The Story of the Little Critter That Causes Big Problems!
No one is immune to the everyday villain that often goes unnoticed to the human eye. This annoying bacterial spirochete, Borellia bourgdoferi (Bb), masquerades as a sly mini vampire who first invades the blacklegged tick (Ixodes scapularis) in order to enter into your bloodstream. Although we may blame the tick, who hungrily scopes us out when we aren’t looking, waiting to feast on our blood, the real issue is when the tick regurgitates his infested saliva back into us that the real horror show begins. The dubious properties of this “Mini-Me” version of terror has allowed it the opportunity to star in its own documentary and earns it place as the number one bacteria responsible for Lyme disease (LD).
According to the Center of Disease Control and Prevention (CDC), “Lyme disease is the most commonly reported vectorborne illness in the United States. In 2013, it was the fifth most common Nationally Notifiable disease.”1
The CDC reports that the disease is not nationwide and is concentrated most heavily in the northeast and upper Midwest with 95% of confirmed cases of Lyme disease isolated to 14 states in 2013 (CT, DE, ME, MD, MA, MI, NH, NJ, NY, PA, RI, VT, VI, and WI). 2
The Non-Lonely Traveler
In recent years, cases of Lyme disease have been popping up in the Northwest, Florida, Georgia, and California.3-5 Furthermore, Bb tends to enjoy companies in his travel. Various other tick-borne pathogens in certain regions can further complicate the picture of diagnosing LD. According to the International Journal of Medical Sciences the following pathogens are also being reported “Anaplasma phagocytophilum, the cause of human granulocytic anaplasmosis, Ehrlichia chaffeensis, the cause of human monocytic ehrlichiosis, Babesia microti, the primary cause of human babesiosis in the U.S., and Rickettsia spp.”3
The CDC offers a more comprehensive list of diseases that result from the various pathogens that ticks carry, including anaplasmosis, babesiosis, Borrelia miyamotoi infection, Colorado tick fever, ehrilichiosis, Heartland virus, Lyme disease, Powassan disease, Rickettsia parkeri rickettsisosis, Rocky Mountatin spotted fever (RMSF), STARI (Southern tick-associated rash illness), Tickborne relapsing fever (TBRF), Tularemia, and 364D rickettsiosis.6
Furthermore, co-infections can complicate matters and intensify symptoms.6-9 This means that a single tick could be infected with more than one microbe. These co-infections include Lyme borreliosis, anaplasmosis, babesiosis, and B. miyamotoi infection.
According to Clinical Microbiology Reviews:
The prevalence of dually infected Ixodes ticks appears highest among ticks from regions of North America and Europe where LD is endemic, with reported prevalences of ?28%. In North America and Europe, the majority of tick-borne coinfections occur among humans with diagnosed LD. Humans coinfected with LD and babesiosis appear to have more intense, prolonged symptoms than those with LD alone.9
The estimate of people with LD for 2013 was based on three ongoing studies by the CDC. These projects consisted of referencing medical claims of 22 million insured people annually for six years, a survey of laboratory confirmations, and a self-reported survey of Lyme disease cases.
Although more than 30,000 LD cases were reported to the CDC, earning its place as the most reported tick-borne disease illness in the United States, the newer estimates suggest that the total number of people diagnosed are more likely 10 times higher.
“We know that routine surveillance only gives us part of the picture, and that the true number of illnesses is much greater,” said Paul Mead, M.D., M.P.H, chief of epidemiology and surveillance for CDC’s Lyme disease program. “This new preliminary estimate confirms that Lyme disease is a tremendous public health problem in the United States, and clearly highlights the urgent need for prevention.”10
Symptoms of Lyme disease can include fever, headache, fatigue, and a characteristic bulls-eye-skin rash called erythema migrans.11 The stealth bug can produce a wide array of symptoms due to its ability to evade the immune response through various mechanisms. Therefore, symptoms of LD can manifest differently depending on a person’s unique biochemistry and certain characteristics of the spirochete, and whether a co-infection is present. To further complicate matters, oftentimes symptoms are confused with other illnesses, resulting in a misdiagnosis.12-15 If left untreated, infection can spread to joints (Lyme arthritis), the heart (Lyme carditis), and the nervous system (Lyme radiculoneuritis or mononueritis multiplex, Lyme cranial neuritis, Lyme meningitis, Lyme encephalopathy, and Lyme neuropathies).16
The History Lyme Disease
Just how did the discovery of Lyme come about? In congruence with the stealthy mechanism of the Lyme tick, it being the causative agent for the disease was only discovered when a group of rheumatoid arthritis cases appeared among children in Lyme, Connecticut and two neighboring towns in 1970. When it was determined that most of the children with arthritis lived and played near wooded areas and had symptoms during the height of tick season (summer), the attention was drawn to deer ticks. Researchers began referring to this condition as Lyme in the mid-1970s to help physicians diagnosis the cases. Around the same time, Dr. Wilhelm Burgdorfer was studying Rocky Mountain spotted fever with Jorge Nenach, trying to determine the cause of more than 100 spotted fever cases in NY from 1971-1976.
