Lyme Disease – a personal overview

NB This blog is not finished and represents my personal view.  If it interests you, keep any eye out for additions.

I want to say, right at the start, that any negative comments I make about diagnosis and treatment do not, in the main, apply to me:  I owe my relatively improved health to my excellent GP and his Infectious Disease specialist colleague at my local hospital – when I was living in the Highlands of Scotland.

The second thing I want to say is that there is a lot of bad science, even misinformation, out there.  There are charlatans too.  I am not an expert, I am a victim.  If you have an interest in Lyme Disease, I recommend you look at one of the well-known specialist charities, like Lyme Disease Action.  If you are in the UK, or Europe, the Deutsche Borreliose-Gesellschaft guidelines are worth reading.  See them here

INTRODUCTION

I was diagnosed with Lyme Borreliosis (a.k.a. Lyme Disease, LB or LD) in July 2011.  When I started this, in April 2013, I was not fully recovered and still under treatment. At the time of this update (May 2016) I am no longer under treatment and substantially recovered, but I do not know if I am cured.

LD is a bacterial infection transmitted (mostly) by the bite of an infected tick.  I say ‘mostly’ because, like many features of LD, there is uncertainty (if not full blown disagreement) about whether the Borrelia pathogen can be transmitted in other ways (more on this later).  About the only thing on which there is consensus around the world is that, if diagnosed early enough, LD is curable by a course of antibiotics and that, if not diagnosed early, it can invade the brain and central nervous system leading to permanent disability and, possibly, premature death.  There is disagreement about how early is early enough: it can develop very quickly into a multi-systemic illness that can be hard to treat, never mind cure.  It can mimic many other recognized diseases, like Parkinson’s, Alzheimer’s and Multiple Sclerosis to name only 3.  If you are familiar with the effects of these diseases you will have some inkling of how devastatingly life-changing LD can be.

DIAGNOSIS – First Room in the Hall of Mirrors

Clearly then the really critical thing, for a good outcome, is getting an early diagnosis.  Welcome to the first room in the Hall of Mirrors: for many LD victims, getting a diagnosis of any kind is a challenge.  First of all, assuming the mode of transmission WAS an infected tick, you may not know you were bitten. I had a ‘fastened on’ tick in March 2011 (too early in the year according to ‘the rules’). I became noticeably unwell, with very odd symptoms, in early May 2011.  The symptoms were so bizarre that I began a daily diary.  As a direct result of this evidence, and my general awareness of the potential for Lyme Disease where I lived, I was able to persuade my GP to carry out tests and I was diagnosed in July 2011.  Without that diary I may never have been tested at all, even in Scotland, but recording such detail is a double-edged sword: one doctor thought I was neurotic to be keeping a diary.  In hindsight (while my memory still worked!) I recalled a ‘flu-like’ spring cold – another symptom of early Lyme but, being a “mucus trooper”, had shrugged it off at the time.

Even the nymphal stage of the most common tick Ixodes Ricinus (there are several others) can carry infection; the nymphs can be the size of this fullstop (.) but nearly translucent.  You may only see it if it bites you in a visible place, or when it has started to swell with your blood, or after the bite site has begun to get inflamed. Incorrect removal of the tick may result in giving yourself an infection that you might otherwise have avoided (more on this later).  Similar to the organism that causes Syphilis, the effective agent of the Borrelia pathogen is a spirochete, spiral-shaped: it travels in your blood to any part of the body where it, almost literally, ‘drills’ into your tissues.

The annual number of new cases of LD, in the UK, is disputed.  The official statistics exclude anything directly diagnosed by a doctor, that is to say clinically, without a laboratory test.  Of course what is also excluded from the statistics is the unknowable number of cases that go undiagnosed or misdiagnosed.  Even if the informed, but unofficial, estimates of 3000+ UK cases are correct, many doctors will never have seen a case, ever.  What is not disputed is that the rise in cases, year-on-year, is faster than those of HIV/AIDS which has a much higher public profile.  Recently (since 2015) there has been a change in the official perception of LD as an emerging disease, and the challenges to diagnosis and reatment it presents, but opening the minds of, and offering training to, GPs is slow.

