RICKETTSOSIS AND NEUROLOGICAL ETIOLOGY
Most nervous diseases have been described by symptoms proceeding from observations made by clinicians rather than by histo-pathological and biological studies.
In this paper we want to show how, after fifty years of research on the subject with Henri Barukto, we think we have come to a turning point on neurology, neurological etiology.
Consequently, a number of nervous diseases considered, up to now, as incurable, can be successfully treated for as much as their physical state is not too impaired.
Undoubtedly, most diseases are well known and their etiomolgy has been identified. Nevertheless quite a number of them, for instance the disease of Gilain Bare, syringo-myelie, disease of Creutzfeldt-Jacob, are described as viral affections, due to one of many viruses which attack man during life and are, one after another, being isolated.
Observations which we have kept on since more than fifty years ago, have led us to think that protozoa viruses and bacteria, if associated, may be very important in nervous diseases. (Jadin J.B., Giroud P., Jadin J.M., 1984)
The damage caused on the brain by trypanosoma in Central Africa is well known. Often trypanosoma is not only responsible for the bad physical conditions observed during this terrible disease. Indeed, in many regions, trypanosoma live in symbiosis with man without any effect. For instance, in Zimbabwe where Blair (1939) observed the presence of subjects infected by Trypasonoma Rhodesiense, without any ill effect. In 1963, with Limbos, we isolated a feebly virulent Trypasonoma Gambiense in a healthy subject from Zaire. One should not forget the exceptional case stated by Lapeyssonie, of a woman who, 21 years after a laboratory tested infectio, was still in perfect health. In a recent case originally from Matadi, (Zaire) we have found a very high level of Rickettsial anti-bodies at the same time as Trypasonoma.
This induced us to examine a series of sera coming from subjects infected, some by T. Rhodesiense , others by T. Gambiense. These cases had been parasitologically tested.
Ten sera of T. Rhodesiense came from Zambia while ten sera of T. Gambiense came from patients in the Ivory Coast. These twenty sera all had active anti-rickettsial antibodies, especially for Rickettsia Mooseri. Moreover, four Rhodesiense sera reacted to Coxiella Burneti while two sera of the T. Gambiense group reacted to Chlamhydiae.
We have tried to find out what s the reaction of patients suffering from Chagas sickness. Everyone knows the importance of this parasite in South America. On eight sera o the patients infected by Trypasonoma Cruzi, six had anti Rickettsia Mooseri, while three had active antibodies to C. Burnetti. These facts should make clear the great importance of parasital and bacterial association, where often nervous symptoms are also to be found.
Bearing in the mind the most worldly wide distributed disease, paludism, we are convinced that Plasmodium is not the only reason of high death rate so often caused by cerebral parasitism.
In 1949, together with Paul Giroud, we followed up several cases near Astrida (Butare, Rwanda). Plasmodium Falciparum was found abundantly in all cases, but inoculation of dying people, has allowed us to isolate several strains of Rickettsia Burnetti. In the years following, together with Paul Giroud, we established the role of Chlamydia or neo-rickettsia, during several epidemics occurring in Kivu, of meningo-encaphilitis, encapho-myocarditis where protozoa were observed together with neo-rickettsia (Jadin and Giroud, 1957).
We also want to mention that toxoplasma living inside cerebral cysts, may act differently following a Rickettsial infection. We have thus observed several patients having epileptical fits, rapidly getting cured by antibiotical treatment.
Over forty years we systematically looked for Rickettsia in Europe and Africa. We have made evident, the great importance of those etiologic agents in nervous diseases.
200 000 examinations have confirmed our convictions. Rickettsia and their transmitters are to be found the world over. Though they are less frequent in Western Europe, they are quite as important and totally ignored by many epediomologists.
During epidemics in Russia, as well as in Poland, research made it possible to isolate the infecting agents from sick people as well as from those presenting no symptoms at all. Still, the emigrated people, though not sick themselves but having being exposed to sick people are responsible for introducing the typhus in the USA. This form of disappearing and reappearing disease is commonly known as Brills Disease.
