Chlamydia Pneumoniae, Antibiotics and Reactions
Drawn from materials on www.cpnhelp.org
Chlamydia pneumoniae (Cpn) is an intracellular bacterium, which means that it invades the body cells, and it is an obligate parasite, which means that it cannot supply its own energy source and so takes over the ATP of the body cells it invades for its own reproduction, depleting the host cells and leaving them less functional.
One of the difficulties in eradicating Cpn is that it is a multiphase organism (see more detail on this below). This is not typically understood in standard medical management of Cpn infections, although it is well known that Cpn infections can be “persistent”. Standard medical treatment of Cpn infection utilizes a single antibiotic, typically for a couple of weeks or months. No matter how long a single antibiotic is used, nor how many courses, a single agent cannot kill the Cpn in all of its life phases.
Dr. Charles Stratton’s lab demonstrated that monotherapy antibiotics (use of a single antibiotic such as azithromycin) that kill Cpn in one phase do not necessarily kill it in other phases. So unless a protocol uses agents that cover all three phases of the organism it simply converts to another phase to survive and then takes up reproduction and dissemination in the body once that antibiotic is withdrawn.
- Standard serological tests for Cpn are often false-negative in the face of actual infection, rendering them unreliable indicators. Often treatment response to an empirical course of CAP treatment, when symptoms are suggestive for Cpn, is the best indicator of infection.
- While it is transmitted as a respiratory infection, Cpn can be carried to other parts of the body and infect many other tissues, including nerve tissue, the brain, muscles, kidneys, liver, prostate, the lining of blood vessels and especially the immune cells (macrophages and monocytes). Thus, this single organism can cause a wide array of problems. (See “Cpn & Multiple Diseases” for more on this.)
- Persistence and Resistance- The standard single antibiotic courses (monotherapy) typically used in medicine actually creates persistence of the organism by forcing it to convert into a different phase unaffected by the antibiotic. In addition, repeated courses of single antibiotic increases the risk of creating pools of Cpn resistant to that particular agent. Persistence being the re-emergence of an infection apparently knocked down by treatment; Resistance being the adaptation by a bacterium so that it is no longer susceptible to an antibiotic.
- Combination Antibiotic Protocol- Using the highly sensitive measures they created at Vanderbilt, Dr. Stratton and his colleagues found that the only way to eradicate Cpn completely, avoiding both persistence and resistance, is to take a combination of antibiotics so as to kill it in all of its life phases so that nothing is left behind to re-infect. This is called a Combination Antibiotic Protocol or CAP. This can take a long time depending on the load of Cpn in your system, the organs infected and other variables. Typical courses of 1-3 years are not unusual. It also takes time in many cases because the progression onto full doses of the combined agents must be gradual to avoid precipitating debilitating toxic reactions to bacterial die-off and make the treatment tolerable.
- Treatment reactions: There are three distinct and sometimes strong reactions to killing Cpn with a Combination Antibiotic Protocol that must be considered in its treatment. Calling these reactions collectively a “herx” (short for Herxheimer reactions) is both inaccurate and not useful to treatment, as only one of them is a classical Herxheimer reaction.
- Endotoxin Reaction- Cpn contains at least two endotoxins (LPS and HSP60). Killing Cpn can release significant amounts of these endotoxins typified by drop or increase in body temperature (chills or fever), and cytokine (immune) cascade followed by widespread inflammation. Chronic immune activation and toxic load from long term and hidden Cpn infection also causes hidden tissue damage and disease.
- Secondary Porphyria[i]- Cpn, as an obligate parasite, infects inside your cells and parasitically steals energy (ATP) from your body cells in order to replicate. Many of the cells it infects are responsible for producing heme an important constituent of our blood and used in many places in the body. Heme requires a huge amount of ATP to go from start to finish in its 6 step production process, and any of the intermediate compounds along the way (called porphyrins) are highly neurotoxic and oxidative. Cells parasitized by Cpn will not have enough ATP to carry through this process, and so accumulate these toxic porphyrins.
Killing the Cpn (which often kills the cells infected) releases porphyrins into the blood and other tissues causing symptoms of secondary porpyria: gastrointestinal disturbance, nausea, pain, light and sound sensitivity, anxiety, rapid heart rate, depression, brain fog, and other symptoms.
- The parasitization of infected cells also renders those cells and the organs they are part of less functional over time as Cpn load increases in them. Cpn is well documented to infect the bone marrow, macrophages, monocytes thus rendering immune dysfunction, as well as the fatigue commonly seen in CFIDS.
Phases of the Cpn bacteria and antibiotic agents that effect those phases:
EB’s- Elementary Body What are they? EB’s are spore-like forms that are infectious and have minimal metabolism (aren’t using nutrients, replicating, exchanging with the environment, etc.). They are tough, tiny and reside in the intercellular tissues). EB’s attach to your body cells and invade them. Since there can be more EB’s than can get into cells, EB’s build up in local tissues where their endotoxins cause inflammation and immune response. They are killed by amoxicillin or NAC (N-acetyl cysteine) both destroy the cysteine bonds that hold the EB cell wall together.
