Thursday, July 23, 2009

1 in 100 Australians Autistic with up to 90% Lyme Induced

'ONE IN 100'

Professor Margot Prior says a second independent study from the university [Australia's La Trobe University] found the figure was close to one in 100.

"Well we had 19 autistic children in a sample of 1,900. So that's one in a 100. So again, we believe that the prevalence is certainly greater for whatever reason," she said.

"And of course this is a population, you know, a non-clinical sample, just from the population out there. "

It is still unclear whether there are more cases of autism or whether doctors are just more aware of the condition and likely to pick it up.

While a large study in the United States is looking at possible triggers in the environment, Dr Dissanayake says it is too early to tell what is behind the increase."

Lyme Disease is being touted as a primary cause of autism (purportedly 90% of children with autism are infected with Lyme Disease). I am amazed by this one because I did not know that Lyme Disease was that widespread and did not know that data had been kept correlating LD in some way with Autism. Meanhwile there is actually a Lyme Induced Autism Foundation which has been formed by parents and they are hosting a physician's think tank session January 26-28 in San Diego. Lyme Induced Autism?...Currently, several doctors have stepped forward talking about this. Dr. Warren Levin of Vienna, VA recently appeared on the online radio show on hosted by Duncan called "The Lyme-Autism Connection". He stated that of the 10 children with autism he tested for Lyme disease, 100% of them also came back positive for Lyme disease."
For further information on Lyme Induced Autism go to

Autism Graph from

Saturday, July 11, 2009

2 Million USA Lyme cases per year (CDC reports only 20,000) World wide epidemic...but not in Australia???

When Brian Fallon did a study at Columbia University, which was just done. I forget the exact number, but it was something like he screened through 3700 people to get 37 positive (CDC positive) IGG. Now the number that you see from the CDC is a 10 times difference, like 20 000 is really 200,000. That’s not true according to Brian’s study, it’s 100 times.


Stated Dr Richard Horowitz, who presented on the "Under Our Skin" Panel Discussion on 27 April 2008, as part of the Tribeca Film Festival behind the screen series viewed from:

Richard Horowitz, MD {Vice President ILADS}
Information on his background was found at:

"Dr Richard Horowitz is President of the International Lyme and Associated Diseases Educational Foundation (ILADEF), and he is a founding board member of ILADS. He is a board certified internist and medical director of the Hudson Valley Healing Arts Center in Hyde Park, N.Y., an integrative medical center which specializes in the treatment of Chronic Lyme Disease and other tick-borne disorders. He has treated over 11,000 Chronic Lyme patients in the last 20 years, and has published on the role of co-infections and toxins in Chronic Lyme Borreliosis. He was awarded the Humanitarian of the Year award by the Turn the Corner Foundation for his dedication and research in the treatment of Lyme Disease."

Paralysis Tick Distribution map:

Friday, July 10, 2009

11 Years with Lyme Disease acquired from Australia

Borrelia pics

ELEVEN YEARS have now past since a tick bite in the AUSTRALIAN tropics left me in poor health along with a classic bulls-eye rash internationally indicative of Lyme disease. However the Australian medical community failed to put the pieces together and I was deemed cause and cure unknown, listed as autoimmune, then legally disabled by my 21st Birthday. To mark this my 11th year on the lonely trail of chronic illness and newly learned misdiagnosis, I avow my current understanding of Lyme Diseases which I have been intensely researching for the last 3 months since learning the cause of my infliction.

“Lyme” which is the common term for a Borrellia spirochete bacterial infection, was named after a town in Connecticut in north-eastern USA. This is where a strange arthritis was noted to have inflicted the community during the 70’s. It was found that a number of ticks in the area were infected with this spiral shaped bacteria as frequently depicted, which is a slower replicating cousin of Syphilis, and also resembled African relapsing fever.

In 1982 Willy Burgdorfer, identified one strain of Lyme, it was named Borrellia burgdorferi after his discovery. Since then over 300 species is known word wide, however only 10 species or so have testing much of which is unreliable and more sensitive testing is very expensive. Because the bacteria changes form and is especially capable from hiding from the immune system, it is not unknown for some people who have tested negative on 10 Lyme tests to then show positive.

Mosquitoes, biting flies and various tick species (and other arthropods) have been documented to carry Lyme bacteria (and others disease causing organisms) and likely carry a role in disease transmission to hosts. It is difficult for some labs to culture the bacteria; however an article dated 19 May 2009 titled “UNF professor works to unlock Lyme disease’s mysteries” discusses Prof Kerry Clark from North Florida’s recent techniques used to demonstrate positive Lyme results from previously negative specimens.