It is, therefore, still highly unlikely that any UK doctor will treat for LD following a tick bite without symptoms present.  If you are infected you have 30%+ chance of NOT developing a signature rash, the so-called ‘bullseye’ Erythema Migrans.  Note the word  ‘migrans‘ – spreading.  If it appears, it may not be at the site of the bite, or it can disappear to reappear somewhere else.  If it appears it might be a few days to several weeks after the infecting bite: you may have forgotten about being bitten, or even having been in a location where you might have been exposed to being bitten.  A rash might be large or small, might not be distinct, there may be several.  However, and this is important, the appearance of an EM rash is, by itself, accepted as clinical evidence of LD and your doctor should prescribe antibiotics right away.  Should.  Unfortunately the experience of many LD sufferers is that GPs, even in areas where LD is recognised as endemic, ignorantly misdiagnose even a classic ‘bullseye’ rash as a skin condition or something else.  “Try this cream and come back in 10 days”.  “Let’s try some steroids (the worst thing you can do for Lyme because it interferes with your immune system)”.  If this doesn’t resolve doctors have been known to treat for psychosomatic disorders (stress).  On the other hand, the rash may resolve, leading to the presumption that the diagnosis of psoriasis, ringworm or eczema, was right and you go on your merry way – as do the borrelia organisms.  As it happens I was one of those who didn’t get a rash. So your next chance to get a diagnosis is when you start to exhibit other symptoms: kiss goodbye to early diagnosis and welcome to the second room.

SymptomsSecond Room in the Hall of Mirrors

The list of possible symptoms is enormous, and I’m not going to reproduce it all here, but many of them can be associated with other illnesses or diseases.   Muscle weakness, pain and cramp, twitching, Bells Palsy, joint pain/arthritis, severe headaches, vision and hearing disturbance, loss of co-ordination or the ability to walk, extreme fatigue, inability to think (so-called “brain fog”) are just a few.  The many effects on the central nervous system may be fleeting and move about the body, vague and difficult to describe.  You may have one major symptom, or many.  Your doctor may again think you are over anxious or neurotic.  He/she may diligently set off on a number of tests – all of which take precious time and, confusingly, may unearth another, previously unsuspected, condition which complicates diagnosis and redirects treatment.  Moreover LD is, by nature, a remitting/relapsing disease: you may spontaneously get better, again pre-empting correct treatment.  As a result some victims of LD fight for a diagnosis for YEARS while the disease slowly infiltrates their bodies and becomes ever more difficult to eradicate.

If you are, somehow, tested for LD the blood test(s) may come up negative: the tests are fallible and there is NO test to prove active infection, only a test to show, by presence of antibodies, that you have at some time, been exposed to the infection.  With an equivocal blood test your doctor may adopt a ‘wait and see’ approach.  I have been confirmed twice, by Western Blot blood test, as “weak positive” for LD.  My Lyme-aware GP started treatment immediately we found out but, as bad luck would have it, he was on extended leave when I first got ill, so I was initially seen by 2 locums, one of whom clearly thought I was neurotic (but later apologised).  By the time I started antibiotic treatment crucial months had passed, however this might have been to my advantage as it can take several weeks for the antibodies to appear and a false negative test would have been disastrous.

TreatmentThird room in the Hall of Mirrors

With a firm diagnosis of LD you would think your troubles are over.  Indeed many sufferers (some of whom will have begun to doubt their own sanity) express profound relief that they at least know what is wrong.  This relief is likely to be very short-lived, as the next battle will be over getting a treatment that works.  The fact is that the science on Lyme Borreliosis is both developing and mired in controversy.  Until 2016 Public Health England (PHE), and Health Protection Scotland (HPS) based UK treatment guidelines on the American model promoted by their Centre for Disease Control (CDC), and the Infectious Disease Society of America (IDSA).  Although the PHE clearly stated that adherence to the guidance is not mandatory for clinicians they, the General Medical Council (GMC) and the British Medical Association (BMA), behaved as if it were.  This left clinicians who diverged from the guidelines open to disciplinary action, which they naturally avoided.  Unfortunately the CDC/IDSA guidance is founded on the species of ticks, infective pathogens, and potential co-infections, found in America.  The most common of these is Borrelia burgdorferi whereas in the UK and Europe generally you are more likely to be infected by Borrelia afzelii or Borrelia garinii. These agents affect, and may need to be treated and tested for, differently: the American experience is not necessarily relevant but the HPA/HPS continued to base treatment guidelines on those of the CDC/IDSA.  At last PHE is reviewing and revising its guidance, acknowledging the uncertainties of diagnosis and treatment, but it may be a long time before hard-pressed GPs approach LD with a more open mind than hitherto.

