Re: Cellulites

June 16, 2001

Dear Erma, It is treatable and should be by insurance with Hyperbaric Oxygen

therapy, anti Biotic and Hyperbarics,

cellulitus

List,

I just meet someone that has cellulitus. Doctors put him on antibiotics of

course when this flares up. Anyone know how to treat this? I would say to

do a parasite cleanse first?

Erma

OxyPLUS is an unmoderated e-ring dealing with oxidative therapies, and other

alternative self-help subjects.

THERE IS NO MEDICAL ADVICE HERE!

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June 16, 2001

Will ozone sauna treat it? Not close to HBO......if I ever get an extra

$10,000, I will have a unit of my own so I can heal everything with God's help.

Erma

At 08:44 AM 6/16/01 -0700, you wrote:

>Dear Erma, It is treatable and should be by insurance with Hyperbaric Oxygen

>therapy, anti Biotic and Hyperbarics,

>

> cellulitus

>

>List,

>

>I just meet someone that has cellulitus. Doctors put him on antibiotics of

>course when this flares up. Anyone know how to treat this? I would say to

>do a parasite cleanse first?

>

>Erma

>

>OxyPLUS is an unmoderated e-ring dealing with oxidative therapies, and other

>alternative self-help subjects.

>

>THERE IS NO MEDICAL ADVICE HERE!

>

>This list is the 1st Amendment in action. The things you will find here are

>for information and research purposes only. We are people sharing

>information we believe in. If you act on ideas found here, you do so at your

>own risk. Self-help requires intelligence, common sense, and the ability to

>take responsibility for your own actions. By joining the list you agree to

>hold yourself FULLY responsible FOR yourself. Do not use any ideas found

>here without consulting a medical professional, unless you are a researcher

>or health care provider.

>

>You can unsubscribe via e-mail by sending A NEW e-mail to the following

>address - NOT TO THE OXYPLUS LIST! -

>DO NOT USE REPLY BUTTON & DO NOT PUT THIS IN THE SUBJECT LINE or BODY of the

>message! :

>

> oxyplus-unsubscribeegroups

>

> oxyplus-normalonelist - switch your subscription to normal mode.

>

June 16, 2001

Jim,

That's a great idea. The question is how do you find people who would be in

the area that would want to do this? Is there anyone in the Seattle area

interested in getting a group co-op for purchasing a sauna?

Jacqui

June 16, 2001

Erma,

You don't need $10,000. Ten people w/$1000 would also work. A co-op of

50 people could have access for $200 each. Think about it.

jim

Erma Seabaugh wrote:

>

> Will ozone sauna treat it? Not close to HBO......if I ever get an extra

> $10,000, I will have a unit of my own so I can heal everything with God's

help.

>

> Erma

-----

The TRUTH in 11 words:

Inside every older person is a younger person wondering what happened!

-- anon

jlambert@... http://www.entrance.to/madscience

http://www.entrance.to/poetry

June 16, 2001

OR, sense Most insurances pay for HBOT for Cellulites, you could go an have

it treated right away. Plus it really works

www.hbot4u.com

Re: cellulites

> Jim,

> That's a great idea. The question is how do you find people who would be

in

> the area that would want to do this? Is there anyone in the Seattle area

> interested in getting a group co-op for purchasing a sauna?

> Jacqui

>

June 16, 2004

Thanks Sandy. We did end up taking her in and she does have cellulites in

two spots. One on her cheek and one on her arm pit. The one on her cheek

covers her whole cheek and the one on her arm is slightly smaller. She has

received three dosages of the anti-biotic now and I think that it is

helping. The one on her cheek is still huge, but I can tell the other one is

getting smaller.

Our pediatrician also told us to spray her with bug spray EVERY time she

goes outside and subsequently to bathe her every night (obviously!). She

also told us that the FDA has approved all bug sprays for kids ages 2 and

older so to start using that since the kid stuff isn't very effective...

Thanks again for bringing this up. I hope someone is able to answer your

question. Our ped. just told us to come in for a recheck if it got worse or

started pussing..

Alia and Caroline, age 2, Poly and Uveitis

Re: cellulitis

Alia - I am the original poster about this topic ( recently anyway).

Emma had two mosquito bites but the rash was completely around both

and down to her ankle. It was about the size of my hand. It

reminded me of the skin poison I get from being in the sun- but there

was also visible swelling. I would not be too concerned if it is

just a bite. Emma's looked very odd and distinctive. You might call

or go in to get peace of mind. Best of luck.

Emma is three and on the small side so a rash the size of my hand on

her calf and thigh was quite noticable.

I wonder if those who responded last time might give me an idea about

how long this takes to resolve. I can still see about a tennis ball

size circle of " rash " and she should be done with her antibiotic on

Friday. I cancelled her follow up appt. for last Friday b/c it was

healing rather quickly and now I regret it. Thanks again!

Sandy - mom to Emma 3 - poly

> I hope this doesn't post twice - I messed up and am starting over.

