Tuesday, December 31, 2013

Happy new year, everybody!

Dear readers,

It's been a pleasure corresponding with many of you over this past year. I was just sitting here answering a few more questions sent to me by people who are looking for various Lyme-literate doctors, dentists, and so forth. I happened to look out the window and saw the last sunset of the year. I thought I would share it by posting it here on the blog. May this mark the beginning of a new year of healing for you and for those you love. 


Sunday, December 29, 2013

Brainstem abnormalities and vestibular nerve enhancement in acute Neuroborreliosis

Nadja A Farshad-Amacker*, Hans Scheffel, Thomas Frauenfelder and Hatem Alkadhi

Author Affiliations

Diagnostic and Interventional Radiology Department, University Hospital of Zurich, Raemistrasse 100, Zurich 8091, Switzerland

For all author emails, please log on.

BMC Research Notes 2013, 6:551  doi:10.1186/1756-0500-6-551

The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1756-0500/6/551

Received:31 July 2012
Accepted:16 December 2013
Published:21 December 2013

© 2013 Farshad-Amacker et al.; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.



Borreliosis is a widely distributed disease. Neuroborreliosis may present with unspecific symptoms and signs and often remains difficult to diagnose in patients with central nervous system symptoms, particularly if the pathognomonic erythema chronica migrans does not develop or is missed. Thus, vigilance is mandatory in cases with atypical presentation of the disease and with potentially severe consequences if not recognized early. We present a patient with neuroborreliosis demonstrating brain stem and vestibular nerve abnormalities on magnetic resonance imaging.

Case presentation

A 28-year-old Caucasian female presented with headaches, neck stiffness, weight loss, nausea, tremor, and gait disturbance. Magnetic resonance imaging showed T2-weighted hyperintense signal alterations in the pons and in the vestibular nerves as well as bilateral post-contrast enhancement of the vestibular nerves. Serologic testing of the cerebrospinal fluid revealed the diagnosis of neuroborreliosis.

Borreliosis; Brain stem; MRI; Neuroborreliosis; Vestibular nerve enhancement


Borreliosis (Lyme disease) is a world wide distributed disease, transmitted by ticks, with particular focus in Europe and North America. Borreliosis can be classified in three clinical stages (Table 1). Only 40-60% of patients present with erythema chronicum migrans as an initial pathognomonic sign (stage I) [1]. Flu-like symptoms, such as fever, headaches, neck stiffness and arthralgia may be followed by meningeal irritation, encephalitis and/or neuritis (stage II) and further, cardiac involvement may develop. The final stage (stage III) may include arthritis, encephalomyelitis and acrodermatitis chronica atrophicans [2] (Table 1).

Table 1. Stages of borreliosis

The diagnosis of neuroborreliosis is often challenging, particularly if the pathognomonic erythema chronicum migrans does not develop or is missed. Thus, it seems emergent to call for vigilance in case of unspecific presentations of the disease which might have devastating consequences if not recognized and treated early. In neuroborreliosis, magnetic resonance imaging (MRI) may show meningeal and cranial nerve enhancement after contrast administration [3-5] and/or signal abnormalities in the white matter of the brain, although rarely reported [6].

We present a 28-year-old patient infected with neuroborreliosis in whom MRI showed T2-weighted (T2w) hyperintense signal alterations in the pons and vestibular nerves as well as bilateral post-contrast vestibular nerve root enhancement.

Case presentation

A 28-year-old Caucasian female presented with headaches and fever of unknown origin lasting for two weeks. The patient noticed a tick bite two weeks prior to the onset of fever and headaches. Past history and family history were otherwise unremarkable.

At the time of an ambulatory exam by a general practitioner (about three weeks after the tick bite), laboratory investigation e.g. complete blood cell count (CBC), C-reactive protein (CRP), electrolytes, liver enzymes, albumin, creatinin, lactate dehydrogenase (LDH), thyroid stimulating hormone (TSH), free thyroxine (free T4), glucose and Borrelia serum screening test were shown within normal limits. No abnormalities of the skin were noted. The patient was treated with non-steroidal analgetics and returned home.

