Lyme is all around us but I believe we will help many more if we give up on blaming everything on the tick related introduction of more pathogens than we had the day before we are bit.  It is confusing to people, as too often Lyme tests are inconclusive. So let’s rename the condition LIMES (Lowered Immune Metabolic Encephalopathy Syndrome) or LIMNS (for Neuropathy, as in MS like conditions) or LIMAS (Arthropathy when it is more arthritic in presentation), as these names move us closer to seeing the true picture.

It is sad to turn patients away with these devastating symptoms when the Infectious Disease Association guidelines force us to say it is Lyme. I am certain broadening the approach to Food sensitivities, other Infections, Genetics, Heavy metals and Hormones and Toxins would wind up with better results than the low batting average that is reported from long-term IV antibiotics, which are often reported as low as 33% about which Lyme critics point out is the response rate to placebos. If we focus on my F.I.G.H.T. program and do something to help deal with the obvious issues that can be found in almost anyone in any of these categories, we can be more cost effective and actually help more patients, as they will stop looking just for a doctor that will interpret their test as positive for Lyme.

Realize that everyone today will fail the Mount Sinai School of Medicine $4900 test for toxins. So let’s blame the neurotoxins and endocrine disruptors just like we blame the total body burden of infection, as properly tested everyone will have some Chlamydia or CMV or Coxackie or Candida and so on.

No one will pass the test at Harvard for bone lead levels. They have shown that the level in bone is in equilibrium with most other tissues in the body including the eye so there is a direct correlation with how high lead in bones is and how soon you develop a cataract. So there is no one on earth that does not need some lead out and since Lead makes Mercury as much as 100 times more toxic, who needs tons of tests to know what to do in most of the categories my F.I.G.H.T. program acronym represents.

So would it not be better medicine to offer some oral detoxification for the Heavy metals and the Toxins, with ZeoGold and BIOE’NR-G’Y C, Beyond Fiber, and some organic Greens and some Maca and help people eliminate suspect foods for a time. Before letting the outcome of the patient’s intervention with the doctor pass on the results of unreliable negative lab tests for Lyme, because of immune suppression until some treatment is started for awhile and then the test for Lyme often changes to positive. What a waste to not simply realize we are confronted with an epidemic of autoimmune diseases that has so many different presentations that over 100 conditions are now considered to be autoimmune related. These conditions deserve meaningful intervention and my F.I.G.H.T. program protects patients from Johnny One Note health care providers who focus only on one aspect of my program and thus only help a small percentage of patients.

Let’s broaden our approach and help everyone with empowering knowledge. Everyone we see today needs help to optimize every one of the categories in F.I.G.H.T. If we expand the FIGHT concept we would make F stand for FOCUS on positive thinking not just Food and H for hormones and Heavy metals and then really the G is not just Genetics but also the entire new field of Epigenetics where exposures to BISPHENOL A have led to overnight changes in Gene activation. They are permanent until treated with aggressive methylation support, as with the MSM and TMG found in BIOE’NR-G’Y C and the active forms of Folic Acid found in Beyond B12.

We all remember AIDS is acquired immune deficiency so now I recommend that this new epidemic just be renamed LOWERED IMMUNE METABOLIC ENCEPHALOPATHY SYNDROME or LIMES then we can start to be much more cost effective in improving the health of many who suffer without excess reliance on some lab test for Lyme related infections.

This link to MEDSCAPE may help broaden your knowledge regarding some aspects of this new epidemic. By putting LIMES category into a new AUTOIMMUNE RELATED condition it forces us to broaden our approach beyond antibiotics can help our patients who still will not be covered by insurance but at least they will not be turned away without receiving real help and we will not waste time with medical board fights. Patients will be taught something that I am confident for most will help them improve their health more than getting 6 months of IV antibiotics even if it were fully covered by their insurance company. It is not just an antibiotic deficiency we are encountering; read the book BEYOND ANTIBIOTICS!

It is like the old adage TEACH a man to fish or give him a fish; I prefer the teaching approach. Knowledge of what is really wrong with our health can be empowering but to put everything on one infection or one toxin and ignore leaky gut and food sensitivities, etc I feel  means we provide little long-term meaningful help to patients who deserve a broader understanding of what is really going wrong with their health.

