Atteinte de la borréliose chronique persistante , babesia et bartonella ; le déni est grand , battons nous pour la faire connaitre la borréliose de lyme et ses coinfections ; 8 ans de bi et tri therapies d'antibiotiques auxquels j'ai ajouté une partie du protocole Buhner et autres http://francelyme.fr
Maladie de Lyme, mythes et réalités
https://www.lapresse.ca/debats/opinions/201906/26/01-5231771-maladie-de-lyme-mythes-et-realites.php?fbclid=IwAR0OOOklKinsby7es8JhGne8QiwC9Pb36kfT1X_TpnRiUoSB0V43RqvjI7Irealites.php?fbclid=IwAR0OOOklKinsby7es8JhGne8QiwC9Pb36kfT1X_TpnRiUoSB0V43RqvjI7I
Laura Arnal, son combat contre la maladie de Lyme
vivrefm.com
Laura Arnal publie "J'ai surmonté la maladie de Lyme", aux Editions Odile…
the first BBC Scotland documentary coverage on Lyme disease.
À propos de ce site web
youtube.com
the first BBC Scotland documentary coverage on Lyme disease. This
occurred because of of the hard work of Lyme advocates. The BBC
documentary is now available through YouTube. This is worth your time.
Its great how the person in charge of the Lyme testing is very open
about how poor the tests are and how other persons ''in authority'
describe how Lyme patients are marginalized.
Sarreguemines. Réflexions autour de la maladie de Lyme
À propos de ce site web
republicain-lorrain.fr
Nicole Trisse, députée, copréside à l’Assemblée nationale un groupe…
Deadly ticks carrying Ebola-like Congo fever 'found in UK after spreading across Europe'
traduction semi-automatique
Tiques mortelles porteuses de fièvre congolaise semblable à l’Ebola «découvertes au Royaume-Uni après une propagation en Europe »
Gemma Mullin, reporter numérique sur la santé 19 juin 2019,
Une tique capable de transporter des virus meurtriers de type Ebola a été découvert au Royaume-Uni après s'être répandu en Europe, ont annoncé des responsables de la santé. La tique suceuse de sang Hyalomma rufipes ne se trouve généralement qu'en Afrique, en Asie et dans certaines régions du sud de l'Europe.
Selon Public Health England, l'un d'entre eux, 10 fois plus grand que la moyenne, a été découvert dans le Dorset l'année dernière. Des tests ont montré que la créature portait la fièvre tachetée de Rickettsia, pouvant provoquer des maux de tête, des crampes et des ampoules chez l'homme. Mais on sait également que les tiques sont porteuses du virus mortel du virus de la fièvre hémorragique de Crimée-Congo (FHCC), une maladie mortelle surnommée le "prochain virus Ebola". L'horrible virus, également connu sous le nom de fièvre du Congo, entraîne la mort dans environ deux cinquièmes des cas - et il n'existe aucun vaccin prouvé pour le prévenir. Ceux qui ont la malchance d’attraper la maladie souffrent souvent de saignements internes, avant que la défaillance d’un organe ne frappe le patient. Le virus Ebola est également classé comme virus de la fièvre hémorragique, selon l'Organisation mondiale de la santé. Une récente épidémie de la maladie en Ouganda a fait deux morts, dont un garçon de cinq ans, alors que près de 1 400 sont morts au Congo depuis août. Tique trouvée dans le Dorset La tique a été retirée d'un cheval par un vétérinaire à The Barn Equine Surgery à Wimborne, dans le Dorset, en septembre dernier, puis envoyée à PHE pour analyse. Kayleigh Hansford, qui dirigeait l’équipe de surveillance des tiques de l’agence, a écrit: «C’est la première fois que Hyalomma rufipes est signalé au Royaume-Uni. "L'absence de déplacement du cheval - ou de tout autre cheval en contact avec un autre contact - suggère que ceci pourrait également être la première preuve de la mue réussie d'une nymphe Hyalomma au Royaume-Uni." Elle a dit qu'il était soupçonné que la tique avait attelé un oiseau migrateur avant de se poser au Royaume-Uni. Ni le cheval infesté, ni les autres chevaux de l'écurie n'avaient voyagé et aucune autre tique n'a été détectée sur aucun des chevaux. On pense que la tique a probablement voyagé sur une hirondelle parce qu'elle a tendance à nicher dans les écuries des chevaux et à migrer de l'Afrique vers le Royaume-Uni pendant l'été. "Menace pour la santé publique" Cette découverte inquiétante pourrait "représenter une menace pour la santé publique au Royaume-Uni", a déclaré le PHE. On ignore si d'autres tiques ont été découverts en Grande-Bretagne cette année, mais jusqu'à présent, six cas ont été rapportés en Allemagne. Les experts à Munich croient que les insectes ont muté pour survivre aux hivers rigoureux - et ne croient pas qu'ils auraient pu être introduits dans le pays par des oiseaux. Le Dr Ute Mackenstedt, parasitologue à l'Université de Hohenheim, a déclaré: "Si le cycle de développement est pris en compte, cela ne peut pas être le cas ici, car les tiques auraient dû être introduites à un moment où les oiseaux migrateurs n'avaient pas même arrivé. "Selon les dernières preuves, nous devons supposer que ces animaux sont capables de survivre aux hivers allemands." Mais il a également souligné que cela ne signifie pas que les Hyalomma sont cultivés chez nous.
Qu'est-ce que la fièvre hémorragique de Crimée-Congo? La fièvre hémorragique de Crimée-Congo (FHCC) est une maladie répandue causée par un virus transmis par la tique. Il est généralement porté par un large éventail d'animaux sauvages et domestiques tels que les bovins, les ovins et les caprins. Le virus est transmis aux personnes par morsures de tiques ou par contact avec du sang d'animal infecté La majorité des cas sont survenus chez des personnes travaillant dans le secteur de l'élevage, telles que des ouvriers agricoles, des ouvriers d'abattoirs et des vétérinaires.
La transmission interhumaine peut survenir suite à un contact étroit avec le sang, les organes ou les fluides corporels d'une personne infectée. Signes et symptômes Le délai entre l'apparition de l'infection et l'apparition des symptômes est généralement d'un à trois jours. Fièvre Douleur musculaire Vertiges La douleur du cou Mal au dos Mal de tête Yeux irrités La nausée La diarrhée Douleur d'estomac Gorge irritée Sautes d'humeur Confusion Après deux à quatre jours, l'agitation peut être remplacée par la somnolence, la dépression et la douleur à l'estomac peut s'être déplacée. Parmi les autres signes cliniques, on peut citer une fréquence cardiaque rapide, une hypertrophie des ganglions lymphatiques et une éruption pétéchiale, provoquée par un saignement dans la peau, sur les surfaces muqueuses internes, telles que la bouche et la gorge, et sur la peau. Il y a généralement des signes d'hépatite et les patients gravement malades peuvent présenter une détérioration rapide des reins, une insuffisance hépatique subite ou une insuffisance pulmonaire après le cinquième jour de la maladie. Le taux de mortalité est de 30%, le décès se produisant au cours de la deuxième semaine de maladie. Chez les patients en convalescence, l'amélioration commence généralement le neuvième ou le dixième jour suivant l'apparition de la maladie.
Le Dr Mackenstedt a ajouté: "Pour que la population augmente, il faut que la tique mâle et la femelle se retrouvent. C'est très difficile avec un si petit nombre." Cependant, cinq des tiques de Hyalomma ont été retrouvées sur un cheval dans une écurie, ce qui signifie qu'il est possible qu'un jumelage soit possible - et par conséquent, l'émergence d'une population indépendante. L'année dernière, des scientifiques allemands ont mis en garde contre plusieurs tiques tropicales vivant dans le pays, probablement à cause de la hausse des températures. Les scientifiques ont enregistré un total de sept spécimens du genre Hyalomma en Basse-Saxe et dans la Hesse en août 2018. Entre temps, seules deux tiques tropicales ont déjà été trouvées en Allemagne, une en 2015 et une en 2017. Les tiques Hyalomma sont très visibles et peuvent atteindre jusqu'à 2 cm, beaucoup plus grandes que la tique commune des bois. Ils se reconnaissent à leur taille inhabituelle et à leurs jambes rayées. Hyalomma est originaire d'Iran ou du sud de l'ex-Union soviétique et s'est répandu en Asie, au Moyen-Orient, dans le sud de l'Europe et en Afrique. Les morsures de tiques peuvent causer un certain nombre de maladies qui, dans certains cas, peuvent être fatales, telles que l'encéphalite à tiques et la maladie de Lyme. Les espèces Hyalomma peuvent également être atteintes de fièvre hémorragique de Crimée-Congo, qui a déjà fait une victime britannique en 2012. L’homme de 38 ans est décédé quelques heures après son mariage en Afghanistan. Il a été soigné pour la fièvre de Crimée-Congo et transféré dans une unité spécialisée à Londres où il est décédé 96 heures plus tard. Il existe plusieurs types de tiques au Royaume-Uni, mais le plus courant est la tique de mouton, connue scientifiquement sous le nom d'Ixodes ricinus. On les trouve partout au Royaume-Uni, mais les zones à haut risque comprennent les zones herbeuses et boisées du sud de l'Angleterre, de l'est de l'Angleterre, des landes du Yorkshire et des Highlands écossaises.
Une tique capable de transporter des virus meurtriers de type Ebola a été découvert au Royaume-Uni après s'être répandu en Europe, ont annoncé des responsables de la santé. La tique suceuse de sang Hyalomma rufipes ne se trouve généralement qu'en Afrique, en Asie et dans certaines régions du sud de l'Europe.
