WHY DO MY SYMPTOMS IMPROVE ON ANTIBIOTICS BUT DETERIORATE WHEN I STOP?

Why does my arthritis get better when I take antibiotics but deteriorate when I stop?
Why does my muscle weakness get better on antibiotics but deteriorate when I stop?
Why does my fatigue and Fibromyalgia get better when I take antibiotics but deteriorate when I stop?
Why do my chronic symptoms improve on antibiotics for urinary tract infection and then deteriorate when antibiotics stop?
Why do my neurological symptoms get better on antibiotics and deteriorate when I stop?

I hear these questions all the time from people with RA, ME/CFS, Fibromyalgia, MS, Parkinson's - read any Facebook site for these illnesses and you see it over and over.

Well in my case it turned out that I had Lyme Disease but no doubt there are other bacterial infections that are not cleared by just a couple of courses of antibiotics.

Biofilms is one reason why Borrelia ( Lyme Disease) can persist despite long term antibiotics. 

Dr MacDonald pathologist and researcher of Lyme Borreliosis gives us a good lesson on Biofilms of Borrelia- from Lymenet Europe here


We now have entered a third era in Lyme Borreliosis - namely the Biofilm Era. 
Biofilms of borrelia burgdorferi were undreamed of until year 2006 and proven to exist in vitro and recently In ViVO in human skin biopsies of Erythema Migrans and in living Ixodid Tick midguts.
Biofilm science is radically different from Planktonic microbiology. Biofilms are part of the 
repertoire of over 99.9% of microbes. Biofilms form from planktonic microbial forms, but
biofilms provide mechanisms for microbial survival under adverse conditions which would eliminate
planktonic microbes. Biofilms explain Chronic antibiotic resistance. Biofilms are the mechanism
for Chronic Infections of many organ systems. The diagnostic names - infected artificial medical
device, bacterial endocarditis, Helicobacter pylori chronic gastritis, Dental root canal infections,
and may more- have the concept that these infections are solely due to biofilmsand the persistence of 
biofilms in humans despite administration of antibiotics/
In biofilms the microbes {planktonic forms} undergo specialization and are no longer
identical to Planktonic [single free living microbes]. Biofilm microbes are biochemically specializing
(ie have a different biochemistry, different cell wall structure, have cell to cell intercommunications
[nanowires and nanotubes] which enable cell to cell communication between the cytoplasmic compartments, and form water channels to facilitate the flux of nutrients and the removal of waste
from the biofilm community. An envelope of Extracellular matrix invests biofilm communites. This matrix is derived from once living --now dead members of the biofilm community. For Borrelia biofilms
the matrix investment includes Sloughed Outer Surface Membrane {slime layer} of Bb, Extruded 
DNA [eDNA], alginate-like material, and liposomes {micro vesicles} [blebs].

Biofilm communities may be and often are POLYMICROBIAL.

Biofilm communities spread from their sessile site of naissance to the body sites by
two mechanisms:
1. pieces of the Sessile community [Matrix invested specialized microbes] actually break apart
from the parent community and METASTASIZE to other sites.
2. Planktonic Showers rain from the sessile community from time to time and these
planktonic showers re-establish new communities in the mammalian host.

So in the year 2102, we have now entered into the 3rd era of Borrelia pathobiology;
namely the Biofilm Era.

Implicit in the biofilm concept is the ability of DNA transfer/exchange
[lateral DNA Transfer/ horizontal DNA transfer] among specialized members of the biofilm.
With DNa exchange, there is a mechanism for transfer of new virulence factors and new
modalities in antibiotic resistance. Persistence of biofilm infection in mammalian hosts
is in part due to PERSISTER microbes, which may reside within biofilm communities or which may reside intracellularly, or which may reside in so called "Sanctuary Sites"

The clinical spectrum of Lyme borreliosis continues to expand into areas of medicine
in which NAMED diseases of unknown cause [idiopathic diseases] are now incorporated within
the Lyme borreliosis disease complex. The number of skin conditions which are now Lyme disease
cutaneous manifestations has increased, thanks to the work of Dr Klaus Eisendle and Dr Bernhard Zelger to include many new entities, [ and more to be added with the use of FFM techniques]
I summarize these in my lecture on the International Cutaneous and Molecular Dermatopathology
of Lyme Borreliosis [attached , Boston Mass , Date November 4,2012]

In parallel with the expansion of cutaneous Borreliosis conditions, is the expansion of lymphoid
neoplasias linked to chronic Borrelia infections [ analogy with Helicobacter pylori induced
Malignant Lymphomas], Sarcoidosis in China as a borreliosis infection, Idiopathic lethal fibrosing
illnesses [Retroperitoneal Fibrosis, and Mediastinal fibrosis], borrelia to human Tranfections
mimicking human spontaneous gene mutations, Cardiomyopathies secondary to chronic Lyme borreliosis, giant cell arteritis [temporal arteritis] due to borrelia infection, Abdominal aortic aneurysms due to borrelia aortitis, and various intra-ocular inflammations {uveitis, optic neuritis},
Demyelination syndromes secondary to borrelia infections, and transplacental transmission of borrelia with possible lethal outcomes in the fetus in untreated conditions. The list above is only partial and will be added 
to as future medical research utilizing molecular Tools such as DNA probes fleshes out the full spectrum of
Lyme borreliosis and related co-infections.

It is truly a great time to be alive.

With all good wishes,
Alan

An earlier post on biofilms and Borrelia here

Dr Alan B MacDonald has already earned a Nobel Prize several times over in my view for the services he has done to the science and medicine in the field of Lyme Borreliosis I hope I am still around to see him recognised for those services.