Migratory birds, lizards, mammals including humans are some of many animals host this disease life cycle. Some are carriers with no symptoms which is concerning for imported stock into Australia including Deer and Texas Longhorn bullock. The longhorn was notorious in the southern states of USA for infecting other cattle and other animals with Master’s Disease also known as Southern Tick Associated Rash Infection (STARI) in the area and there was even stock route restrictions applied to Texas to try and curve the Lonestar Tick invasion.

Ed Master’s the discoverer fought hard to get Masters Disease/STARI a Borrellia spirochete to also be recognised a new Lyme species (Borrellia lonstarii) to bring to light the magnitude of the epidemic prior to his sad passing away last month. In Feb 2009, an article “Discovery of new Lyme strains invalidates current tests” from

Benjamin Luft, M.D., Professor of Medicine at Stony Brook University Medical Center, discovered that four highly virulent mutations of Borrelia burgdorferi, the spirochete that causes Lyme disease, may account for the alarming increase in cases for the past 20 years. Luft’s investigation and findings were initially reported in Emerging Infectious Diseases.

This genetic drift of the organism could explain why current Lyme disease tests, which were defined nearly two decades ago, are missing approximately 75% of the confirmed positive Lyme cases, according to a recent Johns Hopkins study.
Pam Weintraub, author of “Cure Unknown: Inside the Lyme Epidemic,” recently interviewed Luft for the Psychology Today website about his findings:

“What we will find,” says Ben Luft of Stony Brook, “are proteins we never tested for on our ELISAs and Western blots—proteins we were never even aware of. But they will be the critical markers for invasive, infectious Lyme disease. Perhaps people who test negative on the old tests will become positive when we look for the right markers.”

Some viruses including “Sindbis” (which I tested positive for) and also stress from migration has been shown to reactivated Lyme bacteria in many birds that also carry ticks including the Lonestar species. Hosts infected with any of the Borrellia spirochete bacteria have the potential to have their blood, brain, central nervous system and all bodily tissues invaded, just as Syphilis has been documented as being as accomplished in.

Is Lyme also sexually transmitted? This is yet to be determined. There is evidence of Lyme surviving blood transfusion processes, and organ transplants. Lyme has been documented to have been passed congenitally in-utero and via breast-milk from mother to child and has caused foetal death. There is a strong disposition for autoimmune mothers to have children within the autistic spectrum. There are also many cases of autism recovery from long term antibiotic protocols, suggesting a possible infectious causal link to many syndromes, such as autoimmune or degenerative disorders including Alzheimer’s Disease. Many trailing Antibiotics have seen improvement in conditions recently.

The bacteria morphs between spiral form (that can cloak itself with your own proteins or create ones that mimic it which may lead to a state of autoimmunity in the body) to an cell wall free state known as L-form (which invades cells) and also a cyst form which continues to replicate while laying dormant.

Cysts around throughout the body as a defence mechanism and have been found in hostile environments such as human saliva. In animal studies, cyst forms have been demonstrated to convert back into spirochetal form when serum favourable to the bacteria was added.

Tick-less transmission has been document in controlled mouse studies, where infection has crossed to non infected mice, though this could have had numerous pathways such as urine, blood, saliva or sexually.

Mice studies have also been conducted where alziemer’s plaques were induced by infecting the mice with borrellia spirochete. There are some pretty convincing scientific studies if you google “lyme alziemer’s disease” that demonstrating the correlation, if you can handle the jargon.

Australia apparently is not an endemic region for Lyme Disease or it’s carrier the American Lonestar tick. Well, I came across a travellers log from Western Australia where the writer documented and photographed a ‘bush tick’ in the area and commented lucky there’s no Lyme in Australia. This drew my attention as it looked identical to the lonestar tick I had been researching about. Not the one with the well known star on its back, but the male version.

Just because there is inadequate vector surveillance, lack of research, and poor laboratory testing procedures, doesn’t mean that it is not a widespread unidentified problem in Australia, just as it is worldwide. It has higher infection rate and severity of disease than AIDS and there is no excuse why there should not be an equally high level of government funding allocated for research and public education for Lyme or as our Health Department calls it “Lyme-Like”.

The Lyme documentary "UNDER OUR SKIN" recently commenced Cinema screenings in America. I would highly recommend gaining access to this video when available.

Saturday, July 4, 2009

My Lyme Symptoms - Stage III (Dec 01 – Apr 09)

This photo depicts how my hands looked for around a year before presenting to my initial Rheumatologist appointment in Dec 2001. More blood tests were ordered by my Rheumatologist and presumed MCTD. Brutal introduction to chronic disease and treating symptoms, and to adjust to the fact as there is no cure. Prednisone 10mg and Plaquenil 400mg a day was to commence during my next appointment, 2 months later, and I was informed to avoid sunlight and come back the following month.

