CPn as a cause of recurrent optic neuritis in a twelve year old boy
CPni as a cause of recurrent optic neuritis in a twelve year old boy.
http://tinyurl.com/qk33f
Pohl D, Rostasy K, Gieffers J, Maass M, Hanefeld F.
Department of Paediatrics and Paediatric Neurology, Georg August University Gottingen, Germany.
It has been suggested that Chlamydia pneumoniae (C. pneumoniae) is involved in the pathogenesis of diverse diseasesi of the central nervous system (CNSi), including multiple sclerosis. We report the case of a 12-year-old male with isolated recurrent optic neuritis and an associated CNS infection with C. pneumoniae. The patient presented with three attacks of optic neuritis within 5 months. A positive polymerase chain reaction for C. pneumoniae in the cerebrospinal fluid led to the diagnosis of a CNS infection with C. pneumoniae. After treatment with the antibiotic rifampicin, he experienced no further attacks during the follow-up period of 6 years. These findings suggest the possibility of a C. pneumoniae infection as a contributing factor or even causative event for the development of optic neuritis.
Dev Med Child Neurol. 2006 Sep;48(9):770-2.
PMID: 16904026 [PubMed - in process]
I thought this was interesting because optic neuritis is the first symptom of so many people with MSi..........Sarah
Started the Wheldon regime in August 2003, due to very aggressive SPMSi. Moved to intermittent therapy after one year. In May 2006 still take this, two weeks every two months. EDSSi was about 7, now less than 2.
http://tinyurl.com/qk33f
Pohl D, Rostasy K, Gieffers J, Maass M, Hanefeld F.
Department of Paediatrics and Paediatric Neurology, Georg August University Gottingen, Germany.
It has been suggested that Chlamydia pneumoniae (C. pneumoniae) is involved in the pathogenesis of diverse diseasesi of the central nervous system (CNSi), including multiple sclerosis. We report the case of a 12-year-old male with isolated recurrent optic neuritis and an associated CNS infection with C. pneumoniae. The patient presented with three attacks of optic neuritis within 5 months. A positive polymerase chain reaction for C. pneumoniae in the cerebrospinal fluid led to the diagnosis of a CNS infection with C. pneumoniae. After treatment with the antibiotic rifampicin, he experienced no further attacks during the follow-up period of 6 years. These findings suggest the possibility of a C. pneumoniae infection as a contributing factor or even causative event for the development of optic neuritis.
Dev Med Child Neurol. 2006 Sep;48(9):770-2.
PMID: 16904026 [PubMed - in process]
I thought this was interesting because optic neuritis is the first symptom of so many people with MSi..........Sarah
Started the Wheldon regime in August 2003, due to very aggressive SPMSi. Moved to intermittent therapy after one year. In May 2006 still take this, two weeks every two months. EDSSi was about 7, now less than 2.
An Itinerary in Light and Shadow Berger.
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Very interesting and bang up to date too. More grist to the mill...
Michele: on Wheldon protocol since 1st May 2006 for a variety of long standing ailments, also spokesperson for Ella started Wheldon protocol 17th March 2006 for RRMSi
Sussex, UK
Michèle (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse.
Sarah, Fortunate me (sort of). My first attention-getting event was optic neuritis and that's what caused me to be immediately diagnosed as 'probable MSi' a year ago this month. While my acuity returned to normal, my depth-perception has been affected, which shows how important it is to get treatment for cpni as soon as possible. The cause can be killed off, but the ultimate damage it does may be difficult to reverse, so better to bite the head off the bugs as soon as one can! Nice find. I'm off to read the entire thing now...
The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi
The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi
MacK, for the moment that is the entire thing: it is still in process, due in the September issue. I guess DW will order the full paper when he finishes his break. I'm glad I never got it, just a slight dimming of colour in one eye for a couple of weeks, so I still don't need glasses......Sarah
Started the Wheldon regime in August 2003, due to very aggressive SPMSi. Moved to intermittent therapy after one year. In May 2006 still take this, two weeks every two months. EDSSi was about 7, now less than 2.An Itinerary in Light and Shadow Berger.
Compston DA, Batchelor JR, Earl CJ, McDonald WI. Factors influencing the risk of multiple sclerosis developing in patients with optic neuritis. Brain. 1978 Sep;101(3):495-511.
One-hundred and forty-six patients who had presented with optic neuritis but without evidence of demyelinationi elsewhere in the nervous system, and in whom no specific cause could be identified, were reassessed clinically between one month and twenty-three years after the onset. Fifty-eight patients (40 per cent) had developed MS. All 146 patients were HLA-typed. Three factors were identified which were significantly associated with the development of MS: positive typing for the HLA antigen BT 101, winter onset of the initial attack of optic neuritis in BT 101-positive patients only, and recurrent attacks of optic neuritis. The application of these results to the individual patient is of limited use. However, recurrent attacks of optic neuritis should be given the same significance in the clinical classification of MS as episodes of demyelination occurring elsewhere in the central nervous system in a patient with a previous attack of optic neuritis. The results suggest that optic neuritis is caused by two different environmental agents or groups of agents and that the agent which is most common in the winter leads to the development of MS in the genetically susceptible individual. The agent more common in the summer is much less likely to cause MS in either suscetible or non-susceptible individuals. The biological role of the HLA system in the handling of foreign antigens is discussed and it is suggested that the presence of the HLA antigens associated with MS confers a specific disadvantage on individuals in the ability to handle infection by the MS causative agent and that this allows damaging immunological processes to develop.