Garry F. Gordon MD,DO,MD(H)
President, Gordon Research Institute
www.gordonresearch.com
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

A Case of Ascending Paralysis: the Signs and Symptoms of Tick Paralysis
Menyoli Malafa, MSII; Veronica Tucci, JD, MS IV; Albert Vincent, PhD; Sajeel Chowdhary, MD
Posted: 03/26/2009; American Academy of Emergency Medicine.
2009;16(1):22, 26, 27 © 2009 American Academy of Emergency Medicine
http://www.medscape.com/viewarticle/589591

Summary
Tick paralysis (TP), a response to the neurotoxic effects of the salivary secretions produced by attached hard ticks (Ixodidae), is a syndrome that mimics a large number of better known neurological disorders. TP is a sporadic, seasonal, rural disorder in which acute ataxia often develops five to six days following a history of walking in grass or low brush, followed by ascending flaccid paralysis. Recognition and timely removal of the tick usually leads to complete resolution of symptoms, whereas continued feeding can lead to respiratory arrest and death. Follow-up includes species determination and patient surveillance for tick-borne infectious disease.

Discussion
TP is a worldwide disease, occurring in Australia, Europe, South Africa and throughout North America. In the United States, most cases occur in the Rocky Mountain states and the Pacific Northwest, including Washington, Montana, Oregon, Idaho, Wyoming, Nevada, Utah, Colorado and the northern parts of Arizona, New Mexico and California. However, cases have also been reported in central, southern and eastern states, including Texas, Oklahoma, Mississippi, Florida, Georgia, North Carolina, South Carolina, Virginia, Washington, D.C., Pennsylvania and New York. In Canada, most cases are encountered in the western part of the country, primarily southern British Columbia.[1,2] More than 60 species of ticks are known to cause paralysis, but only a handful are responsible for most cases. In North America, the disease is associated primarily with six species: Dermacentor andersoni (‘Rocky Mountain wood tick’), D. variabilis (‘American dog tick’), Amblyomma americanum (‘Lone Star tick’), A. maculatum (Gulf Coast tick), Ixodes scapularis (formerly I. dammini, ‘Blacklegged tick’) and I. pacificus (‘Western Black-legged tick’). Peak incidence occurs between April and June when nymphs and mature adults abound in low vegetation and climb upward, questing for their next host by extending their anterior pairs of legs.[1,3,4] Paralysis is a response to a neurotoxin secreted by the salivary glands of the arachnid.[1,5] The biochemistry and pharmacology of the specific paralysis- inducing toxins produced in North American ticks are yet to be fully elucidated, but current evidence points to a mechanism by which the toxins inhibit presynaptic acetylcholine release at the neuromuscular junction.[1,3,6] TP presents more often and more severely in children, suggesting a concentration-dependent relationship between toxin levels and symptom expression.[1,4] Signs and symptoms of TP begin about five to six days after the parasite has attached, when neurotoxin is secreted at its peak levels. These prodromal symptoms include restlessness, irritability, fatigue, nausea, paresthesias and possibly ataxia. Over the next 24-48 hours, the patient develops ascending symmetrical flaccid paralysis and weakness in the lower extremities. Over the course of the next day or two, paralysis and weakness may ascend to involve the trunk, axial and upper limb muscles. Cranial nerves may also become involved in an ascending pattern, resulting in bulbar, facial and/or extraocular paralysis. Patients demonstrate diminished or absent deep tendon and superficial reflexes while, aside from occasional paresthesias, their sensory exam remains normal. Pain and fever are absent. Death ensues following paralysis of the respiratory muscles.[1,5,7,8,9] Atypical presentations reflect variations in the site of tick attachment. There may be ataxia and associated cerebellar deficits without accompanying muscle weakness. The disorder may also present as an isolated facial paralysis without trunk or limb involvement. Another group of atypical presentations is unilateral paralysis and/or weakness, including isolated unilateral facial paralysis.[1,8] Tick paralysis is treated by removal of the tick. Although the site of attachment is most often the head and neck region, the entire body should be scrutinized, including ear canals, nostrils and genitalia. Multiple ticks should be suspected, and all must be removed.[1,4,7,10] Applications of petroleum jelly, nail polish, alcohol, a needle and heat are inappropriate. These measures may result in infection and cause the parasite to salivate or regurgitate more of its bodily fluids.
The tick should be grasped with blunt, angled forceps as close as possible to the skin and to the embedded mouthparts (hypostome). Wearing protective gloves, slowly pull the organism straight outward with a gentle and steady traction, without twisting its body. Do not burst the tick. The hypostome is usually deeply and firmly embedded and should be removed surgically should it come detached. Antiseptic solution is then applied to the wound, and the recovered tick and severed mouthparts may be preserved in 75% ethanol for identification. The patient should be instructed to return in the event of additional illness and educated on protective measures against ticks.
The symptoms of TP, at least those caused by North American species, typically resolve rapidly following removal of all ticks from the patient. Improvement in the condition of the patient subsequent to tick removal is confirmatory for the diagnosis. Species found in some other parts of the world, notably Ixodes holocyclus of Australia, produce a very potent neurotoxin and symptoms may not subside as quickly, even worsening after removal.[5] The prognosis depends on clinical presentation prior to removal. If all ticks were removed prior to the onset of bulbar weakness, the patient often makes a full recovery within the first 24 hours. However, if onset of bulbar symptoms occurs during continued feeding, the likelihood of fatal respiratory paralysis increases to 10%. Therefore, prompt of diagnosis and tick removal are paramount.[1,5,7,8] Because ticks are both vectors and reservoirs for various infectious diseases, it is important to educate the patient about this added risk for possible concurrent illnesses. Table 1 displays the geographical location and infectious diseases associated with North American tick species which are also known to cause TP.[1,8,11,12]

