Expert Opinion

“Virtually all patients that I diagnose with chronic persitent Cpn (Chlamydophila pneumoniae) infection have a raised LDL level. If they are treated with a statin from the begining, they will frequently have typical muscle and joint symptoms. If however they are commenced on the appropriate antibiotic protocol and diet first, then recheck their LDL level, it usually reduces a little, perhaps enough to get to the level I am after. If it doesn’t reduce enough – often it is quite high, I commence them on a low dose of rosuvastatin and they don’t get the statin side effects. At that stage many get by with a low dose of statin. If they respond well to the treatment and I have evidence that the Cpn infection has been eliminated or suppressed enough, they can come off the statin. So the statin is acting like an antibiotic. Cpn needs cholesterol for its outer membrane but can’t manufacture it itself. It has genes to manipulate human cholesterol metabolism in the liver (stops its secretion) and also oxidises LDL in circulating macrophages. This is one of the mechanisms by which it contributes to vascular disease. The other mechanism is its ability to increase platelet aggregation. Cpn is transmitted from person to person by prolonged close contact and this is why one sees high prevalence in situations such as army barracks. However, I suspect the main transmission comes from within the family and may be the reason why many diseases appear to have a “genetic” – you catch it off your parents. It is of interest that the neurologists are now trailing the use of statins in MS! Unfortunately they just understand why statins may be of beenfit in this situation.” Dr Paul Thibault (in conversation with science journality Maryanne Demasi), vascular specialist, Facebook, Australia, Apr 2019.


The concern I have is that people (medical doctors, patients, and the general public) will become disillusioned by the many studies (including Zamboni et al), which refute the use of venoplasty to achieve a “cure” for MS. Zamboni has highlighted the connection between MS and a chronic venous disease, which I appreciate. However, since 2011 I have suspected his theory that venous obstructions cause demyelination (due to iron-deposition which accompanies vascular reflux) to be incorrect.

In a published pilot study (4), we showed that venoplasty appeared to improve cerebral perfusion and I feel this is the mechanism which explains why some pwMS experience symptomatic improvement following venoplasty. But this effect was short term in most, and only occurred in approximately 30% of those treated. We analysed 2 pilot studies in NSW, one at St Vincents Hospital and a later one at Prince of Wales Private Hospital. Both came to the conclusion that venoplasty was generally ineffective in improving the symptoms of pwMS in the long term. The major participants had no enthusiasm for publishing negative results from pilot studies, and no randomised placebo controlled trials were planned. We abandonded venoplasties for CCSVO (Chronic CerebroSpinal Venous Obstruction) in MS in 2012. At that stage, we had performed over 200 procedures. Never-the-less, the objective diagnostic ultrasound examination that we developed (5) to diagnose obstructive venous disease in the neck veins (in contrast to the subjective Zamboni ultrasound) appeared to be accurate, reproducible and indicated that the venous obstructions were due to a chronic inflammatory venous condition that resulted in obstructions to both the internal jugular veins AND the vertebral veins. Interestingly, the vertebral veins have been largely ignored by Zamboni and others – perhaps because they can’t be treated by venoplasty. After seeing David Wheldon’s website suggesting that a chronic persistent chlamydophila pneumonia infection was the likely cause of disease in a large sub-group of pwMS, I developed the theory that MS was due to a chronic infective cerebrospinal phlebitis and venulitis (published in Phlebology in 2012.). From that time, we have treated pwMS with the combined antibiotic protocol developed by the Stratton group (Vanderbilt University, Nashville) and David Wheldon. My observations are that the results have been superior to venoplasty, particularly in RRMS with positive serology to Cpn, with relapses completely suppressed and only rare instances of new lesions developing on MRI examinations. Our 6-month follow-up with ultrasound flow measurements in the affected neck veins (published in Phlebology) (6) shows significant improvements in those with positive serology testing to chlamydophila pneumonia (Cpn) infection. This article also highlights the possibility that chronic persistent infection with Cpn is widespread in the community but only a small percentage go on to develop MS. Some other factor, such as a genetic or concurrent infection with an agent like EBV, is likely to be involved at a critical time early in life. Therefore CCSVI (O) is likely to be observed in many “normal” people who are included in randomised trials, which explains why so many studies have shown that the neck vein obstructions are observed in the “normal” population, but generally not at the rate found in pwMS. This is consistent with the epidemiology studies of the most famous MS neurologist, Prof John Kurtzke who concluded that MS was caused by an infection that was widespread through the community, but only a SMALL proportion went on the exhibit MS.

