What is Lyme Disease
Lyme Disease is the most common tick borne infection in British Columbia and the most common disease transmitted by insects in Canada. Recent estimates by the CDC show that current statistics on Lyme Disease do not include the unknown number of people who are infected but who are not adequately diagnosed and treated. Lyme disease British Columbia is a fast growing epidemic that can be treated by a Lyme literate doctor.
Even when Lyme is treated early and appropriately with standard doses of antibiotics, these infections often produce chronic symptoms and disease that can affect almost any organ of the body, from the brain to the skin.
In a prospective study by Johns Hopkins, 35% of patients who were treated with standard antibiotics in early Lyme Disease had new or persistent symptoms 6 months after completing treatment. Those with symptoms had developed significant impairment in life function, making it clear that Lyme Disease is an important cause of chronic illness.
Lyme is transmitted by ticks that live on deer, yet these ticks are also carried on a wide variety of other small animals. The tick is so small, sometimes as small as a poppy seed, and many are not even aware that they were bit by a tick and may never develop a rash at the site of the tick bite.
When To Suspect Lyme Disease in BC
Lyme Disease should be considered in any person with unexplained:
- Fever or muscle pain
- Acute unexplained changes in emotional or cognitive function
- Anyone given a diagnosis of autoimmune or degenerative neurological disease
Signs and Symptoms of Lyme Disease in BC
Common Signs and Symptoms of Lyme Disease :
- Cardiac arrhythmias
- Skin rashes
- Enlarged lymph nodes
- Muscle weakness or paralysis
- Numbness or tingling
- Mood disorders
- Impaired memory or concentration
- GI complaints
Misdiagnosis of Lyme Disease
Lyme Disease is a great imitator and is often misdiagnosed or can be associated with:
- Fibromyalgia/chronic Fatigue Syndrome (over 50% of patients diagnosed with one of these conditions actually has Lyme Disease)
- Rheumatoid arthritis (can be triggered by Lyme Disease, but once properly treated, symptoms can be drastically reduced)
- Crohn’s disease
- Multiple sclerosis
- Positional Orthostatic Tachycardia Syndrome or neurally mediated hypotension
Borrelia Has Many Different Species
Most cases of Lyme Disease are triggered by Borrelia burgdorferi, however, many ticks carry numerous microbes in addition to Borrelia. This makes Lyme Disease one of the most complex multi-layered infectious diseases. Borrelia can exist as a variety of species in addition to Borrelia burgdoferi including:
- Borrelia garini
- Borrelia afzelii
- Borellia hermseii
- Borrelia miyamotoi
Standard blood tests only look for the Borrelia burgdorferi strain, which is why many tests fail to identify Lyme Disease in patients with antibodies to the other Borrelia species.
Lyme Disease and Co-infections
Co-infections are common as deer ticks often carry other bacteria and parasites that cause very distinct patterns of illness and suppress immunity including:
- Anaplasma or Erlichiosis (will often see elevated liver enzymes and sedimentation rates, low WBC and platelets; treated with doxycycline)
- Bartonella (also known to cause Cat Scratch Fever, it invades blood vessels and can raise inflammatory blood vessel markers; enlarged lymph nodes, pain, and fever are also common)
- Babesia (an intra-cellular parasite that will not respond to antibiotics; chills, sweats, fever, anemia, memory lapses, disorientation)
People with Lyme Disease plus a co-infections are often sicker and less responsive to treatments than those infected with Borrelia only. Often, blood tests for Lyme Disease will fail to detect the presence of co-infections and Lyme Disease treatments will often fail to treat these co-infections.
Testing For Lyme Disease
A negative blood test does not rule out Lyme Disease or a co-infection. Most lab tests depend on measuring antibody levels in the blood. People who receive antibiotics very early after becoming infected or who are exposed to steroid medications or severe stress may fail to develop antibodies. Some are genetically unable to develop a normal antibody response to Borellia. There is also great variability in test results among the different laboratories.