> Thank you Elisheva and e for your responses. The Dr. did

draw

> a big circle around the effected area and it seems to be a bit

better

> this morning. The swelling is nearly gone completely. I am off to

> give my girlies a bath and I hope it doesn't wash off.

>

> Also, thanks Elisheva for posting the address of your weblog. I

> enjoyed reading it.

>

> Sandy

>

> > I know I have seen posts about this in the past, but I do not

> remember

> > specifics. My Emma was just diagnosed today after scratching a

> > mosquito bite. Is there anything I should be concerned about?

The

> > Dr. gave her two shots ( one in each thigh) and some oral

> antibiotics

> > as well. We have a follow up appointment on Friday. She didn't

> talk

> > about complications, but of course I read online and it scared me

a

> > bit.

> >

> > Any input is appreciated.

> >

> > Sandy

> > Emma, 3 years poly

>

July 17, 2006

Hi Gloria

Don't know if there is some relation with autoimmune diseases, but it

happens to other folks too. Although folks with poor ciculation or

significant weight problems are more prone to get cellulitis, anyone

who gets pricked by a rose thorn in the garden can get it too. Helps

to wash every skin scrape / cut and dress it to keep it clean.

Sorry your brother has this, it is no fun. -

>

> Hi,

> I am wondering if people with RA are more likely to get

cellulitis. I know my brother who has MS has been in the hospital for

a month with this infection. It just sprang up one day in his left

thigh and now they have had to make a twenty inch cut on his leg and

put some sponges in there to soak up the infection. I remember seeing

someone on the list who had this infection or syndrome or whatever it

is, but I didn't know it was so serious, and I don't know if someone

with RA would be more prone to it.

> Thank you,

> Gloria

>

July 17, 2006

Hi Gloria,have you seen this.It is news from last year butmight help.

Lynne G

--- multiple sclerosis caused by a response to chronic infection:

treatment possiblities

Date: Sat, 25 Jun 2005 21:41:07 -0700

From: lynneandsantos <lynneandsantos@...>

gaboum@...

Hi Sis ,you might want to print this out for your neighbour.Not much new

around here.Desperately praying for rain(again) it has been so hot 35-37

the last few days that I really cannot function.Going from pillar to

post and back again.Started to paint the basement as I can't stand the

smell of cement but had to stop as it would not dry.Want to start the

dining room as soon as possible but can't open the windows as too much

heat comes in.SHEEEESHHH!Lots of work in the gh also but can't do it

either so I'm sort of vegging.What is new up your way?Have to go move

the hose so T.T.F.N. Lynne

http://www.davidwheldon.co.uk/ms-treatment.html

------------------------------------------------------------------------

Message 31st May 2005: To the lady from the US who emailed me today: I'm

afraid

I accidentally deleted your email unanswered. Please feel free to

re-send it.

Empirical antibacterial treatment of

infection with Chlamydophila pneumoniae

in Multiple Sclerosis

Wheldon MB FRCPath

After much controversy there is now powerful evidence for the

respiratory pathogen Chlamydia (Chlamydophila) pneumoniae being a causal

factor in some variants of the neurological illness multiple sclerosis.

A series of remarkable studies finds --

.. the presence of C. pneumoniae gene sequences in the cerebrospinal

fluid of patients who have the disease;

.. an association of new C. pneumoniae respiratory infections with

episodes of clinical relapse;

.. a statistically significant elevation of C. pneumoniae-specific serum

antibody levels when the disease shifts into the progressive form;

.. antibodies to C. pneumoniae in the cerebrospinal fluid of patients

with the disease;

.. evidence of active C. pneumoniae protein synthesis in the central

nervous system, with production of a bacterial protein shown to be toxic

to the cell-type whose death is the first visible event in the genesis

of the acute MS lesion;

.. MRI improvement in antibiotic-treated patients with early disease in a

small but fastidious double-blind trial;

.. MRI improvement, with reduction of the number of Gd-enhancing lesions,

in a second study.

The mainstream neurological establishment does not as yet accept a

chlamydial role in the development of multiple sclerosis, though some

centres actively treat for this. The results have been very promising,

particularly in early disease. (This bacterium causes respiratory

infection and is spread by droplet infection -- coughing and sneezing.

It is not, like another chlamydia, sexually transmitted.)

, my wife, an artist of considerable ability, was given a diagnosis

of MS in July 2003. Her illness in fact stretched back to 1989, when she

experienced a sudden weakness of the right arm. After a fortnight she

recovered its function completely. A few years later she experienced a

slight greying of vision in one eye; this resolved over a few weeks.

Occasional relapses followed, all with a complete recovery. In 1999 the

remissions started to become less complete. Right foot-drop began

insidiously and did not resolve. Then, in 2001, shortly after a

prolonged upper respiratory infection which led to mild new-onset

asthma, began to enter a new, rapidly progressive stage of the

illness. Within two years she was unable able to stand unaided, had to

hold furniture, was unable to hold or use a pencil or paint-brush with

her right hand, and she felt giddy. She said that she seemed to live in

a mental fog: indeed, in the evenings she would fall into a half-sleep

sleep from which she obtained no rest. Her speech was becoming slurred.

