. By 1956 the AKC applied the disqualification to all breeds. Even today some feel that cryptorchidism is an imported or German bloodline problem, forgetting that most working breeds derived from Germany, and not knowing that the SV, and later other breed clubs, really led the way in prohibiting the fault. In fact, cryptorchidism is as common in one country as another, and has about the same incidence in one breed as any other. For those who are considering a sport/working life for such a dog, there should be no deterrent.
The most recent studies on the subject of missing or hidden testicles indicate that there can be several genetic causes. Retractile testicles, a feature of the dog with an overactive or short cremaster, may be due to a genetic determinant quite different from that which causes classic unilateral cryptorchidism, as I have indicated and observed from personal observation. Bilateral cryptorchidism may also be genetically slightly different, since both testes are usually found in almost the same ovarian position as they are in the early fetal life of normal males. It seems that this phenomenon may be caused by two or more genes. Such may be the case in unilateral cases too, although there is reliable data to suggest the possibility of a simple Mendelian recessive in the case of classic unilateral cryptorchidism. If two normal-phenotype dogs actually carry the recessive, on an average one might expect 25 percent of the litter to show the condition. But since about half of each litter is female, the average would only be 12½ percent. With such breedings that produce one-apparent-testicle dogs not being often repeated, it’s difficult to find meaningful statistics. I have observed that when unilateral cryptorchids are bred, there is a high probability of them siring both unilateral and bilateral cryptorchids.
According to one researcher, it is the right testicle that is most often retained, being the more cranial (more toward the head) of the two in the early embryonic stage. The retained testicle in unilaterally affected dogs is usually found near the bladder or at the entrance to the inguinal canal on the inside of the abdominal wall, as if it had been arrested on its way to join its mate. In Angora goats, it is also the right testicle that is commonly retained, though this is not hard evidence that all species have the same genetic cause for the same effect. Similarly, the right ovary of females and the right kidney in both sexes are further forward than the left organs. In the normal male, the left testicle in the scrotum is usually carried slightly higher and behind the right one. (Not always, so don’t write me correction letters on that!) I have checked that out in many a show ring when judging Rotties, American Pit Bull Terriers, and other sizeable, not-heavily-coated breeds.
As mentioned, unilateral cryptorchidism often seems as if it were a simple, recessive, one-gene Mendelian trait, though possibly it is not. If the problem of unilateral cryptorchidism is indeed simply recessive, the occurrence of bilateral cryptorchids might have to be explained by the action of other, modifying genes, and many geneticists today do not find that idea appealing. But for the purpose of explanation, let’s use it as an example. If the pup inherits one gene for the trait from one parent and one normal allele from the other parent, he will not show the disorder but will be a carrier. If the normal gene is represented by the capital letter C, and the defective gene is identified by the lowercase c, his genetic constitution on that chromosome is Cc. On the other hand, if a dog is a cryptorchid, his genetic constitution at that locus on that chromosome is cc (two defective genes). If this dog is bred to a bitch that also inherited two such genes, (she is also a cc), all of their offspring will either be cryptorchids like the sire or homozygous carriers like their dam. It is possible that a testicle found in the scrotum of some very young pups from such a union may later retract and be trapped inside the peritoneum. In some breeds this happens fairly frequently, and some believe it is caused by the same set of genes that cause more typical cryptorchidism. The difference between unilateral and bilateral cryptorchids may also be due to the presence of certain modifier genes.”
In addition, some breeds with brachiocephalic skulls seem to have a much greater than 25 percent incidence of orchidism when “supposed” (phenotypically) normal dogs (who are actually carriers) are bred. Knowing what we do about such breeds and their pituitary defects, would it not be reasonable to say that maybe many breeds and species have in their population a very slight hereditary pituitary defect that acts not only on the development of the spermatic cord and other structures in the genital system, but other traits as well? Breeds that have been selected by fancy to be what Noah would have considered grotesque include the (“English”) Bulldog, said to be a compilation of all the disqualifying and serious faults of most other breeds. The reason for these “defects” stems from genetic defect s in the hypophysis or pituitary gland, the “master gland” deep in the base of the brain. It is the master of the other endocrine glands including those others with functions related to growth of various and all parts of the body. In the GSD, for example, we have a particular defect that results in pituitary dwarfism (see pictures in “The Total German Shepherd Dog,” www.Hoflin.com and other sources) and such dogs, while nearly perfect in proportions, often have serious thyroid gland problems with resultant loss of hair that makes some of them look like Chinese Crested hairless dogs. Remember what I said about the interconnection between endocrine glands. Other defects produce the Bullmastiff face, the Cocker or Corgi dwarf legs, etc.