In 1978, Dr. Burgdorfer was on sabbatical in Switzerland doing research and noticed movement between the cells and tissue of six ticks he dissected. He realized that this movement came from larvae developing into a parasite found in deer.17-18 When none of the American dog ticks studied had helped resolve their mystery of Rocky Mountain Spotted fever, Dr. Burgdorfer suggested they try studying a new tick vector, the deer tick.
The NIH reports:
“Within hours of spotting and confirming the presence of spirochetes in the deer ticks, Dr. Burgdorfer dissected the remaining 124 ticks and found 75 with spirochetes. He cautiously wondered if he had found the cause of both the European skin disorder—erythema migrans—and Lyme disease. After notifying Dr. Benach and receiving serum from recovering Lyme disease patients, Dr. Burgdorfer and his colleagues found antibodies in the patient serum that reacted to spirochetes they had found in the deer ticks.”
It wasn’t until 1981 that NIAID researchers at Rocky Mountain Laboratories (RML) in Hamilton, Montana assisted Dr. Burgdorfer and identified the cause of Lyme disease and discovered the connection between the deer tick and the disease.18 That’s quite a span of time from when the first cases of rheumatoid arthritis appeared in the children in CT.
Now, let’s take a look at suggested testing methods used for Lyme disease. Currently, the CDC recommends a two-tier process for confirming LD, as evidence of antibodies against the Lyme disease bacteria in blood.19
First, the EIA (enzyme immunoassay) or rarely, an IFA (indirect immunofluorescence assay) is used. If negative, no further testing is recommended. With a positive or indeterminate (sometimes called “equivocal”) result, a test called an immunoblot test, commonly known as a “Western blot,” is indicated. Positive results are only confirmed if the EIA/IFA and the immunoblot are both positive.
The CDC recommends that if the Western immunoblot is used during the first four weeks of disease onset (early LD) using both immunoglobulin M (IgM) and immunoglobulin G (IgG) procedures. False positives for IgM test results can occur with those greater than one month of illness, so it is recommended that the IgM only be used acutely.
According to the CDC’s MMWR Weekly (Morbidity and Mortality Weekly Report), those who test negative for Lyme but have suspected early infection can then be further assessed using paired acute- and convalescent-phase serum samples:
“It was recommended that an IgM immunoblot be considered positive if two of the following three bands are present: 24 kDa (OspC) * , 39 kDa (BmpA), and 41 kDa (Fla) (1). It was further recommended that IgG immunoblot be considered positive if five of the following 10 bands are present: 18 kDa, 21 kDa (OspC)*, 28 kDa, 30 kDa, 39 kDa (BmpA), 41 kDa (Fla), 45 kDa, 58 kDa (not GroEL), 66 kDa, and 93 kDa (2).”20
Standard of care may also include a polymerase chain reaction (PCR) to test for bacterial DNA in fluid drawn from an infected joint in those with chronic Lyme arthritis or for those with persistent infection in the cerebrospinal fluid and who have nervous system symptoms.21
Controversy Heats Up
Up until this point, I have been giving you the facts based mostly confirmed in conventional treatment for LD. However, there is much controversy around various topics in LD, including:
- Chronic Lyme Disease
- Methods of Treatment
Borrelia burgdorferi (Bb) is a sneaky critter that has adapted well to surviving and persisting in its host, despite a strong antibody response.22-23 It has long been known to be capable of forming aggregates and colonies. In vitro studies have determined that these aggregate formations can change related to a hostile environment by this pathogen. One study tested these aggregates to determine if Bb formed biofilms, which would contribute to their immune evasion. The researchers tested for several features of a biofilm (including substrate matrices and secretion of protective extracellular polymeric substance (EPS) matrix). They concluded, “…we have found substantial evidence that Borrelia burgdorferi is capable of forming biofilm in vitro. Biofilm formation by Borrelia species might play an important role in their survival in diverse environmental conditions by providing refuge to individual cells.”23
Even more interesting, it seems that the clinical manifestations of LD may vary related to differences in pathogenicity of certain Bb strain characteristics.24-26 The plamid-borne, highly polymorphic outer surface protein (ospC) and the 16S-23S rRNA intergenic spacer (IGS) are the most commonly measured, but certain restriction fragment length polymorphisms in these genetic markers may be factors that account for the pathogenicity of LD. 24