Lyme Disease Diagnosis
The CDC and IDSA agree that the diagnosis of Lyme Disease is a clinical diagnosis based on:
- Signs or symptoms compatible with Lyme Disease
- The likelihood of exposure to deer ticks
It is important to note that deer ticks are NOT carried by deer alone. White footed mice may also be responsible for most transmission to humans, and this makes it a possibility for Lyme to be acquired in an urban environment, not just in wooded or grassy areas.
Lyme Disease can also be transmitted at any time of the year, not just in the summer as previously thought.
The Two Faces of Chronic Lyme Disease
The first face is someone with a previously undiagnosed, chronically ill and have untreated late stage Borrelia infection. Often, these patients have been diagnosed as autism, fibromyalgia, different autoimmune disorders, MS, arthristis, and neuropathies.
The other face is recurrent or relapsing chronic illness following antibiotic therapy after Lyme treatment. This stage may occur after treatment of early or late stage Lyme disease. Many patients in late stage Lyme disease relapse after stopping antibiotic treatment.
Causes of Chronic Lyme-related Illness
- Bacterial persistence
- Autoimmunity and reactive inflammation – Often, reactions occur to bacterial debris left in tissue or to damaged cells and the formation of autoantibodies results, which provokes an inflammatory response. Peripheral, central, and autonomic neuropathies often result from damage.
- Antibiotic induced side effects and illnesses
- Neural sensitization and pain syndromes
- Psychosocial fall out – Lyme induced chronic illness places a huge strain on relationships, work, and home life and depression is often a side effect of being chronically ill.
Bacterial persistence is when the bacteria find ways to survive, which is a major problem in the treatment of chronic Lyme Disease. There are several different mechanisms for this persistence.
- Inappropriate dosing of antibiotics. For this reason, there is no one established antibiotic protocol for each patient. Different strains respond differently to a variety of antibiotics and doctors must be wiling to change up their treatment plans if they are not working.
- Intracellular translocation and acidification. Borrelia typically starts out as an extracellular pathogen but it can move inside the cells and hide in cell compartments called vacuoles, and these become acidic. When the cell is acidic, antibiotics cannot penetrate the cell to kill the Borrelia inside. Plaquenil (Hydrochloroquine) is used to prevent the acidification of the intracellular area, which enables antibiotics to penetrate the cell and ultimately kill the Borrelia.
- Formation of persister organisms. These can occur spontaneously amongst many species, and are slow growing cells which are not killed by most antibiotics. They may provoke an ineffective but symptom producing immune response because they hide themselves in vacuoles. Their presence may be increased by prolonged use of antibiotics. Most bacteriocidal antibiotics work because they damage the biochemical mechanics of the pathogen and getting the pathogen to produce its own free radicals, which causes self destruction. Persister cells do not do this in response to antibiotics, but they are very susceptible to antibiotics in the presence of oxygen.
Maintaining adequate levels of oxygen to the tissues becomes highly important in the treatment of chronic Lyme in conjunction with antibiotics and antimicrobial herbs. Cyst formations are likely live bacteria persister cells that can be killed by “cyst busters” such as Metronidazole (Flagyl), Tinidazole (Tindamax), Plaquenil (Hydrochloroquine), Rifampin/rifabutin and Grapefruit seed extract.
Other treatment strategies include improving oxygenation and micro-circulation with oxidative therapies such as hyperbaric oxygen, ozone, and artemisinin, in conjunction with antibiotics. Proteolytic enzymes can help to improve circulation by breaking up the tiny blood clots in the tissues which occur as a result of infection and inflammation This phenomenon can be measured in the blood by thrombin, anti-thrombin complexes, pro-thrombin fragments.
- Biofilm formation. Biofilms are present throughout the body and act as a protective shield for pathogens. Biofilms may be disrupted by azithromycin, rifampin, proteolytic enzymes, cat’s claw, Otoba bark, and garlic.