I believe it is safe to say that cryptorchidism is genetic, that it is in some way recessive, and that there is some sort of connection between bilateral cryptorchids and unilateral ones. Perhaps there is also a connection between the pituitary and floating testicles. At any rate, the unilateral condition at least is so widespread in many families and breeds that an all-out effort to combat it would take our minds and efforts away from more serious disorders, which would consequently increase. It’s just a minor thing we have to put up with. Simply remove the affected ones from the gene pool, and shift your preference away from breeding any (including females) that come from litters in which the defect occurred.
Since cryptorchidism is sex-limited (only affected males, not carrier females, show it) it is likely to persist at about the same prevalence in the breed for a long, long time. In Germany and many other countries, where registration is denied cryptorchids and sanctions are made against their parents, more than half of the “VA” (top show) GSDs in a 20-year period sired cryptorchids and hence were carriers. In England, the prevalence is higher, and probably that’s because for a long time such dogs were not penalized in the show ring.
Effects on the Dog
It is not uncommon for retained testicles to give a dog a grouchy, sour, or miserable personality, and the condition also seems to be associated with a higher than normal percentage of testicular cancers or tumors on the retained gonad. For both reasons, many veterinarians recommend castration even if the testicles are undescended. That can be a difficult operation; sometimes the vet gives up without ever finding the little undescended bugger. The vets who operate make some money as they do on any surgery, but there are many such cases when they cannot even find it. The question of whether to have a vet open him up and look for it is a personal one, based on many factors. A third possible effect is cryptorchidism’s reported connection with early fetal death of females in litters with affected males, with these females either resorbed or, in some cases, mummified. The gene or genes may be semi-lethal ones which are only sometimes expressed in the death of the female embryo, and which sometimes cause the surviving bitch pups to be sterile if they are homozygous (cc). Mummy puppies can cause great difficulties in abortions of later pregnancies, lack of or decreased contractions, and stillborn pups in subsequent litters. So if there is a connection with cryptorchidism, that’s another reason to avoid families in which it appears.
Dogs that are castrated early in life do not have the same development of bulk and other attributes of masculinity that intact males do. This is primarily because the primary source of testosterone and other “male hormones” has been cut off — literally. Remember that all the endocrine glands (those producing hormones) and “connected” in a way analogous to a network of businessmen, electricity generator grids, etc. When one is affected, almost all the others “feel” it. Many hormones are required to make endocrine glands in another part of the body function optimally. Sometimes the hormones normally generated by a specialist gland can be produced in small quantities by other glands when the principal supplier is lost. Still, for normal development of the various organs, all the endocrine glands should be present and healthy.
Partial castration (removal of only the retained testis) or complete castration produces very few other noticeable effects if the dog is allowed to mature before the operation. By then, the testosterone and other hormones have had their intended effect and the dog has developed into a large enough, masculine enough dog suitable for anything an intact dog would be used for. Perhaps those wishing to have an impressive dog that could take down a Schutzhund helper might want to postpone such an operation until the dog is older and fully developed.
According to Canine and Feline Theriogenology by Johnston, Kustritz, & Olson, there is a link between patellar luxation (common in toys) and undescended testicles. I have not researched this, though, so I don’t know if anyone else has seen this link, or what the reason for the coincidence. It may be a pleiotropic phenomenon.
Depending partly on the breed, cryptorchidism is a fairly common condition; it is seen more often in toy and miniature breeds. Most affected dogs have one testicle that is not descended. Dogs that are cryptorchid have a much increased risk of testicular cancer (it has been said to be approximately tenfold). However, the literature I have researched so far does not give a starting incidence to multiply by that factor of ten. Castration will of course eliminate this risk. On the other hand, many dogs never have any adverse reactions to leaving the undescended testicle in. It’s up to you to research further, ask, and decide.
One reference work stated, “The only treatment for this condition is removal of both testicles.” and... “Affected dogs should not be bred. It is best not to breed their parents as well, who carry the gene.” But I disagree with that. There is no good reason except convenience to remove the testis that is in the scrotum. Just take out the one that gives the higher risk of cancer.
There is the definite risk that the vet will not be able to find the retained testicle... I have seen this happen and have heard of it many times. If it were my own dog, I would not operate. But everyone has to make his own decision after weighing all the pros and cons.
