Lyme disease surveillance in the United States: Looking for ways to cut the Gordian knot
Authors: M. L. Cartter, R. Lynfield, K. A. Feldman, S. A. Hook, A. F. Hinckley
First published: 12 February 2018 DOI: 10.1111/zph.12448
Disclaimer: The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention.
Summary
Current surveillance methods have been useful to document geographic expansion of Lyme disease in the United States and to monitor the increasing incidence of this major public health problem. Nevertheless, these approaches are resource-intensive, generate results that are difficult to compare across jurisdictions, and measure less than the total burden of disease. By adopting more efficient methods, resources could be diverted instead to education of at-risk populations and new approaches to prevention. In this special issue of Zoonoses and Public Health, seven articles are presented that either evaluate traditional Lyme disease surveillance methods or explore alternatives that have the potential to be less costly, more reliable, and sustainable. Twenty-five years have passed since Lyme disease became a notifiable condition – it is time to reevaluate the purpose and goals of national surveillance.
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**Comment**
Yes, please! Cut the Gordian Knot! Better yet, take an ax to the thing!
Thanks to the enduring popularity of the Alexander fable, the phrase “Gordian knot” has entered the lexicon as shorthand for an intricate or intractable obstacle. One of its earliest appearances came in the Shakespeare play Henry V, where the titular character is praised for his ability to “unloose” the Gordian knots of politics. Likewise, the saying “cutting the Gordian knot” is now commonly used to describe a creative or decisive solution to a seemingly insurmountable problem.
LYME DISEASE, TRANSPLACENTAL TRANSMISSION AND FETAL DAMAGE
The two sides of the coin in pregnancy and LYME DISEASE
Hello friends of the network DERMAGIC EXPRESS, I bring you today another topic for what I call the “SAGA” on LYME DISEASE, in this case the controversial issue of TRANSPLACENTAL TRANSMISSION AND FETAL DAMAGE AND DEATH in pregnant women and infected with the feared BORRELIA BURGDORFERI.
I have found numerous references; most claim that BORRELIA in pregnant women with LYME DISEASE traverses the placenta and reaches the fetus and can cause multi organic damage, including the death of the same, intrauterine or a few hours or days after birth. Other authors say that this is false.
The CDC (Center of Control of Infectious Diseases) affirms that if the pregnant woman with LYME does her treatment, the child will be born healthy and recommends the use of the antibiotic AMOXICILLIN, because DOXYCYCLINE can cause damage to the developing fetus. The question here is what would happen if the BORRELIA species is resistant to AMOXICILLIN? Or the antibiotic to which BORRELIA is sensitive cannot be indicated because it would harm the fetus?
BORRELIA BURGDORFERI was discovered in 1982 by the aforementioned Willy Burgdorfer, the causal agent of the ERYTHEMA MIGRANS or LYME DISEASE, and only 1 year later the first study in 1983 described that it is suspected that this ESPIROCHETE can cross the placenta and infect the fetus, study published by Shirts SR, Brown MS, and Bobitt JR. under the name of “Listeriosis and borreliosis as causes of antepartum fever”. (8)
Later in the year 1985 Schlesinger PA, Duray PH, Burke BA, Steere AC, Stillman MT published a paper called “Maternal-fetal transmission of the spirochete of Lyme disease, Borrelia burgdorferi” where they report a case of a woman who developed LYME DISEASE and did not receive treatment with antibiotics. The child was born at 35 weeks of pregnancy and died of congenital heart disease the first week of life. The autopsy revealed the LYME ESPIROCHETE in the SPLEEN, KIDNEYS AND BONE MARROW. (2)
Later, the same WILLY BURGDORFER the discoverer and “father” of the ESPIROCHETE BORRELIA, who along with Dr. Alan Mc Donald and Jorge Benach PhD, published in the year 1987 (31 years ago) a work they called “stillbirth following maternal LYME DISEASE.” and I quote from the conclusions of these scientists: (24.)
