Archive for the ‘Heart Issues’ Category

Advanced Heart Block in Children With Lyme Disease

Advanced Heart Block in Children with Lyme Disease

Meena Bolourchi, Eric S. Silver, Leonardo Liberman




The clinical course of children with advanced heart block secondary to Lyme disease has not been well characterized.


To review the presentation, management, and time to resolution of heart block due to Lyme disease in previously healthy children.


An IRB approved single-center retrospective study was conducted of all patients < 21 years old with confirmed Lyme disease and advanced second or third degree heart block between 2007 and 2017.


Twelve patients (100% male) with a mean age of 15.9 years (range 13.2–18.1) were identified. Six patients (50%) had mild to moderate atrioventricular valve regurgitation and all had normal biventricular function. Five patients had advanced second degree heart block and 7 had complete heart block with an escape rate of 20–57 bpm. Isoproterenol was used in 4 patients for 3–4 days and one patient required transvenous pacing for 2 days. Patients were treated with 21 days (n = 6, 50%) or 28 days (n = 6, 50%) of antibiotics. Three patients received steroids for 3–4 days. Advanced heart block resolved in all patients within 2–5 days, and all had a normal PR interval within 3 days to 16 months from hospital discharge.


Symptomatic children who present with new high-grade heart block from an endemic area should be tested for Lyme disease. Antibiotic therapy provides quick and complete resolution of advanced heart block within 5 days, while steroids did not appear to shorten the time course in this case series. Importantly, no patients required a permanent pacemaker.




Yes, go ahead and test but realize testing misses half of all cases.  

Since 3rd degree heart block can be fatal, this is a big deal.  Don’t let fear of antibiotics keep you from treating these poor kids.  They say 5 days of antibiotics does the trick, but these patients need follow-up.  Coinfections also need to be taken into consideration as certain antibiotics will not work on all pathogens.  If they have Babesia, for instance, they need anti-malarials.

There are many out there giving “natural” protocols and dissing the use of antibiotics.  This study on serious heart issues is a prime example of the fact that Lyme can kill & time is of the essence.  

More on heart issues with Lyme:



Advanced Heart Block in Children With Lyme Disease

Advanced Heart Block in Children with Lyme Disease

Meena Bolourchi, Eric S. Silver, Leonardo Liberman


Original Article




The clinical course of children with advanced heart block secondary to Lyme disease has not been well characterized.


To review the presentation, management, and time to resolution of heart block due to Lyme disease in previously healthy children.


An IRB approved single-center retrospective study was conducted of all patients < 21 years old with confirmed Lyme disease and advanced second or third degree heart block between 2007 and 2017.


Twelve patients (100% male) with a mean age of 15.9 years (range 13.2–18.1) were identified. Six patients (50%) had mild to moderate atrioventricular valve regurgitation and all had normal biventricular function. Five patients had advanced second degree heart block and 7 had complete heart block with an escape rate of 20–57 bpm. Isoproterenol was used in 4 patients for 3–4 days and one patient required transvenous pacing for 2 days. Patients were treated with 21 days (n = 6, 50%) or 28 days (n = 6, 50%) of antibiotics. Three patients received steroids for 3–4 days. Advanced heart block resolved in all patients within 2–5 days, and all had a normal PR interval within 3 days to 16 months from hospital discharge.


Symptomatic children who present with new high-grade heart block from an endemic area should be tested for Lyme disease. Antibiotic therapy provides quick and complete resolution of advanced heart block within 5 days, while steroids did not appear to shorten the time course in this case series. Importantly, no patients required a permanent pacemaker.



Two things stick out 1) These are all kids 2) They need to be followed for a much longer period of time.  There is a third thing as well and that’s the ineffectiveness of steroids, which has long been known, as catabolic steroids will suppress the immune system allowing the infection to worsen.  Many a Lyme/MSIDS patient has had to learn that fact the hard way.  The next question begging to be asked is are these kids were infected with other TBI’s (tick borne infections) such as Bartonella, Babesia, Mycoplasma, and numerous viruses?  After all, one tick bite could give you 18 and counting different infections:  This link shows the importance of overlapping treatment with many antimicrobials to effectively treat a pleomorphic (shape-shifting), complex bacteria(ish) organism that pretty much defies all convention in the infectious world.  It’s complexity has never been taken seriously by main-stream medicine.

Myopic and limited research such as this worries me greatly.  These kids are young and have full lives ahead of them.  Due to the lack of recognition and acceptance of the complexity of the organisms involved, these children in my mind are in harm’s way and are in great risk of developing serious issues in the not so distant future.  

Please spread the word!

For more on Lyme:

Key Quote: “Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes.”

And I’ll bet that 65% is still low….

Study Shows Lyme/MSIDS Patients Infected With Many Pathogens and Explains Why We Are So Sick (Please see comment at end of article)

Evaluating polymicrobial immune responses in patients suffering from tick-borne diseases

Kunal Garg, Leena Meriläinen, Ole Franz, Heidi Pirttinen, Marco Quevedo-Diaz, Stephen Croucher & Leona Gilbert
Scientific Reportsvolume 8, Article number: 15932 (2018)

There is insufficient evidence to support screening of various tick-borne diseases (TBD) related microbes alongside Borrelia in patients suffering from TBD. To evaluate the involvement of multiple microbial immune responses in patients experiencing TBD we utilized enzyme-linked immunosorbent assay. Four hundred and thirty-two human serum samples organized into seven categories followed Centers for Disease Control and Prevention two-tier Lyme disease (LD) diagnosis guidelines and Infectious Disease Society of America guidelines for post-treatment Lyme disease syndrome. All patient categories were tested for their immunoglobulin M (IgM) and G (IgG) responses against 20 microbes associated with TBD. Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes. We have established a causal association between TBD patients and TBD associated co-infections and essential opportunistic microbes following Bradford Hill’s criteria. This study indicated an 85% probability that a randomly selected TBD patient will respond to Borrelia and other related TBD microbes rather than to Borrelia alone.

