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Time to recognise Congenital Lyme: an open letter to the WHO

Updated: Mar 3, 2023

On behalf of Borrelia positive patients, expert clinicians and scientists working in the field of Borrelia clinical and laboratory research.

Dear Dr. Tedros Ghebreyesus,

We are writing to you today to protest at the removal of code 1C1G.2, for ‘Congenital Lyme borreliosis’, from the new ICD-11 codes, and to ask for you to support its reinstatement as a ‘stand-alone’ category.

With the current letter (previous communications not responded to), we once again hope to raise your awareness of significant concerns regarding congenital Lyme disease, and would ask the WHO to embrace the science, rather than ignoring it as has been done in the ICD-11 process with regards to congenital Lyme infection to date.


A request to have ‘Congenital Lyme borreliosis’ listed as a ‘stand-alone’ category in the new ICD-11 codes was made by the Ad Hoc Committee for Health Equity in ICD-11 Borreliosis Codes, submitted March 27, 2017 by Jenna Luché-Thayer and other authors. Following a WHO directed scientific review, the code 1C1G.2, for ‘Congenital Lyme borreliosis’, was released as part of WHO's June 2018 announcement of ‘stable codes' - meaning they had been thoroughly vetted and accepted as stable.

Following its acceptance in June 2018, the WHO’s Medical and Scientific Advisory Committee (MSAC) apparently conducted a second review of this ‘stable code’, and recommended removal of the code at a meeting in October 2018 (1). The Ad Hoc Committee lead by Jenna Luché-Thayer were not informed about the meeting or the removal of the code. Only by chance was the deletion discovered on the WHO website. No reason was provided when members of the Ad Hoc Committee investigated this covert and unexplainable deletion. However, correspondence from a member of the WHO committee communicated that “This was in response to a request for the removal of Congenital Lyme borreliosis by the Public Health Agency of Canada (PHAC) ...”.

Following the deletion of ‘congenital Lyme borreliosis’ from the ICD-11 codes, between July and October of 2019, multiple communications requesting clarification were made by Dr John Lambert, members of the Ad Hoc Committee, concerned citizens, Members of Parliament, members of the UK House of Lords, and MEP’s from around the world to ‘responsible’ individuals within the WHO who administrate the ICD-11 codes. There has been no satisfactory explanation for the deletion of ‘Congenital Lyme borreliosis’. One communication stated that since congenital Lyme disease does not have a ‘congenital syndrome’ it does not need a stand-alone code. However, congenital malaria does not have a ‘congenital syndrome’ but it has a stand-alone code.

Communications in summer of 2019 with Dr Robert Jakob, Team Leader Classifications, Terminologies and Data Standards (ICD, ICF, ICHI), by authors of this letter, were unhelpful. He provided no explanation for the ‘Congenital Lyme borreliosis’ code deletion, but gave ‘alternative’ ways that Congenital Lyme could be coded, in the absence of a ‘stand-alone’ code; and also suggested a new submission to have ‘Congenital Lyme borreliosis’ re-reviewed again. However, our request for ‘transparency’ of process was not addressed. Subsequently, we have sent copies of these communications to Dr Tedros and other members of the WHO. To the best of our knowledge, it has taken until May 2020 to get any response from the WHO to any of our stakeholders to explain the lack of transparency of this process; and the response that was provided in May 2020 shows many flaws within the WHO system that need to be urgently addressed and corrected.

The correspondence from WHO in May 2020 has revealed that:

“The concept of ‘congenital Lyme disease’ was removed from ICD-11 based on a systematic review conducted by UK NICE (2). The decision was later also supported by an independent systematic review by Waddell et al (3) and information available from CDC (4).

“The different proposals in favour of inclusion of ‘congenital Lyme disease’ in ICD-11 included a total of 15 references to literature. We verified these references against ones in the systematic reviews. Of the 15 references, one referred to two different editions of the same textbook, two referred to animal studies. Two were explicitly excluded from the analyses because of their study design. Ten were included in either of the systematic reviews”.