Selon Public Health England, l'un d'entre eux, 10 fois plus grand que la moyenne, a été découvert dans le Dorset l'année dernière. Des tests ont montré que la créature portait la fièvre tachetée de Rickettsia, pouvant provoquer des maux de tête, des crampes et des ampoules chez l'homme. Mais on sait également que les tiques sont porteuses du virus mortel du virus de la fièvre hémorragique de Crimée-Congo (FHCC), une maladie mortelle surnommée le "prochain virus Ebola". L'horrible virus, également connu sous le nom de fièvre du Congo, entraîne la mort dans environ deux cinquièmes des cas - et il n'existe aucun vaccin prouvé pour le prévenir. Ceux qui ont la malchance d’attraper la maladie souffrent souvent de saignements internes, avant que la défaillance d’un organe ne frappe le patient. Le virus Ebola est également classé comme virus de la fièvre hémorragique, selon l'Organisation mondiale de la santé. Une récente épidémie de la maladie en Ouganda a fait deux morts, dont un garçon de cinq ans, alors que près de 1 400 sont morts au Congo depuis août. Tique trouvée dans le Dorset La tique a été retirée d'un cheval par un vétérinaire à The Barn Equine Surgery à Wimborne, dans le Dorset, en septembre dernier, puis envoyée à PHE pour analyse. Kayleigh Hansford, qui dirigeait l’équipe de surveillance des tiques de l’agence, a écrit: «C’est la première fois que Hyalomma rufipes est signalé au Royaume-Uni. "L'absence de déplacement du cheval - ou de tout autre cheval en contact avec un autre contact - suggère que ceci pourrait également être la première preuve de la mue réussie d'une nymphe Hyalomma au Royaume-Uni." Elle a dit qu'il était soupçonné que la tique avait attelé un oiseau migrateur avant de se poser au Royaume-Uni. Ni le cheval infesté, ni les autres chevaux de l'écurie n'avaient voyagé et aucune autre tique n'a été détectée sur aucun des chevaux. On pense que la tique a probablement voyagé sur une hirondelle parce qu'elle a tendance à nicher dans les écuries des chevaux et à migrer de l'Afrique vers le Royaume-Uni pendant l'été. "Menace pour la santé publique" Cette découverte inquiétante pourrait "représenter une menace pour la santé publique au Royaume-Uni", a déclaré le PHE. On ignore si d'autres tiques ont été découverts en Grande-Bretagne cette année, mais jusqu'à présent, six cas ont été rapportés en Allemagne. Les experts à Munich croient que les insectes ont muté pour survivre aux hivers rigoureux - et ne croient pas qu'ils auraient pu être introduits dans le pays par des oiseaux. Le Dr Ute Mackenstedt, parasitologue à l'Université de Hohenheim, a déclaré: "Si le cycle de développement est pris en compte, cela ne peut pas être le cas ici, car les tiques auraient dû être introduites à un moment où les oiseaux migrateurs n'avaient pas même arrivé. "Selon les dernières preuves, nous devons supposer que ces animaux sont capables de survivre aux hivers allemands." Mais il a également souligné que cela ne signifie pas que les Hyalomma sont cultivés chez nous.
Qu'est-ce que la fièvre hémorragique de Crimée-Congo? La fièvre hémorragique de Crimée-Congo (FHCC) est une maladie répandue causée par un virus transmis par la tique. Il est généralement porté par un large éventail d'animaux sauvages et domestiques tels que les bovins, les ovins et les caprins. Le virus est transmis aux personnes par morsures de tiques ou par contact avec du sang d'animal infecté La majorité des cas sont survenus chez des personnes travaillant dans le secteur de l'élevage, telles que des ouvriers agricoles, des ouvriers d'abattoirs et des vétérinaires.
La transmission interhumaine peut survenir suite à un contact étroit avec le sang, les organes ou les fluides corporels d'une personne infectée. Signes et symptômes Le délai entre l'apparition de l'infection et l'apparition des symptômes est généralement d'un à trois jours. Fièvre Douleur musculaire Vertiges La douleur du cou Mal au dos Mal de tête Yeux irrités La nausée La diarrhée Douleur d'estomac Gorge irritée Sautes d'humeur Confusion Après deux à quatre jours, l'agitation peut être remplacée par la somnolence, la dépression et la douleur à l'estomac peut s'être déplacée. Parmi les autres signes cliniques, on peut citer une fréquence cardiaque rapide, une hypertrophie des ganglions lymphatiques et une éruption pétéchiale, provoquée par un saignement dans la peau, sur les surfaces muqueuses internes, telles que la bouche et la gorge, et sur la peau. Il y a généralement des signes d'hépatite et les patients gravement malades peuvent présenter une détérioration rapide des reins, une insuffisance hépatique subite ou une insuffisance pulmonaire après le cinquième jour de la maladie. Le taux de mortalité est de 30%, le décès se produisant au cours de la deuxième semaine de maladie. Chez les patients en convalescence, l'amélioration commence généralement le neuvième ou le dixième jour suivant l'apparition de la maladie.
Le Dr Mackenstedt a ajouté: "Pour que la population augmente, il faut que la tique mâle et la femelle se retrouvent. C'est très difficile avec un si petit nombre." Cependant, cinq des tiques de Hyalomma ont été retrouvées sur un cheval dans une écurie, ce qui signifie qu'il est possible qu'un jumelage soit possible - et par conséquent, l'émergence d'une population indépendante. L'année dernière, des scientifiques allemands ont mis en garde contre plusieurs tiques tropicales vivant dans le pays, probablement à cause de la hausse des températures. Les scientifiques ont enregistré un total de sept spécimens du genre Hyalomma en Basse-Saxe et dans la Hesse en août 2018. Entre temps, seules deux tiques tropicales ont déjà été trouvées en Allemagne, une en 2015 et une en 2017. Les tiques Hyalomma sont très visibles et peuvent atteindre jusqu'à 2 cm, beaucoup plus grandes que la tique commune des bois. Ils se reconnaissent à leur taille inhabituelle et à leurs jambes rayées. Hyalomma est originaire d'Iran ou du sud de l'ex-Union soviétique et s'est répandu en Asie, au Moyen-Orient, dans le sud de l'Europe et en Afrique. Les morsures de tiques peuvent causer un certain nombre de maladies qui, dans certains cas, peuvent être fatales, telles que l'encéphalite à tiques et la maladie de Lyme. Les espèces Hyalomma peuvent également être atteintes de fièvre hémorragique de Crimée-Congo, qui a déjà fait une victime britannique en 2012. L’homme de 38 ans est décédé quelques heures après son mariage en Afghanistan. Il a été soigné pour la fièvre de Crimée-Congo et transféré dans une unité spécialisée à Londres où il est décédé 96 heures plus tard. Il existe plusieurs types de tiques au Royaume-Uni, mais le plus courant est la tique de mouton, connue scientifiquement sous le nom d'Ixodes ricinus. On les trouve partout au Royaume-Uni, mais les zones à haut risque comprennent les zones herbeuses et boisées du sud de l'Angleterre, de l'est de l'Angleterre, des landes du Yorkshire et des Highlands écossaises.
À propos de ce site web
CHRONIC LYME DISEASE: HOW I CAME TO BELIEVE IT REALLY EXISTS
A
scientist takes an amazing journey by looking methodically at his
daughter's chronic Lyme disease, and questioning every aspect of Lyme
disease research. This is totally worth reading to see how a skeptic
becomes a believer of Chronic Lyme disease and a doubter the CDC's
interpretation's of Lyme disease research through scientific semantics,
and and purposely skewing data. TG
1 CHRONIC LYME DISEASE: HOW I CAME TO BELIEVE IT REALLY EXISTS
I have a buoyant, brilliant, beautiful daughter. Her name is Rebecca. On April 4, 2009, when she was fifteen, she got a headache. But it was no ordinary headache. She woke up every morning with that headache. And she went to sleep with it every night. It didn’t go away for fourteen months. Sometimes it was a “nine” on a scale of zero-to-ten. But she never lost her buoyancy.'
When Rebecca got sick, I just wanted to help her get better. I had no idea I was starting down a path into a medical controversy. Along the way, I have come to believe that Rebecca has chronic Lyme disease. Lyme disease is an infection caused by a bacterium delivered by a tick bite, while “chronic” is added to indicate a persistent infection—not eliminated by antibiotic treatment.
Though Lyme disease is accepted as an illness, the diagnosis “chronic Lyme disease” is controversial. With 300,000 new cases of Lyme disease emerging every year in the U.S., the implications of this unsettled controversy are enormous. The official position of the Centers for Disease Control and Prevention (CDC) and many infectious disease doctors is that chronic Lyme disease does not exist. I will explain why I differ with the CDC. For one, I am a scientist, a molecular biologist, and I’ve read the scientific literature, which has contributed to my reaching a different conclusion. I’m not alone in this regard; others disagree with the CDC, notably members of the International Lyme and Associated Disease Society.
But the truth is, I probably could have read a thousand scientific papers and not have known who to side with. It took a real story—my daughter’s story—to convince me that chronic Lyme disease exists. It’s a gut-wrenching story. And those fourteen months with a continuous headache… That ain’t half the tale. But it has a happy ending—at least for now. * * *
In April, May and June of 2009, my wife, a nurse, and I searched for a diagnosis and explored many kinds of treatments. Many tests were done, including dozens for pathogens—nothing. Brain CT scan—clear. Rheumatology, endocrinology, gynecology, and of course neurology, including with headache specialists—nothing. We tried all kinds of medicine for headaches, from over-the-counter brands to prescriptions for every imaginable headache syndrome—nothing helped. Physical therapies, acupuncture, counseling, biofeedback, vitamins, dietary supplements… Nothing helped.