References
1.Cunha BA, editor. Tickborne Infectious Diseases Diagnosis and Management. New York: M. Dekker; 2000.
2.Meier J, White J. Handbook of Clinical Toxicology of Animal Venoms and Poisons. STATE: CRC Press; 1995.
3.CDC. Tick paralysis – Washington. Morbidity and Mortality Weekly Report 1996; 45(16): 325-6.
4.Schmitt N, Bowmer EJ, Gregson JD. Tick paralysis in British Columbia. Can Med Assoc J 1969 Mar 1; 100(9): 417-21.
5.Meriggioli MN, Howard JF, Howard Jr. JF, Harper CM, Harper Jr. CM. Neuromuscular Junction Disorders: Diagnosis and Treatment. STATE: Informa Health Care; 2003.
6.Grattan-Smith PJ, Morris JG, Johnston HM, Yiannikas C, Malik R, Russel R, Ouvrier RA. Clinical and neurophysiological features of tick paralysis. Brain 1997 Nov;120(Pt 11):1975-87.
7.CDC. Tick paralysis – Colorado. Morbidity and Mortality Weekly Report 2006 Sep 1; 55(34): 933-5.
8.Knoop KJ, Stack LB, Storrow AB. Atlas of Emergency Medicine. STATE: McGraw-Hill Professional; 2002.
9.Biller J. Practical Neurology. STATE: Lippincott Williams and Wilkins; 2002.
10.Gammons M, Salam G. Tick removal. Am Fam Physician 2002 Aug 15; 66(4): 646.
11.Winn WC, Kineman EW, Allen SD, Janda WM, Schreckenberger PC,Procop GW, Woods GL. Koneman´s Color Atlas and Textbook of Diagnostic Microbiology. STATE: Lippincott Williams and Wilkins; 2005.
12.Sonenshine DE, Mather TN. Ecological Dynamics of Tick-borne Zoonoses. STATE: Oxford University Press US; 1994.
13.Greenberg BM. Clinical cases in neurology from John Hopkins. Case 2: acute ascending paralysis in a 4-year-old body. MedGenMed 2003 Apr 9; 5(2): 36.

 This paralleled greater Borreli a burden in
γδ-deficient mice as well as more cardiac inflammation. These findings
are consistent with a model of γδ T cells functioning to promote the
adaptive immune response during infection.

Excerpt:

CONCLUSIONS: We found that the time of the year, associated neurological
symptoms and mononuclear pleocytosis were strong predictive factors for
Lyme neuroborreliosis as a cause of peripheral facial palsy in an area
endemic for Borrelia.

Link: http://www.healthtalkandyou.com/uc-davis-finds-lyme-disease-bacteria-in-lymph-nodes/

Excerpt:

UC Davis Finds Lyme Disease Bacteria in Lymph Nodes
by Maejoy Tutor in Diseases on Jun 15, 2011 

One of the most significant and considered as threatening and rising diseases in US is the Lyme disease. The bacteria which causes this seems to be hiding particularly in lymph nodes. University of California Davis researchers have reported that this can trigger a considerable immune response, except that it is not too strong to defeat the infection.