The letter also states that “When future research would provide evidence for ‘congenital Lyme disease’ a proposal for amendment of ICD could be submitted”.

We object to this process, question the conclusions of the NICE review, as detailed below, and question whether the Waddell publication was indeed a ‘systematic review’; and indeed would suggest that ALL evidence supporting congenital Lyme should be included, not just a limited and ‘exclusive’ data set that was really a ‘means to an end’. And the means to an end was the removal of congenital Lyme, an unacceptable action on these ‘mystery people’ who submitted this request; and an equally unacceptable decision on the part of the WHO to accept such a submission. A subsequent ‘inclusive’ review of the literature on congenital Lyme has been published by Lambert et al. (5).

Indeed, if one looks at the total of the published literature on Congenital Lyme and consider further advances that have taken place over the past two years, we argue that the code should be reinstated based on:

  1. Since WHO reviewed the CDC document, it has been updated (on January 27, 2020), and now states: "Lyme disease acquired during pregnancy may lead to infection of the placenta and possible stillbirth. Therefore, early diagnosis and treatment of Lyme disease is important during pregnancy. However, no negative effects on the fetus have been found when the mother receives appropriate antibiotic treatment” (4). WHO have therefore provided a reference which in fact supports re-instatement. CDC first acknowledged congenital transmission in a communication from 1985 where, referring to research by Schlesinger et al (6), they stated "Transplacental transmission of B. burgdorferi has been documented in a pregnant woman with Lyme disease who did not receive antimicrobial therapy” (7).

  2. The review by Waddell (3) states "Only one case (in Germany) described the full range of expected observations (clinical manifestations in the mother, negative outcome for the child, and laboratory detection of B. burgdorferi in the child) that would give confidence that vertical transmission of B. burgdorferi, with negative consequences for the fetus, occurs”, referring to research by Weber et al (8) and Weber and Neubert (9). However, since the review was co-authored by the CDC and the CDC guidance (4) has changed since its publication, it appears that this has provided sufficient evidence for them to alter their opinion.

  3. Many other cases of congenital Lyme were recorded in the proposals presented by the Ad Hoc Committee. Regarding the two references by Gardner in ‘two different editions of the same textbook’, in actuality these are distinct publications with different content in different editions of a major Pediatric Infectious Disease textbook, and all references from both of these book chapters should be reviewed and included.

  4. The WHO reference to the systematic review by NICE used to justify removal of the code is in fact an outdated draft document published in Sept 2017 (2). The final version of this document was published in April 2018 (10). It is unfortunate that the WHO letter of 11 May 2020 cites a wrong reference to a draft publication. We question, however, both the draft and final publications published by NICE; as the process of ‘exclusion’ by NICE is not a process that WHO should endorse. NICE reviewed congenital transmission only through observational studies that report an incidence or prevalence estimate of Lyme disease through vertical transmission. No use was made of in-vitro or animal studies; studies published in languages other than English; studies published after 3 July 2017; studies from non-OECD countries; or any case studies. In doing so, they reviewed only a very limited set of evidence involving only 12 documents (10). When NICE stated that references were ‘Excluded due to an incorrect study design’, in fact they appear to be referring to their exclusion because these references were case studies. We do not think case studies should be excluded. In fact, we are quite concerned the WHO would endorse the exclusion of studies published in ‘languages other than English’ and studies from ‘non-OECD countries’. NICE’s literature search did not identify the study by Weber and Neubert (9) and by specifically excluding case studies they excluded the research by Schlesinger (6) and Weber et al (8). NICE in fact only reviewed 4 of the 15 submissions which were proposed by the Ad Hoc Committee to WHO as evidence in favour of inclusion. By not reviewing any of the documents which led the CDC and Waddell to conclude that there was vertical transmission with negative consequences for the fetus, the UK NICE have come to a conclusion which cannot be justified.

We therefore maintain that the conclusion reached by UK NICE does not provide justification for overturning the previously carefully considered opinion of WHO and respectfully request that WHO follow the action of CDC in acknowledging 'Congenital Lyme borreliosis' and reinstate the removed code. We also ask, in the name of transparency, for details of who initiated this covert action and any correspondence associated with it for the Ad Hoc Committee to review. To give us an opportunity to respond in a fair and transparent process, an opportunity to this date not provided.


Lyme disease (LD) was first officially described in the State of Connecticut (Old Lyme), when a case series of children with juvenile arthritis were found to have spirochetal infection in 1977 (11). Borrelia burgdorferi was identified as the causative agent of Lyme disease. Following identification of B. burgdorferi sensu stricto, multiple other Borrelia species were confirmed to cause the same or similar clinical manifestations, but still the name ‘Lyme disease’ is used to describe a larger complex of bacteria, Borrelia burgdorferi sensu lato. Today, B. burgdorferi sensu lato complex includes 22 recognized spirochete species, almost half of which have been proved to be, to different extents, pathogenic to humans. Those include Borrelia burgdorferi sensu stricto, Borrelia garinii, Borrelia afzelii, Borrelia bavariensis, Borrelia bissettii, Borrelia kurtenbachii, Borrelia spielmanii, Borrelia lusitaniae and Borrelia valaisiana.

The main vectors of Lyme disease spirochetes are hard ticks that belong to Ixodes ricinus complex: Ixodes scapularis and Ixodes pacificus in North America and Ixodes ricinus and Ixodes persulcatus in Eurasia. Hard ticks also serve as vectors for other bacterial or protozoan pathogens like Ehrlichia, Rickettsiae, Bartonella, and Babesia, and some viruses, e.g., tick borne-encephalitis virus. Often more than one pathogen can be transmitted to the host (including humans) by a tick in a single bite (called co-infections). Nymphal ticks that feed on small mammals and birds represent the most important tick development stage in terms of pathogen transmission. Infected ticks in endemic areas can have a wide range of prevalence’s, ranging from 6-15% in Ireland, to over 50% in many EU countries and in the USA.

Vertical transmission of LD was first suspected in 1983 in a case that described arthritis in a mother. Spirochetes were visualized on a blood film of the newborn who had presented with hyperbilirubinemia. However, no Lyme or syphilis serology was performed in this case (12), limiting conclusions. The first confirmed case with positive Lyme serology was described in 1985 in a 28-year-old mother who had acquired Lyme in the first trimester, who had an erythema chronicum migrans (ECM) rash and delivered at 35 weeks. Symptoms consistent with Lyme disease developed in the mother post-delivery and her LD IFA was positive 1:128. The child died of congenital heart disease and autopsy showed spirochetes infiltrating the spleen, kidneys and bone marrow, but were not found in cardiac tissue (6). A report by MacDonald successfully demonstrated Borrelia burgdorferi in the fetal myocardium using an immunohistochemical technique (13).

In the following years a number of case reports present compelling immunohistological evidence of spirochetaemia in stillbirths where mothers had clinical and/or laboratory confirmed LD, confirming the vertical transmission of B. burgdorferi (8,14). Evidence of clinical LD has been seen in infants in some instances: a 3-week old who developed a skin rash post-partum was found to have B. burgdorferi isolated from biopsy of these skin specimens (15).

A case of neonatal LD was reported whereby Borrelia specific antibodies were discovered in the spinal fluid of an infant with documented neurologic dysfunction. The mother who had LD infection in her second trimester had been treated with oral antibiotics and was reported as being seronegative at the time of delivery (16). A case from Germany described an infant with neonatal onset of maculopapular skin rash, hepatosplenomegaly, anaemia and fever, followed by progressive multi-system manifestations including protruding eyes, bilateral knee arthritis, axillary and inguinal lymph nodes, growth impairment, and developmental delay. Elevated antibody titres against Borrelia were found in the child’s serum; her mother, who had no clinical manifestations, also had positive ELISA titres (17). A case review of 19 women with LD in pregnancy reported adverse events in 5 fetuses suggesting the possibility of congenital transmission (18).

Other suggestions of transplacental transmission pregnancy come from studies of placental tissue tested post-delivery in mothers with LD; in one study of 60 mothers found to have antibodies against Borrelia, 5% had evidence of spirochetes in placenta tissue using silver staining protocol. Two of 3 were PCR positive for Borrelia burgdorferi (19).

A study performed by Strobino et al of over 2000 women from an endemic region who had positive LD serology were compared to a Lyme negative cohort. Worse outcomes when comparing fetal deaths, pre-term delivery and congenital abnormalities were not seen. Furthermore, no risk of adverse outcomes was reported in women with reported (known) tick exposure. In this study only 11 women had positive LD serology, 5 of whom had previously documented LD and who had received treatment (20). It is important to note that congenital defects in babies at 6-month follow-up was the only study marker of adverse outcome in newborns. There was no direct detection testing of placentas or of cord blood of babies born to these seropositive women. Longitudinal health monitoring, and serial serologies in newborns were not performed.

The authors reported ‘a statistically significant association between past miscarriages and history of tick-bite’ and ‘a significant association between having had a tick bite within 3 years of conception and congenital defects.’ Authors also noted that the incidence of cardiac defects was twice as high in children born to mothers residing in towns with a high LD endemicity rate versus low endemic areas. The authors also acknowledged that their study was underpowered and ‘the number of women was too small to draw conclusions about the risk of having a child with a congenital malformation if a woman is seropositive.’ Such findings will only be validated by having recognition of Congenital Lyme as a ‘stand alone’ code.

Gardner analysed congenital Lyme disease in detail, backed up by 888 references, in the 2001 book “Infectious Disease of the Fetus and Newborn Infant” (21). She stated that “As the number of reported cases of Lyme disease continue to increase, there have been increasing reports of gestational Lyme disease associated with adverse outcomes and suspected Lyme borreliosis. Although a homogenous Lyme borreliosis syndrome has not yet emerged, there are several features that are common among the 66 adverse outcomes of pregnancies complicated by gestational Lyme borreliosis … (including miscarriage during the first 20 weeks of gestation with a high frequency of fetal cardiac abnormality; severe early congenital infection with fulminant neonatal sepsis and meningoencephalitis and a high frequency of cardiac abnormality; and late congenital infection with growth retardation, developmental delay and neurologic, cutaneous, dental and skeletal involvement)”.

A recent review on congenital tick-borne diseases by Jasik et al opines, ‘it is possible that B. burgdorferi has a high ability to penetrate mammalian placentae due to its ability of active movement, antigenic and morphological variation, and many other features, which causes diagnostic difficulties and problems. In cases of intrauterine fetal infections among patients with Lyme disease, symptoms are not homogeneous. This suggests that B. burgdorferi s.l. is transmitted trans-placentally. Authors also acknowledge ‘the ability of long-term survival of B. burgdorferi s.l. in tissues and spreading of spirochetes in the body despite antibiotic treatment can contribute to intergenerational spread of Lyme disease’ (22).

In 2018, Waddell et al performed a systematic review of gestational LD and identified 59 cases between 1969-2017 (3). Twelve cases reported miscarriage or fetal death, 8 newborn death and 16 other abnormalities post-delivery including syndactyly, respiratory distress, and hyperbilirubinemia. One case described complete features of clinical and laboratory results consistent with vertical transmission of LD (8). They also summarized epidemiological studies comparing pregnant women in endemic areas with features or serology to non-Lyme pregnancies; their conclusion was that rates of adverse outcomes were not increased. There are discrepancies in the findings and interpretation of studies from the Waddell ‘systematic review’ compared to other publications and reviews on this subject questioning the accuracy of the term ‘systematic’ in the title of their publication. Indeed an ‘inclusive’ PubMed search, and simply just reading Gardner’s book chapter 2001 will identify many more than 59 cases of gestational LD. We would ask that someone within the WHO would take such a task on hand rather than depending on biased, outside consultations.

The most recent review by Lambert, in 2020, concludes that “The failure of recognition of Congenital Lyme both by clinicians caring for their patients, and by the WHO, who have failed to engage with the ICD 11 codes for Congenital Lyme, is a lost opportunity for better science and improved understanding. Such investment could result in improved maternal and child health, a clear purported declaration of the WHO, ‘no child left behind’. Science needs to prevail, and politics rather than science have to date won the day. And the children are losing.” (5).

It is widely accepted that transplacental transmission can occur in infections with tick-borne relapsing fever, another spirochete, even closer to Lyme borreliosis than Syphilis (23,24,25,26). The literature on ‘Congenital Lyme’ is at present incomplete due to lack of intensive investigations, and lack of longitudinal follow up of exposed infants, as has been done for another spirochete, syphilis. There is no doubt that congenital transmission also occurs with Borrelia; whether a congenital syndrome occurs as a result of this in utero infection remains to be further investigated.


So, in summary, recognition of congenital transmission of Lyme disease took place in the 1980’s and 1990’s. It ‘disappeared’ from the radar screen of science in subsequent decades, and indeed was deleted from medical textbooks, is not recognised in the USA ‘Red Book’ publication by the American Academy of Pediatrics, and it is not considered by the Infectious Diseases Society of America, nor by the UK NICE review. This deletion of congenital Lyme from the medical literature is a paradox, as a simple PubMed review will show large number of publications to support its occurrence. However if you delete ‘foreign publications’ and make other arbitrary exclusions, as has occurred in both NICE and Waddell’s reviews, it is an easy task to eliminate most of the world’s literature on this condition.

The work of the Ad Hoc Committee that was submitted in 2017 brought ‘Congenital Lyme borreliosis’ back on the radar screen, with the new ICD-11 code IC1G.2 being established. This code was agreed by the WHO following a transparent and scientific process. However, shortly after the publication of the Waddell article in 2018 (3), the code for ‘Congenital Lyme borreliosis’ was removed from ICD-11 listings, at the covert request of the Public Health Agency of Canada, we were led to believe. In attempts to get transparency, it has taken till May 2020 to get any response from WHO. We now find out that the deletion of ‘Congenital Lyme borreliosis’ from ICD-11 codes was based on a submission of a review by UK NICE. NICE have used flawed methodology to make their conclusions, and the WHO have agreed with this process. Now, as we enter 2020, the situation once again has changed.

The Centers for Disease Control and Prevention website was updated on January 27, 2020 to include mother to fetus as a possible way of transmitting the disease. The site now states: Lyme disease acquired during pregnancy may lead to infection of the placenta and possible stillbirth’ and ‘Spread from the mother to fetus is possible but rare’.

While the ‘politics’ of Lyme play out their course, controlled not by science but by influence and intrigue, children affected and infected by these tick-borne infections continue to suffer.

We ask the WHO to review the process that has occurred between October 2018 and May 2020, and provide the Ad Hoc Committee with names of the members of the WHO committee, and names of correspondents and copies of any correspondence with NICE and PHAC whose actions initiated such a covert action. We additionally ask for copies of the minutes of the meeting at which the WHO chose to have Congenital Lyme deleted as an ICD11 code. We ask for transparency and a fair process, and would ask that WHO Chief Scientist, Dr Soumya Swaminathan, whose position we understand includes science, research, and evidence into policy making, should be called upon to review both the process and the science.

We ask immediately for return of ‘Congenital Lyme borreliosis’ as a ‘stand-alone’ category in the new ICD-11 codes. Only with such a classification, can we truly catalogue the extent of disease caused by Lyme disease (and other co-infections) in pregnancy and their effect on the unborn child. We need prospective studies of pregnant women and longitudinal follow up of children born to these mothers. Better science and financial resourcing will lead to a better understand of this disease process. We ask for science and transparency of process to prevail in addressing ‘Congenital Lyme disease’.

Thank you for considering our point of view. We look forward to hearing from you and anticipate a favourable response from the WHO to assist our efforts to increase the visibility of mothers and babies living with Lyme disease.

Yours sincerely,

Prof. Christian Perronne, MD, PhD

Professor of Infectious and Tropical Diseases Faculty of Medicine Paris-Ile de France-Ouest University of Versailles-St Quentin en Yvelines (UVSQ) Paris-Saclay France

Dr. John S. Lambert, MD, PhD

Professor of Medicine and Infectious Diseases Mater Misericordiae Hospital and UCD School of Medicine Dublin Ireland

cc. Dr. Soumya Swaminathan, WHO Chief Scientist.


  1. World Health Organization – Family of International Classifications (WHO-FIC) Network Annual Meeting, Seoul, South Korea, 22-27 October 2018

  2. NICE Guideline Intervention Evidence Review, Draft for Consultation. Lyme disease: diagnosis and management, [M] Evidence review for person-to-person transmission. UK National Institute for Care and Excellence. Sept 2017.

  3. Waddell LA, Greig J, Lindsay LR, Hinckley AF, Ogden NH. A systematic review on the impact of gestational Lyme disease in humans on the fetus and newborn. PLoS One. 2018 Nov 12;13(11):e0207067.

  4. LYME DISEASE: What you need to know. US Department of Health and Human Services, Centers for Disease Control and Prevention.

  5. Lambert JS. An Overview of Tickborne Infections in Pregnancy and Outcomes in the Newborn: The Need for Prospective Studies. Front. Med. 2020;7:72.

  6. Schlesinger PA, Duray PH, Burke BA, Steere AC, Stillman MT. Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi. Ann Intern Med. 1985;103(1):67-8.

  7. Current Trends Update: Lyme Disease and Cases Occurring during Pregnancy -- United States. MMWR Weekly, June 28, 1985 / 34(25);376-8,383-4

  8. Weber K, Bratzke HJ, Neubert U, Wilske B, Duray PH. Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy. The Pediatric Infectious Disease Journal. 1988;7(4):286-9.

  9. Weber K, Neubert U. Clinical features of early erythema migrans disease and related disorders. Zentralbl Bakteriol Mikrobiol Hyg A. 1986;263(1-2):209‐228.

  10. NICE Guideline Intervention Evidence Review, Final. Lyme disease: diagnosis and management, [M] Evidence review for person-to-person transmission. UK National Institute for Care and Excellence. Apr 2018.

  11. Steere AC, Malawista SE, Snydman DR, Shope RE, Andiman WA, Ross MR, et al. Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three connecticut communities. Arthritis and Rheumatism. 1977;20(1):7-17.

  12. Shirts SR, Brown MS, Bobitt JR. Listeriosis and borreliosis as causes of antepartum fever. Obstetrics and Gynecology. 1983;62(2):256-61.

  13. MacDonald AB, Benach JL, Burgdorfer W. Stillbirth following maternal Lyme disease. New York State Journal of Medicine. 1987;87(11):615-6.

  14. MacDonald AB. Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am. 1989;15(4):657‐677.

  15. Trevisan G, Stinco G, Cinco M. Neonatal skin lesions due to a spirochetal infection: a case of congenital Lyme borreliosis? International Journal of Dermatology. 1997;36(9):677-80.

  16. Dattwyler RJ, Volkman DJ, Luft BJ. Immunologic aspects of Lyme borreliosis. Reviews of Infectious Diseases. 1989;11 Suppl 6:S1494-8.

  17. Lampert F. Infantile multisystem inflammatory disease: another case of a new syndrome. European Journal of Pediatrics. 1986;144(6):593-6.

  18. Markowitz LE, Steere AC, Benach JL, Slade JD, Broome CV. Lyme disease during pregnancy. JAMA. 1986;255(24):3394-6.

  19. Figueroa R, Bracero LA, Aguero-Rosenfeld M, Beneck D, Coleman J, Schwartz I. Confirmation of Borrelia burgdorferi spirochetes by polymerase chain reaction in placentas of women with reactive serology for Lyme antibodies. Gynecologic and Obstetric Investigation. 1996;41(4):240-3.

  20. Strobino BA, Williams CL, Abid S, Chalson R, Spierling P. Lyme disease and pregnancy outcome: a prospective study of two thousand prenatal patients. American Journal of Obstetrics and Gynecology. 1993;169(2 Pt 1):367-74.

  21. Gardner T (2001), ‘Lyme Disease’, in Remington JS, Klein JO (eds.), Infectious Diseases of the Fetus and Newborn Infant, 5th ed. Saunders, pp. 519-642.

  22. Jasik KP, Okla H, Slodki J, Rozwadowska B, Slodki A, Rupik W. Congenital Tick Borne Diseases: Is This An Alternative Route of Transmission of Tick-Borne Pathogens In Mammals? Vector borne and Zoonotic Diseases (Larchmont, NY). 2015;15(11):637-44.

  23. Fuchs PC, Oyama AA. Neonatal relapsing fever due to transplacental transmission of Borrelia. JAMA. 1969, 208, 690–692

  24. Brasseur D. Tick-borne relapsing fever in a premature infant. Annals of Tropical Paediatrics International Child Health Volume 5, 1985.

  25. Yagupsky P, Moses S. Neonatal Borrelia Species Infection (Relapsing Fever) Am J Dis Child. 1985;139(1):74-76.

  26. Steenbarger JR. Congenital tick-borne relapsing fever: report of a case with first documentation of transplacental transmission. Birth Defects Orig Artic Ser. 1982;18(3 Pt A):39-45.


Signed by members of the “Lyme Resource Centre” Crypto-Infections Conference Scientific Committee, prospective delegates of 2nd European Crypto-Infections Conference, Sept 26-27, 2020, Dublin, and others.



Prof. John Lambert, MD, PhD

Mater Misericordiae University Hospital and UCD School of Medicine, Dublin, Ireland and Lyme Resource Centre, Scotland

Prof. Christian Perronne

University Hospital, Garches, France

Jenna Luché -Thayer

Ad-Hoc Committee for Health Equity in ICD11 Borreliosis Codes

Kenneth Sandström, MD

Örebro, Sweden

Michael Cook

Patient representative, Vis-à-vis Symposiums, United Kingdom

Theresa Denham

Oregon Lyme Disease Network, Oregon, USA

Robert C Bransfield, MD, DLFAPA

Rutgers-RWJ Medical School, New Jersey, USA

Dr. Janey Cringean

Trustee and patient representative, Lyme Resource Centre, Scotland

MUDr. Lada Švábová

Benemastr s.r.o., Veterinary Office for Small Animals, Broumov, Czech Republic

MUDr. Anna Ungerová

Benemastr s.r.o., Veterinary Office for Small Animals, Broumov, Czech Republic

MUDr. Michaela Olexová

Benemastr s.r.o., Veterinary Office for Small Animals, Náchod, Czech Republic

Dr. med Ursula Talib-Benz

Spiez, Switzerland

Armin Schwarzbach, MD, PhD

ArminLabs, Augsburg, Germany

Dr. Carsten Nicolaus

BCA-clinic, Augsburg, Germany

Dr. Terezia Heim

BCA-clinic, Augsburg, Germany

Jovet Hollenhorst

Augsberg, Germany

Miranka Mud

Lymevereniging, Netherlands

Petr Dimacek

Institute of Physics of Materials, CAS, Brno, Czech Republic

Petra Dymarková

Borelioza CZ z.s., Czech Republic

Alena Žákovská

Masaryk University, Faculty of Science, Brno, Czech Republic

Jarslav Turanek

Veterinary Research Institute, Brno, Czech Republic

Tomáš Poner

Czech Republic

Klará Smajdová

Naše Srdce pro Boreliózu a koinfekce, Czech Republic

Anna Chitilová

Borelioz cz Z.S., Czech Republic

Jaraslav Polák

IPM AV, Brno, Chech Republic

Jiři Svoboda

IPM, CAS, Brno, Czech Republic

Milan Jarf

IPM, CAS, Brno, Czech Republic

Che Jung Chang

National Tsing Hua University, Taiwan

Yvonna Jirásková

IPM, CAS, Brno, Czech Republic

Jiři Melzer

MELZER s.r.o., Czech Republic

Inka Melzerová

MELZER s.r.o., Czech Republic

Jaroclav Martinák

IPM, CAS, Brno, Czech Republic

Josef Hlaváč

MORSA s.r.o., Czech Republic

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