Thursday, May 24, 2018

Lyme arthritis and reactive T cells

A friend told me that a new mouse study gave us the answer regarding Lyme arthritis. 
Not quite.  The study was done at the University of Utah (U of U) in mice.  Mice with Lyme arthritis had severe inflammation with thickened synovium. Low levels of spirochetes, referred to as residual bacteria were usually found in the joints. The pathology and immunology revealed the basis for the inflammation was abnormal T cells. This has been described in the past. 
The germ response immune system has two primary legs:  Killer T Cells vs antibodies (behaving badly).  Most autoimmune diseases -- based on current knowledge are due to antibody responses. 
The first leg, the T cell leg is referred to as the innate immune system.  The antibody side -- connected with B cells comprises the acquired immune responses.  
This is the simplest and easiest way to understand the dichotomy.
Patients may go to rheumatologists and report they have fully tested, they don’t have any autoimmune diseases. Rheumatologist only test for things like rheumatoid factor, CCP antibodies, ANA antibodies and a host of other antibodies. Antibodies which attack our healthy tissues. Not poorly acting T cells.  Commercially available tests only measure autoimmune antibodies. 
There likely exist numerous autoimmune disorders for which there is no available test. The rheumatologist should say that based on currently available tests there is no evidence of an autoimmune disease. 
Lyme arthritis is autoimmune without antibodies.  We know the immune system frequently struggles to make Lyme antibodies, explaining some negative tests in Lyme infected individuals.  
There is no test, especially one that would be agreed upon.
The autoimmune, inflammatory reactions were associated with a small number of residual Lyme bacteria.   Small numbers of spirochetes, stubborn and hard to eradicate may cause a lot of inflammation as we have long suspected. 
There are two belief systems here.
One can choose to believe that the T cell response is part of a self-perpetuating process irrespective of residual or germ. In this case, powerful immune suppressing drugs and/or surgical removing of the synovium, the joint lining is the way to go. Not my opinion.
I have found that long term antibiotics, including IV antibiotics work for most patients. 
This is the rub:  Lyme bacteria are the oxygen which feed the fire – the inflammatory T cell medicated response.  Take away the oxygen and the fire goes out -- the joints improve. 
Lyme is in Utah.
Of course, people (most people,) are not mice. You cannot necessarily generalize mice data to people.

Of course in the film “A hitchhiker’s guide to the galaxy” (spoiler) we ultimately learn that white mice run the world and we humans are the guinea pig test subjects. 
You never know.

Tuesday, May 8, 2018

Lyme: my new and improved approach to patient care.

