The other day a patient a seemingly simple question: "Doctor, why is my case of Lyme disease so mild." Perhaps the answer to this question can lead us down the path of understanding Lyme disease.
The standard(LLMD)paradigms would suggest that the Lyme disease syndrome is the product of a multi-pathogen state. The co-infections, including Bartonella and Babesia are additional tick borne pathogens which contribute to the character and severity of the illness. But is this right? Perhaps not. What I have seen in very ill patients, consistently, is the presence of other, to date unrecognized "germs," swimming in the blood of such patients, undeterred- in the face of large and prolonged courses of antibiotics. Some of these organisms for example look like Toxoplasmosis. The existence of "Toxo like organisms" has been touched on in medical literature. Others are small gram negative bacteria which resemble Bartonella but are not Bartonella. In fact such "mystery bacteria" resembles hundreds of other bacteria which might stain in the same way. There exists a plethora of bacteria which share a similar morphology; for now, these are unknowns. Are these blood organisms seen in Lyme patients really tick borne pathogens?. Perhaps not. I propose that these anomalous bugs are pre-existing endogenous organisms, normally contained by the host immune system- prior to the onset of the illness- until the genie is let out of the bag.
Before chronic Lyme, or post-Lyme as some like to call it there was chronic fatigue syndrome. CFS became CFIDS: chronic fatigue and immunodeficiency syndrome. It has been pointed out by numerous observers that the two syndromes have much in common. The CDC has defined criteria for the syndrome. It usually starts after a "flu like illness." It has a new onset: it is not lifelong. It is associated with fatigue not relieved with rest. It is associated with: impaired memory or concentration, unrefreshing sleep, muscle pain, joint pain, headaches, sore throat and tender lymph nodes. Many other symptoms may occur as well. It is characterized by impaired immune responses. It is understood to be a "multi-system" disease. Its cause is not understood and it has a poor prognosis. Does this sound familiar?
Let us shift gears to chronic Toxoplasmosis. The seroprevalence of Toxoplasmosis is incredibly high. Most of the world's population is colonized by this parasite and they are ostensibly asymptomatic. It is thought that the "normal" immune system keeps it in check. Numerous symptoms may be associated with chronic Toxo. These include: fever, malaise, swollen lymph glands, eye symptoms and more. In immunocompromised patients, including the population with AIDS, symptoms include: fever, chills, skin rash, brain symptoms, heart and lung symptoms, confusion, headache, tremor, muscle weakness and more.
The existence of immunosuppression is one hall mark of Lyme disease or what is now called tick borne disease. I have repeatedly spoken of the "opportunistic" nature of co-infections. Evidence of immune compromise is regularly seen seen in patient lab studies. Many patients have low white blood cell counts with low neutrophils and increased lymphocytes. Patients may have low levels of natural killer T cells per the CD57 test. Patients have alterations in vitamin D suggesting a shift in helper cell Th1 and Th2 responses. These patients have a compromised immune system. This compromise is specific and limited. It does not lead to the full blown immunological defects seen in certain inherited disorders or acquired disorders like AIDS. It appears this subtlety has made it difficult for skeptics to appreciates its very existence.
Whereas some point to the Lyme spirochete as the culprit which initiates the cascade leading to immune dysfunction, other advocates point to CPN, Mycoplasma, yeast and other agents as the inciting cause. The disease may go by many names including CFIDS and fibromyalgia.
There are common threads. These chronically ill patients suffer with varying degrees of immunosuppression. The syndromes and their attendant symptoms overlap. Previously innocuous germs perhaps become interwoven into the fabric of a systemic, multi-system disease process. These germs may include: CPN, Mycoplasmas, Toxo like organisms, gram negative bacteria- or Bartonella like organisms if you like, yet unspecified "others" and perhaps a host of viruses including EBV, CMV and HHV6. In many cases the Lyme germ, Borrelia burdorferi may also be an innocent bystander, until something tips the immunological balance in favor of the disease process.
There may be an interplay behind the germs and other environmental factors. Certainly non-infectious proteins such as gluten can trigger abnormal immunological responses. Host factors such as exposure to toxins and stress may very well play an important role in some cases.
But this cannot be the whole story. Per the title of this piece, we are dealing with not only immune suppression, but immune dysregulation. Patients with this disease syndrome suffer with immune consequences impacting both sides of the immunological continuum. We have immunosuppression. On the flip side there is immune system over-activation, leading to the myriad of complex autoimmune responses which complicate the course of the illness more often than not.
Lyme and related organisms have clearly been implicated in a wide host of autoimmune syndromes ranging from inflammatory arthritis to MS and CIDP.
The spirochete dysregulates the immune system at both ends of the spectrum simultaneously- a nasty trick. It creates an environment ideal for opportunistic pathogens while at the same time it contributes to the destruction of erstwhile healthy tissues via an autoimmune process.
Perhaps chronic Lyme disease, fibromyalgia, CFIDS and other related disorders could potentially be combined into a new rubric, forming the foundation of an entirely new class of medical disease.
To get back to the patient's question: why are some people ill while others are not? The answer comes down to an understanding how a complex array of variables interact. As always these include genetic and environmental factors. The end result is seen in each patient's unique clinical syndrome.