The fever resolved spontaneously after two weeks (four weeks after the tick bite), however, the headaches remained and were further accompanied by neck stiffness, fatigue, nausea, weight loss of 5 pounds with decreased appetite, an intentional- and resting tremor, and diffuse disturbances in coarse coordination of the upper extremities. Finally, the patient developed sudden onset of immobilizing vertigo.

Eight weeks after the tick bite, blood laboratory evaluation was repeated. CBC, CRP, electrolytes, liver enzymes and creatinin were all still within normal limits. But at that time the results showed reactive borreliosis (Borrelia screening test: enzyme-linked immunosorbent assay (ELISA)-Immunoglobulin G (IgG)-antibody > 200 U/ml and ELISA-IgM-antibody >100 U/ml; normally each < 9 U/ml; Borrelia confirmation test: Western Blot-IgG and -IgM were also positive, reaction against OspC in IgM-antibody-classes, and against 18kD, OspC and VlsE in the IgG-antibody-classes; Medica, Medical Laboratories Dr. F. Kaeppeli AG, Switzerland).

Lumbar puncture was subsequently performed. Cerebrospinal fluid (CSF) showed an increased protein count (2.006 g/l, normally 0.2-0.4 g/l), increased lactate level (2.5 mmol/l, normally 1.2-2.1 mmol/l), slightly lowered glucose level (2 mmol/l, normally 2.4-4.2 mmol/l) and an increased lymphocyte (252 cells/ul, 99.5% lymphocytes) and IgG-antibody count (0.353 g/l, normally <0.051 g/l). Further, CSF tests for viral agents such as early summer meningoencephalitis (ESME), human immunodeficiency virus (HIV), cytomegalovirus (CMV), enterovirus, epstein-barr-virus (EBV), herpes simplex virus (HSV) and varicella zoster virus (VZV) were negative. However, reactive Borrelia burgdorferi IgG- and IgM-antibodies were positive using an enzyme immunoassay (EIA) test (Immunoblot IgG with recombinant antigens: B. burgdorferi VIsE and p41 positive and Immunoblot IgM with recombinant antigens: B. burgdorferi VIsE, p39, and OspC positive; Institute for Medical microbiology, University Hospital of Zurich, Switzerland).

An MRI of the brain was performed using a 1.5 Tesla MRI unit (Vision, Siemens, Medical Solutions, Erlangen, Germany). Mild hyperintense lesions on T2w TSE images were visible in the pons (Figure 1). Furthermore, strong bilateral T2w hyperintense signal alterations and post-contrast enhancement of the vestibular nerves within the internal auditory canal was noted (Figure 2). No meningeal enhancement, nor any diffusion restrictions were noted.

thumbnailFigure 1. Brainstem abnormalities in a 28-year-old patient. (a) Axial and (b) sagittal T2w- TSE MR- images of the brain show hyperintense signal alterations in the pons (arrows). T2w, T2-weighted; TSE, turbo spin-echo; MR, magnetic resonance.

thumbnailFigure 2. Hyperintense signal alterations and post-contrast vestibular nerve root enhancement in a 28-year-old patient. (a) Axial T2w dark fluid image shows bilateral hyperintense signal in the vestibular nerves. (b) Coronal T1w, post-contrast image shows bilateral enhancement of the vestibular nerves.

Therapy with intravenous ceftriaxone for three weeks was initiated. All symptoms resolved.

Here, we present a patient with hyperintense lesions in the pons and vestibular nerves as well as bilateral vestibular nerves post-contrast enhancement on MRI in a patient diseased with early stage II neuroborreliosis who presented with unspecific encephalopathic symptoms, without the characteristic erythema chronicum migrans and initially normal laboratory parameters but delayed positive reactive Borrelia IgM- and IgG-antibodies.