A paradigm shift is required in current healthcare policies to diagnose TBD so that patients can get tested and treated even for opportunistic infections.
Please see link for full article.  Snippets below:

Tick-borne diseases (TBDs) have become a global public health challenge and will affect over 35% of the global population by 20501. The most common tick-borne bacteria are from the Borrelia burgdorferi sensu lato (s.l.) group. However, ticks can also transmit co-infections like Babesia spp.2, Bartonella spp.3, Brucella spp.4,5,6,7,8, Ehrlichia spp.9, Rickettsia spp.10,11, and tick-borne encephalitis virus12,13,14. In Europe and North America, 4–60% of patients with Lyme disease (LD) were co-infected with Babesia, Anaplasma, or Rickettsia11,15,16. Evidence from mouse and human studies indicate that pathogenesis by various tick-borne associated microbes15,16,17 may cause immune dysfunction and alter, enhance the severity, or suppress the course of infection due to the increased microbial burden18,19,20,21,22. As a consequence of extensive exposure to tick-borne infections15,16,17, patients may develop a weakened immune system22,23, and present evidence of opportunistic infections such as Chlamydia spp.24,25,26,27, Coxsackievirus28, Cytomegalovirus29, Epstein-Barr virus27,29, Human parvovirus B1924, and Mycoplasma spp.30,31. In addition to tick-borne co-infections and non-tick-borne opportunistic infections, pleomorphic Borrelia persistent forms may induce distinct immune responses in patients by having different antigenic properties compared to typical spirochetes32,33,34,35. Nonetheless, current LD diagnostic tools do not include Borrelia persistent forms, tick-borne co-infections, and non-tick-borne opportunistic infections.

The two-tier guidelines36,37,38 for diagnosing LD by the Centers for Disease Control and Prevention (CDC) have been challenged due to the omission of co-infections and non-tick-borne opportunistic infections crucial for comprehensive diagnosis and treatment39,40. Emerging diagnostic solutions have demonstrated the usefulness of multiplex assays to test for LD and tick-borne co-infections41,42. However, these new technologies do not address seroprevalence of non-tick-borne opportunistic infections in patients suffering from TBD and they are limited to certain co-infections41,42. Non-tick-borne opportunistic microbes can manifest an array of symptoms24,29 concerning the heart, kidney, musculoskeletal, and the central nervous system as seen in patients with Lyme related carditis43, nephritis44, arthritis45, and neuropathy46, respectively. Therefore, Chlamydia spp., Coxsackievirus, Cytomegalovirus, Epstein-Barr virus, Human parvovirus B19, Mycoplasma spp., and other non-tick-borne opportunistic microbes play an important role in the differential diagnosis of LD24,29. As the current knowledge regarding non-tick-borne opportunistic microbes is limited to their use in differential diagnosis of LD, it is unclear if LD patients can present both tick-borne co-infections and non-tick-borne opportunistic infections simultaneously.

For the first time, we evaluate the involvement of Borrelia spirochetes, Borrelia persistent forms, tick-borne co-infections, and non-tick-borne opportunistic microbes together in patients suffering from different stages of TBD. To highlight the need for multiplex TBD assays in clinical laboratories, we utilized the Bradford Hill’s causal inference criteria47 to elucidate the likelihood and plausibility of TBD patients responding to multiple microbes rather than one microbe. The goal of this study is to advocate screening for various TBD microbes including non-tick-borne opportunistic microbes to decrease the rate of misdiagnosed or undiagnosed48 cases thereby increasing the health-related quality of life for the patients39, and ultimately influencing new treatment protocol for TBDs.

Positive IgM and IgG responses by CDC defined acute, CDC late, CDC negative, PTLDS immunocompromised, and unspecific patients to 20 microbes associated with TBD (Fig. 1) were utilized to evaluate polymicrobial infections (Figs 2–4). Patient categories included CDC acute (n = 43), CDC late (n = 43), CDC negative (n = 46), PTLDS (n = 31), immunocompromised (n = 61), unspecific (n = 31), and healthy (n = 177).

Polymicrobial infections are present at all stages of tick-borne diseases.

Microbes include Borrelia burgdorferi sensu stricto, Borrelia afzelii, Borrelia garinii, Borrelia burgdorferi sensu stricto persistent form, Borrelia afzelii persistent form, Borrelia garinii persistent form, Babesia microti, Bartonella henselae, Brucella abortus, Ehrlichia chaffeensis, Rickettsia akari, Tick-borne encephalitis virus (TBEV), Chlamydia pneumoniae, Chlamydia trachomatis, Coxsackievirus A16 (CVA16), Cytomegalovirus (CMV), Epstein-Barr virus (EBV), Mycoplasma pneumoniae, Mycoplasma fermentans, and Human parvovirus B19 (HB19V).

In Fig. 2A, 51% and 65% of patients had IgM and IgG responses to more than one microbe, whereas 9% and 16% of patients had IgM and IgG responses to only one microbe, respectively. Immune responses to Borrelia persistent forms (all three species) for IgM and IgG were 5–10% higher compared to Borrelia spirochetes in all three species (Fig. 2B). Interestingly, the probability that a randomly selected patient will respond to Borrelia persistent forms rather than the Borrelia spirochetes (Fig. S2) is 80% (d = 1.2) for IgM and 68% for IgG (d = 0.7). Figure 2A and B indicated that IgM and IgG responses by patients from different stages of TBDs are not limited to only Borrelia spirochetes.

