By Erica Verrillo*
The terms chronic Lyme, Post-Treatment Lyme Disease Syndrome (PTLDS), Late-Stage Lyme, and neuroborreliosis have been used interchangeably, which has produced a great deal of confusion among patients, physicians, and researchers.
Lyme disease is considered chronic by Lyme-literate doctors if disease symptoms don’t disappear with treatment and instead persist long-term. Many patients with Lyme disease may be completely unaware that they have the illness. Symptoms such as headaches, joint pain, trouble concentrating, and fatigue are “non-specific.” That is, they are common to many illnesses, and because Lyme disease follows a relapsing-remitting pattern, symptoms can be written off as transient viral infections, or as “depression.”
However, the Centers for Diseases Control (CDC) and the Infectious Diseases Society of America (IDSA) contend that chronic Lyme disease doesn’t exist, and claim that when symptoms don’t resolve after a short course of antibiotics, then it is because the person has “Post-Treatment Lyme Disease Syndrome,” (PTLDS) – symptoms which are caused by damage to the immune system and the tissues as a result of short-term infection. Yet an abundance of clinical evidence and research shows that chronic Lyme does exist and that the presence of persistent symptoms following treatment is usually caused by ongoing infectious activity, in addition to damage to the tissues/organs and an ongoing inflammatory response. Therefore, Post-Treatment Lyme Disease Syndrome (PTLDS) is simply a term created by these government agencies, most likely to deny the existence, and hence treatment, of an expensive-to-treat epidemic disease.
PTLDS has also been disputed by physicians because the official position taken by the CDC is that a single two to four-week course of antibiotics is sufficient to clear Borrelia and co-infections. Because the CDC has adopted this position, it is also the position taken by most physicians and state agencies, but not Lyme-literate doctors.
Physicians who routinely treat Lyme disease take the contrasting view that symptoms remain because the original infections are still present (and because damage to the body has occurred). They cite several possible reasons why a short course of antibiotics does not resolve Lyme disease.
- Ticks carry many pathogens, which means Lyme disease patients are likely to have several ongoing co-infections, not all of which can be cleared using the same antibiotics or other treatments.
- Like its cousin, syphilis, the Borrelia spirochete has an affinity for nervous system and other organ tissue. Once the infection is established in tissue, it is more difficult to eradicate, especially if the patient has been ill and/or left untreated for a long period of time. The same is true for other Lyme disease infections.
- Borrelia and other infections are adept at hiding from both the immune system and from antibiotics and other treatments. In his review of persistent infection in Lyme disease, Keith Berndtson suggests that Borrelia survives antibiotic treatment by shifting into non-dividing or slowly dividing forms that retain viability “and possibly infectiousness.” He cites evidence of recalcitrant chronic relapsing infection in animal hosts to support this theory.
- A short course of antibiotics is not 100% effective for any infection. The propensity for bacteria to develop resistant strains is well established in medical literature, but even when an antibiotic is considered effective, there is ample proof that some bacteria will survive treatment. For example, Streptococcus bacteria, the infection that causes “strep” throat, can remain in the host weeks after appropriate treatment.
Chronic Lyme disease takes its toll on patients in ways that extend beyond its myriad symptoms. A survey conducted by lymedisease.org in 2014 found that quality of life was poorer for patients with chronic Lyme disease than for those with congestive heart failure, fibromyalgia, depression, and asthma. Over 3,000 patients were polled for the survey.
The survey showed that patients with chronic Lyme disease have high disability and unemployment rates. “Over forty percent of patients with chronic Lyme disease reported that they currently are unable to work because of Lyme disease and 24% of patients report that they have received disability at some point during their illness. This compares with 6% of the US population who are unable to work due to illness.”
Neuroborreliosis refers specifically to the infection of nervous system tissue by Borrelia and co-infections. Many patients with Lyme disease develop pronounced neurological symptoms. These symptoms are due to inflammation in either the peripheral nervous system, the lining of the brain (meninges), and/or the brain itself. Pathology reports from patients have found bacterial infiltration in the dorsal root ganglia along the spine, nerve roots, and in the gray matter of the brain and spinal cord.
Contrary to popular belief, neuroborreliosis can appear early in the disease. According to a review conducted by Fallon et al. (2009), symptoms of neurological involvement can occur one to four weeks after the initial infection. In an experiment performed on rats in 1990, Borrelia burgdorferi were able to induce blood-brain barrier permeability after only 12 hours.
The most common symptoms of neuroborreliosis include: pain radiating from the affected nerve root (radicular pain), numbness, light sensitivity (due to dorsal root ganglia inflammation), fatigue, insomnia, confusion, headaches, cognitive impairments, depression, memory loss and paresthesias (unusual sensations on the skin). In severe cases, patients may experience Bell’s palsy (paralysis on one side of the face), difficulty speaking, stroke-like symptoms, and seizures. In elderly patients, neuroborreliosis can be mistaken for dementia, or Alzheimer’s disease, resulting in a progressive state of neurodegeneration that, sadly, could have been prevented with an accurate diagnosis.
Neuroborreliosis is notoriously difficult to treat, in part because Borrelia burgdorferi can transform into a cyst form that can lie dormant for long periods of time. In this dormant state it can infect the brain, producing inflammation and apoptosis while remaining remarkably resistant to treatment. Researchers have found cystic forms in neuronal cultures after only one week of exposure to Borrelia burgdorferi.