I am excited about my new approach to patient care. 
The EPCDS concept (exhaustion/fatigue, pain and cognitive dysfunction/brain fog has led to a change in philosophy and approach.  
A patient has criteria for CFS, fibromyalgia, POTS, MCAS, Lyme and coinfections. These issues have arisen in the treatment of several patients over the past 2 days. 
First, I address fatigue. (Treating symptoms is not applying a bandaid.  When symptoms improve function improves. When function improves the immune system and other systems work better, facilitating the healing process. These patients are beyond fatigue and exhaustion; getting out of bed is a struggle.  I first look at sleep. I review meds. Many meds contribute to sleep problems and may exacerbate POTS and MCAS.  BP meds can be a problem.  A patient I saw today is taking a BP med Cozaar. Without getting into pharmacology, in some cases Cozaar may contribute to fatigue and exacerbate POTS.  Inderal, a beta blocker taken to prevent migraines may be similarly problematic. Another patient seen today with POTS is taking Abilify for bipolar 2. This med can cause orthostatic hypotension/POTS.  Other options are preferred.  Meds are a problem frequently and must be carefully reviewed. 
Sleep is horrible for these patients. Sleep is fragmented and unrefreshing.  My last patient today falls asleep in front of the TV in the living room at 3 am; wakes up at 6 am to let the dog out; and, it is only then that she goes her bed/bedroom to sleep for another 3 hours. She is nonfunctional without stimulants. Not surprising.  We always have to go back to sleep hygiene and help patients make changes if possible. Changing behavior is not easy. CBT (cognitive behavioral therapy) may help.  Perhaps we fix sleep and the patient will still be exhausted. That’s OK we have still made an important inroad.  There are various medications which may help patient sleep.  I have found that patients with chronic insomnia may only respond to cocktails of meds.  Specific drugs might be considered in each patient.  For example, the sedating muscle relaxer Flexeril has been shown to help patients with tinnitus and may also help fibromyalgia pain. The med may not be tolerated because of a hangover the next day; adjustments can be made.  Patient may only sleep with: Restoril, doxepin, gabapentin and possibly others.  Restoril may help with anxiety. Doxepin may help with mast cell activation. Gabapentin may help with central pain and neuropathic pain.  
We can frequently kill 2 birds with one stone. Sleep, sleep per chance to dream.  When patient report dreams it tells me that REM sleep is present which in some cases is not apparent on sleep studies. Fatigue can certainly be treated with drugs of promote wakefulness like Nuvigil.  Stimulants like Adderall may help.  These drugs are also nootropics and may help improve cognitive dysfunction.  Sleep doctors do not understand the intricacies of such complex patients. 
Pain.  We need to figure out what kind of pain.  The pain may be nociceptive or neuropathic.  The pain may be central.  The pain may be poorly understood as is the case with migraines.  Various pain types are treated differently.  Treating pain and treating sleep may dovetail with each other.  Nociceptive pain, physical pain, is frequently associated with central sensitization – pain amplification.  Patients may have allodynia.  Mild touch causes pain.  These patients do not have a low threshold for pain.  Their pain threshold has been modulated by changes in the central nervous system. An understanding helps the patient and the doctor.   Namenda blocks glutamine and may be effective for fibromyalgia – amplified pain and migraine. Specific drugs target specific types of pain.  Pain drugs can exacerbate or act as a nootropic and relieve brain fog, for example Namenda.  Antidepressant such as amitriptyline and possibly Cymbalta along with anticonvulsants like Neurontin may be helpful.  Other agents such as low-dose naltrexone and medical marijuana are sometimes helpful.  Etc.  Pain is a huge topic and there is much we can do. Unfortunately, many “pain doctors” just hand out prescriptions of Oxys and do their patients a disservice. 
Brain fog I have already touched on.  Treating the underlying illness is important. Still, there are things we can do.  The nootropics, brain drugs mentioned above may be helpful.  Others, for example, magnesium thionate may improve cognition.  Cognitive dysfunction in a young person is something we have to jump on. If neuroborreliosis is the cause intravenous antibiotics may be necessary. In this case, treating the underlying cause takes precedent over managing symptoms. POTS and MCAS can be associated with brain fog and need immediate treatment. We can start MCAS therapy with dietary change and H1, H2 blockers. We may need to prioritize POTS which can be truly disabling. (If MCAS is causing anaphylaxis etc. priorities change). We can juggle many balls if needed. In most cases POTS can be managed well and the treatment is discussed elsewhere.  The treatment of MCAS is discussed elsewhere. Cognitive dysfunction must be carefully evaluated.  If a patient has prominent night sweats, air hunger, bouts of tearfulness and depression babesiosis becomes the first priority. Etc. 
Treatment of chronic infection is addressed from the outset.  However, priorities must be established.  For example, doxycycline alone may be prescribed while sleep and pain and POTS are addressed. Every case is different. 
There is something to be learned from (the best) doctors who treat:  chronic fatigue syndrome, POTS, chronic pain and others. 
What is different in my approach?  I focus on symptoms and function. Patients do much better.  Other specialists may be consulted to cover the bases but sleep specialist, pain specialists and neurologist may not be particularly interested in the care of such patients and label them with: depression – go to the psychiatrist, fibromyalgia – not much can be done or psychosomatic.  The post is intended to give the reader a flavor of the approach and only scratches the surface. These disorders are extremely complex. A lot of thinking and figuring things out is required.

Many disorders may be associated with EPCDS: thyroid disease, adrenal dysfunction, metabolic disorders, genetic disorders, other autoimmune syndromes, cancer, depression, pernicious anemia - B12 deficiency, celiac disease, renal disease, liver disease, heart disease, other chronic infection, sarcoidosis and others. I am sure there are many more. This list is from the top of my head.   The EPCDS syndrome is common. Let's not make assumptions and do our best not to miss anything. 

