ENGLANNIN KONFERENSSISTA

[Bb]

Lähettäjä: Soijuv Lähetetty: 7.7.2004 12:14

Englannin borrelioosikonferenssin luennoilta :


Third Conference on Tick - Borne Diseases, York 2004

Friday 18th June

Dr David Owen

Erythema chronicum migrans is common on the legs and
may appear away from the site of tick bite. (NB: the
picture looks like my erythema migrans.)

The need for treatment must be judged on clinical
grounds. For example, meningitis can be carried
harmlessly in some people, and yet be deadly within
hours in others. Encephalopathy is highly suggestive
of neurotoxins.

Dr Marie Kroun

Spirochetes are associated with psoriasis and other
skin conditions.

She treated herself with Amoxicillin initially. Then
with 10 days of Malarone, and Azithromycin, this
helped, but a longer treatment was not possible due to
expense. She followed up this treatment with
Doxycycline.

Prof Sam Donta

Symptoms
Dr Shattock (female) found in her studies that 30% of
patients with Lyme disease develop a chronic illness,
a CFS type illness. Between 50 to 80% of Lyme disease
patients have neurocognitive symptoms, including
short-term memory loss. There may be psychiatric
manifestations, the seminal work in this area has been
conducted by Brian Fallon. Lyme disease can present
as almost any multisystem illness, and that is the
problem so far as diagnosis is concerned. We need to
be careful because not all patients with Lyme disease
have severe disease, it may be mild or even
asymptomatic. In a study at a psychiatric hospital it
was found that 30 to 50% of patients, compared to 5%
of controls tested positive for Lyme disease. Other
symptoms may be cardiovascular, for example,
palpitations or tachycardia, and this can happen in a
20-year-old. There can also be autonomic problems,
there may be tremors and there can be sensory
neuropathy. Borrelia localise to the nerve roots. In
addition there can be gastrointestinal symptoms, Prof
Dona was surprised at the number of patients
presenting with a picture indicative of IBS. There
can be sleep disorder and many patients with chronic
diseases stop dreaming, then as they are cured they go
through a stage of vivid dreams.

Neuroimaging
MRI scans are mostly normal, with only 5 to 10%
showing abnormalities. SPECT scans are more
informative with up to 75% of patients showing
abnormalities.

Testing
PCR may be too sensitive and pick out even transient
asymptomatic bacteraemia. For Lyme disease PCR
reactivity is rare, and a positive PCR does not
necessarily show active disease. PCR of spinal fluid
is difficult and can yield negative results. In other
words, the Borrelia isn't where we are looking. It is
like the old story of looking for lost keys under a
lamppost when it they were lost elsewhere. Another
disadvantage of PCR testing is the risk of
contamination, for example, the lab technicians may
leave their sandwiches in the fridge with the samples!
In terms of developing an accurate test for the
future, he thinks we need possibly to look for a
metabolite. He also thinks that we need a tissue
registry for PCR testing.

So far as the differential diagnosis of Lyme disease
versus multiple sclerosis is concerned, MRI can't do
this. Abnormal findings on SPECT scans were
trivialised initially, but these patients can be
followed and the changes are reversible with therapy.
At this point, Prof Donta made a comment about which
lobes were particularly affected, I think he
specifically mentioned the temporal and frontal lobes,
can anyone clarify this?

Treatments
First there is the question of whether symptoms are
due to ongoing infection or due to the so-called post
Lyme syndrome. Prof Donta's opinion is that the
symptoms are the same in chronic illness as they were
from the infection, so he thinks symptoms are due to
ongoing infection.

Borrelia is sensitive in vitro to: Penicillins,
Cephalosporins, Tetracyclines, Clarithromycin and the
Macrolide group, and Quinolones. Borrelia is very
sensitive in vitro to the Macrolides. Quinolones have
side effects. Beta lactams don't get into cells.
Prof Donta feels that intracellular antibiotics seem
to work better. Therefore, it appears the infection
has gone intracellular.

