The Basics Page
This site is focused on treatment of chronic disease like Multiple Sclerosis (MSi) Chronic Fatigue Syndromei (CFSi) and Fibromyalgia (FMSi) an many other diseasesi with antibioticsi. Recent research indicates that Chlamydia Pneumoniae (CPni) plays a role in these diseases.
Here are the basics that make it easier for people new to the site to get going (if your brain isn't ready for even this much right now-- we've all been there-- read Cpn Simple first):
Is this a sexually transmitted disease? No. this is chlamydia pneumoniae, a bacteria that can cause pneumonia. It may soon be called chlamydiophilia (meaning in the family of).
Is chlamydia pneumoniae (CPn) rare?
No it is a common cause of respiratory illness, but it has an interesting and abnormal way of existing because it can change forms and inhabit the very cells of your body. It can go into your monocytes (a blood cell), your macrophages i(an immunei cell), microglia (a brain cell that causes immune reaction) endothelial cells (blood vessels) and others and actually take over. We say then it has parasitized the cell. Your cell can't do the work it was meant to do now because it's busy supporting the CPn, all the energy of the cell going to make energy for the CPn and it using that energy to make new CPn cells. For all intents and purposes, your cell is no longer a functional cell and cannot do what it was designed to do.
How does it spread?
From person to person when in the respiratory tract it is spread by droplets; in a cough for example. The form that goes from one to another is the elementary body (EBi), a tough, little tiny bacteria. It may actually cause pneumonia in the respiratory tract. In some cases once inside, the EB will look for a home (cell) to parasitize so it can have an energy source. Once inside the cell the EB turns into a reticular body (RB) which can produce new infective cells (EB's) that can find and parasitize other cells. Gradually the cells of your body lose the ability to do what they were meant to do. They are now supporting CPn lifecycle and not taking care of your lifecycle. If it's a monocyte that's infected for example, it is now a factory for EB's not a functional monocyte. We say then the CPn has parasitized the cell.
Why doesn't my immune system kill it?
This is a complex question. It depends on where the infection is and how advanced it is and what cells have been infected. People who get CPn as a form of pneumonia and do have an active immune response to the bacteria in that instance, though as a form of pneumonia it is mild. Often it is referred to as "walking pneumonia" because people, while ill, are not prostrate with it. Since most people get CPn in their lifetime and get over it as evidenced by rising titers to the bacteria, we can assume that most of the time the immune response is effective enough to for all intents and purposes "get over it."
In some people however, perhaps because of their genetic makeup or some other factor, the bacteria is carried in blood or immune system cells In this case it "goes underground" and infects the tissues far from the origin of the lungs. Key to this discussion is that your immune system cells are some of the ones that now have these nasty little bacteria hiding in them, so where the immune system goes, the CPn goes too and over time may render the immune cells less effective.
Second, the germ is INSIDE the cells. Your immune system can't see them in there. Your immune system "sees" what is "you" and what is "foreign" by looking at the proteins on the outside of the cell wall. The outside of this cell is you. For all your system knows, it is a friendly cell, so your immune system is quiet and unexcited. Meanwhile the stealthy pathogen is hiding, slipping into the cells and taking over one cell at a time, and one cell at a time they are now CPn factories not whatever they were meant to be.
While in some cases CPn is a fairly "benign" germ under certain conditions such as when it is attacked by antibiotics or "starved" it becomes cryptic or shuts down so it can't be harmed or detected. When cryptic it is so quiet and hidden in the body, your body does not really notice it. It then becomes active at some later time causing a "new" infection, perhaps in new parts of the body.
Changing forms of Cpn
This bacteria diabolically can change from any form, EB, RB, Cryptic or persistent, to any other form based on the environment. It will choose the form least affected by whatever is threatening it! If you take an antibiotic, let's say for a bladder infection, the CPn will hide in a non replicating and non metabolizing form until the threat is over and your internal environment is less hostile. Virtually all people will have rising titers to CPn over their lifetime, meaning they have been exposed and make antibodies to it from the occasional experience with it as a respiratory pathogen, but also perhaps because they harbor this cryptic formi which later "wakes up" and then subsides or is treated. But as a cryptic pathogen we know little about it. It is just emerging as a known cause of disease. The Centers for Disease Control list it as an Emerging Pathogen in atherosclerosis. See the slides to see pictures of these germs in the cells.here
Why do steroids help MS then? This question was asked to Dr Wheldon and Dr A. The answer is found here
Why is it true that your doctor does not tell you about this?
This is new understanding and it's not well defined yet. For example why is it cryptic in some people? We are not certain at all. The CPn was first seen in 1965 and was identified as the cause of an outbreak of pneumonia in the early 80's. Before that time we had no research or concept about bacteria with lifecycles that included changing forms from one to another and hiding inside the cells of your body. Bacteria were seen as one form either a cocci, or a spirochete, or a rod and you were given one antibiotic and it would go away. Everyone who was trained in medicine was taught this and spent long hours studying these facts.