“… Two cases of transplacental transmission of the BORRELIA BURGDORFERI were found associated with fetal death and congenital malformations, different anomalies were detected in each case …”
“… We recommend that pathologists study the tissues of stillborn fetuses in search of BORRELIA BURGDORFERI especially those with cardiac anomalies, and clinical doctors investigate the exposure during the first trimester of pregnancy to BORRELIA BURGDORFERI and in these cases determine if cardiac organogenesis is complete by the end of the first trimester of pregnancy”
“… We believe that there is enough evidence to alert women living in endemic areas of LYME DISEASE and doctors to recognize the early signs and symptoms of the disease and to start treatment with PENICILLIN at the same dose of SYPHILIS as used in pregnant women in the first trimester, regardless of the results of the laboratory tests … “
Another study that is worth noting is the one made by the MEDLINE database updated for the year of July 2012, the last revision of November 2012 of 88 journal articles from the PUBMED database, which I summarize as follows:
Maternal-Fetal Transmission of Lyme Disease
RESULTS:
1.) Mothers with active Lyme Disease,Treated: 14.6% of the pregnancies with sequelae,
2.) Untreated: 66.7% of the pregnancies with sequelae,
3.) Unknown as to treatment: 30.3% with sequelae.
4.) Specific adverse outcomes included: cardiac 22.7%, neurologic 15.2%, orthopedic 12.1%, ophthalmic 4.5%, genitourinary 10.6%, miscellaneous anomalies 12.1%, 2nd trimester demise 12.1%. Highest rate of adverse outcome (72.7%) in women with infection acquired prior to or during first trimester.)
Now I will put a summary of the most frequent clinical manifestations described in the studies of children born to mothers with LYME disease, LYME positive
COMMON SIGNS AND SYMPTOMS IN LYME POSITIVE CHILDREN:
=====================================================
1.) LOW GRADE FEVER: 59% -60%
2.) FATIGUE AND LACK OF RESISTANCE: 72%
3.) NOCTURNAL SWEATING: 23%
4.) PALE, DARK CIRCLE UNDER THE EYES: 42%
5.) ABDOMINAL PAIN: 20-29%
6.) DIARRHEA OR CONSTIPATION: 32%
7.) NAUSEA: 23%
8.) CARDIAC ANOMALIES: 23%: PALPITATIONS, (PVC) HERAT MURMUR, MITRAL VALVLE PROLAPSE
9.) ORTHOPEDIC DISORDERS: SENSITIVITY (55%), PAIN (69%) SPASMS AND GENERALIZED MUSCLE PAIN (69%), RIGIDITY AND / OR DELAY OF MOVEMENTS (23%).
10.) RESPIRATORY INFECTIONS OF THE SUPERIOR TRACT AND OTITIS: 40%
11.) ARTHRITIC DISORDERS AND PAINFUL JOINTS: 6% -50-%
12.) NEUROLOGICAL DISORDERS:
A- HEADACHES: 50%
B-) IRRITABILITY: 54%.
C-) BAD MEMORY: 39%
13.) DELAY IN DEVELOPMENT: 18%
14.) SEIZURE DISORDERS: 11%
15.) VERTIGO: 30%
16.) TIC DISORDERS: 14%
17.) INVOLUNTARY ATETOID MOVEMENTS: 9%.
18.) LEARNING DISORDERS AND HUMOR CHANGES: 80%
A-) COGNITIVE SPEAKING: 27%
B-) SPEACH DELAY: 21%
C-) READING-WRITING PROBLEMS: 19%
D.) PROBLEMS OF VOCAL ARTICULATION: 17%.
E-) PROBLEMS OF AUDITIVES / VISUAL PROCESSING: 13%
F-) WORD SELECTION PROBLEMS: 12%
G-) DYSLEXIA: 8%
19.) SUICIDAL THOUGHTS: 7%
20.) ANXIETY: 21%
21.) ANGER OR RAGE: 23%
22.) AGGRESSION OR VIOLENCE: 13%
23.) IRRITABILITY: 54% -80%
24.) EMOTIONAL DISORDERS: 13%
25.) DEPRESSION: 13%
26.) HYPERACTIVITY: 36%
27.) PHOTOPHOBIA: 40-43%
28.) GASTROESOPHAGEAL REFLUX WITH VOMIT AND COUGH: 40%
29.) SECONDARY ERUPTIONS: 23%
30.) OTHER ERUPTIONS: 45%
31.) CAVERNOUS HAEMANGIOMA: 30%
32.) OULAR PROBLEMS: POSTERIOR CATARACTS, MYOPIA, STIGMATISM, CONJUNCTIVE ERYTHEMA (LYME EYES), OPTICAL NERVE ATROPHY AND / OR UVEITIS: 30%
44.) FATIGUE AND LACK OF RESISTANCE: 72%
45.) SENSITIVITY OF SKIN AND NOISE (HYPERACUITY): 36-40%
46.) AUTISM.