There was a continual sense of flickering and worsening neurological

deficit. She suffered tinnitus, hearing the continual sound of distant

machinery. She developed L'hermitte's sign, manifested as an

electric-shock-like pain down the back on bending the head forward and

signifying damage to the cervical spinal cord.

An MRI scan showed many typical active lesions, visible as

variably-sized bead-like hyperintensities in the white matter of the

brain. The neurologist told that she had Multiple Sclerosis; the

disease had entered a secondary progressive phase for which there was no

treatment, and that the illness must be expected to take its course.

I'm much more interventional than he -- this goes with the territory of

being a medical microbiologist -- and I recommended the following oral

antibiotic regime:

doxycycline 200mg once daily

roxithromycin 300mg once daily

Short courses of metronidazole will later be added to this regimen.

We started the doxycycline first, as it was immediately available. The

results were astonishing. For five days she suffered a worsening of her

symptoms; this was accompanied by a flu-like illness, with headache

round the eyes, pains in the large joints (hips and shoulders) and

night-sweats. This is a typical Herxheimer-type reaction; it is caused

when a large bacterial load is broken up by antibiotics or other agents.

After five days she lost the mental fog: indeed, she said she felt

clearer than for two years. The roxithromycin was added three weeks

later, when it became available.

[Note: In some parts of the world roxithromycin is not available.

Combination therapy with oral rifampicin, 300 mg twice a day, may be

considered instead. The combination of doxycycline and rifampicin has

been found to be effective in treating chronic persistent chlamydial

infections of joints.]

Updates on progress may be found here

Article in Hospital Doctor here (warning: large graphic - 629Kb)

------------------------------------------------------------------------

Questions and Answers

What is the evidence that Chlamydia pneumoniae has a causal association

with Multiple Sclerosis?

Chlamydia pneumoniae is known to patchily parasitize the cells which

line small blood-vessels, causing episodes of vasculitis, severe local

inflammation characterised by tiny punctures in the vessel walls and

leakage of blood-components into the surrounding tissue space. The

anatomical distribution of lesions in MS is centred on small blood

vessels; it is most clearly seen in the white matter of the brain and

spinal cord. Examination of the eye reveals retinal vasculitis in about

a third of patients with MS, but it is probably present in far more. It

is especially common after optic neuritis (a common precursor of MS),

and is characterised by leakage of dye in a fluorescein dye test, blood

cells, and cuffing of the vessel walls by inflammatory cells. Where it

is seen, there is a raised likelihood that MS will follow. The very fact

that retinal vasculitis is common in MS casts doubt on the prevailing

notion that the disease is a primary auto-immune disease of nervous

tissue, particularly myelin. Myelin, and the cells which produce it, are

not found at this site.

Demyelination has, in fact, recently been found to be a secondary

phenomenon in the acute lesion of MS: the first visible event in an

acute MS lesion is the sudden, orderly, non-inflammatory local mass

death of oligodendrocytes, the cells which make and support myelin. This

again casts considerable doubt on the notion that MS is a primary

auto-immune disease.

The epidemiology of MS suggests a communicable factor acquired in

adolescence. This is the age when seroconversion to Chlamydia pneumoniae

begins.

Chlamydia pneumoniae has been linked to relapsing-remitting forms of

disease elsewhere in the body, including asthma, reactive arthritis and

coronary artery disease. Causal associations have been made by isolation

of the organism and by detection of diagnostically raised antibody

levels which subside on treatment. MS can be considered an analogue of

these conditions, but, because it represents an intracerebral infection,

shielded from the general circulation, high circulating antibodies are

not to be expected.

Workers at Vanderbilt University, Nashville, Tennessee, were the first

to demonstrate Chlamydia pneumoniae gene-sequences in the CSF of persons

with MS using an amplification method (PCR). Other centres were at first

unable to replicate these results, but since those early days a number

of other laboratories round the world have confirmed the Vanderbilt

workers' findings.

Episodes of relapse in MS patients are associated with new respiratory

infections with Chlamydia pneumoniae; as antibody levels rise, brain

populations of the organism are attacked by host defences. The relapse

is evidence of host 'collateral damage'.

At a population level antibodies to Chl pneumoniae rise as the disease

becomes progressive.

Active transcription of a Chlamydia pneumoniae gene known to code for a

stress-protein (hsp60) has been found in the CSF of persons with MS.

Antibodies to bacterial hsp60 have been found in the CSF of persons with MS.

Specific antibodies to Chlamydia pneumoniae components have been found

in the CSF also (oligoclonal bands).

There is evidence of active synthesis of hsp90 by Chlamydia pneumoniae

in the CSF of persons with MS. hsp90 kills oligodendroctye precursors.