Then one of her physicians looked at some test results and said something like, “She’s on the high side of normal, as if she’s fighting an infection. Let’s test for more exotic pathogens. And she’s only had the inferior test for Lyme disease. Let’s do a better test, a Western blot. (“Western blots” are described later.) In mid-July 2009, the tests for exotic pathogens came back negative, but her Western blot for Lyme was positive. I’ve done Western blotting in my research, so I wanted to see for myself. I talked the testing company into sending me the image of her Western blot. They were right. Rebecca started antibiotics immediately. Within days, she began feeling better. Her headache intensity always varied, but she had moved from highs of eights and nines to threes and fours.
2 I can’t tell you how relieved we felt. We had a diagnosis, and she was improving. She was going to be better. Or so we thought. * * *
The most prevalent Lyme bacterium is Borrelia burgdorferi, which I will call “Lyme/Borrelia.” When a Lyme tick bites someone, it injects saliva containing Lyme/Borrelia, which then multiplies and spreads to many tissues, including brain, muscles, joints and heart, leading to a plethora of possible symptoms, such as joint pain, fatigue and, yes, headaches.
Some people find the tick (the size of a poppy seed) or notice a characteristic bulls-eye rash within a few days of the tick bite. If they take antibiotics right away, they are often cured. For the unlucky others, there is no telltale sign (or it isn’t noticed), and their Lyme disease only becomes apparent when symptoms develop—after the infection has had time to become entrenched. Rebecca was one of those “unlucky others.” A single tick bite can deliver more than just Lyme/Borrelia, including other bacteria (like Anaplasma), protozoa (like Babesia), as well as multicellular parasites.
In fact, co-infections are common, with estimates ranging as high as 50%, which is significant given that antibiotics are ineffective against many tick-borne pathogens, like protozoa. Another complication is that symptoms caused by some common co-infecting agents (such as the protozoan, Babesia) can be similar to those of Lyme/Borrelia itself, making it difficult to be certain which pathogen is causing a particular symptom at a particular time and, thus, what medications to use. * * *
Antibiotic treatment had dramatically improved Rebecca’s headache by the time she started back to high school as a junior in September 2009. She had been on the JV soccer team in 10th grade, and the varsity coach was counting on her to anchor the defense of the varsity team. But her lingering headache made that impossible. In October, her headache got much worse. We feared that the Lyme/Borrelia bacterium had flared up. She was put back on antibiotics. They didn’t help, so her doctor proposed the nuclear option: intravenous antibiotics. A tube was inserted into her right arm that ran up a vein to near her collarbone (a “PIC line”). Twice a day, my wife administered antibiotics. This went on for over three months. * * *
There are multiple controversies regarding Lyme disease. Are laboratory tests for Lyme/Borrelia reliable? Can Lyme disease be chronic? If so, does long-term antibiotic treatment help? Debates about Lyme disease typically focus on what is known in people. In my reading, I discovered a vast scientific literature, often given short shrift in the Lyme debate: studies in model systems, like mice. Model system studies have often proved pivotal in developing an understanding of biology and medicine relevant to humans, importantly because experiments in people can’t be done.
I will weave together Rebecca’s story with findings in a number of key studies that I find particularly revealing. * * * In spite of receiving intravenous antibiotics, Rebecca’s intense headache persisted throughout the last few months of 2009. She finally had to drop out of high school at the end of the first semester.
3 So what did she do? She’d lie still in a dark room, listening to music, watching movies and doing artwork, always trying to distract herself from the constant pain in her head. It was heartbreaking. Though I focus on Rebecca’s headaches—her worst symptom—she has had other symptoms: nausea, night sweats, motion sickness, air hunger, persistent low grade fever, malaise, brain fog, facial flushing and fatigue. These symptoms have varied with time, and severity could change hour-by-hour, day-to-day, etc.
By late 2009, we knew about co-infections, such as with protozoa, like Babesia. We wanted Rebecca treated for a protozoa co-infection. But Rebecca’s physician would not agree without a positive test. Her protozoa tests came back negative. We knew that tests for Lyme/Borrelia, as well as its co-infections, are not definitive, so we realized her protozoa tests might have been false negatives. Since she was incapacitated, and we were desperate, we looked for another doctor—one who would treat her symptoms, rather than her test results. Eventually, we found one.
In March 2010, Rebecca began treatment with anti-protozoa medications. She started feeling better immediately. In May 2010, she said, “For the first time in fourteen months, I don’t have a headache.” I cried. And the headache stayed away. I can’t tell you how relieved we were. She was cured. Or so we thought. * * *
In May 2013, Dr. Stephen Barthold of the University of California, Davis gave the prestigious David B. Schauer Lecture in Infectious Diseases and Global Health at the Massachusetts Institutes of Technology. His seminar was entitled, “There’s Something about Borrelia.” Dr. Bathold described a very important experiment that he and his colleague, Dr. Emir Hodzic, were just finishing. It was published in 2014. Mice were infected with Lyme/Borrelia bacteria, treated with antibiotic for one month, and then evaluated for a persistent infection. Even eight months after antibiotic treatment, the mice showed virtually no signs of Lyme/Borrelia. But at 12 months, evidence showed that Lyme/Borrelia were back again. In fact, they reached a level 20-70% as great (depending on which tissue was evaluated) as the mice that had been infected but never treated with antibiotic.
Researchers had previously tried similar, though not identical, experiments in animal model systems, but the findings were always more suggestive than convincing. I couldn’t think of any way for more Lyme/Borrelia to be present at 12 months than at 8 months, unless the Lyme/Borrelia had survived antibiotic treatment and grown back. This was good evidence for chronic Lyme disease—at least in a model system. Scattered reports in the scientific literature are also consistent with Lyme/Borrelia being present in people following antibiotic treatment. * * *
Rebecca had been headache free for four months when she started her junior year of high school for the second time in September 2010. She was incredibly enthusiastic and passionate about learning. She took delight in everything.
If
4 she had to write a five-page paper, she would write a ten-page paper. And with glee, she’d read it to us. She explained how happy she was to be learning again, given that learning had been ripped away from her in the previous year. She did well during her junior year. * * *
I once had an interesting encounter with the head of infectious diseases at a major hospital. He told me in no uncertain terms that Rebecca did not have Lyme disease. I showed him Rebecca’s Lyme test results and said something like, “If she doesn’t have Lyme disease, then how do you explain these bands in her Western blot?” He seemed baffled, so I asked, “You understand how this test works, right?”
Turns out, he didn’t—he just knew the name “Western blot.” I wondered how he could dismiss her test, especially given her Lyme-like symptoms and her favorable responses to various medications. He said something like, “The company that did that test is not reliable. And besides, she should be IgM negative and IgG positive, since her tests were done months after her alleged tick bite. It’s well known that IgM converts to IgG soon after an infection starts.” IgM? IgG? What was he talking about?
When a pathogen, such as a bacterium or a virus, invades, our immune system fights the infection. Part of the immune system makes antibodies—those carefully crafted proteins that detect a new pathogen with exquisite specificity and target it for destruction. There are several classes of antibodies, but let’s consider the two pertinent ones. The first antibody to appear after an infection is an IgM; they work moderately well, but they are big and clunky, like an old truck. (Call them: “M-antibodies,” for “IgM” or “Moderate.”) But a few weeks after the infection, the body works a miracle and starts making a more effective IgG antibody, which is like a sleek, elegant sports car. (Call them: “G-antibodies,” for “IgG” or “Good.”) G-antibodies are the ones that last, so the body can fight off a new infection by that same pathogen again in the future.
In a typical infection, G-antibodies replace M-antibodies within a few months. I had to admit: that doctor was right. Rebecca was M-antibody positive but G-antibody negative, which is the opposite of expectations at her stage of infection, based on analogy to the standard immune response to a pathogen. I asked him what he thought Rebecca had. He didn’t know. This was typical: doctors dismissing chronic Lyme disease, but having no alternative explanation.
As a scientist, when I am faced with conflicting findings, I try to think in terms of “the weight of the evidence.” Rebecca’s symptoms had been relieved by antibiotics and anti-protozoa medications, which indicates a co-infection with both a bacterium and a protozoan. Only one vector is known to deliver both: a tick. She also had Lyme-like symptoms, as well as no evidence of other maladies. Even though I couldn’t explain her positive M-antibody test result, the weight of the evidence suggested to me that she had chronic Lyme disease. When considering scientific findings that seem baffling, I often recall a quote from Shakespeare: “There are more things in heaven and earth, Horatio, than are dreamt of in your philosophy.”
As
5 unlikely as it seemed, my instincts were that the test was right, but there was something unusual about the immune response to Lyme/Borrelia. * * *
In November 2013, I attended a conference entitled, “Challenges, Controversy in Lyme Disease and Tick Borne Illness Care Symposium” at the Massachusetts General Hospital. I heard a remarkable lecture by Dr. Nicole Baumgarth of the University of California, Davis. Her work was subsequently published in 2014 and 2015. She showed that after mice were infected, Lyme/Borrelia bacteria migrate to lymph nodes, which are sites where much of the immune response occurs.