Now, research on CPn indicates it plays a role in several chronic diseases by using these peculiar and not well understood ways of being in the body. We have to go back to the books and learn a whole new kind of bacterial science where germs evade and hide from our treatments in ways that seem impossible or outlandish based on prior learning and understanding. New knowledge takes time to filter into the mainstream because physicians spend so many years studying biochemistry and microbiology that they feel like experts. This is so different that it sounds "wrong". Also some other research seems to find it is not a factor in chronic illness, which gives the individual physician a sense this is too new to act on yet.
For example, some research in CPn in multiple sclerosis (MS) does not find an increased incidence of CPn in the nervous system in people with MS while other research does find CPn DNA in the nervous system of people with MS. This creates doubt in the minds of physicians and a sense that we need to wait for more definitive research before acting. And finally, medicine is extremely slow to change paradigms.
We have a superb example of this in helicobacter pylori, a bacteria, in peptic ulcer disease. This bacteria was discovered in 1982 by Barry Marshall. He produced a large amount of good research on h. pylorii causing peptic ulcers that went largely ignored. Why? Because "everyone knew" that bacteria could not survive in the stomach (wrong) and he literally had to swallow the bacteria himself and prove that it then caused him an ulcer. When he healed it with antibiotics others to finally accepted his research. It's very difficult to get medicine in general to accept new science, even if it's absolutely correct.
I bet you're thinking that everyone gets antibiotics for ulcers these days, but you'd be wrong. Up to 9 out of 10 ulcers can be healed by treating with appropriate antibiotics for 2 weeks. Yet today, 23 years after the discovery that ulcers are caused by bacteria, not lifestyle or stress, over 50% of ulcers are STILL treated with proton pump inhibitors (medicines that decrease stomach acid)or other palliative measures that do not kill the bacteria, which also may play a role in gastric cancer. This link is to the American Centers for Disease Control detailing these facts HERE There is a serious "blind spot" in medicine about potential infectious causes of chronic disease. Clearly, even a proven fact can still be ignored by doctors.
Why does research say it's not a factor sometimes?
The fact of the matter is that CPn in cryptic form, that means in the cells in an unmetabolizing and non relicating form, is hard to detect. It's virtually impossible to detect without extremely complicated procedures and even in the infectious form it is hard to detect with sensitive DNA (PCRi, below) tests, let alone less sensitive antibody tests. You cannot just see if the person is making antibodies to the bacteria as you would in other infectionsi and as mentioned above, people have rising titers (rising numbers of antibodies) to CPn over their lifetimes as most all of us are exposed repeatedly.
Instead of checking for antibodies a newer advanced kind of technique must be done called polymerase chain reaction (PCR) to see if CPn is in the tissue. This technique uses small amounts of DNA to detect the presence of the bacteria, not the old method of just screening the blood to see if you have antibodies to CPn.
The trouble with this is that just like our understanding of CPn is growing so is our understanding about how to detect it. Labs are developing ways of finding and testing for the DNA fragments, however this is still early days. Some labs use one part of the DNA for detection; others use another. This accounts for discrepancy in results as it has not yet been agreed upon by everyone that one lab's approach is the clear winner for accuracy.
It appears at this time that the Vanderbilt University test is the best at detecting the DNA via PCR. They have doccumented that they have concordance with split samples. In other words, samples tested as positive are positive and negatives are negative in a second test done at another lab. VU finds CPn in the majority of MS cases.
Another reason we have confusion about whether CPn is in chronic disease or not is some research almost inexplicably seems to be set to NOT find it. For example, just testing the antibody titers of people with MS or CFS or FM and people who have no chronic disease is sure to result in no difference between the groups since this is a common bacteria we all will be exposed to over our lives. Yet we still see some "research" doing exactly this; saying that the titers were the same in both the chronic illness group and the normal group and reaching a conclusion that CPn plays no role in the disease. This is silly! The question is not have you been exposed to CPn and do you have a high titer, the question is whether it is an active infection and or whether it has gone cryptic in your particular case. There is no consensus yet as to how to determine that all important question. However evidence is emerging, and in some areas it's substantial (as it is in the area of atherosclerosis) that CPn is the cause of chronic illness. The CDC lists CPn as an emerging pathogen in the cause of atherosclerosis.
What is empirical treatment for Cpn?