A review of the scientific literature, together with references, is

given in this paper (Adobe pdf) which can be printed out and shown to

your doctor.

How might Chlamydia pneumoniae reach the brain?

The organism settles on some part of the respiratory lining and then

invades. A respiratory infection (sinusitis, bronchitis, pharyngitis or

pneumonia) results. Host defence cells mop up the organism; some become

parasitized. Chl pneumoniae can travel round the body in the blood

monocytes - mobile host defence cells - when these are called to deal

with a remote infection - perhaps a transient virus infection. As the

monocytes pass through the blood vessel walls, Chl pneumoniae are shed;

these infect the lining cells. Microcolonies of Chl pneumoniae are set

up. This can happen in the brain, in joints, in the vessels which supply

the great arteries themselves, and in the skin.

MS is a many-staged and complex disorder. How can a simple bacterial

colonisation/infection cause such complexity?

MS has four variants: relapsing-remitting, where neurological deficits

occur suddenly and resolve over a few weeks. Resolution is at first

usually complete; later, it is less so. Although called

relapsing-remitting, most patients gradually accrue deficits. The

disease may change to the secondary-progressive form; remissions are now

unusual and deterioration is the rule. The third variant is the

primary-progressive form, where the disease worsens from the beginning.

The fourth, or so-called benign form, describes rare cases where

resolution is always complete; the deficits themselves may cease to

happen. (It is unwise to use this term as MS can become aggressive

twenty years after its first mild appearance.)

All these forms and stages would correspond well with an established

Chlamydia pneumoniae infection in the brain. In the relapsing-remitting

form the infection is silent until a new respiratory infection provokes

a new host response. This tends to become more severe as time goes on.

(Parallels are seen in the increasing severity of pneumonias caused by

Chlamydia pneumoniae in those who suffer repeated infections after

seroconversion: the severity is caused by the increasing strength of the

host response.) In the progressive forms the host response is

continuously firing, often against an extracerebral bacterial infection;

a patient with early SPMS will often mention chronic sinusitis, chronic

middle ear disease or new-onset asthma which began some time before the

MS began to slide into the progressive phase. experienced a

prolonged respiratory infection followed by new-onset asthma before her

illness became progressive.

MS has a genetic component. It also has a marked geographical

distribution. How do you account for this, given that Chl pneumoniae is

ubiquitous?

MS has a pronounced geographical distribution. It is most common in the

cooler latitudes, becoming rarer as the tropics are approached.

Migration from temperate to tropical areas confers protection, provided

the move is made before adolescence. People who migrate to temperate

areas are more likely to develop MS than those who have remained behind.

The epidemiology of MS is not as simple as this, however. The disease

has an increased incidence in certain groups of women in the Middle

East. The common factor seems to be a seasonal or cultural reduction in

exposure to sunlight; in those with a genetic predisposition a relative

lack of Vitamin D develops. Vitamin D deficiency is indeed found in

those with MS; it is linked to calcium and magnesium deficiency and to

osteoporosis. By contrast MS has not been recorded amongst the Inuit,

who, though living through arctic winters, derive ample Vitamin D from a

fish-rich diet.

Vitamin D is vital for the maintenance of the blood/brain barrier. Not

only may a mild Vitamin D deficiency allow ingress of Chl pneumoniae; it

may also activate quiescent infections. The number of active

white-matter lesions seen on MRI in persons with MS closely follows the

seasonal fluctuation of levels of circulating Vitamin D.

Can a chlamydial cause for MS be proved in an individual patient by

serology?

Not at the moment. This because Chl pneumoniae is a common organism and

infections with the bacterium are common. Antibody levels tend to rise

during life, even in people who are asymptomatic. Patients with

extracerebral infections of some duration (particularly reactive

arthritis) can show high titres in the microimmunofluorescence test; it

is generally reckoned that a titre of 1:512 or above, in the presence of

appropriate clinical findings, is highly suggestive of Chl pneumoniae

disease. MS is different; the pathology is at the blood-brain barrier.

One would not expect an elevation of circulating antibodies unless an

extracerebral component to the infection were also present. This may be

the case in progressive disease; there is a statistical elevation of

antibodies in a group of such patients. This supports the idea of a

chlamydial cause for MS, but makes no prediction in an individual. That

is why treatment must at the moment be empirical.

Antibiotics have been around for more than fifty years: surely they must

have been tried before.

This puzzles me, too. Neurologists have speculated from the late 19th

century that MS might have an infective origin. They were used to

dealing with infections, particularly syphilis. I'm sure that

penicillin, so effective against syphilis, would have been tried in MS.

The intracellular phase of Chlamydia pneumoniae is, however, resistant

to it. The first generation of tetracyclines may well have been tried;

whether they could be given orally in sufficient quantity to enter the

brain is uncertain. By the time doxycycline was invented, neurology, and

the received beliefs about the cause of MS, had changed. Neurologists

now rarely saw patients with underlying infections and MS was considered

an auto-immune disorder. And, too, there is a battle-weariness in the

neurology establishment. So many hopes about finding a treatable cause

for MS have been dashed over the decades. The mind-set of the

neurological establishment needs to be changed. This will happen.