What! Why would an infectious pathogen purposely go to one of the key sites in the body designed to defeat it? It turns out—once in lymph nodes—Dr. Baumgarth showed that Lyme/Borrelia damage the apparatus that creates those “sleek, elegant sports car” G-antibodies. (The apparatus is called the “Germinal Center.”) Once this apparatus is disrupted, G-antibodies are no longer made. Dr. Baumgarth concluded that “(Lyme/Borrelia) causes the structural disintegration of lymph nodes in infected mice…” and “drives (the immune) response away from protective, high-affinity and long-lived antibody responses and toward…short-lived antibodies of limited efficacy.” (M-antibodies are the ones of “limited efficacy.” They are not made in Germinal Centers, and they cannot rid the body of Lyme/Borrelia completely.)
Lyme/Borrelia, thus, goes to lymph nodes to cripple the apparatus that makes the most effective, long-term component of the immune system, G-antibodies. This is the first time that such a mechanism has been described for a pathogen. But it’s worse than that. The mouse immune system is not only crippled for making Lyme/Borrelia-specific antibodies, it is also crippled for mounting an immune response against other pathogens. Dr. Baumgarth studied the response to Influenza.
That is staggering! If it holds true in humans, then individuals with a persistent Lyme/Borrelia infection would be less able to fight off other co-infecting pathogens delivered by the original tick bite, such as protozoa. Furthermore, infected individuals are also expected to be more prone to other infections, such as the flu. Admittedly, no evidence currently exists that this mechanism operates in humans, but it seems likely to me, especially because it provides a plausible explanation for why Rebecca tested M-antibody positive but G-antibody negative. Furthermore, Rebecca is not alone: according to one Lyme testing laboratory, many people tested for Lyme disease are only M-antibody positive. . * * *
In fall 2011, Rebecca started her senior year of high school. She was excited. She was also excited to be thinking about where to apply to college. But in early October—after sixteen months—her headache returned. Was it due to Lyme/Borrelia or to a protozoa? We guessed. Following treatment with anti-protozoa medications, Rebecca felt better almost immediately. It wasn’t long before her headaches were minimal. She did well in her first semester as a senior in high school.
We were
6 optimistic. In January 2012, however, her headache gradually started getting worse again. By March we were sure the anti-protozoa medications had stopped working. This time we guessed “bacteria” and switched her back to antibiotics. * * * But why were we guessing? Why not just do a test? To adequately address that question would require its own article, but the bottom line is that no direct, definitive test for Lyme/Borrelia has been established, and existing tests are complex and not reliable.
First, no simple blood test exists (like for cholesterol). Furthermore, some bacteria can be cultured reliably from blood, like those causing blood poisoning (septicemia), but not Lyme/Borrelia. But even if it could be, Lyme/Borrelia levels can be low in blood, even when it is present in other places, like in connective tissue and/or biofilms (explained below).
Blood samples, however, can be used to detect the presence of the body’s M-antibodies and/or G-antibodies against Lyme/Borrelia, which is an indirect test. The best antibody test is a “Western blot,” though it is very idiosyncratic and complex, especially compared to simple tests, like for cholesterol. (In fact it is actually not a classic Western blot.) Plus, M-antibodies and G-antibodies don’t appear right away, so the test can’t be done immediately after a tick bite. These and other complications have not been adequately addressed or resolved. Rebecca has tested positive four times and negative three times for Lyme/Borrelia. She tested positive one out of four times for Babesia. She also tested positive two out of three times for Anaplasma—another tick-borne bacterium. These tests were not planned as if we were conducting a scientific study, but generally (though not always), her tests were positive when her symptoms were significant and negative when her symptoms were absent or subdued. * * *
The absence of a reliable test has made Lyme disease diagnosis uncertain, complicated and confusing. Doctors make judgments based on their experience with other pathogens and their instincts. I’ve heard a number of doctors state something like, “Your daughter can’t have Lyme disease, because it’s well known that four weeks of antibiotic treatment is sufficient to eliminate a bacterial infection.” That’s certainly true for many infections, but aren’t some pathogens nasty enough to cause persistent infections that are hard to get rid of? If so, does Lyme/Borrelia share anything in common with them?
When I described our immune system, I mentioned antibodies. Our immune response, however, is complex; one component, “innate immunity,” begins immediately after an infection starts. Many pathogenic bacteria that cause persistent infections disrupt innate immunity (e.g., Salmonella), as do viruses (e.g., norovirus). In mice, Lyme/Borrelia has been shown to have two mechanisms to blunt innate immunity. (The OspC protein inhibits macrophages, and the OspE protein disrupts the “complement system.”) Sleeping sickness is actually a coma caused by a tropical trypanosome, which establishes a chronic infection, often resulting in death. The sleeping sickness trypanosome also defeats the immune system, but it uses a very different strategy. Infected individuals generate antibodies
7 against a prominent protein on the cell surface of the trypanosome. But when the trypanosome senses those antibodies, it pulls a clever trick. It changes the amino acid sequence of that cell surface protein, such that the antibody no longer works, and the immune system has to start over. And when the trypanosome senses that new antibody, it changes the amino acid sequence again. And again. And again…
Guess what? In mice, Lyme/Borrelia does the same thing with one of its cell surface proteins (VlsE). Hiding is another strategy used by pathogens to establish a persistent infection. For example, some bacteria hide inside a protective sack composed of a “biofilm,” which they make, like a cocoon. Biofilm sacks block the penetration of both antibodies and antibiotics. Cystic Fibrosis is a genetic disorder that leads to excessive mucous buildup in the lung.
This mucous provides a rich broth, which the bacteria Pseudomonas aeruginosa colonizes as a biofilm sack, thus allowing it to survive antibiotics and the immune system. The persistent Pseudomonas infection eventually contributes to the premature death of individuals with Cystic Fibrosis. Evidence shows that Lyme/Borrelia also form biofilm sacks, which (by analogy) could provide a reservoir to perpetuate a chronic infection.
There are other hiding mechanisms. The immune system eventually eliminates most cells infected by the chickenpox virus, but it hides in nerve ganglia, which are not monitored by the immune system. Later in life, the latent virus can emerge from its hiding place in response to various stresses and cause shingles. Lyme/Borrelia also does this, using its DbpA protein to hide in connective tissues, which have a low blood supply. Low blood levels result in low exposures to antibodies and antibiotics. A great place to hide. I have mentioned five mechanisms by which pathogens can create a persistent infection. (There are others.) Lyme/Borrelia has all five. No one knows where this places it on the scale of pathogens best equipped to cause a persistent infection, but it is certainly no slouch in terms of having well-established mechanisms to establish persistence. In the absence of antibiotics, Lyme/Borrelia only has to defeat the immune system in order to develop a persistent infection—and it clearly can. But does having these five mechanisms mean that it can establish a chronic infection when antibiotics are added to the battle? Dr. Barthold showed that it does in mice. But what about in people? Indirect evidence (e.g., persistent symptoms) certainly suggests it can.
But in all honesty, I would characterize the direct evidence in people currently as being strongly suggestive, but not ironclad. Nevertheless, each of those five mechanisms make it harder for the body to rid itself of Lyme/Borrelia. And, remember, it’s a self-renewing life form, so even one surviving microbe can in principle initiate a new round of infection. Nothing is known about how many Lyme/Borrelia must survive to start a new infection, but a few pathogens need but a single microbe to start an infection, while others only need 10-100 microbes. * * *
After switching back to antibiotics in March 2012, Rebecca’s headaches began getting better, which suggested that indeed it had been her Lyme/Borrelia bacterial infection that had flared up again. Her symptoms varied from being barely noticeable to being bad. But she maintained her
8 buoyancy, and managed to limp across the finish line and graduate from high school. Rebecca was accepted into college and began her studies in fall 2012. Given her situation, she decided to take only two courses. The rigors of college were challenging, and she struggled with both occasional headaches and other symptoms, notably fatigue, which often left her so exhausted she had to nap during the day. About halfway through her first semester, school got to be too much. She stopped going to class. Professors were contacted. They were understanding.
One anecdote stands out. She attended no classes in her introductory psychology class between the first and second exam. But she felt better during the Thanksgiving break, so she taught herself the material. She asked her psychology professor to give her a makeup exam. She got an A-. I couldn’t believe it. When I asked, she said something like, “I’m used to teaching myself. How do you think I finished high school?” * * *
The Centers for Disease Control and Prevention (CDC) does not accept the existence of chronic Lyme disease, though it does recognize that some people formerly with Lyme disease can experience ongoing Lyme-like symptoms after antibiotic treatment. They call it “Post-Treatment Lyme Disease Syndrome” (PTLDS). CDC acknowledges that the “cause of PTLDS is not yet known,” but they favor that “lingering symptoms are the result of residual damage to tissues and the immune system that occurred during the infection.” An example of what they mean is that Lyme/Borrelia might trigger an autoimmune response. * * *
If the CDC’s preferred hypothesis for PTLDS is correct, then it must somehow be reconcilable with Rebecca’s history. Their hypothesis implies that patients with lingering Lyme-like symptoms not only don’t have a chronic bacterial infection, they also don’t have a chronic co-infection. Rebecca has had five major headache flare-ups, each of which was significantly relieved—twice by antibiotics and three times by anti-protozoa medications.
Furthermore, on several occasions, we know that one medication (for protozoa) worked, while another (for bacteria) did not, and vice versa. How could antibiotics and anti-protozoa medications have an impact on “residual damage to tissues and the immune system that occurred during the infection…”? A number of physicians have suggested that some antimicrobials have anti-inflammatory effects, which may have helped Rebecca. This is the most commonly offered rationale that is consistent with the CDC’s preferred hypothesis.