There are numerous studies showing a clear EVIDENCE that the BORRELIA BURGDORGFERI in pregnant women is able to cross the placenta and infect the fetus. I could get tired here of giving you the description of each of them. But I will give you ALL the BIBLIOGRAPHIC REFERENCES that I found from the year 1983 until the year 2017, first the ones I found and then a chronology of ALL of them.
I close this issue which is HIGHLY DISCUSSED TODAY, with a post by Angélica Johansson, a great fighter against THIS PLAGUE that I found in my LINKEDIN network about the future of the planet and the LYME DISEASE … I quote:
“…”1 million people are predicted to get infected with Lyme disease in the USA in 2018. Given the same incidence rate of Lyme disease in Europe as in the USA, then 2.4 million people will get infected with Lyme disease in Europe in 2018. In the USA by 2050, 55.7 million people (12% of the population) will have been infected with Lyme disease. In Europe by 2050, 134.9 million people (17% of the population) will have been infected with Lyme disease. Most of these infections will, unfortunately, become chronic.
The estimated treatment cost for acute and chronic Lyme disease for 2018 for the USA is somewhere between 4.8 billion USD and 9.6 billion USD and for Europe somewhere between 10.1 billion EUR and 20.1 billion EUR. If governments do not finance IV treatment with antibiotics for chronic Lyme disease, then the estimated government cost for chronic Lyme disease for 2018 for the USA is 10.1 billion USD and in Europe 20.1 billion EUR.
If governments in the USA and Europe want to minimize future costs and maximize future revenues, then they should pay for IV antibiotic treatment up to a year even if the estimated cure rate is as low as 25%. The cost for governments of having chronic Lyme patients sick in perpetuity is very large….”
But what you see every day is a fight between IDSA and ILADS, CDC and others on the subject of whether it is a simple tick bite and you take an antibiotic and you cure or that it is a disease of difficult diagnosis and high cost of treatment. Between believers and non-believers to summarize. The truth is that it is spreading all over the world in leaps and bounds.
And if you have doubts that this ESPIROCHETE may or may not harm the fetus of pregnant women, cause birth defects, and many other consequences including, stillborn babies, read this “MOUNTAIN” of references that I leave here.
Approx. 25 Min.
Sue Faber, RN and Co-Founder of LymeHope speaks to pregnancy and Gestational Lyme at the LymeHope Education Event, Oakville, Ontario on November 3, 2017.
Dr. Elena Frid, a board-certified NYC neurologist and specialist in Lyme disease & other vector-borne diseases, discusses congenital Lyme disease.
**Comment** In reference to Dr. Frid’s comment that congenital Lyme is rare, I would disagree. We have not been keeping track of numbers and there are probably way more than is being acknowledged.
CONCLUSION: BORRELIA BURGDORFERI, not only transmitted by the tick bite, is TRANSMITTED by sexual contact, fluids and can also colonize the fetus of pregnant women if there is no effective treatment able to eradicate it during the same. And it is not exclusive to the Northern Hemisphere. The BORRELIA is also in the Southern Hemisphere.
2.) Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi. Ann Intern Med. 1985 Jul;103(1):67-8. [PUBMED]. Schlesinger PA, Duray PH, Burke BA, Steere AC, Stillman MT.
3.) Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy. Pediatr Infect Dis J. 1988 Apr;7(4):286-9. [PUBMED]. Weber K1, Bratzke HJ, Neubert U, Wilske B, Duray PH.
4.) Neonatal skin lesions due to a spirochetal infection: a case of congenital Lyme borreliosis? Int J Dermatol. 1997 Sep;36(9):677-80. [PUBMED]. Trevisan G1, Stinco G, Cinco M.
5.) Confirmation of Borrelia burgdorferi spirochetes by polymerase chain reaction in placentas of women with reactive serology for Lyme antibodies. Gynecol Obstet Invest. 1996;41(4):240-3. [PUBMED]. Figueroa R1, Bracero LA, Aguero-Rosenfeld M, Beneck D, Coleman J, Schwartz I.
6.) Detection of Borrelia burgdorferi DNA in urine of patients with ocular Lyme borreliosis.