To date, then, the first-line response to an early diagnosis, say by erythema migrans rash, is a single course of a tetracycline antibiotic (usually Doxycycline) at 200mg per day for 14 days.  Once this course is completed, some clinicians will not prescribe further courses.  Some will prescribe the same dose for 28 days, as a first course, or as a further course if the first course fails.  Some doctors say that all of this is ineffective for disseminated disease because the blood concentration resulting from these dosages is too low to be bactericidal for LD, and of too short a duration.  Very few doctors will follow the European guidelines, e.g. Deutsche Borrelia Gesselschaft, or those of the International Lyme and Associated Disease Society of America (ILADS) which suggest a more appropriate dose is at least 3 or 400mg/day for one, two, three, or even many more, months.

For so-called “late stage” and strongly neurological LD, the “silver bullet” is suggested to be several weeks of intravenous antibiotics, commonly Ceftriaxone.  As I said before, everything from the particular strain of your infection to your age, general health, and physiology may make one treatment succeed where another fails, and vice-versa, but the authorities persist in following a “one size fits all” approach.

Persistence of Infection – Fourth Room in the Hall of Mirrors

The official position is that once “appropriately” treated (i.e. according to the guidelines) LD will have been cured, and that any persistent symptoms or relapses are either due to something else or re-infection.  For those people who live in tick ‘hotspots’ re-infection is always a possibility and cannot be discounted.  However there is no blood test to show that your symptoms are caused by a new infection only, as before, that you have been infected sometime.  So this is unhelpful in determining persistence.  The “something else” list is long. The main theory is that, though the disease is eliminated by the “appropriate” treatment, there is long-lived, even permanent, damage to the central nervous system or an over sensitive auto-immune response.  If you want to see the experience of one UK individual who has persistent Lyme, you could do a lot worse than follow this link.

If you want to read a brief, learned, exposition of the two sides of the persistence debate, try this link.

The main ways currently used to determine whether you have viable spirochetes in your system is by biopsy, or spinal fluid examination; sequential brain scanning might show continuing scarring implying ongoing disease.  These tests are invasive, expensive and, consequently, rarely done in the UK.  Some promote the use of various microscopy techniques on live blood smears but the UK health system does not support these. Amongst other candidate reasons for persistent symptoms are residual inflammation of nerves and (surprise, surprise), neurotic focus on otherwise ‘normal’ symptoms; etc., etc.  As previously noted, it is also unfortunately true that the presence of other disease in the victim can cloud the issue:  I had confirmed diagnoses of a virus, and a D.V.T, simultaneously with my Lyme diagnosis.

Of all the areas of medical dispute, perhaps the most contentious is what drugs to use, how often and, especially, for how long.  LD was first named in 1970’s America; after Old Lyme, a town in Connecticut, where a large number of cases of childhood arthritis had appeared.  Although there is evidence that the disease has been around for thousands of years, the infective organism there was isolated by Willy Burgdorfer – hence the most commonly quoted strain is Borrelia burgdorferi.  The American healthcare model is one of private medicine funded, mainly, through insurance: the expensive testing, treatment, and subsequent care of LD is accessible mostly to those with insurance.  Self-evidently the insurance companies have a vested interest in limiting their exposure to, potentially, open-ended care.  Many of the doctors who compose the board of IDSA have direct, or indirect, financial relationships with insurance and drugs companies.  Is it any wonder that the IDSA promotes guidance that has the effect ot supporting the commercial interest?  With a publicly funded healthcare system in the UK, and with very few cases of LD caused by Borrelia burdorferi (which are mostly, if not all, acquired outside the UK) it is hard to understand why the PHE/HPS rigidly promoted adherence to guidelines based almost entirely on the American experience.