The information discussed here is evidence based and discussed in peer reviewed journals.

Appointments available. Paradigm Medicine, Rockville MD.


Tuesday, May 1, 2018

What is POTS? Corecting the record.

What is really going on with POTS?  Is it a neurological disorder, a cardiac disorder?
Probably neither, the answer may lie within the purview of endocrinology?
There is a genetic component. This is clear. For example, patients with hypermobile joints are more likely to develop POTS.
Nobody knows what causes POTS.  Apparently 10 different theories have been proposed.  It is not due to direct dysfunction of sympathetic and parasympathetic nerves.  It is not due to nerve damage such as what you might find in diabetic autonomic neuropathy. 
Autonomic neuropathy should not be confused with dysautonomia.  The two are quite different. 
The prevailing explanation, according to a recent review, primarily relates POTS to dysfunction of the RAS.  This stands for renin angiotensin system.  Receptors for angiotensin may be off kilter. Angiotensin is messenger molecule or hormone known to be associated with the regulation of blood pressure, constriction of blood vessels and retention of salt and water.  This what I remember from physiology.  It turns out that Angiotensin and its associated receptors have wide reaches effects in a wide array of organs and organ systems– including the cardiovascular and nervous systems. 
So, POTS is an endocrine disorder which may or may not be associated with genetic factors.  It has overlap with other specialties including neurology and cardiology.  
Drugs currently prescribed, including Fludrocortisone, DDAVP and Midodrine directly counter aberrant physiology associated with the disorder as viewed through this lens.

Thursday, April 19, 2018

Lyme and the mixing of world views

EPCDS and Lyme:  an evolving paradigm
I have been tossing the idea around in my head.  A Different spin, a new way of thinking, a new acronym. People like acronyms. Exhaustion, Pain, Cognitive Dysfunction Syndrome. These symptoms are the common threads, the bare bones of chronic illness known by different names, depending on your perspective.  I am writing this to introduce the topic, not discuss it in detail. 
What’s in a name?  A universe of thought. Some thinker, group of thinkers, doctors and scientists etc. have looked at a bunch of symptoms and arrived at a name. Many of the names and acronyms are familiar to us all. FMS for fibromyalgia syndrome. CFS for chronic fatigue syndrome. CLD for chronic Lyme disease or PTLDS post treatment Lyme disease. POTS for postural orthostatic tachycardia syndrome. Newer acronyms have popped up like MCAS for mast cell activation disorder. 
What these diagnoses and others (without acronym) have in common is that they swirl around EPCDS.  Exhaustion, pain and cognitive dysfunction or brain fog.  
They are all described in medical literature and associated with contemporary notions of evidence-based or science-based medicine.  In each case it looks like advocates of a particular approach think are onto a theory of everything (TOE). Like the unifying field theory that Einstein and others have failed to find in physics. 
Specialists all have blinders on. And – specialists tend to know a lot about their field of interest and read their journals but not the literature from other specialties which are reinventing the same wheel with a different twist. 
Exhaustion. Let’s start here. Fatigue isn’t adequate. In fact, I don’t know a word in the English language which is adequate.  Patients can’t get of bed. Moving a finger, lifting an arm can be a challenge.  Taking a shower an impossibility.  Nobody really understands this, the “pathophysiology.”
A rheumatologist sees fibromyalgia. They see it as a functional illness (whatever that means).  A CFS specialists, perhaps a neurologist sees SEID, systemic exertion intolerance syndrome, something likely post-viral. A sleep specialist may see idiopathic hypersomnia, a sleep disorder similar to narcolepsy. Idiopathic is a big doctor word that means unknown cause (or the doctor’s an idiot and the patient is pathological). A cardiologist, endocrinologist or other POTS specialists may see an impaired autonomic nervous system or dysautonomia.  Perhaps HPA dysfunction (adrenal fatigue) will be stressed. A pain specialist may hone in on central sensitization, alteration in pain-brain pathways as the cause. Those so inclined may always diagnose MCAS, mast cell activation. A Lyme specialist may be convinced that germs are the cause. Others doctors may focus on: genetic issues, poor DNA methylation; toxins; oxidative stress/mitochondrial dysfunction; disruption of the microbiome; autoimmune disease; systemic inflammation; nutritional issues including gluten sensitivity; chemical imbalances within the brain and others. 
Doctors are mostly hammers in search of nails, patients with EPCDS, for example. 
We could repeat the discussion for pain and cognitive dysfunction. The discussions would be very involved, but the same names would likely come up.  This is an introduction to the topic- a preview. 
So far, nothing new. Its not about new; it’s about thinking differently.
Sleep. Let’s back up a step. Disordered sleep is a common denominator. Patients have trouble falling asleep, can’t stay asleep, sleep is fragmented and sleep is unrefreshing.  Time and again I am astonished that such patients have seen scores of specialists and never had a sleep study.  Let’s turn our attention to the sleep specialists. Patients may have narcolepsy. Patients may have abnormal “sleep architecture.”  Most commonly there is a deficit of deep sleep.  Patients may have unexpected sleep apnea – perhaps central sleep apnea.  It is not enough to know Lyme and coinfections. A good Lyme doctor should understand a polysomnogram and MSLT.  Sleep is something we can address.  Therapies for fibromyalgia, dysautonomia, Lyme disease, coinfections and others may completely overlook this.  The notion that the sleep will improve when we fix the Lyme disease is --- well, wrong. Improve function and other things, like a dysregulated immune system or HPA axis may start to heal. Perhaps Lyme was the blow that knocked down the dominoes. While treating Lyme you also try to pick up as many dominoes as possible along the way. We might be able to address fatigue with drugs like Nuvigil or Adderall, at least a start. 
That’s it.
The idea is that a doctor should be a “holistic” Western practitioner at the least. Fuse things together. Read the literature: yes it takes a lot of time. Know a lot about the various specialties and how they think and try to make connections and draw things together.  We should not automatically cut out a specialty because they “don’t believe in Lyme.” That is their problem. Let’s not make it ours. They all have something to offer. Some more than others. 
There is another big plus. The approach gives us a bridge. A common language. When we talk about a dysregulated microbiome, hypersomnia, autonomic neuropathy etc. we are using words that make sense to many colleagues. When we talk to the same highly intelligent colleagues about: Borrelia burgdorferi sensu-stricto, pleomorphic round forms, biofilms, Babesia duncani, anaplasmosis, tickborne bartonellosis and rickettsiosis and Herxheimer reactions we are speaking Greek – gobbled gook.  But this is an aside.
The approach works and has helped many of my patients. 
As a stated. I am introducing the topic. A full discussion would take many pages, if not a book.
What do you think?