And, too, MS sufferers are often seen as people who are difficult to

help. When I was a student it was customary to speak of the 'typical

mental attitude' of those with established MS; this included an

impression of blunted insight, a kind of insouciance, even euphoria. In

these more politically correct days one does not speak like this any

more, but there is an element of truth in it. Now that I think of MS as

an infection, the answer becomes clear: this 'typical mental attitude'

is a state of intoxication with bacterial metabolic products. A similar

state is seen in other chronic infections. In the days before

antibiotics persons with progressive tuberculosis were said to have a

typical mental state. People who were nursing at the time still vividly

remember this.

In addition to this (recalcitrant doctors and recalcitrant patients) the

beginnings of recovery with antibiotics are not pleasant. The early

bacteriolytic (Herxheimer) reaction can be alarming. And, as

found, as-yet unorganised repair can cause function to worsen in the

short term. This could easily lead to an early impression that

antibiotics were unhelpful or even harmful and could have led to their

discontinuance.

Why doxycycline and roxithromycin?

Both are oral, both are active against Chlamydia pneumoniae, both are

relatively inexpensive. They act synergically against test strains of

the organism; giving both together would be the equivalent of giving a

four-fold increase of each drug were it to be given alone. The drugs

work on different steps in the bacterial protein synthesis pathway.

Combination therapy reduces the chance of the emergence of resistance.

Both drugs pass into the brain (roxithromycin is the only drug in its

class to do this.) Both reach good levels inside cells. This is very

important. Both are well tolerated.

Rifampicin may also be considered. It, too, is synergic with

doxycycline, penetrates the brain and is active intracellularly. Its

only disadvantage is that it is suitable for continuous use only.

Why are later short courses of metronidazole to be taken together with

these antimicrobials?

Chlamydiae have a biphasic life-cycle. A small, infectious,

non-replicating extracellular particle (the elementary body, or EB)

spreads the infection both between persons and between host cells. On

gaining entry to a host cell, the EB is able to transmute into a larger,

diffuse form (the reticulate body, or RB) which utilises the host cell's

energy-generating organelles for its own use. It is an energy-parasite.

By this means it is able to replicate rapidly, releasing multitudes of

EBs into the extracellular milieu. Agents which block protein synthesis,

such as doxycycline and roxithromycin, stall this replicating phase, but

do not eliminate the intracellular organism.

Chlamydiae are complex organisms. Long ago their ancestors must once

have been free-living. They must have possessed their own

energy-generating pathways. The transformation from EB to RB is an

active change, and an active change implies the retention of at least

some of these pathways. The ones with the most utility for this purpose

would be anaerobic, and thus susceptible to metronidazole. Metronidazole

should kill the organism while it transformed itself from the EB to the RB.

Doxycycline and roxithromycin block the replicating phase and may be

expected to force the organism to maintain itself by using its own

primitive anaerobic respiratory mechanisms. In this suspended state it

would be susceptible to anti-anaerobic agents such as metronidazole.

This is borne out by clinical evidence. The administration of

metronidazole after doxycycline in a patient with likely high-load Chl

pneumoniae infection causes a bacteriolytic reaction as severe as that

following the original administration of doxycycline.

However, there is a difference: in this leg of treatment there is no

risk of the emergence of resistance, for the organism is unable to

replicate. Metronidazole need thus be given in courses only as long as

can be tolerated. It will be seen that this cyclical treatment regime

allows host cells to be used as a trap; extracellular EBs will enter

cells, to be curtailed at the residual form, where they will be

destroyed when metronidazole is next given.

In this way the total body EB load will gradually be depleted.

Five-day courses of metronidazole at three-week intervals, during

continuous treatment with doxycycline and roxithromycin, would seem

reasonable; at first, metronidazole may be limited to one or two doses

on one or two days to judge the severity of reaction.

The eventual aim would be to give all three agents intermittently. This,

the final leg of treatment, would entail a 14 day course of doxycycline

and roxithromycin, with metronidazole given from day five for five days.

(The reason for continuing doxycycline and roxithromycin for a few days

after the metronidazole has been stopped is because these drugs both

possess anti-inflammatory activity which may prevent a reaction to the

organisms killed by metronidazole.) This course would be given once a

month. After several months the intervals between the antibiotics would

be cautiously extended.

Why this complex antibiotic regime?

The literature is filled with instances of treatment-failure in

serologically-proven chronic Chl pneumoniae infections of non-CNS

systems, whether macrolides, tetracyclines or rifampicin have been used.

When the drug is stopped, even after months of treatment, serology

rises, and the patient relapses.

The intensive cyclical regime of combined antimicrobials outlined here

corrals the pathogen, initially halting replication, then eliminating

stalled intracellular forms. Over a number of cycles it is expected that

the load of extracellular forms will be reduced to negligible levels.