Started the Wheldon regime in August 2003, due to very aggressive SPMSi. Moved to intermittent therapy after one year. In May 2006 still take this, two weeks every two months. EDSSi was about 7, now less than 2.An Itinerary in Light and Shadow Berger.
Sarah fabulous papers! Can't wait for the paper to be out..
marie
On CAPi since Sept '05 for MSi, RAi, Asthmai, sciatica. EDSSi at start5.5.
"Color out side the lines!"
The only thing they are not doing is naming Cpni as a causative agent.
Michele: on Wheldon protocol since 1st May 2006 for a variety of long standing ailments, also spokesperson for Ella started Wheldon protocol 17th March 2006 for RRMSi
Sussex, UK
Michèle (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse.
Marie, I'll keep looking for the publication, but I just read your plans for snow-shoeing on ThisiMS. Wonderful! Take some sticks, though, because the shoes might make you feel clumsier than you are, although they will stop you sinking waist height into the snow, as I did when I jumped off a wall, not realising that the wind had backed the snow up behind it.
Started the Wheldon regime in August 2003, due to very aggressive SPMSi. Moved to intermittent therapy after one year. In May 2006 still take this, two weeks every two months. EDSSi was about 7, now less than 2.An Itinerary in Light and Shadow Berger.
When a family member was finally diagnosed with MSi, after years of mysterious symptoms, I did some research on line. This is about 10 years ago (before Google!), so I am a little fuzzy about the details.
However, I recall that MS patients in Japan are far more likely to have optic nerve involvement than Westerners. In fact, (again, based on my memory of the research), in Japan, the only symptoms of MS are often optic nerve effects.
At the time, I researched down a path involving uric acid levels, which would be impacted by high consumption of soy products. There is some data on uric acid/MS, but no real joy in terms of drawing conclusions. It might have some bearing on this thread, though, so here it is.
Ron
On Stratton protocol for CFSi starting 01/06 (NE Ohio, USA).
Ron
On CAPi for CFSi starting 01/06 (NE Ohio, USA)
Began rifampin trial 1/14/09
Currently: on intermittent
Diagnosed with PPMSi Sept 04. Haven't managed to get ABXi yet, but trying hard! Not a complacent MSer, and I am trying to stir up some sediment. Live in Gibraltar.
"Although the mechanism of multiple sclerosis (MSi) remains elusive, it is generally hypothesized to be an autoimmune disease targeting the central nervous system (CNSi) myelini. Extensive epidemiological and genetic surveys indicate that MS is caused by an interplay between the environment and genetic traits determined by normal polymorphisms in multiple genesi. In Japanese, epidemiological surveys gave the prevalence rates of 0.7 to 8.9/100,000. There is a small but significant north-to-south gradient of MS prevalence rates in Japan, suggesting that environmental factors varying with latitude also play a role in developing MS even in the low prevalence areas. Conventional MS in Japanese is, like MS in Caucasians, associated with HLA-DRB1*1501 whereas opticospinal MS is associated with HLA-DPB1*0501. The ratio of conventional to opticospinal MS has increased rapidly in Japanese born after 1960s, suggesting that the modernization occurred after 1960s in Japan has modifying effects on MS susceptibility and phenotypes."
What have been the main changes in Japan since then? (This isn't a rhetorical question, I'm just asking.)
Started the Wheldon regime in August 2003, due to very aggressive SPMSi. Moved to intermittent therapy after one year. In May 2006 still take this, two weeks every two months. EDSSi was about 7, now less than 2.An Itinerary in Light and Shadow Berger.
Susie, I would hazard a guess here that someone wasn't doing their job properly. It is one thing me going to an orthopaedic surgeon about my walking problems and completely omitting to tell him that I had previously had a problem with my arm (although David did say that he should have asked me if I had ever had any problems with any other limb,) but another thing altogether to go both to an ophthalmic optician and then the eye department of a hospital and no test to be done which would have shown optic neuritis, because if it wasn't optic neuritis it could well have been something far worse. Maybe by the time you had your hospital appointment, it had cleared up, like my temporary dimming of colour vision, they couldn't see a tumour, so it became a mystery. Someone should have realised, though, surely. You maybe could'nt have been diagnosed with MS at that time, but it should have been noted that it might develop at a future date.......Sarah
Started the Wheldon regime in August 2003, due to very aggressive SPMSi. Moved to intermittent therapy after one year. In May 2006 still take this, two weeks every two months. EDSSi was about 7, now less than 2.An Itinerary in Light and Shadow Berger.