However, to be true, not only would secondary anti-inflammatory effects of antimicrobials have to dominate, but also sometimes only the anti-inflammatory effect of an antibiotic must have been effective, while other times it must only have been the secondary effects of an anti-protozoa medication. Furthermore, drugs whose primary purpose is to be anti-inflammatory—which have never helped relieve Rebecca’s symptoms—must have been ineffective for some reason. The notion that Rebecca’s responses could have been due to anti-mircobials working as anti-inflammatories—where only antibiotics work sometimes and only anti-protozoa medications
9 work other times, while true anti-inflammatory drugs don’t work at all—strikes me as virtually impossible. Scientists often think in terms of “parsimony”—what is the most likely explanation for an observation? Parsimony suggests to me that the obvious hypothesis is most likely: Rebecca’s Lyme-like symptoms have been relieved by antibiotics and anti-protozoa medications, because she really has had a chronic bacterial and protozoan infection. * * *
So why are the CDC and others so convinced that chronic Lyme disease does not exist? Historically, they have relied heavily on the interpretation of findings in four scientific studies. (Hereafter, referred to as the “four studies”). In detail, these four studies differed, but the basic approach was similar. Patients (1) with a confirmed history of Lyme disease, (2) who had been treated with antibiotics, but (3) who subsequently experienced persistent symptoms, were treated with an antibiotic (ceftriaxone/rocephin) intravenously (minimum time: 4 weeks), after which their symptoms were assessed subjectively. The authors of those four studies concluded that symptoms did not improve to an extent that was statistically significant and/or clinically relevant, and, thus, antibiotic treatment of patients with ongoing Lyme-like symptoms was not warranted. Based on these studies, the CDC and others extrapolated that if antibiotic treatment didn’t help, implicitly Lyme disease could not be chronic. * * *
After Rebecca’s brief respite from symptoms during Thanksgiving break in 2012, her headache got worse again. There was nothing to do but drop out of college. At that time she was being treated with antibiotics. But what if her protozoa infection had returned? In January 2013, she was switched back to anti-protozoa medications. She responded; her headache improved again. Though she felt better, it was too late to return to college. Plus, she had no confidence that her symptoms would remain stable enough to permit her to cope with the rigors of school. She didn’t know what to do. Fortunately, Rebecca is artistic, and she began to consider being an artist. One of her artistic skills is unusual. She loves doing intricate line drawings, often in symmetrical shapes, reminiscent of mandalas. She found this style of artwork to be soothing; it took her mind off headaches. She started doing a lot of mandala art. In the summer of 2013, unfortunately, her hand developed a tremor. When she tried to draw a fine straight line, it came out jagged and wavy. The mandala artwork, which had become so satisfying and soothing, became impossible. * * *
I’ve come to believe that there are four problems associated with the four studies that the CDC and others have used to conclude that chronic Lyme disease does not exist. The first problem was pointed out by Ms. Allison DeLong, a biostatistician at Brown University, who performed a statistical review of those four studies. There was insufficient evidence to permit a conclusion that antibiotic treatment definitively did not help patients with ongoing Lyme-like symptoms. The major issue was—for the types of statistical methods applied in each
10 of the four studies—too few subjects were included, which is called being “underpowered.”
The second problem was that in fact Ms. DeLong found evidence in two of the four studies of a statistically significant improvement for one symptom, fatigue, when the subjects were subdivided into those with the worst cases of fatigue at the time of enrollment. This is exactly the subpopulation that would be expected to be most revealing about a significant trend. Actually, the authors of those two studies also noted this trend. Why wasn’t it highlighted? The authors believed that all symptoms tested (often three) should improve in parallel, or else the improvement in one symptom (fatigue) must be a red herring. There is no reason to believe that this supposition is necessarily correct. The authors of the other two studies have never released their data, making it impossible for others to reanalyze the data for such a trend. The third problem was the “one size fits all” use of a single antibiotic (ceftriaxone/rocephin) for the subjects in those four studies. Lyme literate physicians have discovered that different patients respond best to different antibiotics, which can also change with time. This has certainly been true for Rebecca, who preferentially responds to antibiotics in the X and Y classes. Why would that be? It is unknown, but may relate to complexities of the infection.
Lyme/Borrelia can hide in different tissues; it can adopt different physical forms (a cork-screw shape, a spherical shape and a biofilm sack); plus, there are different Borrelia species and even different strains within a species.
The fourth problem is most significant to my mind: the implications of co-infections were ignored. Consider this scenario. Imagine that 20% of subjects in those four studies responded significantly to intravenous antibiotics; such a response rate would likely be too low to give a statistically significant outcome. Now imagine that 50% of those subjects didn’t respond because they were primarily suffering from a protozoa co-infection—much like Rebecca in late 2009, when she did not respond to intravenous antibiotics, but she did respond to anti-protozoa medications. If the 50% of subjects with co-infections could be excluded, then the percentage of subjects responding positively to intravenous antibiotics would have doubled from 20% to 40%, which would have significantly improved the chances of detecting statistically significant outcomes for all symptoms. The authors in those four studies had no way of assessing if a subject was primarily suffering from a co-infection. At the very least, though, they should have mentioned this limitation and reflected on its implications.
Based on the scenario in the previous paragraph, 70% of subjects would have a tick-borne illness, and yet none would be treated if the recommendations of those who deny chronic Lyme disease were followed.
Several other studies have been done more recently. One study had more subjects, who were treated longer and were followed longer to assess outcome. The conclusion: “Prolonged intravenous antibiotic therapy is associated with improved cognition, fatigue and myalgias (muscle pain)…” However, this study was only designed to assess whether an “association” exists between treatment and improvement; to establish cause-and-effect would have required even more subjects.
Nevertheless, the “association” was clear. The second study was published in 2016, and the authors argue against chronic Lyme disease. A critique of it would be too involved, so I provide a link to the paper and criticisms, which include that co-infections were not considered, and the “control group” was not proper.
11 * * *
When Rebecca could no longer draw straight lines, because of her hand tremor, she didn’t give up. She had an idea based on a technique called “paper cut art.” She drew her wavy lines, and then cut out the white space between the lines using an exacto knife. Even though her hand shook, she could position the exacto knife precisely, and—when she pressed hard—she could make a non-wavy cut. That’s buoyancy! * * *
When I read scientific papers that support the notion that chronic Lyme disease does not exist, they seem persuasive. In all honesty, if I hadn’t read papers using model systems, and if I didn’t know of the weaknesses in those four studies, I too would probably lean toward the denial of chronic Lyme disease.
More importantly, though, I have had a first hand experience with someone suffering with a chronic disease, so I’ve come face-to-face with having to make real decisions about how to help a real person struggling with pain. I doubt that most deniers of chronic Lyme disease have had such an experience.
Looking back, here’s my perspective. When we followed the hypothesis that Rebecca has chronic Lyme disease, we ended up with a reasonably healthy daughter. But when we followed the alternatives offered by those who believed that something other than chronic Lyme disease was likely, we got nowhere. We vigilantly pursued every possibility they suggested, along with everything else we could think of. They all led nowhere. Rebecca has struggled with Lyme disease and its co-infections for over seven years. Fortunately, for the past three years she has been largely headache free, principally because her current doctor treats her for an ongoing chronic tick-borne illness, which requires vigilant, on-going reassessments and tinkering. Consequently, she has had no major debilitating flare-ups recently. Though she is not cured, her life is more normal—her main symptom now being a lack of stamina (fatigue). She typically rates her overall health as being 75%.
Because of her progress, Rebecca is now making her way as an artist and is also a teacher in an afterschool program. Though her life has not followed the path she once imagined, she is happy, because she loves doing artwork and working with young children. I couldn’t be more proud. Given the intense and often acrimonious debate over chronic Lyme disease, my wife didn’t want Rebecca to be named in this article for fear that she would somehow be targeted. Rebecca insisted otherwise. She wants readers to know that the story I’ve told was neither fabricated nor delivered to me second-hand. She also believes that if telling her story can help even one person avoid what she’s been through then it’s worth it.
1 CHRONIC LYME DISEASE: HOW I CAME TO BELIEVE IT REALLY EXISTS
I have a buoyant, brilliant, beautiful daughter. Her name is Rebecca. On April 4, 2009, when she was fifteen, she got a headache. But it was no ordinary headache. She woke up every morning with that headache. And she went to sleep with it every night. It didn’t go away for fourteen months. Sometimes it was a “nine” on a scale of zero-to-ten. But she never lost her buoyancy.'
When Rebecca got sick, I just wanted to help her get better. I had no idea I was starting down a path into a medical controversy. Along the way, I have come to believe that Rebecca has chronic Lyme disease. Lyme disease is an infection caused by a bacterium delivered by a tick bite, while “chronic” is added to indicate a persistent infection—not eliminated by antibiotic treatment.
Though Lyme disease is accepted as an illness, the diagnosis “chronic Lyme disease” is controversial. With 300,000 new cases of Lyme disease emerging every year in the U.S., the implications of this unsettled controversy are enormous. The official position of the Centers for Disease Control and Prevention (CDC) and many infectious disease doctors is that chronic Lyme disease does not exist. I will explain why I differ with the CDC. For one, I am a scientist, a molecular biologist, and I’ve read the scientific literature, which has contributed to my reaching a different conclusion. I’m not alone in this regard; others disagree with the CDC, notably members of the International Lyme and Associated Disease Society.