Pleyer U1, Priem S, Bergmann L, Burmester G, Hartmann C, Krause A. Br J Ophthalmol. 2001 May;85(5):552-5. [PUBMED]
7.) Culture and identification of Borrelia spirochetes in human vaginal and seminal secretions [version 1; referees: 1 not approved]. Marianne J. Middelveen1, Jennie Burke2, Eva Sapi3, Cheryl Bandoski3, Katherine R. Filush3, Yean Wang2, Agustin Franco2, Arun Timmaraju3, Hilary A. Schlinger1, Peter J. Mayne1, Raphael B. Stricker1
Source: https://f1000research.com/articles/3-309/v1 F1000 RESEARCH
8.) Listeriosis and borreliosis as causes of antepartum fever. Obstet Gynecol. 1983 Aug;62(2):256-61. [PUBMED]. Shirts SR, Brown MS, Bobitt JR.
9.) Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi.
Schlesinger PA, Duray PH, Burke BA, Steere AC, Stillman MT.
10.) Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am 1989 Nov 15:657-77. MacDonald AB. Source: . Rheum Dis Clin North Am 1989 Nov 15:657-77
12) Lyme Borrelia positive serology associated with spontaneous abortion in an endemic Italian area.) Acta Eur Fertil. 1988 Sep-Oct;19(5):279-81. [PUBMED]. Carlomagno G1, Luksa V, Candussi G, Rizzi GM, Trevisan G.
13.) Infection with Borrelia: Implications for Pregnancy. James M O’Brien 1. and 2 Odessa P Hamidi. Division of Maternal Fetal Medicine, Pennsylvania College of Medicine, USA. Department of Obstetrics and Gynecology, Pennsylvania College of Medicine, USA.
SOURCE: http://www.smgebooks.com/lyme-disease/chapters/LD-17-05.pdf
14.) MEDLINE results for: borrelia pregnancy AND human. 88 journal articles in the PubMed
database BDH, July 2012, Latest Revision Novemb
er 2012, http://www.Huismans.de.vu
15.) Infants born to mothers with antibodies against Borrelia burgdorferi at delivery. Eur J Pediatr. 1989 Feb;148(5):426-7. [PUBMED]. Nadal D1, Hunziker UA, Bucher HU, Hitzig WH, Duc G.
17.) Congenital relapsing fever (Borrelia hermsii).Blood, 15 November 2000, Vol. 96, No. 10, pp. 3333-3333William A. Dittman. Sr, Sacred Heart Medical Center, Spokane, WA.
20.) Borreliosis during pregnancy: a risk for the unborn child?. Vector Borne Zoonotic Dis. 2011 Jul;11(7):891-8. doi: 10.1089/vbz.2010.0102. Epub 2010 Oct 6. [PUBMED]. Mylonas I1.
21.) Intrauterine transmission of Borrelia burgdorferi in dogs. Am J Vet Res. 1993 Jun;54(6):882-90. [PUBMED]. Gustafson JM1, Burgess EC, Wachal MD, Steinberg H.
22.) Fetal outcome in murine Lyme disease. Infect Immun. 1995 Jan;63(1):66-72. [PUBMED] Silver RM1, Yang L, Daynes RA, Branch DW, Salafia CM, Weis JJ.
27.) Teratogenic effects of the bacteria Borrelia sp. on the fetuses of pregnant women with Lyme disease. Sliwa, Leopold. Nowa Medycyna 04/2011. (Translation of above article)
28.) Lyme disease in pregnancy: case report and review of the literature. Obstet Gynecol Surv. 2007 Jan;62(1):41-50. [PUBMED] Walsh CA1, Mayer EW, Baxi LV.
29.) Borreliosis During Pregnancy: A Risk for the Unborn Child? VECTOR-BORNE AND ZOONOTIC DISEASES. Volume 11, Number 7, 2011. Mary Ann Liebert, Inc..DOI: 10.1089/vbz.2010.0102. Ioannis Mylonas. Source full text: http://boreliozaonline.pl/publikacje/Borelioza-w-ciazy.pdf BIBLIOGRAPHICAL REFERENCES BY CHRONOLOGY
source:
Lyme Disease and Pregnancy, Maternal Fetal Transmission of Lyme Disease:
1983 Shirts SR, Brown MS, Bobitt Jr. Listeriosis and borreliosis as causes of antepartum fever. Obstet Gynecol 1983;62:256.
1985 Schlesinger PA, Duray PH, Burke BA, Steere AC, Stillman MT. Maternal fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi. (1985) Ann Intern Med, 103, 67-8.