Babesia is an intracellular parasite, which lives in RBC and is similar to Malaria. Acute symptoms include chills, sweats, fatigue, muscle pain, breakdown of red blood cells, shortness of breath, mental confusion, and anemia. Common medications used to treat Babesia include Azithromycin with Atovaquone (Mepron), or Atovaquone with Proguanil (Malarone), or Arthmether with Lumafantrine (CoArtem). Atovaquone works by inhibiting CoEnzyme Q10 synthesis within the pathogen and requires fat for absorption, such as fish oil.
- Anti-malarial herbs such as Artemisia annua and Cryptoleptis sanguinolenta. Artemisinin is a potent pro-oxidant and its actions are enhanced by fish oil but inhibited by Vitamin E. Caution with concurrent anti-oxidants use should be considered.
Bartonella is an intracellular pathogen commonly known to cause Cat Scratch Fever and Trench Fever. There is no classic Bartonella pattern but it may cause fatigue, neuropathic pain of the hand, foot, or ribs, mood swings, and red/purple streaks on the skin. Bartonella relapses are common because antibiotics that have been studied to work in tests tubes may fail inside cells. The most common medications used to treat Bartonella include Co-trimoxazole (Bactrim), Quinolones (Ciprofloxacin, Levofloxacin), Tetracyclines, and Rifampin. Rifabutin is a Rifampin derivative and is the only medication shown to be effective against Bartonella inside the cells. It becomes highly concentrated inside cells and can have positive effects when paired with other agents. Rifabutin (150 mg twice per day) can by paired with Co-trimoxazole (Bactrim) and Fluconazole to help maintain high Rifabutin levels.
Reversing Lyme Induced Autoimmunity
- Hydroxychloroquine is an immune modulatior that potentiates anti-inflammatory and antibiotic effects of macrolides and tetracyclines.
- It is important to restore normal adrenal function, which are important endocrine gland that helps to control inflammation
- Proteolytic enzymes may breakdown immune complexes that are provoking inflammatory reactions
- IVIg can improve patients with neuropathies
- Nutritional gluten free, casein free diet, essential fatty acids
The Lyme Gut Connection
Lyme Disease can infect the GI tract and can often present with irritable bowel disease-like symptoms such as chronic constipation, known as Bell’s Palsy of the gut, which is probably a neuropathic constipation. Lyme can cause autonomic neuropathies with symptoms such as impaired gastric emptying (or gastroparesis), impaired gut motility, and a range of GI related complaints. Patients can be falsely diagnosed with conditions like Chron’s Disease because of ileitis (inflammation of the ileum which is common in Chron’s) and many clinicians find the only way to resolve these conditions is with Lyme treatment.
Side Effects of Antibiotics
- Bacterial dysbiosis can cause diarrhea, Clostridium difficile colitis. Saccharomyces boulardii and probiotics may help.
- Yeast or fungal overgrowth can cause fatigue and brain fog. A low carbohydrate, low sugar diet with anti-fungal herbs and probiotics can help treat.
- Mitochondrial damage can occur with antibiotic therapy because our mitochondrial origin is actually bacterial, which is known as the endosymbiont theory. Bactericidal antibiotic cause mitochondria to generate reactive oxygen species that damage mitochondrial membranes and function. Antioxidant may help to prevent this but can compromise the efficacy of antibiotic therapy. NAC may be the best option as it was shown to not interfere with the antibiotic actions while offering mitochondrial protection. Those with genetic or acquired predisposition are more susceptible to mitochondrial damage. By correcting nutrient deficiencies and addressing heavy metal toxicity, mitochondrial damage can likely be limited.
Complex changes in the brain may cause normal sensory signals to be felt as pain. Chronic Lyme disease often causes this neural sensitization. Common medications used to help with this include membrane stabilization drugs like anti-depressants and pain medications such as gabapentin. Behavioral therapies that involve amygdala or limbic system retraining can be helpful. Nutrients such as B12, methyl folate can enhance methylation and help pain signaling. Low dose naltrexone can increase endorphins to modulate the pain response and lipid exchange (via IV or oral phosphatidylcholine) may stabilize nerve membranes.