So why do some people have such a good result with venoplasty alone? I suspect that they have a “burnt-out” Cpn infection, that has been completely controlled by their immune system, but has left resultant venous obstructions that cause reduced cerebral perfusion. These people test negative to Cpn. This state will be improved by successful venoplasty. As for the other > 90% who have chronic persistent Cpn infection but don’t have MS, they will be prone to other vascular and “auto-immune” disease including coronary artery disease, cerebro-vascular disease, thyroid disease, CFS, polymyalgia, reactive arthritis, thrombo-embolic disease, rosacea and possibly lymphomas of the head and neck. PwMS have a high co-morbidity with these diseases.

So this is why I have entered into this argument, as the only doctor in Australia with a real interest in investigating the association of MS with CCSVO. I will be presenting the evidence at the UIP 2018 meeting to be held in Melbourne in February in a special “Masterclass on CCSVO”. There will also be a demonstration of our Objective Ultrasound Examination, which will show that this is a real entity that needs to be addressed. I apologise that this reply has been so long, but it is an extremely complex problem.”

1 – CCSVI, Chlamydia pneumoniae and multiple sclerosis clarification. Dr Paul Thibault, vascular specialist, Australia, Phlebology, Dec, 2018

2 – Neck vein obstruction : Diagnosis and the role of chronic persistent Chlamydophila pneumoniae infection, Dr Paul Thibault, vascular specialist, Australia, Phlebology, Oct 2018

3 – A prolonged antibiotic protocol to treat persistent Chlamydophila pneumoniae infection improves the extracranial venous circulation in multiple sclerosis, Dr Paul Thibault, Prof John Attia and Dr Christopher Oldmeadow, Phlebology, Jul 2018

4 – Prolonged Antibiotic Protocol to treat persistent Cpn in MS improves Venous Circulation, Dr Paul Thibault, vascular specialist, Australia, Phlebology, Jan 2017

5 – Objective duplex ultrasound evaluation of the extracranial circulation in multiple sclerosis patients undergoing venoplasty of internal jugular vein stenoses: A pilot study, Dr Paul Thibault (vascular specialist), Mr Warren Lewis (sonographer) and Dr Suzanne Niblett (research academic), Phlebology, Mar 2015

6 – Multiple Sclerosis: A Chronic Infective Cerebrospinal Venulitis?, Dr Paul Thibault, vascular specialist, Australia, Phlebology, Aug 2012

Dr Paul Thibault, vascular specialist, Facebook, Australia, Nov 2017

“Minocycline is the first drug that I introduce in the CAP protocol, using the same dose as in the recent Canadian study on treating MS of 100mg twice daily for patients over 75kg weight and reducing that dose for lower weights. It is interesting that in the recently published study, benefit was seen at 6 months, but not at 24 months. This is to be expected. Using Minocycline as the only drug will cause persistence of the Cpn. I add Roxithromycin 300mg daily after 2 weeks, as a “back-up” to the minocycline, then Tinidazole with monthly pulses of 500mg twice daily for 2 days after 1 month to kill the persistent or cryptic form. NAC to treat the extracellular spore is added later as this tends to cause most side effects if introduced too early. I then add in Resveretrol 250mg twice daily and check the patient’s serum lipids. If the LDL is greater than 2.5 I recommend introduction of a statin (usually Rosuvastatin) at a low dose of 5mg, then increasing it slowly over a period of months to aim to get the LDL less than 2.0. (Cpn disturbs lipid metabolism and oxidises LDL). Most of my patients with chronic persistent Cpn have high LDL levels.Of course diet (as proposed by George Jelinek) is important. I aim to wean the patient off the CAP at around 18 months, usually by stopping the minocycline first, then 6 months later the roxithromycin, then finally the Tinidazole. They are then maintained on NAC 600mg – 1200mg twice daily and Resevetrol 250mg twice daily and diet. So that is my current vascular approach to chronic persistent Cpn infection.”, Dr Paul Thibault, vascular specialist, Australia, Facebook, June 2017