No single antimicrobial agent can be expected to achieve this.

What are the expected reactions to the antibiotics?

There seems to be two components to the reactions experienced on taking

the antibiotics.

The first is caused by elimination of bacterial fragments -- endotoxins

-- and is characterised by shivering, influenzal symptoms and general

malaise.

The second is caused by the release of metabolic toxins; waves of

giddiness and feelings of unreality are quite common. They are alarming

if not known about and understood. The strength and duration of these

reactions depends largely on the bacterial load. In MS, particularly

early relapsing-remitting MS, the bacterial load is likely to be small,

and the reaction brief. In other conditions, particularly those with

multi-system involvement, the bacterial load may be large and the

reaction to antibiotics unpleasant and prolonged.

It may seem unlikely that doxycycline, roxithromycin and rifampicin can

cause a Herxheimer-type reaction; they are, after all, considered to be

bacteriostatic agents -- normally they inhibit rather than kill

bacteria. However, intracellular Chlamydia pneumoniae must continuously

elaborate proteins to ensure its own survival within the host-cell; the

three agents above disrupt this.

The reaction to the metronidazole component of treatment is particularly

severe as at this stage numerous bacteria are being killed. For this

reason it may be best to give an initial course of one single day,

followed by review. Prochlorperazine, 10mg orally, may be useful.

The patient can be reassured that a reaction to the antimicrobials are

evidence of bacterial destruction and that they will end. And, too, the

morale induced by physical improvement has to be set against them.

Isn't giving antibiotics for a long time is a bad thing?

That depends on the illness. Long-term doxycycline is used fairly

routinely for certain kinds of gum disease and for acne. Doxycycline is

also used long-term in malaria prophylaxis.

Long-term use of these antibiotics engenders no real risk of an increase

of resistance in other bacteria within the wider community.

Does the fact that antibiotics can roll back MS tell us something about

the nature of the illness itself?

I think it does. Components of MS, at some stages and in some variants,

may be:

A bacterial toxaemia. This may account for the mental fog, blunting of

insight and many other non-specific symptoms which are otherwise hard to

explain, including fatigue. A toxaemia would be expected to resolve

quickly with effective antibiotic treatment, as has happened here.

Early phenomena: local mass oligodendrocyte death and secondary

demyelination. This is the sudden stripping away of the insulation of

the nerve-fibres in the classical MS relapse. It is reversible, but

recovery depends on the replacement of oligodendrocytes, the cells which

produce and sustain myelin. Damage to the nerve fibres occurs even in

early disease, but becomes more severe with time.

Loss of neurones. This has been shown to occur in MS and may cause

eventual dementia. One might speculate that appropriate antibiotic

treatment would prevent further neuronal loss. (Given that neurones are

very susceptible to toxins, and that the brain has evolved an elaborate

defence system for keeping toxins out, it is possible to speculate that

the neuronal loss seen throughout the course of MS might be a direct

result of chronic toxaemia maintained from within the brain itself.)

Until fairly recently it was considered that, in the adult, lost

neurones could not be replaced; there is now a lot of evidence that

neuronal replacement occurs throughout life. In addition, the brain is

known to have considerable functional plasticity.

In what other conditions may chlamydial vasculitis be implicated?

Chl pneumoniae is a common pathogen and almost everyone encounters it.

It is quite likely that a considerable proportion of the population is

chronically but asymptomatically parasitized by this organism. Indeed, a

trivial infection caught in childhood may remain dormant for life, or it

may take decades to develop into a disease form. And, if it does the

latter, the window of opportunity for treatment may be quite narrow.

Systemic illnesses caused by chronic Chl pneumoniae infection have

common features whichever bodily system is affected; indeed, there is an

astonishing overlap between diseases long considered unrelated. MRI

scans on patients with Crohn's disease may show large numbers of

white-matter hyperintensities indistinguishable from those found in MS.

Patients with reactive arthritis may develop uveitis, also seen in some

patients with MS. Whichever system is involved, the disease often takes

a relapsing/remitting course with recurrence of symptoms which tend to

worsen; there is an increased lack of resolution. With time there is a

destruction of the normal anatomy. Finally, the disease becomes 'burned

out': there is the impression that infection has been vanquished, but

with enormous collateral damage. At this stage bacteria may be few, and

there may be little that antibiotics can do to help.

Here is an incomplete list of disorders in which vasculitis due to Chl

pneumoniae may be implicated:

adult-onset asthma; refractory sinusitis, chronic obstructive pulmonary

disease, uveitis, optic neuritis, radiculitis, nerve deafness,

transverse myelitis, Alzheimer's disease, multiple sclerosis, sarcoid,

myocarditis, pericarditis, culture-negative endocarditis, atheromatous

arterial disease, aneurysm, giant-cell (temporal) arteritis,

polyarteritis nodosa, Wegener's granuloma, inflammatory bowel disease,

primary sclerosing cholangitis, reactive arthritis, Reiter's syndrome,

Behcet's disease, interstitial cystitis, cutaneous vasculitides

including pyoderma gangrenosa.