I am available for consultations in my Rockville Maryland office.
301 528 7111

Tuesday, April 10, 2018

Lyme, Babesia, MCAS, FMS, CFS, disordered sleep and PTSD.

A 39-year-old female sought my attention some years ago.  She has a history of PTSD.  She was sexually abused as a small child by numerous close family relatives.  She came to see me for the treatment of Lyme disease.
Many don’t understand PTSD.  It is a specific syndrome with characteristic features:  flashbacks and nightmares.  Time is different for those with PTSD.  Another patient, a former special ops soldier watched a buddy shot gruesomely a few feet away.  With flashbacks it happened 10 minutes ago, not 20 years ago. The flashbacks and nightmares are surreally vivid.  The colors, sounds, smells, adrenalin, fear, sweat and blood are real and now.  PTSD survivors do not trust.  They feel disconnected and depersonalized.  Forming bonds and establishing relationships is difficult at best.

The patient I am discussing ( her PTSD) improved a lot with 14 years of intense therapy.  She is still treated with EMDR and other therapies.

She has always lived in Frederick County Maryland, a Lyme hot spot.  She recalls a lot of tick bites over many years. She never had an EM (bull’s eye) rash and has no recollection of acute symptoms associated with a particular tick bite.  Her chief complaints included FATIGUE, COGNITIVE DYSFUNCTION/BRAIN FOG, POOR SLEEP, ANXIETY and PAIN.  Her pain was diffuse involving small, medium and large joints, upper and lower extremities.