Those that maintain the persistence of LD say that the low dose, relatively short, courses of antibiotics actually cause the spirochetes to ‘hide’ under a so-called biofilm, or transform into a cyst in tissue out of the bloodstream, or other location with a poor blood supply and inaccessible to drugs.  Then they re-appear when conditions are favourable to their continued reproduction.  There are physicians who recommend high dose, intravenous, antibiotics for months – perhaps years.  Over-prescription of antibiotics is widely held to be a cause of drug resistant infection in hospital, some of them potentially deadly like C-Difficile, so their caution is understandable.  Given that Doxycycline is prescribed by doctors for skin conditions (as an anti-inflammatory not as an antibiotic), sometimes for years, it is odd that the same doctors will not give long-term courses for a potentially life-threatening illness like LD – as indeed they would for Tuberculosis (TB).  Of course long-term antibiotic therapies may have unpleasant, even dangerous, side effects that need to be monitored and managed.

Other uncertainties

Vectors and Distribution

World-wide there is an assumption that Lyme Disease is predominantly, if not entirely, limited to a band of the northern hemisphere.  Amongst other things this has led to official denial of its existence (and therefore treatment) in Australia where, nevertheless, cases appear!  In the UK there is a presumption that you would have to visit a ‘hot spot’, and then in spring or summer, to be exposed to Lyme Disease.  The key areas are thought to be heathland, where wild deer, ponies, and sheep roam.  Therefore parts of Wales, the New Forest, the hills and dales of Yorkshire and Derbyshire, the Dartmoor and Exmoor national parks and the Highlands of Scotland, are often quoted as the hotspots.  This is a mistake, based on the common perception that deer, and infected deer ticks, are the only vectors of LD.  In fact deer are not vectors for Lyme Disease at all, they are so-called “dead end hosts”.  They support tick populations by providing a blood meal, and therefore spread ticks, but ticks acquire the disease pathogens from other hosts like mice.

There are several types of tick in the UK and they are all opportunistic feeders: all they need to survive and reproduce is a warm-blooded host to feed from.  They are able to survive temperatures in excess of 40C and, clearly in Scotland, long periods of sub-zero conditions.  Birds (migratory or otherwise), small mammals like mice, rats, rabbits, hedgehogs etc., all can carry ticks and host the pathogens.  All larger mammals like foxes, badgers, cats, dogs, horses, cattle (of course, deer) can also carry ticks.  It is not much of a leap of imagination to say that foxes, birds, hedgehogs and the like, transiting rural corridors, can bring ticks right into your city garden, your urban farm or allotment, or to a park near you.  There is no research to find out the extent of infection being carried in this way, but LD is widespread in continental Europe so is perfectly feasible for a strain of Borrelia, totally unknown in the UK, to be brought right into your house via a migrating bird and then your pet cat or dog.  Recently a tick borne pathogen previously known only in Japan, Borrelia myamotoi, was isolated in Sweden (Gothenburg University).  There is, at time of writing, a furious dispute in Australia where the state government of New South Wales is denying the existence of Lyme Disease in Australia despite growing evidence to the contrary.  The truth is that you may get a tick borne illness anywhere.

Co-Infection

Ticks can carry more than one pathogen, potentially infecting you with more than one disease.  The official position in UK is that so-called co-infection is not a problem.  Some LD specialists and patient support groups disagree on this vehemently, saying that one or more of Anaplasma, Babesia, Bartonella or Erlichia may be transmitted along with the Borrelia.  They say that the overlaying of these diseases means symptoms of LD may manifest differently and will need to be treated differently.  Quite how this affects the treatment of the number of UK residents who acquire Lyme while overseas, where co-infections are accepted to be common, I don’t know.