Conditions which may suggest the possibility of flare-ups of chronic Chl

pneumoniae infection deserving serological investigation include the

following (a multiplicity being more strongly suggestive:)

recurrent sinusitis, recurrent chest infections, chronic fatigue

(especially if following a respiratory infection), focal neurological

deficits, myalgia, muscle fasciculations, recurrent episodes of

bronchospasm, unexplained pleuritic pain, angina, recurrent arthralgia,

unexplained recurrent abdominal pain, unexplained menorrhagia, recurrent

fistula-in-ano, recurrent cutaneous vasculitides.

A brief note on Chronic fatigue and persistent infection with Chlamydia

pneumoniae can be found here.

What might a schedule of treatment comprise?

Antimicrobials

Doxycycline 200mg once daily with plenty of water.

Roxithromycin 150mg twice daily or Rifampicin 300mg twice daily

These are maintained without a break for at least six months.

Two or three months into the treatment regimen, or when the patient is

experiencing few problems with reactions, three-weekly cycles of

intermittent oral Metronidazole are begun. During the first cycle

metronidazole is given only for the first day. If problems with

reactions are found, the period of administration is kept short. When

metronidazole is well tolerated the period of administration in each

cycle is increased to five days.

The dosage of metronidazole is 400mg three times a day. If it is

suspected that a patient may have a heavy chlamydial load a smaller

daily dose may be given.

The eventual aim is to give all three agents intermittently so that the

patient has a respite from antibiotics. This, the final leg of

treatment, may entail a 14 day course of doxycycline and roxithromycin,

with a five day course of metronidazole in the middle. This course is

given once a month. After several months the intervals between the

antibiotics may be cautiously extended.

Rifampicin is not suitable for intermittent use, and azithromycin may be

given instead.

------------------------------------------------------------------------

Adjuncts

The brain has extraordinary powers of repair, but must be provided with

the building-blocks by which to do it.

Vitamin C 1G, B complex, E 800iu daily.

Vitamin D (high dose - 4000iu) (less may be needed in infections other

than MS) Magnesium 300mg and Calcium 500mg supplements in the evening

(remote from the time of taking doxycycline) daily.

Omega 3 fish oil daily.

Selenium 200 micrograms daily.

Vitamin B12 injections once weekly for 3 months, then monthly for the

duration of continuous treatment. (There is now evidence that oral B12

is satisfactorily absorbed, except in patients with pernicious anaemia.

High dose supplementation is recommended.)

Combined Acetyl L-Carnitine 500mg and Alpha Lipoic acid 150mg per day.

(These repair damage to the mitochondria.)

Regular Lactobacillus acidophilus, daily, either as a supplement or in

capsules. This is to maintain bowel flora in the face of antibiotic

treatment. Tablets of Lactobacillus sporogenes spores may be considered.

These have the advantage of getting into the small bowel in large numbers.

This regimen of treatment is epitomised in this pdf file, which may be

copied and printed out.

------------------------------------------------------------------------

A cautionary note must be sounded. All this is very new and much of it

is speculative. It is linking up the work of others. But an empirical

trial of antibiotic treatment is surely worthwhile: it would be

attempted in any other disease were there even indirect evidence of a

treatable pathogen. As an example, one might consider culture-negative

endocarditis, where long-term antibiotics are given (often successfully)

in the absence of a demonstrable pathogen. MS, as it progresses, can be

devastating and antibiotics are very cheap by the standards of

conventional treatment. In comparison with other drugs they are

relatively (but not completely) risk-free.

In treating the disease, it makes sense to use antimicrobial agents

which are effective against other potential pathogens of the CNS

including Borrelia garinii and B burgdorferi. These have been known to

cause a serologically negative MS-like illness. It would also make sense

to cover for Rickettsiae and Mycoplasma sp.and cell-wall deficient

forms. MS and other initially relapsing-remitting but ultimately

progressive diseases may have a polymicrobial phase: the punctured

vasculitis caused by Chl pneumoniae would provide an easy portal of

tissue-entry for blood-borne organisms.

------------------------------------------------------------------------

My own experience from treating several patients with MS is that those

with relapsing-remitting disease and early progressive disease can do

well. Patients with later progressive disease, or who have dense

neurological deficits which have been in place for many years, respond

less well. Generally speaking, the earlier that treatment is begun the

better the result is likely to be.

In considering treatment, one must make an analysis of risk versus

benefit. I believe that a trial of six months' doxycycline is worthwhile

even in late disease; if benefits occur the rest of the treatment can be

added. If no benefit is found then the trial can be stopped. It is

important to go into the trial without undue expectation. Nothing at all

can be guaranteed.