1985 MMWR. Update: Lyme Disease and Cases Occurring during Pregnancy—United States. Vol. 34, No. 25 (June 28, 1985), pp. 376- 378, 383-384
1986 MacDonald A. Human fetal borreliosis, toxemia of pregnancy, and fetal death. Zentralbl Bakteriol Mikrobiol Hyg A. 1986 Dec;263(1-2):189-200.
1986 Burgdorfer, W., The Enlarging Spectrum of Tick Borne Spirochetoses; R.R. Parker Memorial address. Reviews of Infectious Diseases, vol.8, no.6 (Nov-Dec 1986), pp.932940
1986 Markowitz LE, Steere AC, Benach JL, et al. Lyme disease during pregnancy. JAMA.(1986); 255(24), 3394-6.
1987 MacDonald AB, Benach JL, Burgdorfer W. Stillbirth following maternal Lyme disease. N Y State J Med. 1987 Nov;87(11):615-6.
1988 Weber K; Bratzke HJ, Neubert U, Wilske B, Duray PH. (1988) Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy. Pediatr Infect Dis J, 7:286-9.
1988 Carlomagno G, Luksa V, Candussi G, et al. (1988) Lyme Borrelia positive serology associated with spontaneous abortion in an endemic Italian area. Acta Eur Fertil 19(5), 279-81.
1988 Medici F, Benach J, Williams C. Lyme Disease during Pregnancy A Cord Blood Serosurvey. Annals New York Academy of Sciences. Volume 539, Lyme Disease and Related Disorders Pages 504–506.
1988 Health and Welfare Canada. Canada Diseases Weekly Report, June 4, 1988. Lyme disease in Canada.
1988 Lyme disease in Canada. Epidemiologic Report. CMAJ Vol. 139, Aug 1, 1988
1989 MacDonald A. Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am. 1989 Nov;15(4):657-77.
1989 Halperin JJ., Dattwyler R., et al. A Perspective on the treatment of Lyme Borreliosis. Reviews of infectious diseases. Vol. 11 Supp 6. Sept/Oct 1989. S1518-1525
1989 Nadal D, Hunziker UA, Bucher HU, et al. (1989) Infants born to mothers with antibodies against Borrelia burgdorferi at delivery. Eur J Pediatr 148(5), 426-7.
1989 Steere et al. Lyme Seropositivity and pregnancy outcome in the absence of symptoms of Lyme disease. Scientific Abstracts June 12-17, 1989. 53 Annual Meeting of American College of Rheumatology.
1991 Lakos A. Lyme Borreliosis in Hungary in the years 1984 through 1989. Parasit hung., 24;5-51, 1991
1992 ACOG Committee Opinion. Lyme disease during pregnancy. Int J Gynecol Obstet 1992, 39; 59-60.
1992. Bracero LA, Wormser GP, Leikin E. Tejani N. Prevalence of seropositivity to the Lyme disease spirochetes during pregnancy in an epidemic area: A preliminary report. J Matern Fetal Investig. 1992(2): 265-268
1993 Hercogova J, Tomankova M, Frosslova D, Janovska D. Early-stage lyme borreliosis during pregnancy: treatment in 15 women with erythema migrans. Ceska Gynekol 58(5):229-232.
1993 Strobino BA, Williams CL, Abid S, et al. (1993) Lyme disease and pregnancy outcome: a prospective study of two thousand prenatal patients. Am J Obstet Gynecol 169(2 Pt 1), 367-74.
1994 Gasser R. et al. A Most Unusual case of a whole family suffering from late Lyme Borreliosis for Over 20 years. Angiology Vol. 45, No. 1: 85-86.
1994 Trevisan G. Lyme Borreliosis; A general survey. Acta dermatovenerologica A.P.S. Vol 3, 94, No. 1/2 4-12
1994 Elsukova LV, Korenberg EI, Kozin GA., [Pathology of pregnancy and the fetus in Lyme disease] [Article in Russian]. Med Parazitol (Mosk). 1994 Oct-Dec;(4):59-62
1995 Gardner T. Infectious Diseases of the Fetus and Newborn, 4th edition, New York, NY. W.B. Saunders Company (1995) Chapter 11, Lyme Disease. page 447 – 528.
1995 Williams CL, Strobino B, Weinstein A, et al. (1995) Maternal Lyme disease and congenital malformations: a cord blood serosurvey in endemic and control areas. Paediatr Perinat Epidemiol 9(3), 320-30.