But the truth is, I probably could have read a thousand scientific papers and not have known who to side with. It took a real story—my daughter’s story—to convince me that chronic Lyme disease exists. It’s a gut-wrenching story. And those fourteen months with a continuous headache… That ain’t half the tale. But it has a happy ending—at least for now. * * *
In April, May and June of 2009, my wife, a nurse, and I searched for a diagnosis and explored many kinds of treatments. Many tests were done, including dozens for pathogens—nothing. Brain CT scan—clear. Rheumatology, endocrinology, gynecology, and of course neurology, including with headache specialists—nothing. We tried all kinds of medicine for headaches, from over-the-counter brands to prescriptions for every imaginable headache syndrome—nothing helped. Physical therapies, acupuncture, counseling, biofeedback, vitamins, dietary supplements… Nothing helped.
Then one of her physicians looked at some test results and said something like, “She’s on the high side of normal, as if she’s fighting an infection. Let’s test for more exotic pathogens. And she’s only had the inferior test for Lyme disease. Let’s do a better test, a Western blot. (“Western blots” are described later.) In mid-July 2009, the tests for exotic pathogens came back negative, but her Western blot for Lyme was positive. I’ve done Western blotting in my research, so I wanted to see for myself. I talked the testing company into sending me the image of her Western blot. They were right. Rebecca started antibiotics immediately. Within days, she began feeling better. Her headache intensity always varied, but she had moved from highs of eights and nines to threes and fours.
2 I can’t tell you how relieved we felt. We had a diagnosis, and she was improving. She was going to be better. Or so we thought. * * *
The most prevalent Lyme bacterium is Borrelia burgdorferi, which I will call “Lyme/Borrelia.” When a Lyme tick bites someone, it injects saliva containing Lyme/Borrelia, which then multiplies and spreads to many tissues, including brain, muscles, joints and heart, leading to a plethora of possible symptoms, such as joint pain, fatigue and, yes, headaches.
Some people find the tick (the size of a poppy seed) or notice a characteristic bulls-eye rash within a few days of the tick bite. If they take antibiotics right away, they are often cured. For the unlucky others, there is no telltale sign (or it isn’t noticed), and their Lyme disease only becomes apparent when symptoms develop—after the infection has had time to become entrenched. Rebecca was one of those “unlucky others.” A single tick bite can deliver more than just Lyme/Borrelia, including other bacteria (like Anaplasma), protozoa (like Babesia), as well as multicellular parasites.
In fact, co-infections are common, with estimates ranging as high as 50%, which is significant given that antibiotics are ineffective against many tick-borne pathogens, like protozoa. Another complication is that symptoms caused by some common co-infecting agents (such as the protozoan, Babesia) can be similar to those of Lyme/Borrelia itself, making it difficult to be certain which pathogen is causing a particular symptom at a particular time and, thus, what medications to use. * * *
Antibiotic treatment had dramatically improved Rebecca’s headache by the time she started back to high school as a junior in September 2009. She had been on the JV soccer team in 10th grade, and the varsity coach was counting on her to anchor the defense of the varsity team. But her lingering headache made that impossible. In October, her headache got much worse. We feared that the Lyme/Borrelia bacterium had flared up. She was put back on antibiotics. They didn’t help, so her doctor proposed the nuclear option: intravenous antibiotics. A tube was inserted into her right arm that ran up a vein to near her collarbone (a “PIC line”). Twice a day, my wife administered antibiotics. This went on for over three months. * * *
There are multiple controversies regarding Lyme disease. Are laboratory tests for Lyme/Borrelia reliable? Can Lyme disease be chronic? If so, does long-term antibiotic treatment help? Debates about Lyme disease typically focus on what is known in people. In my reading, I discovered a vast scientific literature, often given short shrift in the Lyme debate: studies in model systems, like mice. Model system studies have often proved pivotal in developing an understanding of biology and medicine relevant to humans, importantly because experiments in people can’t be done.
I will weave together Rebecca’s story with findings in a number of key studies that I find particularly revealing. * * * In spite of receiving intravenous antibiotics, Rebecca’s intense headache persisted throughout the last few months of 2009. She finally had to drop out of high school at the end of the first semester.
3 So what did she do? She’d lie still in a dark room, listening to music, watching movies and doing artwork, always trying to distract herself from the constant pain in her head. It was heartbreaking. Though I focus on Rebecca’s headaches—her worst symptom—she has had other symptoms: nausea, night sweats, motion sickness, air hunger, persistent low grade fever, malaise, brain fog, facial flushing and fatigue. These symptoms have varied with time, and severity could change hour-by-hour, day-to-day, etc.
By late 2009, we knew about co-infections, such as with protozoa, like Babesia. We wanted Rebecca treated for a protozoa co-infection. But Rebecca’s physician would not agree without a positive test. Her protozoa tests came back negative. We knew that tests for Lyme/Borrelia, as well as its co-infections, are not definitive, so we realized her protozoa tests might have been false negatives. Since she was incapacitated, and we were desperate, we looked for another doctor—one who would treat her symptoms, rather than her test results. Eventually, we found one.
In March 2010, Rebecca began treatment with anti-protozoa medications. She started feeling better immediately. In May 2010, she said, “For the first time in fourteen months, I don’t have a headache.” I cried. And the headache stayed away. I can’t tell you how relieved we were. She was cured. Or so we thought. * * *
In May 2013, Dr. Stephen Barthold of the University of California, Davis gave the prestigious David B. Schauer Lecture in Infectious Diseases and Global Health at the Massachusetts Institutes of Technology. His seminar was entitled, “There’s Something about Borrelia.” Dr. Bathold described a very important experiment that he and his colleague, Dr. Emir Hodzic, were just finishing. It was published in 2014. Mice were infected with Lyme/Borrelia bacteria, treated with antibiotic for one month, and then evaluated for a persistent infection. Even eight months after antibiotic treatment, the mice showed virtually no signs of Lyme/Borrelia. But at 12 months, evidence showed that Lyme/Borrelia were back again. In fact, they reached a level 20-70% as great (depending on which tissue was evaluated) as the mice that had been infected but never treated with antibiotic.
Researchers had previously tried similar, though not identical, experiments in animal model systems, but the findings were always more suggestive than convincing. I couldn’t think of any way for more Lyme/Borrelia to be present at 12 months than at 8 months, unless the Lyme/Borrelia had survived antibiotic treatment and grown back. This was good evidence for chronic Lyme disease—at least in a model system. Scattered reports in the scientific literature are also consistent with Lyme/Borrelia being present in people following antibiotic treatment. * * *
Rebecca had been headache free for four months when she started her junior year of high school for the second time in September 2010. She was incredibly enthusiastic and passionate about learning. She took delight in everything.
If
4 she had to write a five-page paper, she would write a ten-page paper. And with glee, she’d read it to us. She explained how happy she was to be learning again, given that learning had been ripped away from her in the previous year. She did well during her junior year. * * *
I once had an interesting encounter with the head of infectious diseases at a major hospital. He told me in no uncertain terms that Rebecca did not have Lyme disease. I showed him Rebecca’s Lyme test results and said something like, “If she doesn’t have Lyme disease, then how do you explain these bands in her Western blot?” He seemed baffled, so I asked, “You understand how this test works, right?”
Turns out, he didn’t—he just knew the name “Western blot.” I wondered how he could dismiss her test, especially given her Lyme-like symptoms and her favorable responses to various medications. He said something like, “The company that did that test is not reliable. And besides, she should be IgM negative and IgG positive, since her tests were done months after her alleged tick bite. It’s well known that IgM converts to IgG soon after an infection starts.” IgM? IgG? What was he talking about?
When a pathogen, such as a bacterium or a virus, invades, our immune system fights the infection. Part of the immune system makes antibodies—those carefully crafted proteins that detect a new pathogen with exquisite specificity and target it for destruction. There are several classes of antibodies, but let’s consider the two pertinent ones. The first antibody to appear after an infection is an IgM; they work moderately well, but they are big and clunky, like an old truck. (Call them: “M-antibodies,” for “IgM” or “Moderate.”) But a few weeks after the infection, the body works a miracle and starts making a more effective IgG antibody, which is like a sleek, elegant sports car. (Call them: “G-antibodies,” for “IgG” or “Good.”) G-antibodies are the ones that last, so the body can fight off a new infection by that same pathogen again in the future.
In a typical infection, G-antibodies replace M-antibodies within a few months. I had to admit: that doctor was right. Rebecca was M-antibody positive but G-antibody negative, which is the opposite of expectations at her stage of infection, based on analogy to the standard immune response to a pathogen. I asked him what he thought Rebecca had. He didn’t know. This was typical: doctors dismissing chronic Lyme disease, but having no alternative explanation.
As a scientist, when I am faced with conflicting findings, I try to think in terms of “the weight of the evidence.” Rebecca’s symptoms had been relieved by antibiotics and anti-protozoa medications, which indicates a co-infection with both a bacterium and a protozoan. Only one vector is known to deliver both: a tick. She also had Lyme-like symptoms, as well as no evidence of other maladies. Even though I couldn’t explain her positive M-antibody test result, the weight of the evidence suggested to me that she had chronic Lyme disease. When considering scientific findings that seem baffling, I often recall a quote from Shakespeare: “There are more things in heaven and earth, Horatio, than are dreamt of in your philosophy.”
As
5 unlikely as it seemed, my instincts were that the test was right, but there was something unusual about the immune response to Lyme/Borrelia. * * *
In November 2013, I attended a conference entitled, “Challenges, Controversy in Lyme Disease and Tick Borne Illness Care Symposium” at the Massachusetts General Hospital. I heard a remarkable lecture by Dr. Nicole Baumgarth of the University of California, Davis. Her work was subsequently published in 2014 and 2015. She showed that after mice were infected, Lyme/Borrelia bacteria migrate to lymph nodes, which are sites where much of the immune response occurs.