There are only a few cases reporting neuroborreliosis with brainstem abnormalities. In a recent case report, hyperintense lesions in the pons in a patient with neuroborreliosis having a 2-month history of neck pain, wasting, and fatigue followed by gait disturbance, dysarthria and dysmetria were shown [7]. Another report has described a case of borreliosis involving the brainstem in a 28-year-old man, showing symmetric patchy areas of hyperintensity involving the cerebellar peduncles eventually extending to the pons and cerebellar white matter [8]. Unfortunately, no contrast media was administered in this case [8].

Meningeal and/or cranial nerve enhancement has been reported thus so far. Right trigeminal nerve enhancement in a 15-year-old boy was previously described in a case report [5]. Further, simultaneous enhancement and thickening of the third and sixed cranial nerve [9] in a 57-year-old woman and also bilateral enhancement of cranial nerves III-V, as well as of cranial nerves VII and VIII on the left side in a 12-year-old girl [10] have been reported.

A retrospective study of 66 patients revealed that positive neuroimaging findings on MRI of patients with neuroborreliosis are relatively unusual and the authors concluded that findings are usually focal lesions in the white matter of the brain or nerve-root or meningeal enhancement [4]. Unlike previously reported studies, nerve-root or meningeal enhancement was detected in a substantial percentage of patients [4].


Patients with neuroborreliosis may present with unspecific neurologic symptoms and an MRI as a noninvasive imaging tool showing brain stem abnormalities and/or nerve root enhancement may help in establishing the diagnosis, especially since Borrelia antigens/antibodies are not routinely assessed in CSF. If the disease is missed and left untreated it might end in devastating consequences.


Written informed consent was obtained from the patient for the publication of this report and any accompanying images.

Competing interest

The authors declare that they have no competing interests.

Authors' contributions

All authors drafted and corrected the manuscript. All authors read and approved the final manuscript.


  1. Nadelman RB, Wormser GP: Erythema migrans and early Lyme disease.

    Am J Med 1995, 98:15S-23S. PubMed Abstract | Publisher Full Text OpenURL

  2. Nau R, Christen H-J, Eiffert H: Lyme disease–current state of knowledge.

    Dtsch Arztebl Int 2009, 106:72-81. PubMed Abstract | Publisher Full Text | PubMed Central Full Text OpenURL

  3. Nelson JA, Wolf MD, Yuh WT, Peeples ME: Cranial nerve involvement with Lyme borreliosis demonstrated by magnetic resonance imaging.

    Neurology 1992, 42:671-673. PubMed Abstract | Publisher Full Text OpenURL

  4. Agarwal R, Sze G: Neuro-lyme disease: MR imaging findings.

    Radiology 2009, 253:167-173. PubMed Abstract | Publisher Full Text OpenURL

  5. Köchling J, Freitag HJ, Bollinger T, Herz A, Sperner J: Lyme disease with lymphocytic meningitis, trigeminal palsy and silent thalamic lesion.

    Eur J Paediatr Neurol 2008, 12:501-504. PubMed Abstract | Publisher Full Text OpenURL

  6. Krüger H, Heim E, Schuknecht B, Scholz S: Acute and chronic neuroborreliosis with and without CNS involvement: a clinical, MRI, and HLA study of 27 cases.

    J Neurol 1991, 238:271-280. PubMed Abstract OpenURL

  7. Haene A, Troger M: Diffuse hyperintense brainstem lesions in neuroborreliosis.

    Neurology 2009, 73:326-326. PubMed Abstract | Publisher Full Text OpenURL

  8. Kalina P, Decker A, Kornel E, Halperin JJ: Lyme disease of the brainstem.

    Neuroradiology 2005, 47:903-907. PubMed Abstract | Publisher Full Text OpenURL

  9. Lell M, Schmid A, Stemper B, Maihöfner C, Heckmann JG, Tomandl BF: Simultaneous involvement of third and sixth cranial nerve in a patient with Lyme disease.