She felt like she was always walking through fog.  She was distractible and confused.  Simple tasks were onerous.  She was in bed for 12-14 hours but slept only 5.  Sleep was not refreshing. She experienced regular night sweats and bouts of air hunger.  She experienced irritability and mood swings with episodes of random tearfulness. She experienced weird dizziness, difficult to explain – but she felt like her head was disconnected from the rest of her. She experienced numbness and tingling and bouts of weakness. She had a boatload of other symptoms, circling most symptoms on my symptom inventory form.
She previously worked as a special ed teacher but had been on leave for several years.  A previous doctor had diagnosed Lyme 3 years before and treated her with supplements, IV Myer’s cocktails and low doses of pulsed antibiotics:  such and such MWF, something else TuTh and something else one weekends with off weeks over the course of a month. This treatment went on for over a year.  She never got better and was referred to me.

Something key in her history proved very helpful.  She admitted to frequent episodes of flushing and itching. She had dermatographia: when you scratch her skin the color changes from white to red and stays red.  She also suffered with orthostatic intolerance.  When she stood up she felt like she had to sit down again after a few minutes.

Physical exam remarkable for paired tender spots associated with fibromyalgia, decreased sensation lower extremities peripheral neuropathy pattern and facial flushing and dermatographia (writing on her back legible 40 min later). Lyme Western Blot from Stony Brook:  IgM 18,41,64,93. A sleep study showed absent stage 3-4 sleep with alpha wave intrusion. A brain SPECT showed decreased perfusion diffusely.
The main diagnoses were:  Lyme, Babesia, MCAS, FMS, CFS, disordered sleep and PTSD.

One of the turning points of therapy was treating mast cell activation. Different drugs were best for different people. Yesterday a patient responded miraculously to Claritin. For this patient ketotifen has been key.  Klonopin, a benzodiazepine has been very effective.  Mast cells have benzodiazepine (BZD) receptors and BZDs and similar like Ambien may be very helpful.  As with other patients she has not responded well to typical antidepressants like Cymbalta. (SSRI/SNRI antidepressants are prescribed without thought and patients are usually not informed that getting off these drugs is frequently fraught with severe withdrawal symptoms).
We went to IV antibiotics for quickly and she responded very well to several months of Rocephin and others.   Babesia was treated with high doses of several agents and improved after many months.

MCAS treatment was as described in other posts. She also did well with cannabis. She obtained CBD which helped pain and anxiety tremendously.  (Cannabinoids are MCAS stabilizers). THC also helped with pain and sleep.  
Sleep is key for most patients.  Many need multiple agents. (Doxepin, Ambien, Neurontin, others).
She certainly has chronic fatigue syndrome.  Antibiotics quashed cognitive dysfunction and helped to significantly reduce pain.  She was able to get 9 hours of decent sleep.  She was still tired. The sleep study showed typical problems of disordered sleep “architecture.”  Without deep sleep, and this has been studied in college students, everyone develops chronic fatigue (syndrome).  A sleep specialist might use the term hypersomnolence or narcolepsy-like. It’s the same thing.  Drugs like Nuvigil and Adderall were/are indispensable for improving quality of life. 
She has the criteria for fibromyalgia. She has the tender spots. Pain doctors now call this central sensitization.  What you call it depends on your perspective bias.
CFS vs Fibromyalgia vs MCAS vs central sensitization vs hypersomnolence vs chronic Lyme disease etc. Perhaps it is important to listen to each camp since they may have something to offer.  The syndrome names are used above descriptively. FMS is used when discussing tender spots and pain and CFS is used when discussing fatigue. 

Luckily her pain level went from 9 to 3 with antibiotics and MCAS therapy.   Neuropathy also improved. 
Here are a few key points:  NSAIDS don’t usually work; antidepressants may help or make things worse – norepinephrine effect is needed, low doses of older TCA and antidepressants like Elavil may be effective without awful side effects; anticonvulsants, especially Neurontin may or may not work; cannabinoids, mostly CBD with some THC can be very effective.
PTSD is a very serious disorder and specialized care – not run of the mill mental health care is required. 
After more than a year with me:
She works full time -- sleeps OK, has no brain fog, fatigue is managed, MCAS is controlled and pain is managed.  She has a good quality of life and smiles a lot.

Wednesday, April 4, 2018

Deconstructing the Herxheimer (and Lyme toxins)

It is common knowledge that many patients feel much worse for a time when they start treating Lyme disease.  This temporary worsening of symptoms is known as Herxheimer reaction or simply Herx.  Commonly the reaction is attributed to “toxins” and it is commonly held that treatment which removes toxins – detox, alleviates symptoms. 