1995 Schmidt, B. et al. Detection of Borrelia burgdorferi DNA by Polymerase Chain Reaction in the Urine and Breast Milk of Patients with Lyme Borreliosis. DIAGN MICROBIOL INFECT DIS 1995;21:121-128.
1995 Alexander, J. Cox, S. Lyme disease and Pregnancy. Infectious diseases in Obstetrics and Gynecology 3?256-261 (1995)
1996. Figueroa R. et al. Confirmation of Borrelia burgdorferi Spirochetes by Polymerase Chain Reaction in Placentas of Women with Reactive Serology for Lyme Antibodies. Gynecol Obstet Invest 1996; 41?240-243
1996. Maraspin V, Cimperman J. Treatment of Erythema Migrans during Pregnancy. Clinical Infectious Diseases 1996; 22?788-93
1997 Silver H. (1997) Lyme Disease During Pregnancy. Inf Dis Clinics of N. Amer. Vol 11, No 1.
1997 Trevisan G, Stinco G, Cinco M. Neonatal skin lesions due to a spirochetal infection; a case of congenital lyme borreliosis? International Journal of Dermatology 36; 677-99
1999 Norris C., Gardner T. Aseptic Meningitis in the Newborn and Young Infant. Am Fam Physician 1999 May 15;59(10):2761-2770
2001 Elliot D, Eppes S., Klein J. Terratogen Update; Lyme disease. TERATOLOGY 64?276 – 281 (2001)
2001 Gardner T. Chapter 11, Lyme Disease. Remington and Klein: Infectious diseases of the Fetus and Newborn, Fifth edition. New York, NY. W.B. Saunders Company 2001 pgs. 519-641
2001 Gardner T. Lyme disease in pregnancy. Program and abstracts of the 14th International Scientific Conference on Lyme Disease and Other Tick-Borne Disorders; April 21-23, 2001; Hartford, Connecticut.
2003 Goldenberg, R. L and C. Thompson (2003). “The infectious origins of stillbirth.” Am J Obstet Gynecol 189(3): 861-73.
2003 Salvato, WT, Salvato P. Lyme disease: ancient engine of an unrecognized borreliosis pandemic? Medical Hypotheses 60(5): 742-759.
2005 Onk G, Acun C, Kalayci M, Cagavi F, et al. (2005) Gestational Lyme disease as a rare cause of congenital hydrocephalus. J Turkish German Gynecology Association Artemis, 6(2), 156-157.
2005 Jones CR, Smith H, Gibb E, Johnson L (2005) Gestational Lyme Disease: Case Studies of 102 Live Births. Lyme Times. Gestational Lyme Studies 34-36
2005 Goldenberg et al. Maternal Infection and Adverse Fetal and Neonatal Outcomes. Clin Perinatol 32 (2005) 523–559.
2006 Walsh et al. Lyme disease in pregnancy. Obstetrical and Gynecological Survey. CME Review Volume 62, Number 1.
2007 Bransfield, Robert C. et al. The association between tick borne infection, lyme borreliosis and autism spectrum disorder. Medical hypotheses (2007)
2008 Hercogova J, Vanousova D. Syphilis and borreliosis during pregnancy. Dermatol Ther 21(3), 205-9.
2008 Theiler RN, Rasmussen, S. et al. Emerging and Zoonotic infections in women. Infect Dis Clin North Am 2008 December ; 22(4): 755–viii
2009 Lakos et al. Maternal Lyme borreliosis and pregnancy outcome. International Journal of Infectious Diseases 14 (2010) e494–e498
2009. Hulinska D, Votypka J, Vanousova D, Hercogova J, Hulinsky V, Drevova H, Kurzova K, Uherkova L. Identification of Anaplasma phagocytophilum and Borrelia Burgdorferi sensu lato in Patients with Erythema Migrans. Folia Microbiol. 54(3), 246-256 (2009)
2011 Mylonas I. Borreliosis During Pregnancy: A Risk for the Unborn Child? Vector Borne Zoonotic Dis. 11?891-8.
2011 Sliwa, Leopold. Teratogenny wplyw bakterii Borelli sp. Na ploy matek chorujacych na borelioze z Lyme. Zaklad Biologi Rozwoju Czlowieka. Instytus Pielegniarstwa.