    Neuroradiology 2003, 45:85-87. PubMed Abstract | Publisher Full Text OpenURL

  10. Huisman TA, Wohlrab G, Nadal D, Boltshauser E, Martin E: Unusual presentations of neuroborreliosis (Lyme disease) in childhood.

    J Comput Assist Tomogr 1999, 23:39-42. PubMed Abstract | Publisher Full Text OpenURL


Thursday, December 26, 2013

Severe tick disease virus investigated in Mass., Maine patients

I have decided to reprint this entire article (I hope it's okay with the Boston Globe as a public service) because of the level of danger of the microbe described.

By Kay Lazar
Boston Globe Staff
(c) Boston Globe
December 26, 2013

Disease trackers in Massachusetts and Maine are investigating two apparent cases of a rare and severe tick-borne illness, providing new evidence of the suffering that can be inflicted by ticks and prompting warnings that the threat can persist into December.

Investigators suspect that the infections were caused by Powassan virus or a related virus, which can spawn headaches, vomiting, confusion, seizures, memory loss, and long-term neurological problems in those who survive the infection. The virus is believed to be fatal in 10 to 15 percent of those who are exposed.

Blood tests show that a Maine woman who died last week was infected with the virus. Health officials said it appears the woman, from mid-coast Maine, had not been traveling and probably was infected locally.

Massachusetts health authorities are investigating a suspected Powassan infection in a resident who became ill in October. Dr. Catherine Brown, state public health veterinarian, declined to identify the patient, or the county where the person lives, to protect confidentiality, but said the person survived.

Brown said the Massachusetts and Maine cases should serve as reminders to residents to continue checking themselves for ticks and tick bites, even during the winter.

Yet there are aspects of the recent cases that remain mysterious to investigators — most prominently, the type of tick responsible for the infections.

Powassan typically is spread by the woodchuck tick, but disease investigators are concerned that the more common deer tick may be the culprit in the Maine and Massachusetts cases, raising concerns because deer ticks are prevalent throughout the Northeast, already inflicting widespread misery as the major carrier of Lyme disease.

Sam Telford III, an infectious disease professor and tick specialist at the Cummings School of Veterinary Medicine at Tufts University, published a study in 1997 that identified a virus in Massachusetts ticks similar to Powassan, but spread by deer ticks. He called it deer tick virus.

Telford and colleagues then hunted for Massachusetts residents infected with that virus, but could not find any, and concluded it was perhaps not a risk to humans.

But about five years ago, another published study identified the case of a New York resident who died from a deer tick virus similar to Powassan.

Since then, health officials have been on the lookout for this Powassan-like variant spread by deer ticks. The hunt comes amid increasing reports of patients in several states, notably New Hampshire, New York, Minnesota, and Wisconsin, infected with Powassan virus. Roughly 50 cases of the virus have been reported to the US Centers for Disease Control and Prevention in the past decade.

There is no treatment for the disease.

Maine’s last confirmed Powassan case was in 2004, but Dr. Sheila Pinette, director of Maine’s Center for Disease Control and Prevention, said state health officials were watching for the illness because of a reported case in New Hampshire in August.

She said Maine health care providers are not required to report suspected Powassan to the state, a rule that is likely to be changed to better track the illness. “If we know we have one, we recognize we may have others,” Pinette said, “so we need to track it to understand the prevalence and if it’s increasing in our state.”

A new rule in Massachusetts that became effective last week requires health care providers to report suspected Powassan cases to the Department of Public Health, Brown said.

“It’s not something that’s been on people’s radar, but we know that there is increasing awareness these days of diseases that could be introduced here,” she said.

The state had no documented Powassan cases in the past decade, but anecdotal reports suggest there may have been a handful in that period, she said.

Current testing methods to confirm Powassan illness, which look for signs of the virus in patients’ blood or spinal fluid, cannot distinguish whether the disease was caused by deer ticks or woodchuck ticks, Telford said. Consequently, researchers believe that some, if not many, of the reported Powassan cases have actually been deer tick virus, caused by the more common deer tick.

The only way to distinguish the two illnesses, he said, is to obtain tissue samples from a patient, then grow samples of the virus from that tissue and study the genetic components of that material.

Telford said he is expecting to receive tissue samples from the Maine patient to determine whether she died from Powassan, or from deer tick virus.

“I suspect it’s deer tick virus because there are no woodchuck ticks out this time of year,” he said. Woodchuck ticks are typically active from April through September, he said, but deer ticks are much hardier and known to be active into the winter.

Brown, the Massachusetts public health veterinarian, agrees. “We know that the adult deer ticks can be out and active if temperatures are above freezing,” she said.

Kay Lazar can be reached at Kay.Lazar@globe.com Follow her on Twitter @GlobeKayLazar.

Straight from the Boston Globe:

Monday, December 23, 2013

Depression, suicide and inflammation

A rather technical abstract, but an important study about depression and suicidality. As you kay know, a major cause of sickness and aging turns out to be low-grade, systemic inflammation. Lyme disease (among other bacterial and microbial invaders of the body) can cause such low-level inflammation. Here's a brief summary of a scientific study linking inflammation andr suicide.

AnNeuropsychopharmacology. 2013 Apr;38(5):743-52. doi: 10.1038/npp.2012.248. Epub

2012 Dec 3.


Connecting inflammation with glutamate agonism in suicidality.


Erhardt S, Lim CK, Linderholm KR, Janelidze S, Lindqvist D, Samuelsson M,

Lundberg K, Postolache TT, Träskman-Bendz L, Guillemin GJ, Brundin L.


Author information:

Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm,



The NMDA-receptor antagonist ketamine has proven efficient in reducing symptoms of suicidality, although the mechanisms explaining this effect have not been detailed in psychiatric patients. Recent evidence points towards a low-grade inflammation in brains of suicide victims. Inflammation leads to production of quinolinic acid (QUIN) and kynurenic acid (KYNA), an agonist and antagonist of the glutamatergic N-methyl-D-aspartate (NMDA) receptor, respectively. 

We here measured QUIN and KYNA in the cerebrospinal fluid (CSF) of 64 medication-free suicide attempters and 36 controls, using gas chromatography mass spectrometry and high-performance liquid chromatography. We assessed the patients clinically using the Suicide Intent Scale and the Montgomery-Asberg Depression Rating Scale (MADRS). We found that QUIN, but not KYNA, was significantly elevated in the CSF of suicide attempters (P<0.001). 

As predicted, the increase in QUIN was associated with higher levels of CSF interleukin-6. Moreover, QUIN levels correlated with the total scores on Suicide Intent Scale. There was a significant decrease of QUIN in patients who came for follow-up lumbar punctures within 6 months after the suicide attempt. In summary, we here present clinical evidence of increased QUIN in the CSF of suicide attempters. An increased QUIN/KYNA quotient speaks in favor of an overall NMDA-receptor stimulation. The correlation between QUIN and the Suicide Intent Scale indicates that changes in glutamatergic neurotransmission could be specifically linked to suicidality. Our findings have important implications for the detection and specific treatment of suicidal patients, and might explain the observed remedial effects of ketamine.


PMCID: PMC3671988

PMID: 23299933  [PubMed - indexed for MEDLINE]


Sunday, December 22, 2013

Detection of Lyme Borrelia... in Louisiana

Detection of Lyme Borrelia in Questing Ixodes scapularis (Acari: Ixodidae) and Small Mammals in Louisiana

Authors: Leydet, Brian F.; Liang, Fang-Ting

Source: Journal of Medical Entomology


Lyme borreliosis is caused by spirochetes from the Borrelia burgdorferi sensu lato species complex. In the United States, B. burgdorferi sensu stricto (s.s.; Johnson, Schmid, Hyde, Steigerwalt, and Brenner) is the most common cause of human Lyme borreliosis. With >25,000 cases reported annually, it is the most common vector-borne disease in the United States.

Although approximately 90% of cases are contained to the northeastern and Great Lake states, areas in Canada and some southern states are reporting rises in the number of human disease cases. Louisiana records a few cases of Lyme each year. Although some are most certainly the result of travel to more endemic areas, there exists evidence of locally acquired cases.

Louisiana has established populations of the vector tick, Ixodes scapularis (Say), and a wide variety of potential reservoir animals, yet Lyme Borrelia has never been described in the state. Using culture and polymerase chain reaction, we investigated the presence of Lyme Borrelia in both mammals and questing ticks at a study site in Louisiana. Although culture was mostly unsuccessful, we did detect the presence of B. burgdorferi s.s. DNA in 6.3% (11 of 174) of ticks and 22.7% (five of 22) of animal samples.

To our knowledge, this is among the first evidence documenting B. burgdorferi s.s. in Louisiana. Further investigations are required to determine the significance these findings have on human and animal health.
Keywords: Borrelia; LA; Lyme disease; small mammal; tick

DOI: http://dx.doi.org/10.1603/ME12273

Affiliations: Department of Pathobiological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803

Appeared or available online: December 9, 2013

Poughkeepsie Journal to report on Lyme carditis deaths

I received this in my email today and wanted to pass it along. -Bob

Dear Friends and Associates,

Please share this with others.

Last week the CDC announced  information about deaths due to Lyme Carditis:

Once again Mary Beth Pfeiffer (of the Poughkeepsie Journal (http://www.poughkeepsiejournal.com/) is following up on this with a story which is so important for awareness of both physicians and residents!

Although the CDC reports this as rare at 1%, it may be more common than that. Even if only 1% that is at least 3,000 people when there are over 300,000 a year who contract Lyme disease. We need our medical community on heightened awareness to save unnecessary fatalities.

Additionally, 17 year old honor student Joseph Elone's death attributed to tick-borne disease was front page news in this region in Aug. and Sept. Then we heard nothing more. I hope Mary Beth has an answer for us about what happened to him. If it was Lyme disease, the BIG question we will never know, would his death have been avoided by treatment? Joesph lies in a grave, perhaps a tragedy that could have been avoided for him and his grieving family!

Thanks to the CDC and Mary Beth for bringing awareness to this serious symptom caused by the Lyme spirochete! Let's save lives and let's get these cases reported so we know the true incidence of sudden death from Lyme carditis!

Get Monday's newspaper or online version. Thank the reporter by recommending and commenting. Much gratitude to the CDC for bringing awareness to this!

I always have to add: It is well past time for our government to focus on serious research to reduce tick numbers or STOP their ability to transmit disease pathogens to us (Such research is no longer funded by the NIH. Does that make any common sense? No, of course not!)

Wishing you all the Joys of the Holidays and a Happy, HEALTHIER New Year!

Jill Auerbach
Hudson Valley Lyme Disease Association, Chairperson
Dutchess County Legislative Task Force on Tick and Lyme Disease Reduction, Member
Stop Ticks On People (S.T.O.P.), Board Member
"What's the problem? Well it's the ticks of course!"
PS: If the story does not cover all the other links about this. I will follow up with additional information the CDC sent to myself and others on this topic.

Friday, December 20, 2013

Depression and Autoimmunity: The Biological Connection

This is a very interesting article about depression and inflammation. This fits with my experience, that's for sure. When my body has been undergoing inflammation due to infection (for example, a flu, or a Lyme flareup), I get depressed. The tendency is to think I'm doing something wrong, mentally, emotionally. I can become very self-critical about my entire life, choices I've made, etc. I believe that if I just do something different, I will stop my depression. Trained as a psychotherapist, this makes sense, of course. But what if I'm wrong? What if this is just 'the disease talking' ? Well, it looks as though that just might be right. - Bob

Depression and Autoimmunity: The Biological Connection
August 21, 2013

Comorbid depression is common with chronic inflammatory illnesses such as rheumatoid arthritis and psoriasis. The cycle of symptoms even appears to track simultaneously: For instance, it has been known for some time that depression accompanies psoriasis flares, and resolves when the flares subside.

New research suggests that this depression is no mere reactive consequence of the "frustration and discouragement associated with the illness," as Andrew J. Cutler MD puts it in this recorded interview. It is a "true, underlying biological process" recognizable by measuring mediators of inflammation.

Here Dr. Cutler sheds light on the relationship between neurotransmitters, mediators of inflammation, depression, and chronic disease. He is board certified in internal medicine and psychiatry. Dr. Cutler is on the clinical faculty in the Department of Psychiatry at the University of Florida. He is also CEO and Chief Medical Officer of the Florida Clinical Research Center in Bradenton.

Key quotes:

  • Depression is not only an illness that is seen by psychiatrists. All physicians need to be aware of this, especially as we learn more about the common underlying biologies and the relationships between some very common illnesses and depression.
  • People who have chronic medical conditions such as ... rheumatoid arthritis or autoimmune conditions ... are at risk for depression. What's been under-appreciated is that this is not just a reactive depression ... We now know that the same biologic conditions that are causing the primary condition ... can cause changes in the brain that induce depression.
  • The brain is loaded with hormone receptors and also cytokine receptors, and we know that some of these inflammatory cytokines have a negative effect on the brain's ability to make ... the neurotransmitters serotonin, norepinephrine, and dopamine. ... involved with the pathogenesis of depression. We also know that inflammation can prevent neurogenesis and be toxic to nerve cells. 
  • Charles Raison ... treated a group of patients with depression with infliximab. ... He found that overall the drug did not beat placebo at treating depression. However, he found that when markers for inflammation were elevated, those patients did respond and the depression got better. This is the first time we have a biologic treatment rather than the standard antidepressants.

Read the rest of the story: http://www.musculoskeletalnetwork.com/rheumatic-diseases/content/article/1145622/2155014?GUID=4DB58E07-09DF-49B8-A2C3-4704E7037D8C&rememberme=1&ts=22082013

Wednesday, December 18, 2013

Critique of potential upcoming Lyme vaccine

Important reading about probable upcoming Lyme vaccination

Lyme disease vaccination: safety first

In the Article by Nina Wressnigg and colleagues1 and the related Comment by Paul Lantos2 describing a novel Lyme vaccine, the authors attempt to avoid discussion of the side-effects of the previous Lyme vaccine, LYMErix (SmithKline Beecham, Pittsburgh, USA). This approach to safety issues bodes ill for the new Lyme vaccine candidate.

LYMErix was put on the market in 1998 and withdrawn by the manufacturer in 2002, ostensibly because of poor sales. However, the so-called poor sales were related to safety concerns raised in a class-action lawsuit by more than 400 patients who claimed that they developed Lyme-like symptoms after vaccination with LYMErix.3, 4 Subsequent studies showed that outer surface protein A (OspA), the antigenic component of Borrelia burgdorferi used to create both LYMErix and the new candidate vaccine, induced joint-reactive and nerve-reactive antibodies in animals and human beings vaccinated with the protein antigen.3—6  

Even more disturbing, other studies indicated that LYMErix induced reactivity against multiple target antigens that were never characterised, and these studies called into question the OspA specificity of the vaccine.7, 8 By withdrawing LYMErix when it did, the manufacturer avoided releasing phase 4 post-marketing data that probably would have shown increased side-effects related to the vaccine.9 The data have never been disclosed, and this lack of disclosure has fostered persistent patient mistrust of Lyme vaccine manufacturers.

Wressnigg and colleagues provide minimum safety data about the new OspA-based Lyme vaccine, whereas Lantos glosses over the "largely unsubstantiated safety concerns" about LYMErix. Adoption of this view by Lyme vaccine manufacturers, regulators, and promoters has shaken patient confidence in Lyme vaccines despite the fact that this patient population is generally pro-vaccination.10 Any new Lyme vaccine will need extensive safety testing, more transparency about side-effects, and improved patient communication on the part of the vaccine manufacturer to allay valid patient concerns about safety.4, 10 Let's hope that history does not repeat itself because Lyme vaccine manufacturers, regulators, and promoters once again underestimate or ignore justified patient concerns about Lyme vaccination risks.

RBS serves without compensation on the medical advisory panel of QMedRx Inc. He has no financial ties to the company. LJ declares that she has no conflicts of interest.


1 Wressnigg N, Pöllabauer E-M, Aichinger G, et al. Safety and immunogenicity of a novel multivalent OspA vaccine against Lyme borreliosis in healthy adults: a double-blind, randomised, dose-escalation phase 1/2 trial. Lancet Infect Dis 2013; 13: 680-689.Summary | Full Text | PDF(256KB) | CrossRef | PubMed
2 Lantos PM. Lyme disease vaccination: are we ready to try again?. Lancet Infect Dis 2013; 13: 643-644. Full Text | PDF(94KB) |CrossRef | PubMed
3 Stricker RB. Lymerix risks revisited. Microbe 2008; 3: 1-2. PubMed
4 Smith P, Gaito A, Marks DH. Transcript of FDA Lymerix meeting, BethesdaMD.http://www.lymediseaseassociation.org/index.php?option=com_content&view=article&id=532: lymerix-meeting&catid=129: hhsfood-a-drug-administration-fda&Itemid=531. (accessed Nov 29, 2013).
5 Souayah N, Ajroud-Driss S, Sander HW, Brannagan TH, Hays AP, Chin RL. Small fiber neuropathy following vaccination for rabies, varicella or Lyme disease. Vaccine 2009; 27: 7322-7325. CrossRef | PubMed
6 Marks DH. Neurological complications of vaccination with outer surface protein A (OspA). Int J Risk Saf Med 2011; 23: 89-96.PubMed
7 Molloy PJ, Berardi VP, Persing DH, Sigal LH. Detection of multiple reactive protein species by immunoblotting after recombinant outer surface protein A Lyme disease vaccination. Clin Infect Dis 2000; 31: 42-47. CrossRef | PubMed
8 Fawcett PT, Rose CD, Budd SM, Gibney KM. Effect of immunization with recombinant OspA on serologic tests for Lyme borreliosis. Clin Diagn Lab Immunol 2001; 8: 79-84. PubMed
9 Nardelli DT, Munson EL, Callister SM, Schell RF. Human Lyme disease vaccines: past and future concerns. Future Microbiol2009; 4: 457-469. CrossRef | PubMed
10 Smith P. Remarks to Vaccines and Related Biological Products Advisory Committee, BethesdaMD.http://www.lymediseaseassociation.org/index.php?option=com_content&view=article&id=262: vaccine-remarks&catid=80: controversy&Itemid=76. (accessed Nov 29, 2013).

Response from the development team:
Lyme disease vaccination: safety first — Authors' reply

We refute the assertion by Raphael Stricker and Lorraine Johnson that we avoided discussion of the side-effects of the previously licensed Lyme vaccine, LYMErix, in our report of a novel multivalent candidate vaccine against Lyme borreliosis.1 In our introduction, we provide a full and balanced description of the hypothesised safety concerns associated with the monovalent outer surface protein A (OspA) vaccine LYMErix, and we present and discuss in detail the safety data generated in our phase 1/2 trial of the new multivalent vaccine.  

Conflict of interest statement:
All authors are employees of Baxter. PNB, BAC, NW, and GA own stock and share options in Baxter, and have planned, pending, or issued patents for Lyme vaccines.