Critics of this reasoning say it is a lot of hogwash. What toxins? There are no toxins. Bacterial endotoxins occur with gram negative bacteria not spirochetes. And detoxing? Complete mumbo-jumbo. 

Let's take a look.
There is a lot of stuff we don’t know. A great thing about science is we are always learning new stuff. 
We know that Herxheimer reactions are modulated by cytokines – the traffic cops that direct a very busy immune system hither and thither.
Its true. Lyme spirochetes do not process traditional endotoxins. Classic bacterial endotoxins are comprised of lipopolysaccharides (LPS). I have read this critique many times.  Lyme bacteria have something else: membrane derived lipoproteins. These molecules are not endotoxins but may be equally problematic.  Killed spirochetes spill these molecules into the circulation. These molecules wildly overstimulate usual immune responses leading to unbridled production of inflammatory cytokines. This is called a cytokine storm. 
A Herxheimer reaction, a well described scientific phenomenon, is caused by a cytokine storm. Unregulated cytokines cause chaos within a usually well-ordered machine.  There is a yin-yang balance within immune responses to kill germs. Some inflammation is necessary but this must be balanced against greater forces that diminish inflammation.  In a cytokine storm inflammation is unchecked.  Effector mechanisms (ways the immune system kills germs), T cell responses, B cell responses and complement activation become poorly regulated.  Germs are being killed but tissues cannot tolerate the excess inflammation. 
Inflammation is in part modulated by such molecules as histamine, leukotrienes, prostaglandins, enzymes and others, in part due to excess mast cell activation. This is something that can be limited with medical management. Cellular debris accumulates in the face of destroyed tissues, blood vessels and immune cells. Oxidative stress and mitochondrial dysfunction lead to an accumulation of intracellular toxins. Tissue damage may be associated with a build up of lactic acid. Macro toxins in excess, those eliminated by kidneys and liver may tax the system.
Let’s get to “detoxing.”  Two things are commonly recommended:  Lemon water and Alka-Seltzer Gold.  A gazillion patients have told me it works.  The first question is: what do lemon juice and Alka-Seltzer Gold have in common?  Citric acid. Citric acid has established anti-inflammatory properties. A recent study reported citric acid decreased the production of inflammatory cytokines: tumor necrosis factor, interleukins and cyclooxygenase (promotes prostaglandins) in LPS stimulated macrophages. The next question is why only Alka-Seltzer Gold? The main difference is aspirin. Regular Alka-Seltzer contains  aspirin, sodium bicarbonate and citric acid. The “Gold” version substitutes aspirin with potassium bicarbonate.  What’s wrong with aspirin? Isn’t it an anti-inflammatory? The answer is not always. Aspirin has different properties from other NSAIDS.  Peer reviewed studies have shown that in the presence of bacterial antigens aspirin has proinflammatory effects.  Sodium bicarbonate is best known as baking soda. It is also an antacid. Studies show that athletes who consume sodium bicarb  prior to intense exercise have improved performance. Our cells function best in the buffered blood pH of 7.4, slightly alkaline.  As in the case of Herxheimer responses, the athlete's tissues run out of available oxygen and Lactic acid accumulates. The blood become slightly acidic and metabolic functions suffer. Baking soda partially restores pH (acid-base) balance. Cellular metabolic dysfunction improves. 
How about those Epsom salt baths?  I have read various explanations and none make sense. It’s supposed to be about the magnesium which has healing powers. Its been scientifically shown that magnesium from Epson salts can’t get through the dermal barrier – the skin and therefore into tissues.  That’s not it.  Maybe it’s just the bath?  Hot water. Heat. Heat dilates blood vessels. Heat is well known to have healing properties. That is how saunas work. The process facilitates egress of inflammatory wastes from injured tissues. So, it’s just the water. The magnesium is for show – or is it?  When you mix molecules, they interact.  Magnesium sulfate “Epsom salts” is a salt.  Salt crystals have a particular physical characteristic. They hold on to heat.  Epsom soaks have a higher average temperature and stay warmer for longer than tap water baths.   
There are other detox strategies many of which seem helpful.  There is always a mechanism, an explanation, even if we do not yet know it.