Veterinarians are sometimes asked to surgically correct cryptorchidism by moving the testicle(s) down into the scrotum, but this is an extremely difficult and delicate operation with very little chance of success because of the length of the spermatic cord, the effect on attached tissues and blood vessels, and other technical reasons. An easier alternative is to implant a synthetic testicle—glass, silicone, or whatever—and veterinarians are quite often asked to do this. However, nine times out of ten the owner’s motives are questionable at best. Usually he wants the surgery so his dog can compete in shows, or so he can fool owners of bitches into paying for stud service from what is supposedly a normal dog. Best to keep cryptorchidism in perspective, and be above-board in your data and honest in your statements and dealings. Educate your puppy buyers if you are a breeder, and they will acknowledge that such recessive traits will always be in the breed. They will also learn that if you do the selective breeding I recommended your kennel’s incidence will be lower than the average in the general population.
Typical Reader Questions (these are from GSD owners)
Q. Consider your simplified example of Mendelian recessive unilateral cryptorchidism in two normal-phenotype dogs. What outcome (affected/carriers/clear) would you expect if you bred the following combinations?
(a) Carrier Cc male with a clear (CC) bitch;
(b) Clear (homozygous non-carrier) male with a Cc bitch;
A. First, remember that anything genetic is not as “simple” as mathematics... every chromosome and every gene is affected in some degree by others close to it as well as by various other factors. Use the Punnett Square examples in my GSD book to work out approximate percentages, however. Second, divide the figures below in half, because there will be half females and therefore no chance of knowing phenotypically whether you have C or c or combinations thereof. Regarding (a.): Assuming C is “Clear” and dominant, you would get 50% CC (homozygous clear... non-carriers) and 50% Cc heterozygous “clear” (not affected but carriers); Re (b.), What’s the difference from (a)? Unless it is a trait on the X or Y chromosome (and this isn’t), it matters not which parent has what genotype.
(c) a clear male with a cc bitch;
A. All will be Cc (no other combination possible... all will be carriers.
(d) a Cc male with a Cc bitch?
A. 50% Cc (carriers), 25% clear CC, 25% homozygous “affected.” Of this 25%, remember, half on average will be females, so really 12.5% of such litters will be affected (obvious) males... you just can’t see the homozygous “affected” females’ genes or their zero effect on their phenotype.
Q. Assume normal phenotype dogs -- is it impossible to have affected puppies? How about if both dam and sire are carriers?
A. Yes. GIGO: Garbage In, Garbage Out. You can’t get something unless the parents give it to you (them). The second part of this question is answered under (d.) above.
Q. Bilateral cryptorchidism is thought to be affected by some additional modifier genes but they are thought to be related conditions, right?
A. I agree. There may be a few genes at work, but one main type. Some may affect the shortening of the cremaster muscle or the spermatic cord to varying extents.
Q. In example (d) above, would you expect to see both unilateral AND bilateral cryptorchids in the same litter?
A. If these dogs had those additional modifier genes. Based on observation, it seems that the more recent and the more numerically the affected dogs in the pedigree, the more likely you are to find bilateral cryptorchids pop up. There are not enough statistics of litters bred for this bad trait for us to be positive, but I would guess that the likelihood of having a bilateral in a litter might increase in proportion to the number of unilateral cases in the recent ancestry.
Q. You mention that the SV prohibits registration of cryptorchids. Is there an effective way for the SV to enforce this?
A. Nobody tries to breed-survey such dogs, obviously, and registration is granted when the breed warden visits at 7-8 weeks, at which time some are not willing to be premature in their evaluation of cryptorchidism. If a dog were presented later for registration, or happened to be evaluated in a breed survey (Truly, some people never check their own dogs’ testicles until a show or survey!) and were found to be missing one, it would be recorded (and published in the Zeitung) as Einhoden, (one testis) and ineligible for registration. The papers (Ahnentafeln) are the property of the SV (though they remain in the dog-owner’s possession and care), and must be returned. Even if the paper is lost, the dog is in the records as not being allowed to have registrable offspring.
Q. What kind of “sanctions” can be brought against the parents of litters that include cryptorchids?
A. None. It happens in the best of families, and that would cause a riot and revolution.
Q. How does the SV find out about cryptorchids?
A. As I said, there really are such people here and there who enter a show (or breed survey) and have never “counted the cajones.” You will notice that although the incidence is relatively high, the number of reported cases in the Zeitung is very small. Almost all published registration revocations are for “severe HD.” The SV obviously does not hear of most of the “einhoden” cases.
Q. The statistic that more than half the VA dogs over a 20-year period sired litters that contain cryptorchids surprised me. Was that a recent 20-year period?
A. I don’t think it was very recent. But like other studies and surveys the SV has taken, the percentages have not changed much in 100 years.
Q. How does the SV/other source track that information?
A. I can’t answer that except to say that Europeans, and especially Germans, keep almost everything in some files somewhere. That’s how many WW2 Nazis were nailed... voluminous record-keeping.