------------------------------------------------------------------------

return to previous page

return to home page

*(Roxithromycin is available on prescription in Europe. Although it is

not listed in the British National Formulary it can be prescribed by any

registered medical practitioner; a delay of about ten days must be

allowed for its importation. It is not available in the US.

The combination of doxycycline and rifampicin is likely to be as

effective in chronic chlamydial infections.)

First uploaded 29th November 2003; last updated 25.06.2005

Gloria M. Tate wrote:

> Hi,

> I am wondering if people with RA are more likely to get cellulitis. I

> know my brother who has MS has been in the hospital for a month with

> this infection. It just sprang up one day in his left thigh and now

> they have had to make a twenty inch cut on his leg and put some

> sponges in there to soak up the infection. I remember seeing someone

> on the list who had this infection or syndrome or whatever it is, but

> I didn't know it was so serious, and I don't know if someone with RA

> would be more prone to it.

> Thank you,

> Gloria

>

July 17, 2006

Yes Gloria, Any person who has a compromised immune system is suseptible to

infection and cellulitis is one of the worst ones to get rid of. Is your

brother on Steroids or MTX, Remicaid, Humira, Thalidomide or any of those

medications that suppress the immune system? If so, then that is the reason why

he has a problem with any infection. I have R/A & Scleroderma. Those drugs

were prescribed to me last year when I was diagnosed after a miserable 4 years

in pain for which they could not give me a diagnosis. Because of my nursing

background, 40 years and now semi-retired I knew how bad the side effects these

drugs can cause, so I did my research which led me to Antibiotic Protocol. Been

on Minocin for 7 months and I have taken an upturn for the better. I am no

longer in pain, nor anemic and can move about like anyone else. I am on Minocin

200mg. /day. 100mg in the a.m. & p.m. I hope your brother can recover quickly.

Seek out a doctor who will prescribe the

antibiotics he needs and when he is better, seek out an A/P doctor who will

also wean him off these terrible meds. Good luck, Dolores

" Gloria M. Tate " <miss.gloria@...> wrote: Hi,

I am wondering if people with RA are more likely to get cellulitis. I know my

brother who has MS has been in the hospital for a month with this infection. It

just sprang up one day in his left thigh and now they have had to make a twenty

inch cut on his leg and put some sponges in there to soak up the infection. I

remember seeing someone on the list who had this infection or syndrome or

whatever it is, but I didn't know it was so serious, and I don't know if someone

with RA would be more prone to it.

Thank you,

Gloria

July 18, 2006

Such a broad affliction, I'm certain that the degree of severity and the

approach to treatment is going to vary greatly from person to person.

Certainly those with compromised immune systems are susceptible to

cellulitis, but there are other reasons.....for me its circulation or even a

small cut. An infection is present, but the imflammation can be the much

worse component, with me it is. That is why for me, in addition to the

antibiotics (IV if needed), an expedient round of high dose prednisone and

several cycled strong anti-inflammatories make a huge difference. The

difference between about a 10 day battle or a five week all-out war,

including an ER visit, but not including the complimentary five and a half

hours of CNN waiting room blather thrown in at no additional charge. Not

fearing the smart use of effective medications and having a physician

exceedingly skilled in their application is a great benefit.

Jeff

----Original Message Follows----

From: mike rosner <martysfolks2004@...>

Reply-rheumatic

rheumatic

Subject: Re: rheumatic Cellulites

Date: Mon, 17 Jul 2006 20:21:57 -0700 (PDT)

Yes Gloria, Any person who has a compromised immune system is suseptible to

infection and cellulitis is one of the worst ones to get rid of. Is your

brother on Steroids or MTX, Remicaid, Humira, Thalidomide or any of those

medications that suppress the immune system? If so, then that is the reason

why he has a problem with any infection. I have R/A & Scleroderma. Those

drugs were prescribed to me last year when I was diagnosed after a miserable

4 years in pain for which they could not give me a diagnosis. Because of my

nursing background, 40 years and now semi-retired I knew how bad the side

effects these drugs can cause, so I did my research which led me to

Antibiotic Protocol. Been on Minocin for 7 months and I have taken an upturn

for the better. I am no longer in pain, nor anemic and can move about like

anyone else. I am on Minocin 200mg. /day. 100mg in the a.m. & p.m. I hope

your brother can recover quickly. Seek out a doctor who will prescribe the

antibiotics he needs and when he is better, seek out an A/P doctor who

will also wean him off these terrible meds. Good luck, Dolores

" Gloria M. Tate " <miss.gloria@...> wrote: Hi,

I am wondering if people with RA are more likely to get cellulitis. I know

my brother who has MS has been in the hospital for a month with this

infection. It just sprang up one day in his left thigh and now they have had

to make a twenty inch cut on his leg and put some sponges in there to soak

up the infection. I remember seeing someone on the list who had this

infection or syndrome or whatever it is, but I didn't know it was so

serious, and I don't know if someone with RA would be more prone to it.

Thank you,

Gloria

July 19, 2006