In Fig. 3 sub-inlets, more than 50% of the patients reacted to only the individual Borrelia strains suggesting that Borrelia antigens are not cross-reactive. If patients were cross-reacting among antigens, a larger percentage of the patients would be seen with the combination of all three species (Fig. S2). These results provide evidence to suggest that the inclusion of different Borrelia species and their morphologies in current LD diagnostic tools will improve its efficiency.

The study outcome indicated that polymicrobial infections existed at all stages of TBD with IgM and IgG responses to several microbes (Fig. 2). Results presented in this study propose that infections in patients suffering from TBDs do not obey the one microbe one disease Germ Theory. Based on these results and substantial literature11,15,16,17,27,49,50,51 on polymicrobial infections in TBD patients, we examined the probability of a causal relationship between TBD patients and polymicrobial infections following Hill’s nine criteria47.

An average effect size of d = 1.5 for IgM and IgG (Fig. 4A) responses is considered very large52. According to common language effect size statistics53, d = 1.5 indicates 85% probability that a randomly selected patient will respond to Borrelia and other TBD microbes rather than to only Borrelia. Reports from countries such as Australia27, Germany49, Netherlands11, Sweden50, the United Kingdom51, the USA15,16, and others indicate that 4% to 60% of patients suffer from LD and other microbes such as Babesia microti and human granulocytic anaplasmosis (HGA). However, previous findings11,15,16,27,49,50,51 are limited to co-infections (i.e., Babesia, Bartonella, Ehrlichia, or Rickettsia species) in patients experiencing a particular stage of LD (such as Erythema migrans). In contrast, a broader spectrum of persistent, co-infections, and opportunistic infections associated with diverse stages of TBD patients have been demonstrated in this study (Fig. 2). From a clinical standpoint, the likelihood for IgM and IgG immune responses by TBD patients to the Borrelia spirochetes versus the Borrelia persistent forms, and responses to just Borrelia versus Borrelia with many other TBD microbes has been quantified for the first time (Fig. S2).

Borrelia pathogenesis could predispose individuals to polymicrobial infections because it can suppress, subvert, or modulate the host’s immune system18,19,20,21,22 to create a niche for colonization by other microbes54. Evidence in animals55 and humans11,15,16,27,49,50,51 frequently indicate co-existence of Borrelia with other TBD associated infections. Interestingly, IgM and IgG immune levels by patients to multiple forms of Borrelia resulted in immune responses to 14 other TBD microbes (Fig. 4B). In contrast, patient responses to either form of Borrelia (spirochetes or persistent forms) resulted in reactions to an average of 8 other TBD microbes (Fig. 4B). Reaction to two forms of Borrelia reflected an increase in disease severity indicating biological gradient for causation as required by Hill’s criteria47.

Multiple microbial infections in TBD patients seem plausible because ticks can carry more than eight different microbes depending on tick species and geography56,57. Moreover, Qiu and colleagues reported the presence of at least 18 bacterial genera shared among three different tick species and up to 127 bacterial genera in Ixodes persulcatus58. Interestingly, research indicates Chlamydia-like organism in Ixodes ricinus ticks and human skin59 that may explain immune responses to Chlamydia spp., seen in this study (Fig. 2). Additionally, prevalence of TBD associated co-infections such as B. abortus, E. chaffeensis, and opportunistic microbes such as C. pneumoniae, C. trachomatis, Cytomegalovirus, Epstein-Barr virus, and M. pneumoniae have been recorded in the general population of Europe and the USA (Table S2). However, true incidence of these microbes is likely to be higher considering underreporting due to asymptomatic infections and differences in diagnostic practices and surveillance systems across Europe and in the USA. More importantly, clinical evidence for multiple microbes has been reported in humans11,15,16,27,49,50,51, and livestock55 to mention the least. Our findings regarding the presence of polymicrobial infections at all stages of TBD further supports the causal relationship between TBD patients and polymicrobial infections (Fig. 2). Various microbial infections in TBD patients have been linked to the reduced health-related quality of life (HRQoL) and increased disease severity39.

An association between multiple infections and TBD patients relates well to other diseases such as periodontal, and respiratory tract diseases. Oral cavities may contain viruses and 500 different bacterial species60. Our findings demonstrate that TBD patients may suffer from multiple bacterial and viral infections (Fig. 4). In respiratory tract diseases, influenza virus can stimulate immunosuppression and predispose patients to bacterial infections causing an increase in disease severity61. Likewise, Borrelia can induce immunosuppression that may predispose patients to other microbial infections causing an increase in disease severity.

Traditionally, positive IgM immune reaction implies an acute infection, and IgG response portrays a dissemination, persistent or memory immunity due to past infections. Depending on when TBD patients seek medical advice, the level of anti-Borrelia antibodies can greatly vary as an Erythema migrans (EM) develops and may present with IgM, IgG, collective IgM/IgG, or IgA62. This study recommends both IgM and IgG in diagnosing TBD (Figs 5 and S4–S6) as unconventional antibody profiles have been portrayed in TBD patients. Presence of long-term IgM and IgG antibodies have been reported in LD patients that were tested by the CDC two-tier system. In 2001, Kalish and colleagues reported anti-Borrelia IgM or IgG persistence in patients that suffered from LD 10–20 years ago63. Similarly, Hilton and co-workers recorded persistent anti-Borrelia IgM response in 97% of late LD patients that were considered cured following an antibiotic treatment64.

Similar events of persistent IgM and IgG antibody reactions were demonstrated in patients treated for Borrelia arthritis and acrodermatitis chronica atrophicans65, chronic cutaneous borreliosis66, and Lyme neuroborreliosis67. A clear phenomenon of immune dysfunction is occurring, which might account for the disparities in LD patient’s antibody profiles and persistence. Borrelia suppresses the immune system by inhibition of antigen-induced lymphocyte proliferation18, reducing Langerhans cells by downregulation of major histocompatibility complex class II molecules on these cells19, stimulating the production of interleukin-10 and anti-inflammatory immunosuppressive cytokine20, and causing disparity in regulation and secretion of cytokines21. Other studies have demonstrated low production or subversion of specific anti-Borrelia antibodies in patients with immune deficiency status22.

In the USA alone, the economic healthcare burden for patients suffering from LD and ongoing symptoms is estimated to be $1.3 billion per year69. Additionally, 83% of all TBD diagnostic tests performed by the commercial laboratories in the USA accounted for only LD70. Globally, the commercial laboratories’ ability to diagnose LD has increased by merely 4% (weighted mean for ELISA sensitivity 62.3%) in the last 20 years71. This study provides evidence regarding polymicrobial infections in patients suffering from different stages of TBDs. Literature analyses and results from this study followed Hill’s criteria indicating a causal association between TBD patients and polymicrobial infections. Also, the study outcomes indicate that patients may not adhere to traditional IgM and IgG responses.



For the first time, Garg et al. show a 85% probability for multiple infections including not only tick-borne pathogens but also opportunistic microbes such as EBV and other viruses.

I’m thankful they included Bartonella as that one is often omitted but definitely a player.  I’m also thankful for the mention of viruses as they too are in the mix.  The mention of the persister form must be recognized as well as many out there deny its existence.

Key Quote:  Our findings recognize that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes.”

But there is another important point.

According to this review, 83% of all commercial tests focus only on Lyme (borrelia), despite the fact we are infected with more than one microbe.  The review also states it takes 11 different visits to 11 different doctors, utilizing 11 different tests to be properly diagnosed.

This is huge.  Please spread the word.


Lyme Carditis Presenting With Atrial Fibrillation

Case Reports in Cardiology

Volume 2018, Article ID 5265298, 5 pages

A Case of Lyme Carditis Presenting with Atrial Fibrillation

Peter J. Kennel,1 Melvin Parasram,2 Daniel Lu,3 Diane Zisa,1 Samuel Chung,1 Samuel Freedman,1 Katherine Knorr,1 Timothy Donahoe,1 Steven M. Markowitz,3 and Hadi Halazun3

Published 2 September 2018

Academic Editor: Kjell Nikus


We report a case of a 20-year-old man who presented to our institution with a new arrhythmia on a routine EKG. Serial EKG tracings revealed various abnormal rhythms such as episodes of atrial fibrillation, profound first degree AV block, and type I second degree AV block. He was found to have positive serologies for Borrelia burgdorferi. After initiation of antibiotic therapy, the atrial arrhythmias and AV block resolved. Here, we present a case of Lyme carditis presenting with atrial fibrillation, a highly unusual presentation of Lyme carditis.



Sigh….there it is again – “highly unusual presentation of Lyme carditis……”

Nothing about Lyme is rare.  It’s just not reported.  Please remember, most of these patients for the past 40 years have been told they are imagining their symptoms and, “it’s all in their head.”  Autopsies have rarely been done on these people and they have faced denial the entire time.

For more on heart-related symptoms with tick borne infections:  Trust me, folks have been dying from this for a long time.  It’s just now beginning to make the radar.  If you have Lyme/MSIDS and heart issues, speak loudly about it.

Microbiologist Tom Greer has a fantastic article about how post-mortem work is one of the only ways we are going to get to the bottom of the Lyme Wars:
For information on preparing for brain and tissue donations upon death for Lyme research, please see:

Lyme, BTW, is NOT the only tick borne illness that can cause heart issues:  (cases listed here)

Most common parasites causing carditis:

  • Borrelia burgdorferi
  • Ehrlichia species
  • Babesia species
  • Trypanosoma cruzi (Chagas Disease)
  • Bartonella (My addition due to the following…..)


Bartonella Infective Endocarditis With Dissemination: A Case Report & Literature Review

Bartonella henselae infective endocarditis with dissemination: A case report and literature review in Southeast Asia.

Noopetch P, et al. IDCases. 2018.


Bartonella is among the most common causes of culture-negative infective endocarditis, with B. henselae being one of the most frequently reported species. The clinical presentation of Bartonella endocarditis is similar to that of subacute bacterial endocarditis caused by other bacteria and the diagnosis can be challenging since the organism is difficult to isolate using standard microbiologic culture techniques. In clinical practice, Bartonella endocarditis is usually diagnosed based on serology. To date, only a handful of cases of infective endocarditis caused by Bartonella have been reported in Thailand. Here, we report the case of 51-year-old Thai male with B. henselae endocarditis with dissemination to the lungs, bones, subcutaneous tissue (below dermis, and is primarily loose connective tissue and lobules of fat), epididymis (coiled tube at the back of the testes), and lymph nodes with a successful outcome.



Please notice the dissemination to lungs, bones, testes, lymph nodes, and area below skin.  Bartonella does not play nice.

This right here is an example of why Lyme/MSIDS patients can suffer so.  Nobody is considering the implications of Bartonella with Lyme.  

For more:

Humana Bartonellosis: Perspectives of a Veterinary Internist


Edward B. Breitschwerdt, DVM, DACVIM
Chief Scientific Officer, Galaxy Diagnostics, Inc.
Professor, Internal Medicine, NCSU, Raleigh, NC
Adjunct Professor of Medicine, Duke University Medical Center
Bartonella species are fastidious gram-negative bacteria that are highly adapted to a mammalian reservoir host and within which the bacteria usually cause a long-lasting intraerythrocytic bacteremia.  1-3  These facts are of particular importance to veterinarians and physicians, as an increasing number of animal reservoir hosts have been identified for various Bartonella species. Among numerous other examples, Bartonella henselae has co-evolved with cats, Bartonella vinsonii subsp. berkhoffii has co-evolved with dogs and wild canines, and Bartonella bovid has co-evolved with cattle.  1-2  Importantly, the list of reservoir-adapted Bartonella species, including a large number of rodent species that might serve as “pocket pets,” continues to grow exponentially, as new Bartonella spp. are discovered. Prior to 1990, there were only two named Bartonella species, whereas there are now at least 24 named and numerous unnamed or candidatus species, based upon deposited Gen Bank sequences or preliminary reports, respectively, seventeen Bartonella spp. including B.alsatica, B. bacilliformis, B. clarridgeiae, B. doshiae, B. elizabethae, B. grahamii, B. henselae (Houston 1 and San Antonio 2 strains), B. koehlerae, B. melophagi, B. quintana, B. rochalimaea, B. tamiae, B. vinsonii subsp. berkhoffii (Genotypes I, II and III), and B. washoensis have been associated with an expanding spectrum of human diseases.
Epidemiological evidence and experimental flea transmission studies support an important role for fleas in the transmission of B. henselae, B. clarridgeae and most likely B. koehlerae among cats. 1  Three other Bartonella species, B. bovid, B. quintana and B. vinsonii subsp. berkhoffii have been isolated from cat blood, but the modes of transmission and the reservoir potential of these species in felids has not been definitively established. Recently, we isolated Bartonella vinsonii subsp. berkhoffii from a cat with recurrent osteomyelitis spanning an eighteen month time period. 2  Thus, cats can maintain a chronic bacteremia with at least six Bartonella spp., of which five are known zoonotic pathogens.  1-3 In addition to fleas, an increasing number of arthropod vectors, including biting flies, keds, lice, sandflys and ticks have been implicated in the transmission of Bartonella species. Although there is clinical and epidemiological evidence to support tick transmission of B. vinsonii subspecies berkhoffii to dogs and coyotes, the mode of transmission of this Bartonella subsp. to cats and dogs has not been determined. Recent evidence supports tick transmission of B. henselae by Ixodes scapularis and Ixodes ricinus. Considering the diversity of Bartonella species and subspecies, the large number of reservoir hosts and the spectrum of arthropod vectors, the clinical and diagnostic challenges posed by Bartonella transmission in nature may be much more complex than is currently appreciated in human and veterinary medicine.
In the natural reservoir host, such as a cat or rodent, chronic bacteremia with a Bartonella species can frequently be detected by blood cultre or PCR in outwardly healthy individuals.  1-3  In contrast, the diagnostic detection of a Bartonella spp. in a non-reservoir adapted host, such as a dog, horse or human patient, can be extremely difficult. Most, although not all diseases caused by Bartonella spp. occur in accidental hosts and these organisms are being increasingly implicated as a cause of zoonotic infections.  4-8  It is important to recognize that strains of a Bartonella sp. vary in their virulence. Therefore, highly pathogenic strains of B. henselae, for which the cat is the primary reservoir, can induce granulomatous myocarditis in cats, presumably following flea transmission.  Until recently, mechanisms that facilitate persistent Bartonella bacteremia in mammals were not well understood. Recent reports have identified an intra-endothelial, as well as intra-erythrocytic localization for these bacteria, which represents a unique strategy for bacterial persistence. Non-hemolytic intracellular colonization of erythrocytes in conjunction with the ability to invade and replicate within endothelial cells would preserve the organisms for efficient vector transmission, protect Bartonella from the host immune response, and potentially contribute to decreased antimicrobial efficacy. Although the clinical implications are not understood, other in vitro studies indicate that Bartonella spp. can infect dendritic cells, microglial cells, monocytes and CD34+ bone marrow progenitor cells.
For over a century regional lymphadenopathy has been associated with animal contact, particularly cat scratches. Over the years, numerous microorganisms were implicated as the cause of CSD. In 1992, Regnery and colleagues at the Centers for Disease Control, identified seroreactivity to B. henselae antigens in 88% of 41 human patients with suspected CSD compared to 3% of controls.  Subsequently, additional support for B. henselae as the predominant cause of CSD was provided when Bartonella DNA was amplified from lymph node samples of 21 of 25 (84%) patients with suspected
CSD, using a polymerase chain reaction assay. A similar study from Sweden identified B. henselae DNA, but failed to identify A. felis DNA, in a large number of patients with suspected CSD. Prior to the
recognition of B. henselae as the cause of CSD, Afipia felis, named for the Armed Forces Institute of Pathology, was considered the sole cause of CSD. Subsequently, we blood cultured B. henselae or B. clarridgeae
from 17 of 19 cats owned by 14 patients with CSD, which indicated that bacteremia is a frequent occurrence in cats that transmit B. henselae
to a human being. 1-2
Historically, atypical manifestations of CSD have included tonsillitis, encephalitis, cerebral arteritis, transverse myelitis, granulomatous hepatitis and/or splenitis, osteolysis, pneumonia, pleural effusion, and thrombocytopenic purpura. With the advent of specific diagnostic techniques, (culture, serology, and PCR), there has been a dramatic increase in reports describing human patients with “atypical” manifestations of CSD. Osteomyelitis, granulomatous hepatitis and granulomatous splenitis have been increasingly recognized in children infected with B. henselae, who frequently lack the classical lymphadenopathy of CSD. Previously, Bartonella infection would not have been considered a likely differential diagnosis by the physician in patients lacking a history of lymphadenopathy or animal contact. As evidenced by reports in the past four years, the spectrum of human disease associated with the genus Bartonella continues to expand, requiring periodic reassessment as new information becomes available. On a comparative medical (“One Health”) basis, our research group has documented many of the same CSD atypical manifestations in cats or dogs, including encephalitis, transverse myelitis, granulomatous hepatitis, osteolysis, pleural effusion, and thrombocytopenic purpura. In this context, a highly prevalent, naturally-occurring human disease (CSD) can be used as a “model” to determine the potential behavior of these bacteria in companion animal patients.
Because cat scratch disease generally denotes a self-limiting illness characterized by fever and lymphadenopathy and because the recognized spectrum of human disease manifestations associated with Bartonella infections (which may not include fever or lymphadenopathy) has expanded considerably in recent years, it is becoming obvious that the designation CSD lacks clinical, microbiologic and zoonotic utility. Although cats are a major reservoir for B. henselae, B. clarridgeiae, and B. koehlerae, some patients deny the possibility of a cat scratch or bite wound, or indicate no contact with cats. Transmission from environmental sources, various arthropod vectors, perinatally or by other animal hosts is probable and the more inclusive term bartonellosis may facilitate enhanced future understanding of diseases caused by members of the genus Bartonella. As physicians have been taught that CSD is self-limiting, there is an ongoing lack of appreciation that B. henselae can cause chronic, asymptomatic or intermittently symptomatic illness, accompanied by persistent bacteremia in people. In this context, the documentation of chronic, relapsing bacteremia in cats, dogs and other animal species provides a “model” for better understanding human bartonellosis.
Endocarditis can be induced by a spectrum of Bartonella species in dogs and human patients and is the best example of documented disease causation for this genus. Historically, Bartonella species have been a cause of culture-negative endocarditis in people and dogs because the diagnostic methods used by microbiology laboratories were not adequate to isolate these bacteria. Now, by using
specialized techniques, a spectrum of Bartonella species have been identified in research and diagnostic laboratories in different parts of the world—in heart valves or in blood cultures from dogs
and people with endocarditis. 3  It is important for physicians and veterinarians to recognize that some of these Bartonella species are found in the blood of cats, dogs, rats, ground squirrels, and rabbits.
Because conventional microbiological techniques lack sensitivity, bartonellosis is usually diagnosed by PCR amplification of organism specific DNA sequences and/or through serological testing. Recently, the development of a more sensitive isolation approach, using BAPGM (Bartonella alpha Proteobacteria growth medium) followed by PCR has greatly facilitated the molecular detection or isolation of Bartonella species from the blood of sick or healthy animals, including cats, dogs, horses and human beings. Most importantly, the use of this enrichment growth medium prior to PCR testing has allowed our research group to confirm that immunocompetent human patients, in particular veterinarians and veterinary technicians, can have chronic intravascular infections with Bartonella spp. 4-5 Information relative to this EnrichmentPCRTM testing platform for animal and human patients is available at
It is increasingly clear that no single diagnostic strategy will confirm infection with a Bartonella sp. in the immunocompetent patient population.  As described in studies from our NCSU laboratory, B. henselae, B. koehlerae and B. vinsonii subsp berkhoffii seroreactivity was found in only 58.6% of the patients in which Bartonella spp. infection was confirmed by EnrichmentPCR TM and sequencing. Therefore, Bartonella serology lacks sensitivity and can only be used to implicate prior exposure to a Bartonella sp. Even when serum from cat scratch disease patients, which is caused by B. henselae, is used in various diagnostic laboratories for IFA testing, test sensitivities have ranged from 14 to 100%.
Previously, we described B. quintana bacteremia in a woman who was tested following the development of an infected cat bite lesion involving the hand. 6  Two months later, the feral cat that had
induced the bite wound was captured and was also shown to be B. quintana bacteremic. In a cumulative study involving 392 patients with occupational animal contact or extensive arthropod exposure 31.9% were bacteremic with one or more Bartonella spp., when blood, serum and BAPGM enrichment culture PCR results were combined. Although this high prevalence of bacteremia is biased by testing at risk, sick individuals, it clearly demonstrates that intravascular infection with Bartonella sp. is much more common in immunocompetent patients, than was previously suspected. By IFA testing, only 75 out of 128 (58.6%) PCR positive patients were seroreactive to a panel consisting of five Bartonella sp. test antigens.
In a recent study, Bartonella vinsonii subsp. berkhoffii, Bartonella henselae or DNA of both organisms were amplified and sequenced from blood, BAPGM enrichment blood cultures or autopsy tissues from four family members. 7  Historical and microbiological results derived from this family support human perinatal transmission of Bartonella species. To date, there have been a limited number of studies that address the potential impact of intravascular infection with a Bartonella sp. on reproductive performance, however, studies involving experimentally-infected cats, rodents and naturally-infected cows with various Bartonella sp. have identified decreased reproductive performance involving both males and females. The parents of these children had attempted to conceive children for several years prior to resorting to in vitro fertilization.
We have also described a veterinarian, who experienced a needle stick while obtaining a fine needle aspiration sample from a cutaneous histiocytic neoplasm. 8  Subsequently symptoms, including headaches, fatigue and intermittent paresthesias (numbness) developed. This patient seroconverted to B. vinsonii subsp. berkhoffii genotypes I and III and B. vinsonii subsp. berkhoffii genotype I DNA was amplified and sequenced from sequentially obtained blood samples, whereas genotype III DNA was amplified from the cytological specimen. All symptoms resolved following antibiotic treatment.
It is increasingly evident that dogs can serve as a source for human infection with B. vinsonii subsp. berkhoffii. Bartonella vinsonii subsp. berkhoffii genotype II was amplified and sequenced from
a liver biopsy from a patient with epithelioid hemangioendothelioma (soft tissue tumor considered a vascular cancer), after which the organism was isolated by BAPGM blood culture. 9  The unique capability of Bartonella to invade and induce long lasting intraerythrocytic and intraendothelial infections, in conjunction with the ability of at least three Bartonella spp. (Bh, Bq, and B. bacilliformi) to induce VEGF-mediated vasoproliferative disease in immunocompromised or immunocompetent individuals suggests that these novel emerging bacterial pathogens might contribute to the development of vascular tumors.
Bartonella koehlerae bacteremia was documented in eight immunocompetent patients by PCR amplification and DNA sequencing, either prior to or after BAPGM enrichment blood culture.10  Presenting symptoms most often included fatigue, insomnia, joint pain, headache, memory loss, and muscle pain. Four patients were also infected with Bartonella vinsonii subsp. berkhoffii genotype II. Bartonella koehlerae antibodies were not detected (titers<1:16) in 30 healthy human control sera, whereas five of eight patient samples had B. koehlerae antibody titers of 1:64 or greater. Studies are needed to determine if B. koehlerae is a cause or cofactor in the development of arthritis, peripheral neuropathies or tachyarrhythmias in human patients. Co-infection with B. henselae and two hemotropic Mycoplasma variants resembling Mycoplasma obis were also found in the blood of a veterinarian with a historical diagnosis of multiple sclerosis. 11
Due to extensive contact with a spectrum of animal species, veterinary professionals appear to have an occupational risk of infection because of frequent exposure to Bartonella spp., therefore these individuals should exercise increased precautions to avoid arthropod bites, arthropod feces (i.e. fleas and lice), animal bites or scratches and direct contact with bodily fluids from sick animals. As Bartonella spp. have been isolated from cat, dog or human blood, cerebrospinal fluid, joint fluid,aqueous fluid, seroma fluid and from pleural, pericardial and abdominal effusions, a substantial number of diagnostic biological samples collected on a daily basis in veterinary practices could contain viable bacteria.
The increasing number of defined Bartonella spp., in conjunction with the high level of bacteremia found in reservoir adapted hosts, which represent the veterinary patient population, ensures that all veterinary professionals will experience frequent and repeated exposure to animals harboring these bacteria. Therefore, personal protective equipment, frequent hand washing and avoiding cuts and needle sticks have become more important as our knowledge of this genus has improved and various modes of transmission have been defined.
Physicians should be educated as to the large number of Bartonella spp. in nature, the extensive spectrum of animal reservoir hosts, the diversity of confirmed and potential arthropod vectors, current limitations associated with diagnosis and treatment efficacy, and the ecological and evolving medical complexity of these highly evolved intravascular, endotheliotropic bacteria.
1  Chomel BB, et al. Vet Res 2009;40:29.
2  Breitschwerdt EB, et al. J Vet Emerg Crit Care 2010; 20:8.
3  Chomel BB, et al. Ann N Y Acad Sci 2009;1166:120.
4  Breitschwerdt EB, et al. J Clin Microbiol 2008;46:2856.
5  Breitschwerdt EB, et al. Parasit Vectors 2010;3:29.
6  Breitschwerdt EB, et al. J Clin Microbiol 2007;45:270.
7  Breitschwerdt EB, et al. J Clin Microbiol 2010;48:2289.
8  Oliveira AM et al. J Vet Intern Med 2010;24:1229.
9  Breitschwerdt EB, et al. J Clin Microbio 2009;47:1957.
10 Breitschwerdt EB, et al. Parasit Vectors 2010;3:76.
11 Sykes JE, et al. J Clin Microbiol 2010;48:3782.

Lyme Carditis: Heart Block & Other Complications of LD

**Please see independent tick researcher John Scott’s comment regarding climate change and tick expansion after the article.**

Lyme Carditis: Heart Block and Other Complications of Lyme Disease

by Adrian Baranchuk, MD, FACC ,FRCPC, FCCS, and Cynthia Yeung, BSc

The incidence of Lyme disease, a tick-borne bacterial infection, is rapidly increasing in North America. Risk modeling suggests that the incidence of Lyme disease will continue to rise as the migratory birds that are responsible for transmitting the Ixodes tick are affected by climate change and consequently, contribute to the expansion of at-risk regions. Lyme disease can affect many organ systems, including the heart, nerves, and joints.

In this article, the authors intend to highlight one of the most dramatic complications of Lyme disease, early dissemination Lyme carditis.

How Common Are Lyme Disease And Lyme Carditis?

Lyme disease is the most commonly reported vector-borne disease in North America, with an annual incidence of approximately 25, 000 confirmed cases in the United States. However, estimates suggest that the true incidence is closer to 300, 000 cases annually. Lyme disease affects the heart in 0.3-10% of cases.

Lyme Carditis: How Spirochetes Affect The Heart

In Lyme carditis, Borrelia burgdorferi (the spirochete responsible for Lyme disease) directly affects the heart. Damage to the heart tissue occurs from the direct invasion by the bacteria, as well as from the body’s exaggerated immune response to the infection.

In 90% of cases, the most common consequence of Lyme carditis is heart block. Electrical signals from the upper chambers of the heart are not properly relayed to the lower chambers of the heart, which can dramatically slow down the heart rate.

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.

Symptoms Of Lyme Carditis

Patients with Lyme carditis may report light-headedness, fainting, shortness of breath, palpitations, and/or chest pain. Conversely, patients with Lyme carditis may also experience no symptoms, which contributes to the elusive nature of the diagnosis.

Systematic Approach For Lyme Carditis

To help healthcare providers consider Lyme carditis as a potential cause for heart block, our research team developed the Suspicious Index in Lyme Carditis (SILC) score.

It allots points for specific risk factors. The resulting score classifies patients into low, intermediate, and high-risk categories for the likelihood that the heart block is due to Lyme carditis. The variables in the SILC score can be associated with the mnemonic “CO-STAR”: Constitutional symptoms, Outdoor activity/endemic area, Sex (male), Tick bite, Age (< 50 years), and Rash.

Table 1. The Suspicious Index in Lyme Carditis (SILC) score evaluates the likelihood that a patient’s high-degree heart block is caused by Lyme carditis. The total score indicates low (0-2), intermediate (3-6), or high (7-12) suspicion of Lyme carditis.

Variable                                                               Value
Age < 50 years                                                     1
Male                                                                     1
Outdoor activity/endemic area                             1
Constitutional symptoms*                                    2
Tick bite                                                              3
Erythema migrans rash                                    4

* fever, malaise, arthralgia, and dyspnea

Patients with high-degree heart block and a SILC score of three or higher should be investigated immediately for Lyme disease. They should also receive antibiotic treatment while awaiting the results of testing.

Importance Of Prompt Recognition And Treatment Of Lyme Carditis

The standard protocol for high-degree heart block calls for implanting a permanent pacemaker. However, the heart block in Lyme carditis will most likely resolve with antibiotic therapy. Thus, identifying Lyme carditis as the underlying cause of the heart block can prevent the unnecessary implantation of permanent pacemakers.

The battery of a pacemaker lasts 7-10 years. Thus, a missed diagnosis could subject an otherwise young, healthy patient to 5-7 battery replacements over a lifetime—with each procedure bringing potential adverse events. These risks associated with the initial pacemaker implantation can be mitigated by intravenous and oral antibiotic treatment for heart block caused by Lyme carditis.

Educating Healthcare Providers

We aim to raise awareness about the cardiac manifestations of Lyme disease in endemic areas, so that healthcare providers are educated and alert about Lyme carditis. The conduction disorders associated with Lyme carditis can progress quickly. Patients often seek medical attention several times before Lyme carditis is suspected. The prompt diagnosis and treatment of Lyme carditis is essential to prevent unnecessary implantation of permanent pacemakers and further complications of Lyme disease.

Additional resources

  1. Wan D, Baranchuk A. Lyme carditis and atrioventricular block. CMAJ 2018;190:E622.
  2. Fuster LS, Gul EE, Baranchuk A. Electrocardiographic progression of acute Lyme disease. Am J Emerg Med 2017;35:1040 e5-1040 e6.
  3. Wan D, Blakely C, Branscombe P, Suarez-Fuster L, Glover B, Baranchuk A. Lyme Carditis and High-Degree Atrioventricular Block. Am J Cardiol 2018;121:1102-1104.

Dr. Baranchuk, a cardiologist and professor of medicine at Queen’s University, Kingston, Canada, is one of the world’s leading experts on Lyme carditis. Cynthia Yeung is a medical student.


Birds, not climate change, brought ticks

Re: “Balance key to addressing climate change: expert,” Jan. 19.

I do not agree with Roberta Bondar’s statement: “The migration of deer ticks [blacklegged ticks] into the Kingston area, and the increased incidents of Lyme disease is an example of the kind of environmental changes that climate change is bringing.”

My peer-reviewed scientific research shows that migratory songbirds import blacklegged tick larvae and nymphs into Canada, and are widely dispersing them countrywide. In fact, a heavily tick-infested songbird can initiate a new blacklegged tick population. The number of immature blacklegged ticks on migratory song birds has remained constant for decades — long before climate change was coined. Furthermore, the adult female blacklegged tick does not migrate at all, and crawls a maximum of six metres in her lifetime.

I believe federally funded researchers who publish peer-reviewed papers on tick expansion numbers, ascribed to being caused by climate change, are wasting millions of taxpayer dollars. Moreover, their research is not helping patients get diagnosed and treated in a timely manner. Alarmingly, we have 3,000 patients going to the United States for diagnosis and treatment of Lyme disease and associated tick-borne diseases.

Any daily temperature increases are not putting any extinction stressors on the blacklegged female. She lays her eggs in the cool, moist leaf litter, where she has typically laid them for millennia, and is very comfortable in this microhabitat. She does not have extinction stress in this environment and, thus, does not lay more eggs. The seemingly more ticks in the Kingston area, and everywhere else, is not because of climate changing. In reality, public awareness is the key factor because more people, veterinarians and pet groomers are looking for them.

John D. Scott

Fergus, Ontario

Please know there’s a ton of money when it is ear-marked with the words “climate change,” but regarding tick expansion and therefore the spread of Lyme, it isn’t being honest and it’s taking valuable resources and money away from things that really matter.  Scott goes as far to say it’s a nefarious plot protecting authorities from the lack of helpful research and care for patients that’s occurred over the span of 40 years. This pdf by Lyme Advocate Jill Auerbach shows that while there were only 5,700 cases of WNV in 2012, research dollars were $29 million, whereas, Lyme cases in 2012 were 312,000 but received only $25 million.  Another stark contrast is Hepatitis C in 2012 with 1,300 cases but with $112 million in research dollars.

While the number of the infected continue to soar, the research dollars for Lyme are radically reduced in successive years.  Go here for a quick table comparing research dollars for various diseases:


Don’t kid yourself.  Words mean things and any research ear marked with the words “climate change” have not and will not help patients one iota.

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