If you are tested as positive for Cpn either through antigen or PCR testing, then you clearly know you need to treat it. In that case, know that the standard two week course of a single antibiotic may be inadequate to kill the Cpn in some of it’s life-phases, and re-infection can occur unless a combination antibiotic protocol such as the Vanderbilt or Wheldon protocolsi, is followed. But if you have any of the diseases in which Cpn has been implicated (see list on Home page), it may be worth doing an “empirical” (based on symptoms) course of a combination antibiotic protocol even if your tests for Cpn are negative or uncertain. The antibiotics used are not considered harmful, even for long courses. If you have Cpn involved in your disorder and try this protocol you will likely experience the following: an inflammatory reaction or worsening of some of your symptoms (caused by the bacteria dying and releasing it’s toxin in larger amounts), followed by a gradual improvement in your disease symptoms. Reactions to treatment can range from mild, if your load of Cpn is not great, to very strong and uncomfortable. In the latter case, you have to go very slowly to get to full dose of the protocol. Similarly, improvements in your condition depend on how long you have been infected, and what your total load of Cpn is, and how much permanent damage it might have created to your body.
Why are there so many antibiotics?
CPn exists in your body in several different forms. The first is the elementary body. It is small hard and is not actively replicating or metabolizing. It is "looking" for a cell to adhere to and be absorbed by. At this stage amoxicillini can force the EB into the cells.
Once inside a cell, the EB goes through a transformation becoming metabolically active and replicating. To make this transformation, proteins are used and reassembled to cause the change. It grows huge compared to it's EB size and when the transformation is complete, it takes over the cell's energy system, robbing all the energy for it's own purposes. At this point the tetracycline antibiotics block one of the proteins used in the transformation process (that's how antibiotics work; by blocking proteins used to replicate) so the EB is stuck halfway transformed to an RB (replicating body).
Now, one of the problems we have with antibiotics in general is that bacteria are very crafty and they have "learned" to resist different antibiotics by replicating using different pathways than before so the blocked protein is no longer needed. This is what we mean by resistance. A certain bacteria is no longer stopped by a certain antibiotic from replicating. The concern about CPn resistence can be stopped in it's tracks by adding a macrolide antibiotic such as rifampin, azithromycin or roxithromycin in addition to tetracyclines because it blocks protein synthesis in a second part of it's pathway. It is effectively impossible for CPn to develop resistance with this double whammy.
Both the tetracyclines and the macrolides are considered bacteriostatic. They do not kill germs outright, but stop replication so your body can clean up and win the battle without a growing bacterial population to deal with. In the case of CPn however, the EB is stuck halfway converted. It is not able to take over the cell's energy system, so it's on it's own. It has some rudimentary ability to survive on it's own in this anaerobic (without oxygen) state, but not much. As a result a number of the CPn germs will die causing an endotoxini reaction (see below) even though at this stage you are only taking bacteriostatic drugs.
However a good number of the bacteria will survive even though many die under the stress of living stuck halfway between EB and RB, reducing the overall bacterial loadi by a good margin. This brings us to flagyl (metronidazole). This antibiotic kills the CPn outright, causing for some people a big reaction to the endotoxin, depending on how extensive the bacterial load still is for them as they begin it's use. For this reason, many people wait a number of months after starting the bacteriostatics before taking their first dose of flagyl. Then, they may take flagyl for only one dose the first time they take it, then wait for the body to recover a bit before dosing again. Pulsing the flagyl kills off some germs, then gives the body and tissues reacting to the released LPSi a rest.
The Wheldon regimen recommends using the flagyl for 5 days once every three weeks while continuing to take the other antibiotics. Effectively the CPn is stuck by the bacteriostatic agents waiting to be killed by your next flagyl pulse, though some die simply waiting. The VU protocol recommends flagyl without rest in between and amoxicillin to force the EB's into the cells where they can be killed by the flagyl. This can result in a fairly vigorous LPS reaction (below). Dr A stated in his interview he has no probelm with people pulsing flagyl if they wish to do so.
What is endotoxin and how is that related to "herxheimer"?
Endotoxin is a lipopolysaccharidei (LPS), the protein that is on the outside of every gram negative bacteria. A gram negative bacteria is one that does not take gram stain. LPS is very immunogenic meaning it causes a brisk reaction by the immune system to it's presence. When gram negtive bacteria die, either naturally or by antibiotic, the resulting load of LPS floating around is toxic to the person. "Toxic shock syndrome" is a reaction to LPS in a gram negative bacteria. The kinds of reactions to LPS vary a bit depending on the bacteria in question, some being more toxic than others. CPn LPS is not very toxic as far as LPS goes, though it does cause a noticable reaction, it's not threatening as other LPS can be.
Syphilis as another gram negative bacteria. When antibiotics were first applied to this dread disease, the patients got markedly worse as the LPS built up in thier systems. This was named for the doctors that described it as "Jarisch Herxheimer Reactions". It has been specualted that the phrase "you have to get worse before you get better" came from this phenomenon. Today the term herxheimer or herx has been in common usage to mean any reaction to a gram negative bacteria. I have even heard of people using the phrase in relation to the die off of candida after appropriate anti-yeast drugs have been taken.What diseases has it been implicated in?