These facts would seem to support that individuals with different genetic variations and immune robustness will respond differently to an infection with the spirochete. Still, the Infectious Disease Society of America (IDSA) does not believe in chronic Lyme and typically will not treat a Lyme patient beyond acute management. On the other hand, the International Lyme and Associated Diseases Society (ILADS) group does believe that Lyme can and often persists beyond a few weeks, and are willing to treat someone beyond the four-week period. These two groups represent the schism in LD and differ in treatment.27
According to Interdisciplinary Perspectives on Infectious Disease, the evidence for chronic Lyme Disease (CLD) is robust, 28-35 and recognizing it could facilitate efforts to avoid diagnostic delays of two years and durations of illness 4.7-9 years:
Despite the above documented evidence, the 2006 Infectious Diseases Society of America (IDSA) LD treatment guideline panel questioned the existence of CLD . The IDSA panel concluded, “Considerable confusion and controversy exist over the frequency and cause of this process and even over its existence” . The IDSA panel referred to chronic manifestations of LD as Post-Lyme disease syndrome (PLDS), PTLD and CLD. There are shortcomings for each term. The PLDS nomenclature implies that an active LD has been successfully treated, that any remaining symptoms are merely harmless vestiges of previous illness, and that the patient has been cured. The term PTLD merely implies that LD has been treated with antibiotics for 10 to 30 days. The CLD nomenclature implies that chronic manifestations of LD are present with or without evidence of active infection that cannot be reasonably explained by another illness. 28
Testing Part II
The controversy on testing for Lyme with integrative health care practitioners versus conventional diagnostics exists for a variety of reasons.36-40 According to ILADS, the CDC surveillance criteria for Lyme disease were devised in order to track a narrow band of cases for epidemiologic purposes and states the ELISA screening is unreliable. The CDC states that the 65% sensitivity statistic is unreliable due to the fact that negative testing can occur because of individuals who receive antibiotics and do not develop a robust antibody response or testing too early.36
The ILADs also reports:
Of patients with acute culture-proven Lyme disease, 20–30% remain seronegative on serial western blot sampling. Antibody titers also appear to decline over time; thus while the western blot may remain positive for months, it may not always be sensitive enough to detect chronic infection with the Lyme spirochete. For “epidemiological purposes” the CDC eliminated from the western blot analysis the reading of bands 31 and 34. These bands are so specific to Borrelia Burgdorferi that they were chosen for vaccine development. Since a vaccine for Lyme disease is currently unavailable, however, a positive 31 or 34 band is highly indicative of Borrelia Burgdorferi exposure. Yet these bands are not reported in commercial Lyme tests. 36
Various specialty tests have been used by integrative doctors that are more liberal in reporting of antibodies to the spirochete36 due to the fact that the various differences exist among those with a chronic immune trigger. Furthermore, it has been shown that Bb can take on various forms – cystic, intracellular, and extracellular.41-44
A newer assay of an in vitro diagnostic test for Bb antigens is based on the detection of antigen-specific effector/memory T cells that respond to stimulation by Bb antigens. This test accounts for the fact that an infection includes both the B cell and T cell response. This test measures frequency of antigen-specific T-cells for Lyme antigens. The result is based on measurement of interferon gamma (IFN- ?) secreted by T cells in response to stimulation by the B. burgdorferi antigens DbpA, OspC, p100, and VlsE-1.38-39
Other tests include PCR testing, FISH, and various Lyme cytokines.41-44 Conventional labs can also indicate a chronic infection such as anemias (especially with Babesia co-infections), high ferritin and CRP as markers of inflammation, and various markers of immune deregulation such as complement testing and CD50 count. However, these tests are not specific for LD.
Support for LD
Lifestyle factors such as optimizing sleep,45 reducing stress, decreasing toxic exposures (especially mold),46-47 and modulating immune balance are paramount for LD sufferers. Due to the morphological shifts of spirochetes and the co-infections, symptoms can wax and wane and the use of various combinations of botanical and prescription antimicrobials that are cycled related to the changing shapes of Bb have been used by experts in LD treatment, such as wormwood (Artemisia annua), 48-49 bearberry (Berberis vulgaris)50-51 and grapefruit.
Supplements specific for LD’s current symptoms, such as neurological or cardiac, should also be utilized. Furthermore, the impact of the microbiome cannot be underestimated. Dietary support with plenty of whole foods and fiber should be incorporated along with probiotics for gastrointestinal health.
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