RB's- Reticulate Body Once an EB enters a host cell it transforms into a form that can replicate new EB’s that is called a Reticulate Body or RB. The RB has no energy source of it's own for this, so it must steal energy (ATP) from the host cell, leaving the host cell weakened and less functional. The RB also inhibits the natural cell death (apoptosis) of the host cell so that it can survive while it replicates. After the production of many new EB's the host cell bursts and dies, spreading the infectious new EB's into the surrounding tissue. RB's are inhibited in replicating by various antibiotics principally: doxycycline, azithromycin, roxythromycin, Isoniazid (INH), rifampin.
Cryptic persistent form When RBs face an environment that threatens their survival (lack of food, antibiotics, etc) they can transform into a “Cryptic” form that stays inside the cell, but is in hibernation, so to speak. In this form Cpn is not vulnerable to regular antibiotics as it is not replicating or metabolizing, and can reside there until conditions change, then converting back to an RB again, replicating and reinfecting with EBs.
As the Cryptic form is anaerobic, it is killed by Flagyl (metronidazole) or Tinactin (tinidazole). These drugs can be hard to tolerate for various reasons, and so are commonly “pulsed” by taking a course of them while continuing the regular antibiotics (protein synthase inhibitors), for 5 days every 3-4 weeks, rather than taken continuously. Some protocols may eventually have one of these drugs taken continuously for some period as the patient can tolerate. Patients may experience fatigue; nausea, bowel upset, deep joint achyness and muscle pain as the cryptic organisms are killed and the immune system engages in clean up.
Amoxicillin and NAC kills the infectious spore-like EB forms which build up in the tissues.
Rifamcin kills EB’s transforming to RB’s in a vulnerable enzyme transformation phase.
Doxycycline and either Roxythromycin or Azithromycin, are used in combination to interfere with the RB’s ability to replicate. Two are usually used concurrently, as they work on different proteins and so together minimize chances of creating antibiotic resistance.
Metronidazole or tinidazole will infiltrate the cells and kill the cryptic Cpn.
Supplements are recommended to help counter the impact of Cpn on the body, and of the inflammatory effect of the die off during treatment.
The Combination Antibiotic Protocol (CAP) for Cpn therefore consists of building up gradually to:
- Two protein synthase inhibitors continuously (such as 200mg doxycycline daily plus 250mg azithromycin 3x per week)
- Alternately, daily Rifampin and/or Isoniazid
- 2400mg NAC daily or amoxicillin
- 5-day pulses of 1000-1500mg Flagyl or Tinidazole every 2-4 weeks.
- A regimen of supplements to enhance body function, detoxification, counter oxidation and inflammation, and enhance cell replacement.
Treatment can take months to years to completely eradicate Cpn from the body.
What diseases has Chlamydia pneumoniae been implicated in? The following are just a few of the diseases associated with Cpn, more and more are being discovered all the time. Cpn is a vascular disease and therefore can affect all parts of the body.
· Alzheimer's disease
· Cardiac disease
· Chronic fatigue
· Chronic refractory sinusitis
· Crohn's disease
· Inflammatory bowel disease
· Interstitial cystitis
· Multiple sclerosis
[i] Secondary Porphyria-
One of the significant discoveries made at Vanderbilt is that Cpn infection causes secondary porphyria, with significant effects on the nervous system, gut, and other tissues. Cpn interferes with heme production, a multiphase chemical process in the body that requires considerable ATP, by stealing the ATP from the host cell. Without adequate ATP, heme production is stopped at the point where unstable porphyrins, highly toxic, oxidizing and neurotoxic, build up.
Highly simplified, heme synthesis looks like this:
Heme precursors >> porphrinogens>> transformation to heme >> increased cellular transport including ATP production.
Instead, Cpn interferes with this normal process, and this happens:
Heme precursors >> porphrinogens >> inadequate ATP does not allow full transformation to heme >> build up of unstable heme precursors and porphyrins inside and outside cells >> free radical damage and further reduced ATP (energy) synthesis.
When infected host cells already loaded with accumulated porphyrins are killed (apoptosis) by antibiotic treatment, these are dumped en masse into the bloodstream precipitating porphyric reactions such as nausea, intestinal disturbance and spasm, and neurological reactions including anxiety, neuropathy, profound fatigue, depression, “fogginess” and so on. Some of what has been mislabeled as a “herx” reaction to treatment is actually acute porphyria reaction and not a reaction to bacterial endotoxin– which is what a true Herxheimer reaction is about.
Porphyrins are cleared only with difficulty from the body. Some are water-soluble and are excreted in urine. Others are fat-soluble and are processed by the liver and dumped into the bowel where they further aggravate bowel problems. Significant portions are actually reabsorbed from the bowel unless bound to a substance like activated charcoal or Questran. Re-absorbtion further burdens an already toxic overload.