Link: http://iai.asm.org/cgi/content/full/73/2/1014

Excerpt:

Our in vitro model of the human BBB mimics many of the important features of in vivo B. burgdorferi interactions with the BBB. Hence, this model should be an important tool for identifying the cellular and molecular elements implicated in B. burgdorferi interactions with the BMEC, as well as for helping characterize the biochemical mechanisms by which the bacteria cross the BBB.

Full aritcle: http://www.newhaven.edu/news-events/82773.pdf

Excerpt:

 Our results demonstrated that both herbal agents, but not doxycycline, had very significant effects on all forms of B. burgdorferi, especially when used in combination, suggesting that herbal agents could provide an effective therapeutic approach for Lyme disease patient. 

Lyme disease, the multi-system infection caused by the tick-borne
spirochaete Borrelia burgdorferi, can involve the nervous system, most
commonly causing, alone or in combination, lymphocytic meningitis or
abnormalities of cranial or peripheral nerves, the latter most typically
presenting as a painful radicular syndrome. Diagnosis is based on
appropriately used, standard serological tests; in instances where the
central nervous system is involved, cerebrospinal fluid assessment for
organism-specific antibodies can be useful. Treatment with any of several
standard regimens of oral or parenteral antimicrobials is highly effective.
Prolonged treatment beyond four weeks is rarely if ever warranted, and
carries significant risk.

Link: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21127770&retmode=ref&cmd=prlinks

Excerpt:

Results-Sensitivity and specificity of the in-clinic ELISA for detection of
heartworm antigen (99.2% and 100%, respectively), antibodies against B
burgdorferi (98.8% and 100%, respectively), and antibodies against E canis
(96.2% and 100%, respectively) were similar to results for a similar
commercial ELISA. In samples obtained from dogs in the northeast and upper
Midwest of the United States, sensitivity and specificity of the in-clinic
ELISA for antibodies against Anaplasma spp were 99.1% and 100%,
respectively, compared with results for an immunofluorescence assay. Samples
from 2 dogs experimentally infected with the NY18 strain of A
phagocytophilum were tested by use of the in-clinic ELISA, and antibodies
against A phagocytophilum were detected by 8 days after inoculation.
Antibodies against Anaplasma platys in experimentally infected dogs
cross-reacted with the A phagocytophilum analyte. Coinfections were
identified in several of the canine serum samples. 
Conclusions and Clinical Relevance-
The commercially available in-clinic ELISA could be used by veterinarians to
screen dogs for heartworm infection and for exposure to tick-borne
pathogens.

Excerpt:

 The epidemiology of vector-borne zoonotic diseases is determined by
encounter rates between vectors and hosts. Alterations to the behavior of
reservoir hosts caused by the infectious agent have the potential to
dramatically alter disease transmission and human risk. We examined the
effect of Borrelia burgdorferi, the etiological agent of Lyme disease, on
one of its most important reservoir hosts, the white-footed mouse,
Peromyscus leucopus. We mimic natural infections in mice using the vector
(Black-legged ticks, Ixodes scapularis) and examine the immunological and
behavioral responses of mouse hosts. Despite producing antibodies against B.
burgdorferi, infected mice did not have elevated white blood cells compared
with uninfected mice. In addition, infected and uninfected mice did not
differ in their wheel-running activity. Our results suggest that infection
with the spirochete B. burgdorferi has little impact on the field activity
of white-footed mice. Lyme disease transmission appears to be uncomplicated
by pathogen-altered behavior of this reservoir host.

Excerpt:

Antibiotic-refractory Lyme arthritis may result from Borrelia
burgdorferi-induced autoimmunity in affected joints. Such patients usually
have certain HLA-DRB1 molecules that bind an epitope of B. burgdorferi
outer-surface protein A (OspA), and cellular and humoral immune responses to
OspA are greater in patients with antibiotic-refractory arthritis than in
those with antibiotic-responsive arthritis. Recent work in a mouse model
suggests that, during B. burgdorferi infection, OspA in genetically
susceptible individuals stimulates a particularly strong T(H)1 response,
which may be one of several factors that can help set the stage for a
putative autoimmune response in affected joints. However, vaccination with
OspA did not induce arthritis in this mouse model, and case and control
comparisons in human vaccine trials did not show an increased frequency of
arthritis among OspA-vaccinated individuals.
Thus, a vaccine-induced immune response to OspA does not replicate the
sequence of events needed in the natural infection to induce
antibiotic-refractory Lyme arthritis.