What! Why would an infectious pathogen purposely go to one of the key sites in the body designed to defeat it? It turns out—once in lymph nodes—Dr. Baumgarth showed that Lyme/Borrelia damage the apparatus that creates those “sleek, elegant sports car” G-antibodies. (The apparatus is called the “Germinal Center.”) Once this apparatus is disrupted, G-antibodies are no longer made. Dr. Baumgarth concluded that “(Lyme/Borrelia) causes the structural disintegration of lymph nodes in infected mice…” and “drives (the immune) response away from protective, high-affinity and long-lived antibody responses and toward…short-lived antibodies of limited efficacy.” (M-antibodies are the ones of “limited efficacy.” They are not made in Germinal Centers, and they cannot rid the body of Lyme/Borrelia completely.)
Lyme/Borrelia, thus, goes to lymph nodes to cripple the apparatus that makes the most effective, long-term component of the immune system, G-antibodies. This is the first time that such a mechanism has been described for a pathogen. But it’s worse than that. The mouse immune system is not only crippled for making Lyme/Borrelia-specific antibodies, it is also crippled for mounting an immune response against other pathogens. Dr. Baumgarth studied the response to Influenza.
That is staggering! If it holds true in humans, then individuals with a persistent Lyme/Borrelia infection would be less able to fight off other co-infecting pathogens delivered by the original tick bite, such as protozoa. Furthermore, infected individuals are also expected to be more prone to other infections, such as the flu. Admittedly, no evidence currently exists that this mechanism operates in humans, but it seems likely to me, especially because it provides a plausible explanation for why Rebecca tested M-antibody positive but G-antibody negative. Furthermore, Rebecca is not alone: according to one Lyme testing laboratory, many people tested for Lyme disease are only M-antibody positive. . * * *
In fall 2011, Rebecca started her senior year of high school. She was excited. She was also excited to be thinking about where to apply to college. But in early October—after sixteen months—her headache returned. Was it due to Lyme/Borrelia or to a protozoa? We guessed. Following treatment with anti-protozoa medications, Rebecca felt better almost immediately. It wasn’t long before her headaches were minimal. She did well in her first semester as a senior in high school.
We were
6 optimistic. In January 2012, however, her headache gradually started getting worse again. By March we were sure the anti-protozoa medications had stopped working. This time we guessed “bacteria” and switched her back to antibiotics. * * * But why were we guessing? Why not just do a test? To adequately address that question would require its own article, but the bottom line is that no direct, definitive test for Lyme/Borrelia has been established, and existing tests are complex and not reliable.
First, no simple blood test exists (like for cholesterol). Furthermore, some bacteria can be cultured reliably from blood, like those causing blood poisoning (septicemia), but not Lyme/Borrelia. But even if it could be, Lyme/Borrelia levels can be low in blood, even when it is present in other places, like in connective tissue and/or biofilms (explained below).
Blood samples, however, can be used to detect the presence of the body’s M-antibodies and/or G-antibodies against Lyme/Borrelia, which is an indirect test. The best antibody test is a “Western blot,” though it is very idiosyncratic and complex, especially compared to simple tests, like for cholesterol. (In fact it is actually not a classic Western blot.) Plus, M-antibodies and G-antibodies don’t appear right away, so the test can’t be done immediately after a tick bite. These and other complications have not been adequately addressed or resolved. Rebecca has tested positive four times and negative three times for Lyme/Borrelia. She tested positive one out of four times for Babesia. She also tested positive two out of three times for Anaplasma—another tick-borne bacterium. These tests were not planned as if we were conducting a scientific study, but generally (though not always), her tests were positive when her symptoms were significant and negative when her symptoms were absent or subdued. * * *
The absence of a reliable test has made Lyme disease diagnosis uncertain, complicated and confusing. Doctors make judgments based on their experience with other pathogens and their instincts. I’ve heard a number of doctors state something like, “Your daughter can’t have Lyme disease, because it’s well known that four weeks of antibiotic treatment is sufficient to eliminate a bacterial infection.” That’s certainly true for many infections, but aren’t some pathogens nasty enough to cause persistent infections that are hard to get rid of? If so, does Lyme/Borrelia share anything in common with them?
When I described our immune system, I mentioned antibodies. Our immune response, however, is complex; one component, “innate immunity,” begins immediately after an infection starts. Many pathogenic bacteria that cause persistent infections disrupt innate immunity (e.g., Salmonella), as do viruses (e.g., norovirus). In mice, Lyme/Borrelia has been shown to have two mechanisms to blunt innate immunity. (The OspC protein inhibits macrophages, and the OspE protein disrupts the “complement system.”) Sleeping sickness is actually a coma caused by a tropical trypanosome, which establishes a chronic infection, often resulting in death. The sleeping sickness trypanosome also defeats the immune system, but it uses a very different strategy. Infected individuals generate antibodies
7 against a prominent protein on the cell surface of the trypanosome. But when the trypanosome senses those antibodies, it pulls a clever trick. It changes the amino acid sequence of that cell surface protein, such that the antibody no longer works, and the immune system has to start over. And when the trypanosome senses that new antibody, it changes the amino acid sequence again. And again. And again…
Guess what? In mice, Lyme/Borrelia does the same thing with one of its cell surface proteins (VlsE). Hiding is another strategy used by pathogens to establish a persistent infection. For example, some bacteria hide inside a protective sack composed of a “biofilm,” which they make, like a cocoon. Biofilm sacks block the penetration of both antibodies and antibiotics. Cystic Fibrosis is a genetic disorder that leads to excessive mucous buildup in the lung.
This mucous provides a rich broth, which the bacteria Pseudomonas aeruginosa colonizes as a biofilm sack, thus allowing it to survive antibiotics and the immune system. The persistent Pseudomonas infection eventually contributes to the premature death of individuals with Cystic Fibrosis. Evidence shows that Lyme/Borrelia also form biofilm sacks, which (by analogy) could provide a reservoir to perpetuate a chronic infection.
There are other hiding mechanisms. The immune system eventually eliminates most cells infected by the chickenpox virus, but it hides in nerve ganglia, which are not monitored by the immune system. Later in life, the latent virus can emerge from its hiding place in response to various stresses and cause shingles. Lyme/Borrelia also does this, using its DbpA protein to hide in connective tissues, which have a low blood supply. Low blood levels result in low exposures to antibodies and antibiotics. A great place to hide. I have mentioned five mechanisms by which pathogens can create a persistent infection. (There are others.) Lyme/Borrelia has all five. No one knows where this places it on the scale of pathogens best equipped to cause a persistent infection, but it is certainly no slouch in terms of having well-established mechanisms to establish persistence. In the absence of antibiotics, Lyme/Borrelia only has to defeat the immune system in order to develop a persistent infection—and it clearly can. But does having these five mechanisms mean that it can establish a chronic infection when antibiotics are added to the battle? Dr. Barthold showed that it does in mice. But what about in people? Indirect evidence (e.g., persistent symptoms) certainly suggests it can.
But in all honesty, I would characterize the direct evidence in people currently as being strongly suggestive, but not ironclad. Nevertheless, each of those five mechanisms make it harder for the body to rid itself of Lyme/Borrelia. And, remember, it’s a self-renewing life form, so even one surviving microbe can in principle initiate a new round of infection. Nothing is known about how many Lyme/Borrelia must survive to start a new infection, but a few pathogens need but a single microbe to start an infection, while others only need 10-100 microbes. * * *
After switching back to antibiotics in March 2012, Rebecca’s headaches began getting better, which suggested that indeed it had been her Lyme/Borrelia bacterial infection that had flared up again. Her symptoms varied from being barely noticeable to being bad. But she maintained her
8 buoyancy, and managed to limp across the finish line and graduate from high school. Rebecca was accepted into college and began her studies in fall 2012. Given her situation, she decided to take only two courses. The rigors of college were challenging, and she struggled with both occasional headaches and other symptoms, notably fatigue, which often left her so exhausted she had to nap during the day. About halfway through her first semester, school got to be too much. She stopped going to class. Professors were contacted. They were understanding.
One anecdote stands out. She attended no classes in her introductory psychology class between the first and second exam. But she felt better during the Thanksgiving break, so she taught herself the material. She asked her psychology professor to give her a makeup exam. She got an A-. I couldn’t believe it. When I asked, she said something like, “I’m used to teaching myself. How do you think I finished high school?” * * *
The Centers for Disease Control and Prevention (CDC) does not accept the existence of chronic Lyme disease, though it does recognize that some people formerly with Lyme disease can experience ongoing Lyme-like symptoms after antibiotic treatment. They call it “Post-Treatment Lyme Disease Syndrome” (PTLDS). CDC acknowledges that the “cause of PTLDS is not yet known,” but they favor that “lingering symptoms are the result of residual damage to tissues and the immune system that occurred during the infection.” An example of what they mean is that Lyme/Borrelia might trigger an autoimmune response. * * *
If the CDC’s preferred hypothesis for PTLDS is correct, then it must somehow be reconcilable with Rebecca’s history. Their hypothesis implies that patients with lingering Lyme-like symptoms not only don’t have a chronic bacterial infection, they also don’t have a chronic co-infection. Rebecca has had five major headache flare-ups, each of which was significantly relieved—twice by antibiotics and three times by anti-protozoa medications.
Furthermore, on several occasions, we know that one medication (for protozoa) worked, while another (for bacteria) did not, and vice versa. How could antibiotics and anti-protozoa medications have an impact on “residual damage to tissues and the immune system that occurred during the infection…”? A number of physicians have suggested that some antimicrobials have anti-inflammatory effects, which may have helped Rebecca. This is the most commonly offered rationale that is consistent with the CDC’s preferred hypothesis.