As early as 1911, Charles Nicolle noted the extreme importance of unapparent diseases, firstly noted in Guinnea pigs and later on, in man (Nicolle, 1925). Rickettsia are, without doubt, the cause of many nervous troubles. Multiple Sclerosis is among those we have done most research one. Following Paul Giroud and Paul Le Gac, we have shown the presence of anti-Rickettsial antibodies in quite a number of patients suffering from M.S. In some cases, we could find which Rickettsia was the cause. (Jadin, 1962).
P. Le Gac associates treatment with large spectrum antibiotics, proves to be a decisive argument. Hundreds of patients can walk, see and live a normal life again, once more.
These last months, together with fellow workers, we have shown that many other diseases such as epilepsy, Parkinsons Disease, caracterial children are nearly always due to Rickettsia. (Le Gac 1986; Bottero, 1986).
With all these facts in mind, Henri Baruk comes to the conclusion that they lead to a turning point in neurology and thus to its treatment if a patient is not in too poor a condition.
In the evolution of humankind, diet refined sugar is probably the last introduced source of calories.
It comes mainly from sugar cane grown in tropical and sub-tropical countries which reached Europe from the East as early as AD 636 and from beetroot where extraction developed in the early 1800’s, in temperated areas.
Refined sugar was then a luxury item sold in pharmacies. It was consumed in moderation; less than 1kg per year. Today an average person will consume about 40kg per annum. Sugar has become a giant in the global food market aided by advertising and a new culture. Why?
Sweetness and taste buds are not the only elements responsible for this addiction. Our parents have used sugar in the education process as a persuasive tool and a reward, even calling their loved ones sweetie or honey. In French sweeties are called bonbon which means ‘goodgood’.
This phenomenon is recent. For today’s elderly population, Coca-Cola is associated with a birthday party or a sea holiday resort – rare occasions.
Today, a normal shopping trolley will contain a few bottles of cold drink, ice cream, sugar, chocolate, cakes and other sweets, processed food. 80% of which is filled with sugar as an ingredient.
When sugar and carbohydrates are digested, specific enzymes split them a nd the result yields two molecules, glucose and fructose.
Glucose is essential for life. It runs in our blood at a constant level which is strictly maintained by hormones. Glucose is the source of energy for our cells and even with no refined sugar intake, it will be metabolised from glycogene, an unlimited source of sugar embedded in our muscles and our liver.
This is why sugar is so bad for our health. Our cells will use it instead of Glycogene and fat will accumulate causing obesity, cancer, cardio-vascular disease, dental cavities, diabetes and mental disorders. For people suffering from chronic infections, this source of energy boosts the germ division and secondarily weakens the immune response.
Any food package containing refined sugar should have a warning label like a cigarette box. What about Coca-Cole, Fanta etc and other multi-national suppliers?
There is certainly something else to do with sugar cane and sugarbeet. Brazil knows it. Over the last 30 years they have managed to produce 80% of their fuel needs based on ethanol sugar cane, from their plantations.
In the future, we might fill our vehicles with Coke at the bio-fuel station, leaving less sugar on the shelves.
QUESTIONS AND ANSWERS:
Dr C.L. Jadin answers questions related to Rickettsia.
1. What tests are required to determine that one has an active, chronic rickettsial infection, rather than carrying dormant bacteria? How accurate are these tests?
The Rickettsial investigation has to be completed by the following blood tests:
Chlamydiae Non Spec
CRP, RF, ANF
FBE (abs monocytosis)
One germ is normally not enough to impair the immune system. The biological functions tested are those, which are frequently abnormal with intra-cellular organisms’ infections. If these are not relevant, the parasite could be dormant. The blood test can be compared to a photo as opposed to a video, over a period of time. It can only reveal what is passing in the blood taken by a syringe.
2. What causes certain patients with Rickettsia to suffer from constant heart palpitations for long periods of time? What treatment (other than antibiotics and beta blockers) do you suggest?
Rickettsia and Chlamydia are highly associated with producing cardio-vascular diseases like encarditis, valve damage, myocarditis and pericarditis.
3. In cases where progress is slow, do you suggest testing for any other infections, including viral infection?
In every single case, systematically as explained above.
