Submitted by Jim K on Sun, 2006-01-22 08:41

I have culled from Mitchell & Stratton patent #6,884,784 an exhaustive list of diseases where Cpn has been implicated as a possible cause or co-factor (reference: Mitchell & Stratton patent #6,884,784):

Diseases where an association has been discovered between chronic Chlamydia infection of body fluids and/or tissues with several disease syndromes of previously unknown etiology in humans which respond to unique antichlamydial regimens include:

Editorial comment: Strong findings from their research. If you have any of these it suggests to me that at least an empirical course of the combination antibiotic therapy is strongly indicated, with or without serology.

Multiple Sclerosis (MS)
Rheumatoid Arthritis (RA)
Inflammatory Bowel Disease (IBD)
Interstitial Cystitis (IC)
Fibromyalgia (FM)
Autonomic nervous dysfunction (AND neural-mediated hypotension);
Pyoderma Gangrenosum (PG)
Chronic Fatigue (CF) and Chronic Fatigue Syndrome (CFS).

Diseases where Cpn load has been associated where measured, and where treatment can create improvement in the primary condition:

Chronic hepatitis
Systemic lupus erythematosus
Diabetes mellitus
Graves' disease
Beschet's disease and
Graft versus host disease (graft rejection).

Diseases where Cpn may be associated as a secondary or primary factor:

Editorial Comment: The diseases from here on have been associated with Cpn. At minimum it seems to suggest that at least serology  for Cpn should be explored, or where there are other diagnostic indicators of Cpn an empirical course of the combination protocol should be looked at.

Sepsis syndrome
Circulatory collapse and shock resulting from acute or chronic bacterial infection
Acute and chronic parasitic and/or infectious diseases from bacterial
Viral or fungal sources such as a HIV, AIDS (including symptoms of cachexia, autoimmune disorders, AIDS dementia complex and infections) can be treated as well as Wegners Granulomatosis.

Various inflammatory diseases, there are certain features of the inflammatory process that are generally agreed to be characteristic. These include fenestration of the microvasculature, leakage of the elements of blood into the interstitial spaces, and migration of leukocytes into the inflamed tissue. On a macroscopic level, this is usually accompanied by the familiar clinical signs of erythema, edema, tenderness (hyperalgesia), and pain. Inflammatory diseases, such as chronic inflammatory pathologies and vascular inflammatory pathologies, including:
Chronic inflammatory pathologies such as aneurysms
Chronic inflammatory bowel disease
Ulcerative colitis
Crohn's disease and vascular inflammatory pathologies
Disseminated intravascular coagulation
Kawasaki's pathology
Coronary artery disease
Chronic hepatitis
Multiple sclerosis
Peripheral neuropathy
Chronic or recurrent sore throat
Chronic vascular headaches (including migraines
Cluster headaches and tension headaches) and pneumonia when demonstrated to be pathogenically related to Chlamydia infection.

Treatable disorders when associated with Chlamydia infection also include but are not limited to Neurodegenerative diseases including
Demyelinating diseasessuch as multiple sclerosis and acute transverse myelitis;
Extrapyramidal and cerebellar disorders such as lesions of the corticospinal system;
Disorders of the basal ganglia or cerebellar disorders;
Hyperkinetic movement disorders such as Huntington's Chorea and senile chorea;
Drug-induced movement disorders such as those induced by drugs which block CNS dopamine receptors;
Hypokinetic movement disorders
such as Parkinson's disease;
Progressive supranucleo palsy;
Cerebellar and Spinocerebellar Disorders such as astructural lesions of the cerebellum;
Spinocerebellar degenerations (spinal ataxia)
Friedreich's ataxia
Cerebellar cortical degenerations
Multiple systems degenerations (MencelDejerine-Thomas
Shi-Drager and Machado Joseph)); and systemic disorders (Refsum's disease
Abetalipoprotemia, ataxia telangiectasia and mitochondrial multi-system disorder);
Demyelinating core disorders such as:
Multiple sclerosis
Acute transverse myelitis;
Disorders of the motor unit such as neurogenic muscular atrophies (anterior horn cell degeneration) such as
Amyotrophic lateral sclerosis
Infantile spinal muscular atrophy and juvenile spinal muscular atrophy);
Alzheimer's disease;
Down's Syndrome in middle age;
Diffuse Lewy body disease; Senile Dementia of Lewy body type;
Wernicke-Korsakoff syndrome;
Chronic alcoholism;
Creutzfeldt-Jakob disease;
Subacute sclerosing panencephalitis
Hallerrorden-Spatz disease; and
Dementia pugilistica

Malignant pathologies involving tumors or other malignancies such as:
Leukemias (acute chronic myelocytic
chronic lymphocytic and/or myelodyspastic syndrome);
Lymphomas (Hodgkin's and non-Hodgkin's lymphomas such as malignant lymphomas (Burkitt's lymphoma or Mycosis fungoides));
Carcinomas (such as colon carcinoma) and metastases thereof;
Cancer-related angiogenesis;
Infantile hemangiomas;
Alcohol-induced hepatitis.
Ocular neovascularization
Duodenal ulcers
Angiogenesis of the female reproductive tract
can also be treated when demonstrated by the diagnostic procedures described herein to be associated with Chlamydial infection.