Inter-Human Transmission

There is no research to find out if a tick bite is the only way to catch LD. There are alleged cases of trans-placental infection from mother to unborn child; there are suggestions that other body fluids like breast milk, tears and sexual fluids are capable of transmitting infection.  There is a question mark over other, blood-feeding, biting insects.  There is, as yet, no evidence for any of these. Though definitely blood-borne, the UK Blood Transfusion service does not screen donations for Lyme Disease.

Incidence

Since 2010 it has not been a requirement to notify PHE or HPS about a case of Lyme Disease in the UK.  It’s not even reportable unless it has been diagnosed by a laboratory, or occurs in the armed forces, or is acquired “occupationally”, in which latter case it is a matter for the Health & Safety Executive under RIDDOR.  That means all cases which are diagnosed only on the basis of clinical suspicion, perhaps because of an Erythema migrans rash, simply do not figure in the official statistics.  Other European countries, with smaller populations than the UK, report many times the number of cases: they may have different recording systems.  Obviously our governments do not think it worth prioritising scarce resources, or research, on the basis of a few hundreds of cases but if it were many thousands (as suspected by the leading testing laboratory in the UK), then what?

Tick Removal

Unattached

Ticks, especially the adults, are tough and incredibly hard to get off your skin, even if not attached. Unattached they can be hard even to crush between your fingernails.  This is not recommended as you could infect yourself through your skin, especially if broken, but if you get one off you before it attaches, make sure you kill it DEAD.  If you flush it down the toilet, make sure it has really gone.  Wash your hands.

Attached

Once attached you should proceed with great caution.  It is said that a tick is unlikely to pass an infection to you if it has been attached for less than 24 hours, though there are those who say even 12 hours or less is possible.  Even if <24 hours is true, the key word here is “unlikely”: don’t wait, get it off as soon as possible.

Bizarrely, NHS Highland recently pubished advice which encouraged the application of methylated spirits or alcohol to remove a tick!  This is completely wrong.  Do not, under any circumstances, apply creams, fluids, cigarette ends or anything else to an attached tick.  Anything which stresses or crushes the tick may cause it to regurgitate the contents of its mouth or stomach into you, along with any infection it is carrying.

The easiest way is to use a proprietary tick removal tool – there are several on the market.  A problem here is that the proprietary tools are less good at grasping nymph ticks: they are so small.  Better than nothing, but trickier, use a pair of needle nosed (precision) tweezers, NOT the blade ended type you might use for eyebrow plucking.  You must grasp the tick close to the head NOT by the body and pull gently upwards.  Try not to leave the head attached in your skin as this can also result in infection and, in the worst case, septicaemia.  At all costs avoid crushing the tick.  It may seem ridiculous at the time but, if you get an attached tick off, save it in a secure container (an old film canister would do) and mark the date and geographical location where you were bitten.  You can send the tick to be identified and it may even be tested for infection (though this is unusual).  Even if a tick that bites you is found to be carrying the LD pathogen it does not mean you will have been infected but it should encourage your GP to treat you anyway, even without symptoms and even if you haven’t had a positive blood test,.  If nothing else it will add to the knowledge about spread of infected ticks in the UK.  The PHE website has information on how to do this at

http://www.hpa.org.uk/Topics/InfectiousDiseases/InfectionsAZ/Ticks/TickRecordingScheme/

If bitten you should note the date in a calendar or diary, and then watch for early signs of illness.  If it is going to appear, the Erythema migrans rash should be seen within 4 weeks as the infection has a (roughly) 4 week cycle.  If you don’t get a rash but feel like you’ve unaccountably got a mild dose of ‘flu (especially out of season), get odd cramps or twitches, feel excessively fatigued or have trouble concentrating, start a diary and consult a doctor.  Mention the tick bite and ask about Lyme Disease but be prepared to be dismissed – keep your diary going for as long as you are symptomatic.  When I presented my Infectious Diseases consultant with a chart covering 9 months of symptoms and treatment he laughed at my self-description of “mildly obsessive”, but he did agree it was helpful data and added it to my burgeoning file.  Not all doctors would be so open-minded: you need to be cautious about the impression you give to your doctor.

Finally, the web site Wikipedia has a good overview of Lyme Disease and it can be found at http://en.wikipedia.org/wiki/Lyme_disease

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