4. Has your protocol for the treatment of Rickettsia changed since 1999? The information we have regarding your protocol is as follows:
1. Vibromycyn 100 or 200 depending on weight and tolerance
2. Riostaine – f(oxytetracycline) 250 QID, 500 TDS, 500 QTD
3. Minomycin 50mg plus 100mg bd or 100 bd plus Rulide (Macrolide 150mg.)
4. Tetralisal (lymecycliine) – 300mg bd X 7 days plus flagy Metronidazole 200mg bd 400bd
5. Dumoxin 100mg + 50mg daily 100mg bd plus Quinolene =Ciprobay 500mp bd or Maxs wuin BD
6. Dalacin C 150mg or 2 X 4 7 days each treatment to be taken with inteflora (no milk products) – B Complex try nexian 40mg if tolerate go for 12 days/month when travelling take exotin 1/day
The treatment protocol has not changed but the above is not accurate.
5. What treatment protocol do you suggest for patients who test positive for mycoplasma or Chlamydia as well as Rickettsia?
The same antibiotherapy as for Rickettsia.
6. Is it possible that Rickettsia may be in a dormant state before the onset of symptoms, and then become activated at the time of onset of symptoms?
Active Rickettsia and Rickettsial-like infection, will be caused by the symptoms.
7. Can patients with chronic Rickettsia infect others?
No, except through the placenta from Mother to Child
8. Can antibiotic therapy completely eradicate the Rickettsiaor will patients always be prone to recurrent symptoms of Rickettsia?
Like any other chronic infection, (syphilis. Malaria, tuberculosis, leprosy, Aids, herpes, shingles etc.), patients will remain infected.
9. At what point do you recommend stopping the antibiotic treatment? Should this be continued until the patient is completely asymptomatic?
When patients are asymptomatic and when the blood test concerning the differing organic functions and auto-immune factors are normalised. Maintenance treatment is advised to patients that have been presenting auto-immune factors.
10. What are your views on accompanying your protocol with treatments such as oxygen therapy, ionized air, ozone therapy, hypobaric therapy?
Oxygen therapy, ionized air and ozone therapy are not a great help because intra-cellular germs are acting like a screen between the blood and the tissue. I have not much experience in hyperbaric therapy as access to it is not easy in South Africa. Le Gag reported in 1986 some success using it for M.S. Hyperbaric therapy is known to activate cancer.
11. How important is detoxification?
Depending on what type of detoxification. During the treatment – sauna or hot baths are important, as well as large intakes of water. The objective being – to rid the body of particles of antigens released by the antibiotic. A liver booster is advised in case of liver disorder.
12. Do you recommend any other form of treatment to complement your protocolin order to treat symptoms such as brainfrog or cognitive deficits, heart palpitations, sore joints, muscle weakness? This may be especially relevant when antibiotic therapy helps some symptoms but not others.
Piracetam (nootropil) increasing the cerebral vascular net
Peripherical vascular support (betahistine) to improve circulation
Beta blockers for Tachycardia – but be sparing
Anti-inflammatory if necessary
13. Are you aware of any correlation between Rickettsia and Obesity?
Yes and No. Rickettsia produces CFS. CFS patients are tired and spend their life resting. Exercise is not undertaken and obesity could be a result. They are also looking for energy in food. On the other hand, many CFS patients are the opposite.
14. What is the mechanism behind sensitivity to sunlight?
This is a side effect of antibiotics. CFS patients also will be sensitive to any light due to their poor vascularisation.
15. How important is it to take supplements other than Vit B and probiotics?
Not important at all if following a good diet. Apart from the psychological impact of feeling good when taking vitamins, the only definite result and scientific fact will be to preserve your cadaver underground by as much as ten times longer. A cremation will also take more time and therefore be more costly.
16. Are there any prescription medications that should not be taken by Rickettsia patients?
The sulpha group, as they enhance the growth of Rickettsia in guinea pig. So does magnesium and Vitamin A and E are to be avoided because of their tendency to produce intra cranial micro-hemorrhages.
17. Do you have any suggestions for minimising Herxheimer reaction?
To minimise Herxheimer reaction, increase your intake of water. Regular daily exercise for short periods of time will help the circulation of your toxins and hot baths will expel them through the skin.
18. Have you used protocol? If so, is this effective?
I have not heard of Protocol.
The German version of my book under the title CFS has been published without my final consent. The translation does not respect the original version and contains mistakes due to the inappropriate initiatives of Frau Teresa Taddonio. Our working partnership was supposed to be purely administrative, never medical nor scientific.
Last Updated (Sunday, 05 September 2010 17:40)