Metronidazole, why does this have an effect in Lyme
disease patients? Borrelia has no genes to metabolise
Metronidazole, therefore, it can't have any direct
effect. So why do Lyme patients respond to
Metronidazole? Prof Donta thinks that perhaps the
metabolic products of gastrointestinal bacteria must
be detoxified, and that the Lyme patient has become
sensitised to these toxins. This could mean that
Metronidazole, or other antibiotics for that matter
have an indirect effect and work by removing these
toxic gastrointestinal bacteria.

Unlike Doxycycline, Tetracycline is not highly protein
bound. In chronic Lyme disease, it must be used
long-term, over four to six months. He uses
Tetracycline in six-month pulses at which point he may
then instruct the patient to take a break from
treatment and see how they feel. In Lyme disease
there is a two to one female to male ratio, possibly
this is due to the hormonal influence. He also sees
an association between shingles and Lyme disease,
possibly the neuron is challenged by having more than
one infection to deal with.

Before 1992 Prof Donta used only intravenous
Cephalosporins and oral Tetracyclines. He found that
long-term intravenous antibiotics didn't work. For
those patients with two to three years disease
duration a treatment of at least 18 months is normally
required, the good news is that up to 75% of these
patients improve.

Macrolides: there has been some good work done by Dr
Rhodes lab. Prof Donta found that a lysosomotropic
agent is necessary for the Macrolide antibiotics to
work effectively, he uses Hydroxychloroquine at a dose
of 200 mg twice daily or 400 mg once daily.
Specifically he uses Clarithromycin 1000 to 1500 mg
daily, or, Azithromycin 250 to 500 mg daily. There
may sometimes be a Herxheimer reaction but generally
the longer you have been sick, the longer it will take
to improve. If you have been sick over three years it
may take several weeks before you improve.

He often finds that there is IgM reactivity in chronic
disease, this could be due to an antigen excess.

Supplements
Dr Donta feels that we need to be careful here as it
is not scientific and could be seen as quackery.
Research on the Borrelia genome has shown that certain
nutrients are required. The body withholds iron
causing anaemia of chronic disease. Vitamin C is
acidifying and should not be used with
Hydroxychloroquine. Therefore Dr Donta asks his
patients to humour him and not to take any
supplements. Hyperbaric oxygen is something that may
produce a transient improvement. Heat? You can't fry
it!

Questions
Question: I have been recommended 200 mg of
Hydroxychloroquine (Plaquenil) daily is that enough?
Is there a risk of eye toxicity?
Answer: You need to take 400 mg of Hydroxychloroquine
per day, 200 mg is not enough. You can take 400 mg
once per day or 200 mg twice daily. Eventually, you
can go onto a single dose of slow release
Clarithromycin.

Any antibiotic can cause any pleomorphic bacteria to
change form, even putting bacteria into water can do
this.

People first treated with intravenous Ceftriaxone did
worse than those that were started on Tetracycline in
long-term studies. Dr Donta will sometimes add
Tetracycline or Minocycline to Clarithromycin and
Hydroxychloroquine if the patient is not getting
anywhere.

Dr Donta said that silver is toxic to anything, and
perhaps in the future there would be some way to
target the infection.

Regarding long-term antibiotic treatments, Dr Donta
said "try it, you'll like it"!

Regarding co-infections Dr Donta said this was
Pandora's box. He doesn't know if chronic babesia
even exists. He is sceptical about co-infections.
For babesia he would use clindamycin and quinine, he
doesn't use Atovaquone and Zithromax.

His advice regarding vitamin C concerns ascorbic acid,
he is not familiar with Ester C (a type of Calcium
Ascorbate).

Sinusitis would be associated with pain. Nasal
congestion could be something else. It could also
follow antibiotic treatment.


(Lunch)


Dr Raphael Stricker

30% of tick bites are to the leg. NB: June and July
are peak months for reported disease onset (my EM rash
was at the end of May).