Glutathione is the master antioxidant and help mollify oxidative stress and cellular dysfunction.  The problem is that oral forms are ineffective. Patients with IVs do great with IV GTH.  Other available forms, sublingual sprays and nasal spray (may require prescription) can be helpful. 

In my experience, and largely unknown, mast cell approaches can be very helpful for managing Herx responses -- in some patients. 

Monday, April 2, 2018

Is Lyme sexually transmitted?

The CDC says absolutely not. Research shows it does not occur in animal models. It turns out humans, at least most of us, aren’t rodents. Admittedly I have not studied rat copulation but on its face the anatomy and physiology are different.  The amount of body fluid exchanged, the presence of a large mucous membrane, methods and time are different for starters. Observations have been made that Lyme spirochetes have been recovered from human female genital secretion and to a lesser extent male. This is not a surprise since male seminal fluid contains natural antibiotic substances.  The paper in 2014 states the same strains of Lyme were found in both sexual partners. The findings are interesting but not proof. Alternate explanations are feasible: husband and wife did the same activities and were exposed to the same ticks. Retrospective data may be unreliable. We don't know if spirochetes in genital secretions are alive, dead or viable. When passed from a tick spirochetes are wrapped in a protective protein and secreted below the outer epidermis; we don't know if such steps are necessary for transmission. On the other hand, it is clear that vertical transmission occurs: a pregnant mother can clearly transmit Lyme to her unborn child. 
The CDC claims that epidemiology does not support the notion of sexual transmission. I don’t think we have data to support that claim.  Most Lyme infected individuals are asymptomatic and most symptomatic Lyme patients are misdiagnosed. Lyme is slippery and not easy to track like STDs with known calling cards – like gonorrhea. We really don’t know how many Americans are infected with Lyme. There are other STDs that have been missed because of their subtly, like HPV. It took decades for doctors to realize that the majority of the sexually active population is infected since the only manifestation in most cases is cervical cancer. The epidemiology argument does not hold water for now. 
We are left with considerations of biological plausibility. The argument is made that Lyme is like syphilis.  Lyme is a vector borne zoonosis. It resides in host animals and is occasionally passed to humans by specific ticks; the humans become accidental hosts.  It is different from syphilis which is solely sexually transmitted. The two come from different family trees: one is from the genus Borrelia and the other Treponema. Biologically they are different. The two pathogens evolved along very different lines.  After all, syphilis is not transmitted by ticks but humans are the only host of syphilis; this argument is weak. We have to consider other biological specificity. Malaria is transmitted by only one species of mosquito and plague by a specific rate flea. Well – this applies to vector specificity. We know there is Lyme vector specificity. This doesn’t prove anything. The question is: Is it biologically plausible for a vector borne organism to be spread by some other means, such as physical or sexual contact? The answer is maybe. Pathogens adapt. For example, the bubonic plague transmitted only by rat fleas evolved. It became the pneumonic plague transmitted by a cough. 
There are Lyme cases that are difficult to explain without conjuring the hypothesis of sexual transmission. In my practice these seem rare. Two recent patients tested positive for Lyme, one male and one female. One is a city apartment dweller who never goes outside. Her husband is an outdoorsman. The other lives in Colorado, a Lyme free zone and never ventures into the great outdoors. He became ill after an encounter with a female partner who resides in the East Coast. Interestingly, the female was suffering with a flulike illness at the time of the encounter. It is tempting to latch on to data from the 2014 study. I am not there yet. 
I tell my patients not to panic. Sexual transmission if it does occur may be rare. I think.  We don’t really know: is Lyme like hepatitis B – sexually transmitted or hepatitis C – rarely sexually transmitted? 
I think it is irresponsible to categorically stake out a position on this issue. The first order of business is an intelligent proportional, science-based discussion. Perhaps this doesn’t help patients who want a clear yes or no. Perhaps other interested parties who will happily meet that need.  Not me. 
Patients ask: are you a Lyme literate doctor. I answer: that is not important. The question is, are you a Lyme literate patient?  It seems very few things Lyme are black or white. If you don't like dealing with murky shades of gray you picked the wrong disease. 
It is important for us to acknowledge that which we know and that which we do not.