Q. Is it likely that the rate of “carrying” is even higher because some cryptorchids just “disappear” to protect the reputation of the VA sire?
Q. (Several questions from one correspondent) I have a litter of puppies 11 weeks old; there is a testicle problem with ALL of the males—each one is “monorchid.” The paternal grandsire on both sides of the pedigree is the same dog. The granddam produced one unilateral cryptorchid when bred to her cousin. When bred to the dog who is the paternal grandsire of these pups, no resulting pups from the litter were affected although one was slow to descend (4 months). She did not throw any problems when bred to a male of Bxxxx kennel.
A. Your reference to the duplication of great-grandsire in the pedigree indicates the likelihood of your proving the fact again that inbreeding uncovers hidden recessives. That’s how people find out about “problems in my line” as you put it. The Bxxxx dog is probably not a carrier, but your other dogs obviously are.
Q. Her daughter — the dam of the pup’s sire, has had two litters with no testicle problems.
A. This could be coincidence; it could be she is affected (homozygous) but was bred to non-carriers, etc.
Q. However, it was her littermate in that first litter that was the unilateral cryptorchid (dam had been bred to her cousin).
A. I think there is a 66% chance that she is affected when she has an affected littermate. Get Dr. George Padgett’s book on genetic diseases.
Q. Another bitch in that line (a sister to that cousin, and belonging to B.H. in MD) has had multiple litters and has not thrown any testicle problems even when there was an inbreeding.
A. Could be she is not a carrier. In many or most cases, recessives do not give any hint of their presence in the genes.
Q. A brother of the sire of these pups when bred to a half-sister of these pup’s dam, had no problems.
Q. Since this trait is felt to be genetic [is, definitely! --- F.L.], it would seem that there must be carriers and that it would be traced mostly to the paternal grandsire of the pups (sire of both the sire and dam of the pups). We don’t have as much information on him.
A. That’s why open registries (information sharing encouraged) are important.
Q. If these males’ other testicle does not descend, obviously they can’t be used for breeding or showing (and they are outstanding in quality and movement even with a flying trot).
A. That’s the right approach. Why breed known defects when we have enough trouble with the hidden ones?
Q. What about the females of this litter? Would they all be carriers?
A. Can’t tell unless test breedings were done, but there is a high likelihood that littermates are either homozygous or heterozygous for the defect.
Q. And could they (the bitches) be used for breeding?
A. If you have pet homes for affected offspring. Also, if she produces it, you should be willing to spay her and warn the buyers of these females and unaffected males that they probably are carriers.
Q. The genetic makeup doesn’t seem as though it could be cc X cc, as the sire himself is not a cryptorchid; in fact his testicles both descended quite early on.
A. He is not cc, but could be Cc (carrier).
Q. Is it possible that the pup’s dam is a carrier? When outcrossed, her last litter was fine. Would she be a cc?
A. Since cc or Cc females would not show the trait, you can only say “possibly, but unknown until test-bred.” If bred to a normal (unaffected and non-carrier) male, none of the F1 (first-generation) pups would show the trait.
Q. If the sire were a Cc but not himself a cryptorchid, would the dam have to be a Cc or a cc for all of the males in the litter to be cryptorchids?
A. If both are heterozygous (carriers), it is possible for them to produce a litter in which all males are affected (unilateral, bilateral, or a combination). It is also possible that any combination of “unaffected” (heterozygous-defective, or normal) & known “carrier” mates could produce all normal-phenotype male pups. They could also produce a litter of all cryptorchid, or any combination between. You really need to practice drawing those Punnett squares, but keep in mind that this will only show you statistical averages. And it usually takes some extremes to make an average.
Q. & A. (from a Pakistan chat-website): Sajjad Malik wrote about a 50 day-old GSD pup whose testicles have not yet descended normally into the scrotum. In another post I mentioned that I have produced more then 50 litters of GSDs over many years of breeding. I learned how to identify or verify the testicles being normally present and in the scrotum at a very early age... well before 8 weeks of age, which is when I usually let them go to new homes. Grasp the pup in the crook of one arm, supporting it at the chest and elbows, and let it hang suspended thus. With your other hand, use your thumb and a finger to straddle the penile sheath, squeeze slightly, and stroke/press downward until you are able to push the testes into the scrotum. (At young ages, when it is cold, etc., it is common for pups to carry these very small testicles high and close to the abdomen.) If you cannot find (push) both into the scrotal sac, after a few tries, the prognosis is not good. You might want to hold onto that pup for a few weeks longer than you would ordinarily sell puppies, and see if it is a case of a late-descending testicle. Very few come down after that age
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