“…evidence has accrued, strengthening the link between MS and C.pneumoniae. At least five centres in different parts of the world have detected C.pneumonaie gene-sequences in the cerebrospinal fluid of patients with MS; antibodies to the organism are found there; new infection with C.pneumoniae heralds relapse; specific serology becomes statistically elevated as the disease becomes progressive; and the cerebrospinal fluid of patients with MS contains bacterial heat-shock proteins which cause oligodendrocyte precursors to undergo apoptosis…the link between C.pneumoniae and MS is not yet proven, but the evidence is strong. It is heartbreaking to see patients with potentially treatable disease thrown on the scrapheap because simple risk/benefit analyses are not made.”, Dr David Wheldon, microbiologist and neuropathologist, UK, Ignoring the Evidence, Hospital Doctor, June 2005

Even when other associations with viral organisms have been entertained, the degree of association has never been so high as with Chlamydia pneumoniae. We can demonstrate the evidence by a number of means – by culture, or by PCR techniques — that show there are antibodies to this organism present in the spinal fluid of these patients…” Prof Subramaniam Sriram, neuroimmunologist, USA, Pneumonia, MS Link Investigated, Reporter (Vanderbilt University), April, 1999

“the known pathogen that has the greatest likelihood of causing a chronic persistent vasculitis and capable of causing secondary neural injury is Chlamydophila pneumoniae…Optimum management of MS will then involve a complex holistic approach including optimal antibiotic therapy possibly over a prolonged period, minimally invasive angioplasty of significant stenoses, dietary and nutritional management of metabolic effects including but not limited to vitamin D deficiency and secondary focal tissue porphyria, and finally limited use of immunomodulating drugs at appropriate stages of the disease.” Dr Paul Thibault, vascular specialist, Australia, Multiple sclerosis: a chronic infective cerebrospinal venulitis?, August 2012

  “…this pathogen [chlamydophila pneumoniae] may also infect vascular endothelial cells in venous tissues. Such an infection/inflammation of venous vascular tissues could contribute to the inflammatory-autoimmune disease causing the venous abnormalities described in the so-called CCSVI [Chronic Cerebro Spinal Venous Insufficiency – the obstruction of veins draining the brain/spine].” Prof Charles Stratton, Prof Carlo Contini  et al., neurological and infectious disease specialists, USA and Italy, Role of Chlamydophila pneumoniae in the Pathogenesis of Chronic Cerebrospinal Venous Insuffiency in Patients with Multiple Sclerosis, Journal of Multiple Sclerosis, August, 2015

A review of the literature suggests that MS may be triggered by an infectious factor. It is tempting to speculate that MS may actually result from chronic infection associated with autoimmune response against CNS [Central Nervous System] antigens and an altered venous drainage caused by CCSVI [Chronic Cerebro Spinal Venous Insufficiency – the obstruction of veins draining the brain/spine]. We suggest that future research should focus on such hypothetical pathogenetic scenario” Dr Marian Simka et al, vascular specialists, Poland Chronic Cerebrospinal Venous Insufficiency is Unlikely to be a Direct Trigger of Multiple Sclerosis, Multiple Sclerosis and Related Disorders, March 2013

“intraluminal fibrosis could be a result from a past, resolved inflammatory or thrombotic process that involved the wall of the IJV [Internal Jugular Vein]. From this point of view some authors quite recently hypothesized a post infective origin of CCSVI [Chronic Cerebro Spinal Venous Insufficiency – the obstruction of veins draining the brain/spine] in course of MS, focused on clamidia pneumofila” Prof Paolo Zamboni (vascular specialist) et al, Italy, The Pathology of the Internal Jugular Vein in Multiple Sclerosis, Journal of Multiple Sclerosis, 2015

