Semen analysis and Male factor Problems
Male factor issues are common contributors to infertility. Often they are not detected, because either no evaluation is performed, or efforts to detect the problem are inadequate. A sperm count ignores important parameters. How the sperm are formed correlates well with their ability to fertilize eggs.
As the old saying goes, “It takes 2 to tango.” Almost half of infertile couples have a male factor problem impairing fertility. Most of the time, a male factor problem is just one on the list. How do we identify a male factor problem? A simple screening test is a semen analysis. Note I did not say “sperm count”. Sperm count is a small part of the information we need. Below is a chart of what normal semen parameters are:
Normal Semen Analysis
Volume 1.5 -5 ml
Concentration >20 million/ml
Motility >40% rapid forward
Morphology >6% normal forms
What does all that mean? Let’s start with volume. One milliliter (ml) is about 1/5 of a teaspoon. As we noted in our previous discussion, most of that volume of the ejaculate is fluid from the so called accessory glands of the male reproductive tract. Low volume may indicate a blockage of a duct of one of those glands. It may mean that part of the specimen was lost in an effort to make a collection – oops. Do we really need to discuss how a collection is accomplished? Quite frankly, if we need to have a collection performed in the office, I encourage the wife to assist her husband. Guys frequently have problems, under these circumstances.
Concentration refers to the number of sperm per milliliter volume of the ejaculate. Obviously a low count can be a problem. Poor sperm production is common in couples with a male factor problem. Usually, it is not an isolated problem, but found in combination with other problems. This is the sperm count, but as you will see, count, by itself, is inadequate information.
Motility refers to how well sperm are swimming. We want at least 40% swimming rapidly in a fairly straight line. It does not do much good if they are just swimming around in a tight circle. Nor does it help if the are lazily moving in any direction. Worse still, some just quiver, and go nowhere.
Now comes an incredibly important part of a properly performed semen analysis. It is also the part that most labs either ignore, or do poorly. That is the morphology, or how they are formed. A sperm cell consists of a head, with its acrosomal cap, a mid-piece and a tail. The tail is the propeller. Sometimes it is bent or formed abnormally in some other way. The sperm will not swim well in that case. The mid-piece is the engine room. Tiny intracellular organs called mitochondria are in the mid-piece of the sperm. Mitochondria provide energy for cell functions. Finally, the head is the “war head” of the sperm and the acrosomal cap is the “detonator”. The head contains the chromosomes, which must unite with chromosomes of the egg to form a new individual. In order for the chromosomes of the sperm to get to chromosomes of the egg, they must enter the egg. That is where the acrosomal cap is important. The acrosomal cap contains enzymes that alter the sperm cell membrane covering the head of the sperm. Once the sperm cell membrane undergoes the change induced by the acrosomal reaction, the sperm cell membrane can fuse with the egg cell membrane, creating an opening for sperm chromosomes to enter the egg. No, the sperm does not just ram its way in, as folk lore indicates. Nature is usually far more subtle than that.
Semen analysis, if properly performed, is a great screening tool for male factor problems. Other testing of sperm function can provide useful information, but should be reserved for the evaluation of specific problems. One such test is to determine the ability of sperm to actually enter the egg. It is referred to as a sperm penetration assay. If the sperm head is not adequately covered by an acrosomal cap, testing for the ability of sperm to enter the egg may be appropriate, in specimens with borderline abnormal morphology. How is the test done? The testing relies on a peculiarity of eggs from the Syrian golden hamster. Those eggs are very promiscuous. If you strip off the clear protein coat, the zona pelucida, which surrounds the egg, it will allow the normal sperm of any mammal to penetrate the cell membrane, and enter the egg. No, that does not create a funny looking new creature. For a new individual to be created, the egg and the sperm must be from the same species. Hamsters do not even have the same number of chromosomes. Chromosomes from sperm must pair up with chromosomes from eggs to actually fertilize the egg. Actually, we want to see penetrations by multiple sperm into the eggs. The penetration rate of sperm from our male patient is compared to the penetration rate, in the same laboratory setting, of sperm from a known fertile donor. If the penetration rate of our patient is comparable to the fertile donor, even if our patient’s sperm morphology is not great, his sperm can probably fertilize his wife’s eggs without being injected into her eggs.
Over the years, a great deal of discussion has been set forward in literature and conversation about immune problems impairing fertility. Other than conditions where a man is making antibodies to his own sperm, immune problems preventing conception seem to be extremely rare. The things that cause men to make antibodies to their sperm are vasectomy, and, occasionally, trauma to the testicles. There is a way to test for antibodies to sperm. It is called an ImunoBead® test. Tiny latex particles are coated with antibodies to the 3 antibody groups made by the human body. If sperm are incubated with the beads, and stick to them, the sperm have antibodies attached. We can even determine where on the sperm the antibodies are located and which type antibody is attacking the sperm. This is referred to as a direct ImunoBead Test.
Although it has very rarely been found that a woman makes antibodies to her husband’s sperm, we can test for that, too. To perform an indirect ImunoBead test, we must incubate the husband’s sperm in the wife’s serum, before placing sperm with the ImunoBeads. Sperm previously proven not to have antibodies must also be incubated with the wife’s serum as a control, to demonstrate that the antibodies were not already on the husband’s sperm.
Another assessment of sperm, which has been proposed, is examining sperm for breaks in the DNA of the sperm. There are a number of competing tests for DNA breaks, and they all appear to have promise as detection technologies. The problem is that we do not have a reliable treatment for DNA breaks. Research in the area continues, and there will probably be treatment, someday.
I work diligently to detect male factor problems, but I do not treat the male. I am fortunate in that I collaborate with a sub specialty trained urologist, who provides state of the art care for our couples’ male factor issues. Even then, he can improve semen parameters, but often cannot reestablish normal sperm production. Since it takes about 3 months to make a sperm cell, and have it ready to ejaculate, any treatment of the man will take a minimum of 3 months to see any improvement, and 6 to as long as 9 months to see ultimate outcome. Even so, we do have the ability to use the sperm which are available, in treatment of the infertile couple. Treatment of a couple who has a male factor problem also requires treating the woman at the same time. The sperm need help getting to, and into the egg, so we need to make certain eggs are available.
Treatment of male factor problems has advanced at least as much as our ability to identify problems. Previously, all we could offer a couple with a severe male factor problem was donor insemination. Donor sperm is certainly still available, but we have even more options. Intrauterine insemination and the injection of sperm into eggs are topics of other chapters, but provide alternatives to our older technology.