An immunocompromised individual is generally defined as a person who exhibits an attenuated or reduced ability to mount a normal cellular or humoral defense to challenge by infectious agents
e.g., viruses, bacterial, fungi and protozoa. Persons considered immunocompromised include malnourished patients, patients undergoing surgery and bone narrow transplants, patients undergoing chemotherapy or radiotherapy, neutropenic patients, HIV-infected patients, trauma patients, burn patients, patients with chronic or resistant infections such as those resulting from myeloodysplastic syndrome, and the elderly, all of who may have weakened immune systems. A protein malnourished individual is generally defined as a person who has a serum albumin level of less than about 3.2 grams per deciliter (g/dl) and/or unintentional weight loss greater than 10% of usual body weight.

The course of therapy, serological results and clinical improvements from compassionate antichlamydial therapy in patients diagnosed with the diseases indicated were observed and are reported in Example 5. The data provides evidence to establish that treatment of Chlamydia infection results in the serological and physical improvement of a disease state in the patient undergoing combination therapy. These observations were consistent among a variety of different diseases which fall within a generalized disease class.

Other Diseases of Unknown Etiology with New Evidence for a Chlamydia pneumoniae Etiology

Both C. trachomatis and C. psittaci exhibit a protean disease complex dependent on different serovars. One known basis for this diversity to date is the amino acid sequence of the MOMP. FIG. 1 shows a sequence alignment of various Chlamydia MOMPs. Note that the size and sequence are relatively homologous except for the four variable regions that are responsible for the serovar (serotype) basis of classification. Further, it has been discovered that C. pneumoniae infects blood vessel endothelial cells from which EBs are released in the blood stream. In addition, macrophages are known targets for C. pneumoniae and may serve as reservoirs and provide an additional mechanism of transmission. C. pneumoniae is thus able to spread throughout the human body, establishing infection in multiple sites and in multiple organ systems. Infected sites may exist for an extended period without inducing symptoms that are noticed by the patient or by an examining physician. Sequence variability of MOMPs or other chlamydial antigens may provide a basis for organ specificity while other chlamydial proteins, such as the 60K and 70K heat shock proteins or LPS, may influence immune response.

C. psittaci and C. pecorum are known to cause a host of infections in economically significant animals. Thus, the teachings of this invention are relevant to animals. Throughout this application and for purposes of this invention, "patient" is intended to embrace both humans and animals. Virtually all rabbits and mice tested to date have PCR signals for C. pneumoniae. They can be used as appropriate animal models for treatment using specific combination antibiotics to improve therapy. (Banks et al., Ameri. J. of Obstetrics and Gynecology 138(7Pt2):952-956 (1980)); (Moazed et al., Am. J. Pathol. 148(2):667-676 (1996)); (Masson et al., Antimicrob. Agents Chemother. 39(9):1959-1964 (1995)); (Patton et al., Antimicrob. Agents Chemother. 37(1):8-13 (1993)); (Stephens et al., Infect. Immun. 35(2):680-684 (1982)); and (Fong et al., J. Clin. Microbiol. 35(1):48-52 (1997)).

Coupled with these developments are the recently developed rabbit models of coronary artery disease, where rabbits exposed to C. pneumoniae subsequently develop arterial plaques similar to humans (Fong et al., J. Clin. Microbiol. 35:48-52 (1997)). Most recently, a study at St. George's Hospital in London found that roughly 3⁄4 of 213 heart attach victims have significant levels of antibodies to C. pneumoniae antibody and that those that have such antibodies achieve significantly lower rates of further adverse cardiac events when treated with antibiotics (Gupta et al., Circulation 95:404-407 (1997)). Taken together, these three pieces of evidence (the bacteria found in diseased tissue, inoculation with the bacteria causes diseases, and treating for the bacteria mitigates disease) make a case for a causal connection.


My clinical experience also indicates that rosacea and Hashimoto's thyroiditis are also associated with chronic Cpn infection. The common factor with these diseases is that the sufferer will show signs of obstruction in the extra cranial veins of the neck(CCSVI). The left internal jugular vein and vertebral veins are most commonly affected. This is consistent  with my theory that Cpn spreads to the vascular system via the lymphatic system (infected lymphocytes in the thoracic duct) to infect the endothelium of the left internal jugular vein and vertebral vein before spreading elsewhere. There is good evidence at the cellular level as to why this happens. Hopefully I will be able to publish this at a future time.

Wow. This is the first time that I seen macular degeneration linked. As well having optical neuritis I have another, undiagnosed condition. The ophthalmologist says that it is very similar to age related macular degeneration so now the cap should sort that as well. Thanks for the infoSmile