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Late Stage Lyme Disease
The progression of Lyme disease is often broken down into stages:
Stage 1 is called early localized Lyme disease. The infection has not yet spread throughout the body.
Stage 2 is called early disseminated Lyme disease. The bacteria have begun to spread throughout the body.
Stage 3 is called late disseminated Lyme disease. The bacteria have spread throughout the body.
In Late Stage Lyme disease, symptoms can present in a bewildering array. Because the bacteria have spread throughout the body, the immune system releases pro-inflammatory cytokines wherever there is soft tissue – the joints, skin, vascular system, organs, and brain. Pain can be felt in any of these organs (except the brain; headaches are the result of inflammation in the tissue surrounding the brain). Joints and skin may become visibly inflamed, and a host of neurological, gastro-intestinal, cardiac, and neuropsychiatric symptoms (e.g. hallucinations, panic attacks, mood swings) may appear.
It is important to keep in mind that although Stage 3 is referred to as “late stage” Lyme disease, the designation does not imply that it takes years, or even months for the bacteria to spread throughout the body. The Lyme spirochete begins to infect the body as soon as it passes through the saliva of the tick and into the host’s bloodstream. It can produce symptoms within days, or it can lie dormant for months, even years. How quickly it reaches stage 3 is completely dependent on the host’s ability to control the spread of the infection and where the bacteria lodge.
Alan G. Barbour and Stanley F. Hayes. Biology of Borrelia Species.‘Microbiological Reviews’Dec. 1986, p. 381-400. Vol. 50, No. 4. Copyright X3 1986, American Society for Microbiology.
Keith Berndtson. Review of evidence for immune evasion and persistent infection in Lyme disease. Int J Gen Med. 2013; 6: 291-306. Published online 2013 Apr 23. doi: “10.2147/IJGM.S44114.” PMCID: PMC363697.
Brian A. Fallon, Elizabeth S. Levin, Pernilla J. Schweitzer, David Hardesty. Inflammation and central nervous system Lyme disease. Neurobiol Dis. 2010 Mar;37(3):534-41. doi: 10.1016/j.nbd.2009.11.016. Epub 2009 Nov 26. http://www.lymenet.de/literatur/Fallon_Inflammation-and-central-nervous-system-Lyme-disease_2009.pdf.
Garcia-Monco JC, Villar BF, Alen JC, Benach JL. Borrelia burgdorferi in the central nervous system: experimental and clinical evidence for early invasion.J Infect Dis.1990 Jun;161(6):1187-93.
P. Hildenbrand, D.E. Craven, R. Jones, and P. Nemeskal. Lyme Neuroborreliosis: Manifestations of a Rapidly Emerging Zoonosis. AJNR June 2009 30: 1079-1087.http://www.ajnr.org/content/30/6/1079.full
Johnson, L., Wilcox, S., Mankoff, J. and Stricker, RB (2014) Severity of Chronic Lyme Disease Compared to Other Chronic Conditions: A Quality of Life Survey. PeerJ, DOI. 10.7717/peerj.322
MacDonald AB. Alzheimer’s disease Braak Stage progressions: reexamined and redefined as Borrelia infection transmission through neural circuits. Med Hypotheses.2007;68(5):1059-64. Epub 2006 Nov.
Judith Miklossy, Sandor Kasas, Anne D Zurn, Sherman McCall, Sheng Yu, and Patrick L McGeer. Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosis. J Neuroinflammation. 2008; 5: 40. Published online 2008 Sep 25. doi: 10.1186/1742-2094-5-40.PMCID: PMC2564911.
Judith Miklossy. Chronic or Late Lyme Neuroborreliosis: Analysis of Evidence Compared to Chronic or Late Neurosyphilis . Open Neurol J. 2012; 6: 146-157. Published online 2012 Dec 28. doi: 10.2174/1874205X01206010146.PMCID: PMC3551238.
Geeta Ramesh, Juan T. Borda, Jason Dufour, Deepak Kaushal, Ramesh Ramamoorthy, Andrew A. Lackner, and Mario T. Philipp. Interaction of the Lyme Disease Spirochete Borrelia burgdorferi with Brain Parenchyma Elicits Inflammatory Mediators from Glial Cells as Well as Glial and Neuronal Apoptosis. Am J Pathol. 2008 Nov; 173(5): 1415-1427. doi: 10.2353/ajpath.2008.080483.PMCID: PMC257013.
Geeta Ramesh, Lenay Santana-Gould, Fiona M Inglis, John D England, and Mario T Philipp. The Lyme disease spirochete Borrelia burgdorferi induces inflammation and apoptosis in cells from dorsal root ganglia. J Neuroinflammation. 2013; 10: 88. Published online 2013 Jul 18. doi: 10.1186/1742-2094-10-88.PMCID: PMC3721987.
Last Updated: 8/18/15
* Erica Verrillo is ProHealth’s expert editor for the ME/CFS HealthWatch and Natural Wellness newsletters. She is the author of Chronic Fatigue Syndrome: A Treatment Guide, 2nd Edition, available as an electronic book on Amazon,Barnes & Noble, Kobo and Payhip (PDF file). Her website,CFSTreatmentGuide.com, provides practical resources for patients with ME/CFS. She also writes a blog, Onward Through the Fog, with up-to-date news and information about the illness, as well as the full text of CFS: A Treatment Guide, 1st Edition (available in translation).
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