Neurological manifestations
Visual migraine is very common and it is a vascular
phenomenon. There can be acute psychosis and there
may be sleep disorders. This was studied by Eileen
Hilton in New Yor, all patients had a sleep problem
even if they didn't know it. This, on its own could
cause fatigue.

Testing
Re PCR testing: there is a New Jersey physician who
does repeated tests and approximately 1 in 10 is
positive. The LDA test (from Igenex) finds dead
bacteria in urine. He likes to do the CD57 lymphocyte
test. SPECT scanning can show inflammatory and
perfusion defects. There is also neuropsychological
testing which will show cognitive deficits. The
patient may not even be aware of this until testing.
It needs to be done by an experienced tester.

The CD57 test shows decreased numbers of these cells
in chronic Lyme disease. CD57 cells are a subset of
NK cells, distinct from the main CD 56 subset. The
TH1 cytokines down regulate CD57 cells. Studies have
shown that in acute Lyme disease the CD57 count is
normal. However, in chronic Lyme disease,
pre-treatment the CD57 count is low, during treatment
half the patients were low and after treatment all
patients had normal CD57 counts.

In AIDS the CD57 count is normal, despite T-cells
being abnormal. Therefore this abnormality appears to
be specific to chronic Lyme disease. This defect can
persist in chronic Lyme disease and has been
documented in a patient over 10 years. It is a useful
test for monitoring treatment.

Treatment
For neurological disease he uses intravenous
treatments. The treatment must be prolonged. He
rotates antibiotics to reduce the risk of resistance
arising. Intramuscular therapy also appears to work
well for neurological Lyme disease. Doxycycline and
Minocycline have anti-inflammatory properties. He
finds that Amoxicillin and Augmentin are less
effective in chronic Lyme disease.

He uses oral antibiotics in combination. A Macrolide
and a Cephalosporin, for example, Clarithromycin or
Zithromax with Omnicef or Ceftin. Or a Macrolide and
Metronidazole.

Intravenous treatments: it is not only Ceftriaxone
that can cause liver toxicity, it is not well known
that Cefotaxime can also cause liver toxicity and
colitis.

Adjunctive therapy: he uses symptomatic treatments,
for example, Amitriptyline at a low dose, and COX2
inhibitors, including Celebrex, Mobic, and Vioxx.

Other therapies: no proven benefit.

Herxheimer: this may occur in three to four week
cycles. It is caused by a release of Borrelia toxins
and cytokines.

Co-infections
The mouse model shows that co-infections are
significant and must be addressed. A co-infection
will result in more severe symptoms. Babesia is
immuno-suppressive and is associated with symptoms
such as sweating. He thinks that antibody or FISH
testing by Igenex is a better method of testing than
PCR.

Closing comments
Treatment must be very prolonged, this is the case in
other chronic infectious diseases such as tuberculosis
where 2 antibiotics are used for 18 months.

[Bb]

Lähettäjä: jukka61 Lähetetty: 8.7.2004 22:24

Mielenkiintoinen tuo Dontan juttu. Milloinkohan vastaava kongressi saataisiin Suomeen (ja samalla tietoa)?

Meillähän käytäntö on, että oireiseltakin potilaalta (lähes aina) evätään hoito, jos sen kerran tai kaksi on saanut, vaikka yhä enenevässä määrin tutkimukset osoittavat, että Borre on krooninen juttu osalle ja hoitoa tarvitaan, silloin, kun on oireita ja hoitoa pitäisi jatkaa vielä senkin jälkeen tarpeeksi pitkään (3kk), kun on ollut oireeton.

Metron käytöstä meidän (infektio)lääkäreille ei harmainta aavistusta.

Eli meillä "lyödään sellainen rätinki eteen, että kaikki tarvittavat hoidot on saatu, mitäs vielä valitat" ja siirrytään eri kipulääkkeillä (vast.) "saattohoitoon". Mitäköhän MS-, reuma-, syöpä-, diabetes-, jne. potilaat (ja heidän etujärjestönsä) sanoisi, jos hoito lopetettaisiin, kun sitä on "saatu" tarvittavan pitkään.