However, to be true, not only would secondary anti-inflammatory effects of antimicrobials have to dominate, but also sometimes only the anti-inflammatory effect of an antibiotic must have been effective, while other times it must only have been the secondary effects of an anti-protozoa medication. Furthermore, drugs whose primary purpose is to be anti-inflammatory—which have never helped relieve Rebecca’s symptoms—must have been ineffective for some reason. The notion that Rebecca’s responses could have been due to anti-mircobials working as anti-inflammatories—where only antibiotics work sometimes and only anti-protozoa medications
9 work other times, while true anti-inflammatory drugs don’t work at all—strikes me as virtually impossible. Scientists often think in terms of “parsimony”—what is the most likely explanation for an observation? Parsimony suggests to me that the obvious hypothesis is most likely: Rebecca’s Lyme-like symptoms have been relieved by antibiotics and anti-protozoa medications, because she really has had a chronic bacterial and protozoan infection. * * *
So why are the CDC and others so convinced that chronic Lyme disease does not exist? Historically, they have relied heavily on the interpretation of findings in four scientific studies. (Hereafter, referred to as the “four studies”). In detail, these four studies differed, but the basic approach was similar. Patients (1) with a confirmed history of Lyme disease, (2) who had been treated with antibiotics, but (3) who subsequently experienced persistent symptoms, were treated with an antibiotic (ceftriaxone/rocephin) intravenously (minimum time: 4 weeks), after which their symptoms were assessed subjectively. The authors of those four studies concluded that symptoms did not improve to an extent that was statistically significant and/or clinically relevant, and, thus, antibiotic treatment of patients with ongoing Lyme-like symptoms was not warranted. Based on these studies, the CDC and others extrapolated that if antibiotic treatment didn’t help, implicitly Lyme disease could not be chronic. * * *
After Rebecca’s brief respite from symptoms during Thanksgiving break in 2012, her headache got worse again. There was nothing to do but drop out of college. At that time she was being treated with antibiotics. But what if her protozoa infection had returned? In January 2013, she was switched back to anti-protozoa medications. She responded; her headache improved again. Though she felt better, it was too late to return to college. Plus, she had no confidence that her symptoms would remain stable enough to permit her to cope with the rigors of school. She didn’t know what to do. Fortunately, Rebecca is artistic, and she began to consider being an artist. One of her artistic skills is unusual. She loves doing intricate line drawings, often in symmetrical shapes, reminiscent of mandalas. She found this style of artwork to be soothing; it took her mind off headaches. She started doing a lot of mandala art. In the summer of 2013, unfortunately, her hand developed a tremor. When she tried to draw a fine straight line, it came out jagged and wavy. The mandala artwork, which had become so satisfying and soothing, became impossible. * * *
I’ve come to believe that there are four problems associated with the four studies that the CDC and others have used to conclude that chronic Lyme disease does not exist. The first problem was pointed out by Ms. Allison DeLong, a biostatistician at Brown University, who performed a statistical review of those four studies. There was insufficient evidence to permit a conclusion that antibiotic treatment definitively did not help patients with ongoing Lyme-like symptoms. The major issue was—for the types of statistical methods applied in each
10 of the four studies—too few subjects were included, which is called being “underpowered.”
The second problem was that in fact Ms. DeLong found evidence in two of the four studies of a statistically significant improvement for one symptom, fatigue, when the subjects were subdivided into those with the worst cases of fatigue at the time of enrollment. This is exactly the subpopulation that would be expected to be most revealing about a significant trend. Actually, the authors of those two studies also noted this trend. Why wasn’t it highlighted? The authors believed that all symptoms tested (often three) should improve in parallel, or else the improvement in one symptom (fatigue) must be a red herring. There is no reason to believe that this supposition is necessarily correct. The authors of the other two studies have never released their data, making it impossible for others to reanalyze the data for such a trend. The third problem was the “one size fits all” use of a single antibiotic (ceftriaxone/rocephin) for the subjects in those four studies. Lyme literate physicians have discovered that different patients respond best to different antibiotics, which can also change with time. This has certainly been true for Rebecca, who preferentially responds to antibiotics in the X and Y classes. Why would that be? It is unknown, but may relate to complexities of the infection.
Lyme/Borrelia can hide in different tissues; it can adopt different physical forms (a cork-screw shape, a spherical shape and a biofilm sack); plus, there are different Borrelia species and even different strains within a species.
The fourth problem is most significant to my mind: the implications of co-infections were ignored. Consider this scenario. Imagine that 20% of subjects in those four studies responded significantly to intravenous antibiotics; such a response rate would likely be too low to give a statistically significant outcome. Now imagine that 50% of those subjects didn’t respond because they were primarily suffering from a protozoa co-infection—much like Rebecca in late 2009, when she did not respond to intravenous antibiotics, but she did respond to anti-protozoa medications. If the 50% of subjects with co-infections could be excluded, then the percentage of subjects responding positively to intravenous antibiotics would have doubled from 20% to 40%, which would have significantly improved the chances of detecting statistically significant outcomes for all symptoms. The authors in those four studies had no way of assessing if a subject was primarily suffering from a co-infection. At the very least, though, they should have mentioned this limitation and reflected on its implications.
Based on the scenario in the previous paragraph, 70% of subjects would have a tick-borne illness, and yet none would be treated if the recommendations of those who deny chronic Lyme disease were followed.
Several other studies have been done more recently. One study had more subjects, who were treated longer and were followed longer to assess outcome. The conclusion: “Prolonged intravenous antibiotic therapy is associated with improved cognition, fatigue and myalgias (muscle pain)…” However, this study was only designed to assess whether an “association” exists between treatment and improvement; to establish cause-and-effect would have required even more subjects.
Nevertheless, the “association” was clear. The second study was published in 2016, and the authors argue against chronic Lyme disease. A critique of it would be too involved, so I provide a link to the paper and criticisms, which include that co-infections were not considered, and the “control group” was not proper.
11 * * *
When Rebecca could no longer draw straight lines, because of her hand tremor, she didn’t give up. She had an idea based on a technique called “paper cut art.” She drew her wavy lines, and then cut out the white space between the lines using an exacto knife. Even though her hand shook, she could position the exacto knife precisely, and—when she pressed hard—she could make a non-wavy cut. That’s buoyancy! * * *
When I read scientific papers that support the notion that chronic Lyme disease does not exist, they seem persuasive. In all honesty, if I hadn’t read papers using model systems, and if I didn’t know of the weaknesses in those four studies, I too would probably lean toward the denial of chronic Lyme disease.
More importantly, though, I have had a first hand experience with someone suffering with a chronic disease, so I’ve come face-to-face with having to make real decisions about how to help a real person struggling with pain. I doubt that most deniers of chronic Lyme disease have had such an experience.
Looking back, here’s my perspective. When we followed the hypothesis that Rebecca has chronic Lyme disease, we ended up with a reasonably healthy daughter. But when we followed the alternatives offered by those who believed that something other than chronic Lyme disease was likely, we got nowhere. We vigilantly pursued every possibility they suggested, along with everything else we could think of. They all led nowhere. Rebecca has struggled with Lyme disease and its co-infections for over seven years. Fortunately, for the past three years she has been largely headache free, principally because her current doctor treats her for an ongoing chronic tick-borne illness, which requires vigilant, on-going reassessments and tinkering. Consequently, she has had no major debilitating flare-ups recently. Though she is not cured, her life is more normal—her main symptom now being a lack of stamina (fatigue). She typically rates her overall health as being 75%.
Because of her progress, Rebecca is now making her way as an artist and is also a teacher in an afterschool program. Though her life has not followed the path she once imagined, she is happy, because she loves doing artwork and working with young children. I couldn’t be more proud. Given the intense and often acrimonious debate over chronic Lyme disease, my wife didn’t want Rebecca to be named in this article for fear that she would somehow be targeted. Rebecca insisted otherwise. She wants readers to know that the story I’ve told was neither fabricated nor delivered to me second-hand. She also believes that if telling her story can help even one person avoid what she’s been through then it’s worth it.
Disulfiram (Tetraethylthiuram Disulfide) in the Treatment of Lyme Disease and Babesiosis
A
drug called Disulfiram, used to treat alcohol use disorder by making
patients sick when they consume alcohol, was identified in a drug
screening project as a possible treatment for #Lymedisease.
This new paper presents three case studies. Further research is needed,
including proper clinical trials to establish limits of clinical
utility and safety.
Maladie de Lyme: une chambre hyperbare pour soulager Jules
|
Près
d'Alençon dans l'Orne,le petit Jules est atteint d'une forme sévère de
la maladie de Lyme,une infection causée par les tiques. Depuis quelques
mois,il ...
france3-regions.francetvinfo.fr
|
PRÉVENTION | Les tiques dans le viseur de l'INRA
radiodreyeckland du 11.06.19: podcast CITique...
À propos de ce site web
radiodreyeckland.com
Des acteurs du milieu sportif et des accueils collectifs (comme les centres…
La section Saône et Loire de France lyme tiendra un stand samedi 15 juin de 9 à 13 h , quartier de Bellevue , 71300
La section Saône et Loire de France lyme tiendra un stand samedi. Venez nous rencontrer et échanger avec nous
Mother left paralysed and blind after catching Lyme disease
À propos de ce site web
dailymail.co.uk
Christine Jennings, 57, of Leicester, was bitten by an infected tick 25…
Inscription à :
Articles (Atom)