I noticed rapid deterioration of my skin at that time. It turned thin and translucent, it aged really fast. I would scar badly as it now took my body a lot longer to respond to injury and to commence healing. If I burnt my hand, it wouldn’t blister for 3 days, and then it would take a month to heal. My joints inflammation increased again and I increased my prednisone to 15mg a day.

I noticed an increase in little red blisters I would get on my arms mainly and then got a terrible case of shingles on my right arm radiating from my back to my 3 small fingers, due to the steroids. I now know blister increase means to low immune system and monitor myself better. For the six weeks I had shingles followed by 12 months of unbearable post neuelgia. Tramadol was the best to give relief at the time and I continue to use this a day or two almost monthly when I have bad symptoms and pain that I cannot sleep. Neurontin helped though my CK jumped to 1000 which is toxic to my liver so I ceased that drug. When I was on it I had strange black-head like / hair follicle king of skin eruptions, mainly where I had scars from my shingles. I don’t know what that was about possibly dead nerves or toxin accumulation or simply natural exfoliation after 6 weeks painting sores with a pink lotion (?camomile). I was then given low dose antidepressants were given to aid sleep during pain. The nerve sensitivity lessened, and is now generally tolerable when it gets irritated.

My jaw involvement flared up on one occasion where I was frequently yawning from tiredness. The first time it took me 10 hours to fix a painful off centred jaw. Then later in the day I instinctively yawned again and ditto. It only took 1 hour that time, and the next 10minutes. My jaw was obviously very tender and now was giving me sharp stabbing nerve pain intermittently. The dentist took several x-rays and revealed my wisdom teeth were stuck behind my back teeth with the small roots growing in the nerves. Given my risk of infection in my current medical situation, it was preferable to wait and see if they remained stuck and to only have the surgery if absolutely necessary.

On occasion I had irritated eyes, conjunctivitis, inflammation and also. At one point approx 2003 I had a lump under the centre of one top eyelid like a cyst, placing pressure on my eye and affecting vision temporarily. That I eventually cleared up and then on other occasions I would get infected eyelash follicles, which I needed to clean with ‘J&J baby shampoo’ or medicated eye drops. My eyes get dry and annoyed easily so I try to only use the likes of clean wet ear buds or separate tissues for use around the area. Around 2004 I again noticed vision issues. I was seeing double vision 10-20m away. It was minor and I only noticed it on occasion. An optometrist said glasses were not required at the time.

I felt I wasn’t really managed well for a couple of years and sort out a new Rheumatologist despite the travel involved. I suspected I may have had infectious arthritis possible a mycoplasma infection, not purely Rheumatoid Arthritis. This was due to the fact that apart from symmetrical anthrelgia I also continued to have unsymmetrical inflammation and joint dislocations. My new Rheumatologist gathered my history and conducted further testing including baseline x-rays to check for erosion and bone density tests. There was concern as I had been on prednisone for a few years by this stage which wasn’t very good. I was interested in long-term antibiotic protocol which had some positive results in RA patients.

My new specialist understood my position, however wanted to try in addition to continuing plaquenil, the chemotheraputic drug Methotrexate in low weekly doses (followed by folic acid supplement). This reduces the inflammation response, rather than the steroid treatment which just processes the existing inflammation and can lead to osteoporosis. This was tolerated enough to wean off the corticosteroids over the next 2-3 year period, however over time the current treatment has had discomforting side effects including ulcers and digestive issues.

My overall inflammation has been better managed since this treatment regiment; however I have noted development of skin spots and increased neurological symptoms over the last 2 or so years. There could be several explanations for this, including the chemo-brain effect as it is referred to, or neuro-borreliosis or Lyme in the brain continuing to progress due to the limited drug crossover due to the blood brain barrier despite the rest of body treatment. I also noted increased vision deterioration since late 2007. On one occasion, if felt like my optic nerve was inflamed and/or spamming and all I could see was blur for over 30 minute on work day. I had been quite stressed at the time and this really scared me.

I finally ceased prednisone in late 2008, and had an especially hard year with night tremors and withdrawal symptoms increasing exponentially, and peaking 1 month after my last dose. For 1 week solid I had vivid nightmares or negative dreams, and would wake with tightly clenched hands and muscle spasms. Then it reduced to every 2nd night for a couple of weeks, then every third and decreased over several months.

Since April 2009 my eyes have been very irritable with increased light sensitivity, dryness, swelling and distance vision problems or with extended reading. I also started to have facial twitching at times. My left upper eyelid and my lower right eyelid have been twitching when I have been quite tired. It is very noticeable to me; however in the mirror it doesn’t seem so obvious. Interestingly enough, this is where I had cysts on my eyelids in the past. It seams that I could stop the left upper eyelid twitching by pressing a certain spot on my forehead. It is also interesting that I have a large 3-4mm diam red skin spot I have had for a few years on this exact location.

Photo of Acrodermatitis Chronica Atrophicans from: