Archive for the ‘research’ Category

Detection of Potentially Pathogenic Bacteria From Castor Bean Ticks Carried By Italian Pets

Detection of potentially pathogenic bacteria from Ixodes ricinus carried by pets in Tuscany, Italy

Affiliations expand

Free PMC article


Background: Ticks are vectors of disease-causing pathogens that pose a serious threat to animals and people. Dogs and cats are exposed to tick infestation in multiple ways and can easily transport infected ticks into domestic environments and potentially transfer them to people. Pet owners are at increased risk of picking up ticks from their pets and developing tickborne diseases. This study aims to detect the presence of pathogens of potential public health interest in ticks removed from cats and dogs in Tuscany, Italy.

Methods: The collected ticks were screened for the presence of protozoan (Theileria species and Babesia species) and bacterial (Rickettsia species, Anaplasma species, Ehrlichia species, Chlamydia species, Bartonella species and Coxiella burnetii) pathogens using PCR.

Results: PCR and sequencing analysis revealed that

  • 3% of the ticks were PCR-positive for the presence of Rickettsia helvetica DNA
  • 5 %of ticks were PCR-positive for Bartonella henselae DNA
  • 46% of ticks were PCR-positive for Chlamydia psittaci and Chlamydia abortus DNA
  • None of the examined ticks was PCR-positive for Theileria species, Babesia species, Anaplasma species, Ehrlichia canis or Coxiella burnetii DNA

Conclusion: The results of this preliminary study highlight the importance of monitoring companion animals as indicators to evaluate the health status of their owners. Preventive measures are necessary to limit the spread of zoonotic pathogens from companion animals to people within the home environment.



Ixodes ricinus, aka the castor bean tick is considered a  European species of tick that can transmit the following:

Now, there is the potential of two strains of Chlamydia to be added the growing list, with nearly half of the ticks in the study carrying it.

What does this mean to patients?  Good question.  We may never know because researchers are too busy studying ‘climate change,’ to have time for such silly endeavors as uncovering the effects of polymicrobial illness on patients.

This isn’t the first time we’ve heard of ticks carrying chlamydia:

Here, researchers identify chlamydia along with other pathogens in Alzheimer’s:


Great read on the types of chlamydia: The first two are mentioned in the abstract:

  • Chlamydia trachomatis can be passed from one person to another via unprotected sexual intercourse. Pain English: this is a STD.
  • Chlamydia pneumoniae (C. pneumoniae), a nonsexually transmitted disease that infects the lungs and causes bacterial pneumonia.
  • Chlamydia psittaci is another chlamydia strain that can lead to a rare condition called psittacosis, aka “parrot fever.”  Excerpt:


For more:  Great resources within link for tick prevention methods

More Evidence of Lyme Organism Persistence. Peptidoglycan is only Produced by Metabolically-Active Spirochetes.


Front. Cell. Infect. Microbiol., 07 October 2020 |

Mechanisms of Dysregulated Antibody Response in Lyme Disease

  • 1Global Lyme Alliance, Inc., Stamford, CT, United States
  • 2Edge Bioscience Communications, Sherborn, MA, United States


Lyme disease (LD), caused by the spirochetal bacterium Borrelia burgdorferi, is transmitted by the black-legged tick Ixodes scapularis (Hu, 2016). LD is the fastest growing global tick-borne disease and annually affects >300,000 people in the U.S. alone (Steere et al., 2016). The economic impact is a staggering $1.3 billion dollars per year (Adrion et al., 2015). LD can cause long-term, debilitating symptoms, including arthritis, carditis, and neurological complications (Hu, 2016; Steere et al., 2016). A longstanding question is why antibodies produced during primary infection are not able to completely clear spirochetes or confer protective immunity (Barbour et al., 2008). Antibody titers can remain for years in some LD patients while in others, they wane over time or never develop at all (Kalish et al., 2001). Herein, we describe animal studies that reveal mechanisms behind dysregulated development of adaptive immunity and provide insights that may be relevant to human immunity to B. burgdorferi infection.

Role of Lymphocytes and Antibodies in Lyme Disease Pathogenesis

Antibodies produced through B and T cell interactions either within or outside germinal centers are termed T cell-dependent (TD) whereas those produced without the aid of T cells are T cell-independent (TI). One mechanism whereby B. burgdorferi attempt to evade adaptive immunity is by continuously changing the sequence of a unique surface protein called variable major protein-like sequence (VlsE) (Norris, 2015). Such sequence variation generates a large repertoire of antigenically-distinct spirochetes that become unrecognizable to the antibodies that are mounted against a previous version of this protein. This may allow B. burgdorferi to persist for months or years if not effectively cleared through innate immune response and/or early diagnosis and treatment with antibiotics. Another defensive strategy relies on switching which immunogenic proteins are surface expressed [e.g., Outer Surface Protein A (OspA) and OspC], as spirochetes transit from one environment to another. OspA and OspC are predominately expressed when spirochetes are in the tick vs. the mammalian host, respectively. Notably, whole-proteome microarray analysis revealed that while relatively few B. burgdorferi open reading frames (~15%) encode immunogens, those that do elicit the same detectable antibodies in naturally infected humans and wild white-footed mice (Peromyscus leucopus), the predominant maintenance reservoir for B. burgdorferi (Barbour et al., 2008). Interestingly, a spectrum of disease severity has been observed in different mouse strains, reflecting their unique genetic composition, which controls the magnitude of humoral responses during B. burgdorferi infection (Weis et al., 1999).

Despite strong antibody responses in animals experimentally-infected with B. burgdorferi and in many LD patients, this does not translate to robust disease-resolving and long-term immunity (Barthold and Bockenstedt, 1993; Aguero-Rosenfeld et al., 1996). In order to explore the mechanisms through which B. burgdorferi infection impacts the immune system and gain an understanding of the role of B and T cells in LD pathogenesis, researchers have conducted studies in mice lacking either or both of these lymphocyte populations.

Pathologies associated with B. burgdorferi infection of mice often spontaneously resolve, although animals may never completely clear spirochetes. In contrast, after infection with B. burgdorferi, severe combined immunodeficient (SCID) and recombination activating gene (RAG)-deficient mice, both of which lack B and T cells, developed severe, persistent arthritis that remained unresolved (Hastey et al., 2012). While B cells regulate disease progression and resolution in wild-type mice (McKisic and Barthold, 2000), adoptive transfer of CD4+ T cells into RAG-deficient mice prior to B. burgdorferi infection increased arthritis and carditis severity (unless B cells were co-transferred), and CD8+ T cell transfer increased arthritis severity (McKisic et al., 2000). Conversely, adoptive transfer of serum from immunocompetent B. burgdorferi-infected mice into SCID mice ameliorated both arthritis and carditis (Barthold et al., 1997; McKisic and Barthold, 2000). Transfer of immune serum into naive recipient mice either prior to or at the time of inoculation also prevented B. burgdorferi infection (Barthold et al., 1997). Immunization of mice with late-stage LD patient sera that demonstrated strong antibody reactivity to several B. burgdorferi proteins, including OspA and B, provided partial protection against B. burgdorferi challenge (Fikrig et al., 1994). These findings reveal that humoral immune responses generated in experimentally-infected mice and LD patients play an important role in the resolution of some of the most commonly reported clinical manifestations (arthritis and carditis), which are driven principally by activation of inflammatory T cells and release of potent inflammatory mediators.

Researchers found unusually strong and persistent TD and TI IgM antibody production in lymph nodes during early infection and in bone marrow later on in the course of murine infection (Hastey et al., 2012; Richards et al., 2015). IgG-secreting plasma cells, on the other hand, accumulate slowly in the bone marrow. Only about 50% of the IgG response is clearly TD and, coupled with IgM, is thought to contribute to the reduction but not elimination of B. burgdorferi from tissues (Hodzic et al., 2003). This TD repertoire of IgG contributes minimally to long-term antibody-mediated immunity, unlike the typical humoral response to bacterial pathogens (Hastey et al., 2012; Tracy and Baumgarth, 2017).

Mechanism(s) of Immune Dysfunction in Lyme Disease

To dissect the mechanisms behind this dysregulated response, Hastey et al. (2012) elucidated distinct stages of altered immune response using a mouse model of LD. In the first phase of infection, B cells accumulated in lymph nodes and induced antibodies in a TI manner and in the absence of germinal centers. In other infectious diseases, such as mumps and HIV, swollen lymph nodes are a frequent early symptom of infection. Normally, the areas in which T and B cells are found in lymph nodes are well-defined. However, in B. burgdorferi-infected mice, this typical architecture was disrupted, with loss of organized B cell follicles and T cell zones (Tunev et al., 2011). Deterioration of B cell follicles, between days 5 and 10 post-infection occurred together with the presence of spirochetes within the lymph nodes (Hastey et al., 2014). In addition, B cells began to accumulate in large numbers, reaching over 70% in some instances and disrupting normal T/B cell ratios (Hastey et al., 2012).

In the second phase, roughly 2–3 weeks later, short-lived germinal centers developed in lymph nodes. These germinal centers gave rise to relatively few antibody-producing plasma cells within bone marrow, leading to a third phase in which plasma cells only slowly accumulated. Lymph node germinal centers disappeared about 1 month after infection, despite the continued presence of bacteria at these sites. Curiously, B cell accumulation occurred after, not before, destructive changes in lymph node morphology. This suggests that the Borrelia infection, not B cell accumulation, somehow drives lymphoid tissue atrophy (Hastey et al., 2014).

So, while B. burgdorferi infection prompts strong serum antibody levels, and titers increase over the course of infection, the antibody response is ultimately ineffective in completely eradicating spirochetes and/or establishing long-term immunity (Tunev et al., 2011; Hastey et al., 2012; Elsner et al., 2015). B. burgdorferi benefits from this maladaptive immune response. This premise is corroborated by a study of antibiotic-treated human LD patients, which included patients who had persistent symptomatology and those who had returned to health within 6 months after diagnosis and treatment (Blum et al., 2018). The researchers focused on plasmablasts, activated B cells that mature into plasma cells within germinal centers. They found that patients who ultimately recovered their health, as compared to those with persistent symptoms, had significantly more plasmablasts during early infection. The researchers determined this by comparing the percentage of plasmablasts as a total of all B cells at the initial clinic visit, during early infection (even before beginning Doxycycline therapy). In addition, patients who ultimately returned to health had significantly higher titers of antibodies to a diverse array of B. burgdorferi proteins (Blum et al., 2018). Taken together, this is evidence that B. burgdorferi infection redirects the adaptive immune system away from a long-term protective antibody response and toward a less efficacious, rapid and strong, though short-lived antibody response (Richards et al., 2015).

Interestingly, Hastey et al. (2014) also provided evidence that Borrelia infection itself may have broader immunosuppressive effects. They tested this by using influenza virus vaccination as a tool to study TD antibody responses. Two groups of mice were influenza-vaccinated, with one group being infected with B. burgdorferi while the other was not. For the first 3 weeks, both groups of mice produced similar amounts of influenza-specific IgG. However, by 4 weeks, and until the study ended at 26 weeks, the B. burgdorferi-infected animals made significantly less influenza-specific IgG than the uninfected mice. By 9 weeks post-infection, there were far fewer influenza-specific antibody-secreting cells in the bone marrow of the Borrelia-infected animals compared to uninfected influenza-vaccinated mice (Elsner et al., 2015). This finding engenders an intriguing question about whether LD might negatively impact vaccination efficacy.

Implications for Diagnostics

There is more to be done in exploring these mechanisms of dysregulated antibody response in LD patients and there are clear implications for development of improved diagnostic tests. Physicians often follow the CDC-recommended two-tiered testing algorithm to detect B. burgdorferi-specific antibodies in patients suspected of having LD (Marques, 2015). The first-tier test is an enzyme-linked immunosorbent assay or ELISA, and if results are positive or borderline, a confirmatory second-tier test is done; a Western immunoblot analysis to detect IgM and IgG antibodies that are specific for B. burgdorferi proteins. In theory, this test determines if a B. burgdorferi infection is active (Marques, 2015). However, this CDC-recommended serodiagnosis may be misleading. In a small study of 79 patients who no longer had symptoms, but had a history of LD with and without arthritis 10–20 years ago, researchers examined antibody titers using the CDC two-tiered test (Kalish et al., 2001). They found that 10 individuals (13%) currently had IgM responses (reflecting initial exposure) to B. burgdorferi and 34 (43%) had IgG reactivity (reflecting longer term exposure) to B. burgdorferi. Antibody titers were even higher for patients who had LD with arthritis (but were currently asymptomatic), as six of 39 (15%) currently had IgM responses and 24 of 39 (62%) had IgG reactivity. This trend also is seen in infected mice, where IgM antibody levels do not wane but stay relatively high along with the increased IgG response (Hastey et al., 2012).

Theoretically, it would be expected that all recovered patients would lack evidence of IgM and many or all would continue to have circulating IgG. The presence of IgM in 13% of patients would be cause for confusion for physicians as the presence of this class of antibody typically wanes with clearance of the pathogen and recovery from infection. Larger studies need to be done to confirm and to explain the reasons for the continued presence of IgM. Another consideration is that high antibody levels, as discussed, may only offer transient protection, with alterations in germinal center architecture and defective production of long-lived plasma cells and memory cells leading to poor immunoprotection in the long-term (Hastey et al., 2012; Elsner et al., 2015).

Future efforts in Lyme disease diagnosis need to focus on distinguishing between active and inactive infection and improving sensitivity in detecting early disease while maintaining high specificity. Diagnosis would be greatly enhanced with the development and broad adoption of point-of-care testing, and simplified diagnosis. Addition of antigen targets expressed very early in LD (e.g., VlsE1 and pepC10) to current antibody-based diagnostic testing procedures have enhanced performance of the diagnostic assays (Porwancher et al., 2011; Marques, 2015). Additionally, direct detection of B. burgdorferi antigens or nucleic acid rather than antibody testing may eventually be possible with the development of advanced technologies (Branda et al., 2018). Not only might direct detection of spirochetal components be indicative of active infection, but the presence of nucleic acids and certain antigens coincides with the earliest stage of infection, when B. burgdorferi-specific antibodies have yet to be produced. Examples include B. burgdorferi DNA detected using PCR (Mosel et al., 2019) and antigens such as OspC (Ohnishi et al., 2001) or peptidoglycan (Jutras et al., 2019). OspC is expressed on spirochetes as they transit from tick to mammalian host (Ohnishi et al., 2001) while peptidoglycan has been shown to persist in patients long after antibiotic treatment has ceased and patients are theoretically cured of active infection (Jutras et al., 2019).

The latter observation strongly supports the notion of persistence of B. burgdorferi after antibiotic treatment as peptidoglycan is only produced by metabolically-active spirochetes.


There has been significant progress in deciphering the mechanistic foundation of B. burgdorferi’s impact on the adaptive immune response, specifically the B cell response and antibody production. While B. burgdorferi initially elicits a strong immune response, the end result is a failure by the immune system to clear the infection. This could set the stage for B. burgdorferi’s persistence (Tracy and Baumgarth, 2017), which may underlie chronic symptoms such as arthritis, carditis, and skin and neurological complications. The many animal studies conducted to date reveal that B. burgdorferi relies upon multiple strategies to evade and disrupt the normal functioning of the immune system. The end results are inhibition of effective B cell responses, disruption of the formation of stable germinal centers, and dampening the production of optimally protective antibodies and establishment of long-term memory cell populations. Importantly, many of these same evasion strategies appear to be employed by B. burgdorferi in LD patients, particularly those suffering from persistent or chronic disease. These intriguing observations provide an excellent foundation and springboard for further animal and human studies, with the goal of increased understanding of LD pathogenesis, better diagnostics, and ultimately novel and more effective therapeutic options for long-suffering patients.

Author Contributions

DB and TS contributed to the writing of this manuscript. All authors contributed to the article and approved the submitted version.

Funding: Publication of this manuscript was financially supported by Global Lyme Alliance, Inc.

Conflict of Interest

DB is the owner of Edge Bioscience Communications, a freelance, contract scientific/medical writing and consulting company.

The remaining author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.


We would like to acknowledge Drs. Mayla Hsu and Nicole Baumgarth for thoughtful review of this manuscript prior to its submission for review.


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Citation: Sellati TJ and Barberio DM (2020) Mechanisms of Dysregulated Antibody Response in Lyme Disease. Front. Cell. Infect. Microbiol. 10:567252. doi: 10.3389/fcimb.2020.567252

Received: 29 May 2020; Accepted: 02 September 2020;
Published: 07 October 2020.

Edited by:  John M. Leong, Tufts University School of Medicine, United States

Reviewed by:  Rachel Maurie Gerstein, University of Massachusetts Medical School, United States, Ronald Mark Wooten, University of Toledo, United States

Copyright © 2020 Sellati and Barberio. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Timothy J. Sellati,


For more:

Early HCQ Associated with 53% Decreased Risk of COVID-19 Patient Transfer To ICU

Early Hydroxychloroquine but not Chloroquine use reduces ICU admission in COVID-19 patients

Open AccessPublished:September 29, 2020DOI:
This paper is only available as a PDF. To read, Please Download here.


  • After the global push for the use of Hydroxychloroquine and Chloroquine there is ongoing discussion about the effectivity of these drugs.
  • Findings of this observational study provide crucial data on a potential protective effect of Hydroxychloroquine in non-ICU, hospitalized COVID-19 patients.
  • Early treatment with HCQ on the first day of admission is associated with a reduced risk of 53% in transfer to the ICU for mechanical ventilation.
  • This protective effect was not observed for Chloroquine, therefore these drugs cannot be regarded as interchangeable.



The global push for the use of hydroxychloroquine (HCQ) and chloroquine (CQ) against COVID-19 resulted in an ongoing discussion about the effectivity and toxicity of these drugs. Recent studies report no effect of (H)CQ on 28 day-mortality. We investigated the effect of HCQ and CQ in hospitalized patients on the non-ICU COVID-ward.


A nationwide, observational cohort study was performed in The Netherlands. Hospitals were given the opportunity to decide independently on the use of three different COVID-19 treatment strategies: HCQ or CQ, or no treatment. We compared the outcome between these groups. The primary outcomes were 1) death on the COVID-19 ward, and 2) transfer to the Intensive Care Unit (ICU).


The analysis contained 1064 patients from 14 hospitals: 566 patients received treatment with either HCQ (n = 189) or CQ (n = 377), and 498 patients received no treatment. In a multivariate propensity matched weighted competing regression analysis, there was no significant effect of (H)CQ on mortality on the COVID-ward. HCQ however was associated with a significant decreased risk of transfer to the ICU (Hazard ratio (HR) = 0.47, 95%CI = 0.27–0.82, p = 0.008), when compared to controls. This effect was not found in the CQ group (HR = 0.80; 95%CI = 0.55–1.15, p = 0.207), and remained significant after competing risk analysis.


The results of this observational study demonstrate a lack of effect of (H)CQ on non-ICU mortality. However, we show that the use of HCQ – but not CQ – is associated with 53% decreased risk of transfer of COVID-19 patients from the regular ward to the ICU. Recent prospective studies have reported on 28 days all-cause mortality only, therefore additional prospective data on the early effect of HCQ in preventing transfer to the ICU is still needed.



This poor drug has been scrutinized like no other – all because of severe conflicts of interest held by our public ‘authorities’. While it isn’t for everyone, and it must be utilized in a certain way, it has been shown repeatedly to work in certain populations. To ban it from use shows the underhanded way ‘authorities’ have dealt with it.

BTW:  The favored golden calf – the expensive yet lucrative anti-viral Remdesivir our public ‘authorities’ are cashing in on is showing itself to be a dud:  Excerpt:

The highly anticipated WHO drug trial called Solidarity found that Gilead’s COVID-19 treatment, remdesivir, had no substantial effect on a COVID-19 patient’s chances of survival. It also found that three other therapeutics were similarly ineffective.

One of those was HCQ, although it has been shown in numerous other studies that if used appropriately, will benefit patients:

Dr. Zelenko, a New York doctor, has successfully treated 1,450 COVID-19 patients with a 99% success rate using a cocktail of hydroxychloroquine, Zinc Sulfate and Azithromycin:  Video with Zelenko in link.


Chest Palpitations in a Teenager as Unusual Presentation of Lyme Disease: Case Report

Chest palpitations in a teenager as an unusual presentation of Lyme disease: case report

Affiliations expand

Free PMC article


Background: The incidence of Lyme disease (LD) in North America has increased substantially in the past two decades. Concomitant with the increased incidence of infection has been an enhancement in the recognition of LD complications. Here, we report a case of Lyme carditis complicated by heart block in a pediatric patient admitted to our children’s hospital. What is unique about this case is that the complaint of chest palpitations is an infrequent presentation of LD, and what it adds to the scientific literature is an improved understanding of LD in the pediatric population.

Case presentation: The patient was a 16-year-old male who presented with the main concerns of acute onset of palpitations and chest pain. An important clinical finding was Erythema migrans (EM) on physical exam. The primary diagnoses were LD with associated Lyme carditis, based on the finding of 1st degree atrioventricular heart block (AVB) and positive IgM and IgG antibodies to Borrelia burgdorferi. Interventions included echocardiography, electrocardiography (EKG), and intravenous antibiotics. The hospital course was further remarkable for transition to 2nd degree heart block and transient episodes of complete heart block. A normal sinus rhythm and PR interval were restored after antibiotic therapy and the primary outcome was that of an uneventful recovery.

Conclusions: Lyme carditis occurs in < 5% of LD cases, but the “take-away” lesson of this case is that carditis can be the presenting manifestation of B. burgdorferi infection in pediatric patients. Any patient with suspected Lyme carditis manifesting cardiac symptoms such as syncope, chest pain, or EKG changes should be admitted for parenteral antibiotic therapy and cardiac monitoring. The most common manifestation of Lyme carditis is AVB. AVB may manifest as first-degree block, or may present as high-grade second or third-degree block. Other manifestations of Lyme carditis may include myopericarditis, left ventricular dysfunction, and cardiomegaly. Resolution of carditis is typically achieved through antibiotic administration, although pacemaker placement should be considered if the PR interval fails to normalize or if higher degrees of heart block, with accompanying symptoms, are encountered. With the rising incidence of LD, providers must maintain a high level of suspicion in order to promptly diagnose and treat Lyme carditis.



Repeat:  Researchers need to refrain from stating that something is “rare” with Lyme disease as:
  • testing misses more than 70% of cases (thousands go undiagnosed)
  • much fewer report the EM rash than is quoted
  • this is still a misunderstood illness that doctors are woefully uneducated on.  If a patient doesn’t present with the EM rash, doctors unfamiliar with the wide symptom presentation are not going to catching this.

For more:

Click on image to see better. The graph is clear that there is a wide range of those with those finding the EM rash. While the EM rash is diagnostic for Lyme disease, many do not get it. In the first ever patient group in Lyme, Connecticut, only a quarter had the rash:

Again, mainstream medicine continues with abysmal testing and ancient dogma that is hurting patients.

More accurate scientific language would be: “Heart palpitations are rarely reported in the literature.”  What happens in the real world is often quite different than what is reported in the literature – particularly with Lyme as research has been hijacked by The Cabal:

BTW: I had chest palpitations, my husband had chest palpitations, and most of the patients I work with have them.  I don’t think it’s nearly as rare as  is being reported.

It’s a good thing this teen was promptly diagnosed as people have died from this: 

The following statement is quite frightening:

The hospital course was further remarkable for transition to 2nd degree heart block and transient episodes of complete heart block.  Excerpt:

In 90% of cases, the most common consequence of Lyme carditis is heart block. The severity of the heart block can fluctuate rapidly and the progression to complete heart block can be fatal. Importantly, the heart block in Lyme carditis can be transient and usually resolves with antibiotic therapy. Additionally, Lyme carditis can affect other parts of the heart’s conduction system, as well as the heart’s muscle, valves, and outer layer of the heart wall.

These links show heart issues caused by Lyme disease are not rare.

Lyme advocate, Phyllis Mervine, makes a case that autopsies should be performed on those with unexpected, sudden death:

Signs and Symptoms of Lyme Disease

signs and symptoms of lyme disease

The broad range of signs and symptoms of Lyme disease and the varying presentations from person to person make diagnosing the disease challenging. Furthermore, Borrelia burgdorferi spirochete are adept at evading the immune system. The bacterium can travel through the bloodstream, burrow into tissue and remain dormant for days, months, or even years before symptoms arise.

While many people associate Lyme disease with manifestations such as Bell’s palsy, the circular Bull’s-eye rash, and flu-like symptoms, Lyme disease can also cause sensory, cognitive, neurologic, and cardiac complications, even in its earliest stage. But, the signs and symptoms of Lyme disease are all too frequently attributed to another medical condition.

Objective signs of Lyme disease include Bell’s palsy, synovitis of the knee, and the presence of a Bull’s-eye or erythema migrans rash. However, most people exhibit a wide range of signs and symptoms of Lyme disease that may come and go and fluctuate in their intensity.

Initially, Bell’s palsy, also known as idiopathic facial nerve palsy, may not be attributed to Lyme disease. But making the connection early is important, since corticosteroids, a common treatment for facial nerve palsy, can be harmful to patients with Lyme disease.

Furthermore, researchers in the UK remind clinicians to consider Lyme disease in children who present with Bell’s palsy. “In areas endemic with Lyme disease, Lyme disease should be considered as the likely cause of facial nerve palsy in children until proven otherwise.”

Wide range of signs and symptoms of Lyme disease

Studies indicate that at least 50% of patients with Lyme disease do not exhibit the classic Bull’s-eye rash. When a rash is present, it can appear anywhere on the body. It does not always appear at the site of the tick bite. The rash usually appears between 3 – 30 days after the tick bite.

A rash due to Lyme disease is typically not itchy or painful. It may fade and then reappear and it can be confused with a spider bite. Atypical rashes can also occur. And when multiple rashes appear on the body, it may be an indication that the Borrelia burgdorferi spirochete has disseminated beyond the tick bite and the disease is in a more advanced stage.

If left untreated, the infection can spread to other parts of the body, including the brain and central nervous system, cardiovascular system, peripheral and autonomic nervous system, along with the muscles and joints, and eyes.

Neurologic and cardiac manifestations

Lyme disease can cause neurological and cardiac symptoms such as meningitis, encephalitis, and carditis. But, more often symptoms include severe and unrelenting fatigue, joint pain (with or without swelling), sore muscles, neck and back pain, headaches, light, sound and temperature sensitivity, sleep disturbance, night sweats, irritability, anxiety, despair, sadness, lightheadedness, crying, poor memory and concentration, stiff neck, numbness, and tingling sensations.

Although rare, Lyme carditis can cause sudden death. The authors of a case series warn, “These two cases highlight the importance of early recognition. And treatment, even if it’s empirical, may save lives.”

Another researcher reports, “The burden of Lyme disease and Lyme carditis in U.S. children’s hospitals has increased in recent years.” The authors identified 189 children diagnosed with Lyme carditis between 2007 and 2013.