Japan, since the 60's. Well, they've Westernized a lot. Diet and physical lifestyle changes have been huge. Because they travel more, one would suspect greater exposure to cpni than ever before. Protective foods may have fallen away in favor of more processed, less healthy ones. More people working longer hours in offices may also mean less exposure to the sun. Just some guesses.
The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi
The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi
Suzie - I was tentatively diagnosed within minutes! Shame on your eye doctor! I walked into the shop where I buy my eyeglasses and told them what I was experiencing: light sensitivity, diminished color perception in my left eye and pain when looking to the extreme right or extreme left. The doctor looked stricken.
He took me into the back room and showed me a bottle with a shiny red capi. On comparison, it looked less saturated. less 'blue' and the shine was minimal when viewed with my left eye, while the color, shine and saturation were all normal with the right eye. He told me right then I probably had MSi or was about to develop it. He pulled a lot of strings and got me in to see one of Chicago's foremost eye specialists the next day and I was put in the hospital a day later for intravenous steroids (to stop the optic nerve inflammationi in its tracks). By the way, I was on antibioticsi within six weeks of the hospital stay, totally against the wishes of my neurologist.
The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi
The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi
Re the Japanese increase in MSi since the 1960, could that be because there has been an increase in urban population density?
Michele: on Wheldon protocol since 1st May 2006 for a variety of long standing ailments, also spokesperson for Ella started Wheldon protocol 17th March 2006 for RRMSi
Sussex, UK
Michèle (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse.
If I remember correctly, there's some conjecture that the changes in the demographics of MSi in Japan mirror the reduced consumption of soy. Uric acid played a role, I think. It's been a while.
Ron
On Stratton protocol for CFSi starting 01/06 (NE Ohio, USA).
Ron
On CAPi for CFSi starting 01/06 (NE Ohio, USA)
Began rifampin trial 1/14/09
Currently: on intermittent
"Uric acid, an antioxidanti, is reduced in multiple sclerosis (MSi). Patients with gout have a reduced incidence of MS. Optic neuritis (ON), often the first manifestation of MS, is not known to be associated with reduced uric acid..............."
Its from research in Leicester UK, not Japan, but presumably the reduced uric acid comes later, when and if full blown MS develops. Nowadays, with modern MRIs, MS can be diagnosed only at the optic neuritis stage, as MacKintosh found out last year.
I think changes in the pattern of MS in Japan are due to a variety of reasons, as most things are: The move to the city and living in ever more cramped environments, change of dietary habits and so on. As they become more westernised, I guess they do eat less soy, but they must also eat less fish as well, by and large, so less vitamin Di from fish oil and from sunshine, the biggest natural source, due to working all day in offices and factories.
Here is a truly frightening episode which took place in Japan in the 1950s, in a town called Minimata, involving mass poisoning by eating mercury in fish. http://www1.umn.edu/ships/ethics/minamata.htm The mercury was concentrated in that area due to it being dumped in the sea by the local Chisso works, which at that time produce acetaldehyde. When the story came out in 1959, it must have put the wind up the whole country. Warning for MacKintosh that she might be upset by reading this because I know she is very fond of cats......Sarah
Started the Wheldon regime in August 2003, due to very aggressive SPMSi. Moved to intermittent therapy after one year. In May 2006 still take this, two weeks every two months. EDSSi was about 7, now less than 2.An Itinerary in Light and Shadow Berger.
Thanks for the warning, Sarah; I can only imagine where this is going, so I will refrain from reading this particular story.
The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi
The difference between what we do and what we are capable of doing would suffice to solve most of the world’s problems. Mohandas Gandhi
Sarah, I thought the study was saying that uric acid is protective of the spinal nerves and brain, but not the optical nerve. I also got the impression that low uric acid came first, and MSi that attacked the spine and brain if it was low, but attacked the optic nerve even if it was high.
Is that what you were saying, or did you see it the other way around? (i.e., MS causes low uric acid when it attacks the brain and spinal nerves, but not when it attacks the optic nerve.)
Ron
On Stratton protocol for CFSi starting 01/06 (NE Ohio, USA).
Ron
On CAPi for CFSi starting 01/06 (NE Ohio, USA)
Began rifampin trial 1/14/09
Currently: on intermittent
Started the Wheldon regime in August 2003, due to very aggressive SPMSi. Moved to intermittent therapy after one year. In May 2006 still take this, two weeks every two months. EDSSi was about 7, now less than 2.An Itinerary in Light and Shadow Berger.
I posted info about cpnhelp.org under this news at an MSi site, so it would be seen by others with "MS". Optic neuritis is a frequent presentation in early MS.
Case study of chlamydia and optic neuritis
On uric acid, i have seen comparative studies showing that those with gout (high UA) do not also get MS. I believe this is why MS trials are being conducted on the supplementsi Inosine and ferulic acid, to raise levels of UA.
LDNi since 2-04, Wheldon/Stratton protocol 4-06