“Very cool data on chlamydia in CCSVI [Chronic Cerebro Spinal Venous Insufficiency – the obstruction of veins draining the brain/spine] associated to Multiple Sclerosis from a group of neurologists-microbiologists” Prof Paolo Zamboni, vascular specialist, Italy, twitter

The recent molecular, ultrastructural, and cultural advances that have provided evidence that C. pneumoniae is viable and metabolically active in different biological compartments such as CSF [Cerebro Spinal Fluid] and PBMC [Peripheral Blood Mononuclear Cells] from MS patients compared to controls, suggests an association between this pathogen and the disease, particularly in a subgroup of RR [Relapsing/Remitting] MS patients with clinical and MRI [Magnetic Resonance Imaging] disease activity who experience the early inflammatory phase representing the development of the disease [8995108109].” Prof Carlo Contini et al, Infectious Disease and Neurological specialists, Chlamydophila pneumonaie infection and its role in Neurological Disorders, Ferrera Italy, Feb 2010

“MS recovery is not impossible; indeed, many have recovered on this protocol. However, it is long and arduous. Optimizing diet will shorten time to recovery, but it will still take years. MS is not the only disease that may be caused by C. pneumoniae. Alzheimer’s dementia, atherosclerosis, stroke, rheumatoid arthritis, and rosacea are all associated with C. pneumoniae infections and may be treatable by Dr. Stratton’s protocol.” Paul Jaminet, blog entry: The Vanderbilt Protocol for Multiple Sclerosis, Nov 2010

“…in light of the present evidence, empirically treating MS patients for Chlamydia pneumoniae seems reasonable…” Dr David Perlmutter, neurologist, USA, Multiple Sclerosis Functional Approaches. Townsend Letter for Doctors and Patients 244: 66-74; November 2003

“Some of the insults that can contribute to the development of clogging of the veins or arteries include:…chronic low grade infections such as chlamydia bacteria and Epstein-Barr virus…” Dr Terry Wahls, The Wahls Protocol (Chap 2), 2014

“If you are struggling with fatigue and brain symptoms, it may be very helpful to have a comprehensive assessment to test for these types of chronic infections or coinfections, especially if the Wahls Protocol is not resolving issues like chronic fatigue – which could be due to a viral infection (such as Epstein-Barr, herpes 6 virus, and herpes simplex) or bacterial infection (such as Borrelia burgdorferi – Lyme disease – chlamydia, and Bartonella).” Dr Terry Wahls, The Wahls Protocol (Chap 12), 2014

“C.pneumonia can also infect the nervous system, causing the same range of moderate to severe neurological problems. (Meningoencephalitis, multiple sclerosis, Alzheimer’s disease, schizophrenia, autism, vegetative states, and a range of psychiatric disorders)…Vasculitis, for example, often occurs in the brain during MS. There is a sudden death of oligodendrocytes followed by an inflammation-caused removal of the myelin sheath around the nerves. Chlamydia pneumonia have been found in the brain lesions that accompany the disease…” Stephen Harrod Buhner, Healing Lyme, 2015

“When that reaction, after instituting a new antibiotic or dosage increase, or the use of NAC (N-acetyl cysteine, which specifically can kill the EB form of Chlamydia), lasts for a week or more, this is a tip-off to me that we may be dealing with a porphyrin release, which is treated differently. I would encourage readers to check out the website http://www.CPNHELP.ORG to learn more” Dr Neil Nathan, Foreword, Healing Lyme, 2015

“It is very important that we know whether this drug [Minocycline…an antibiotic which is the front line treatment for CPn infection] actually works in MS (which appears almost certain), because it is very cheap, widely available, taken by mouth and has few significant side-effects. On all these counts, it is ahead of the new generation of drugs for MS that are taken by mouth”, Prof George Jelinek, Overcoming Multiple Sclerosis, 2nd edn, 2016

“minocycline […an antibiotic which is the front line treatment for CPn infection] can reduce conversion to MS, and should be considered for initial treatment as well as for combination therapy trials, given both its safety and low cost…This is exciting because it’s oral, it’s low cost, and we have lots of safety data”, Tried-and-True Antibiotic May Block Conversion to MS, MedPage Today, 2015