2011 Sliwa, Leopold. Teratogenic effects of the bacteria Borrelia sp. on the fetuses of pregnant women with Lyme disease. Nowa Medycyna 04/2011. (Translation of above article)
2014 Onyett, H . Lyme disease in Canada: Focus on Children. Paediatr Child Health 2014;19(7):379-83
2014 OʼBrien, JM. Martens MG. Lyme disease in pregnancy; a New Jersey medical advisory. MD advisory, Winter 2014, pgs 24-27
2015 Krysztof PJ et al. Congenital tick borne Diseases: Is this an alternative route of transmission of tick borne pathogens in Mammals? Vector-Borne and Zoonotic Diseases Vol 15, Number 11, 2015.
2015 Hu LT, Tsibris AM, Branda JA. Case Records of the Massachusetts General Hospital: Case 24-2015; A 28 year-old pregnant woman with fever, chills, headache and fatigue. N Engl J Med. 2015 Jul 30;373(5):468-75.
2016 Maldonato, Y, Nizet, V, Klein, J, Remington, J, Wilson, C. Current concepts of Infections of the Fetus and Newborn Infant. Chapter 1. page 6. Infectious Diseases of the Fetus and Newborn Infant. 8th Edition. 2016
2017 OʼBrien, JM. Baum JD. Case Report. The Journal of Family Practice. August 2017; 66(8) pg E9-10 Updated and printed by JC on November 2, 2017
UConn Health researchers led by postdoctoral fellow Ashley Groshong, shown here in UConn Health’s Spirochete Research Lab, are advancing understanding of how the bacteria Borrelia burgdorferi transmits Lyme disease, pointing to the potential for ultimately developing therapeutics to target this system. Courtesy of UConn Office of the Vice President for Research
What Makes the Bacteria Behind Lyme Disease Tick?
Researchers from UConn Health are advancing the understanding of how the causative bacterial agent of Lyme disease, Borrelia burgdorferi (Bb), survives in ticks and mammals.
Connecticut residents are all too familiar with Lyme disease, but the precise mechanisms of how humans become infected are still unclear. Researchers from UConn Health are advancing the understanding of how the causative bacterial agent of Lyme disease, Borrelia burgdorferi (Bb), survives in ticks and mammals.
The findings from Ashley Groshong, a postdoctoral fellow in the Spirochete Research Lab at UConn Health, and her colleagues were recently published in mBio.
Here’s a refresher on the typical steps involved in the spreading of Lyme disease.
An infected black-legged tick (Ixodes scapularis) feeds on and infects a mammal, like a white-footed mouse, to transmit a pathogen (i.e. Borrelia burgdorferi) to its next mammalian host. While the tick may prefer to feed from small rodents or deer, oftentimes humans are an accidental host. In this case, transmission of the bacteria to humans results in disease pathology.
This bacterial pathogen is a spirochete, which means it has a unique spiral shape, and it is slow to replicate. It also depends entirely on its host for nutrients, a unique characteristic that has drawn attention from many Lyme researchers. While previous genetic analyses have suggested that the Bb’s genome encodes a cellular transport system capable of importing nutrients from the host in the form of peptides, the importance of the system for viability and pathogenesis had never been established.
“We wanted to target the energy domain of the system to understand exactly how important this system is for survival and proliferation during infection,” explains Groshong. “If we understand how B. burgdorferi acquires its nutrients from its hosts and which nutrients are essential, it could potentially lead to a novel target for therapeutic intervention.”
The peptide transport system is quite complex, preventing previous evaluation of its role in the bacteria. To better understand the importance of peptides, a source of amino acids, Groshong and the UConn Health team adopted a novel approach. Groshong created a mutant version of B. burgdorferi that effectively blocks the spirochete’s normal methods of consuming peptides by targeting the lynchpin of the transporter, the part of the system that provides energy for peptide transport.
The research showed that spirochetes deprived of peptides failed to replicate, which indicates that peptide uptake is essential for bacterial viability and ability to infect. In other words, Groshong and the UConn Health team have shown that if Bb’s transport system is inhibited, it would be possible to block the proliferation of the bacteria in an infected mammal, such as a human or rodent. Interestingly, this is the only pathogen demonstrated to require peptides for basic viability, making this a unique find in the world of pathogenic bacteria.
Lyme disease research is particularly important for Connecticut residents, where the condition was first recognized in Lyme, Conn., in 1975. According to the Connecticut State Department of Public Health, approximately 30,000 people in the state are diagnosed with Lyme disease each year.
“When it comes to helping Connecticut tackle Lyme disease, UConn is providing support on all fronts,” says Radenka Maric, vice president for research at UConn and UConn Health, “from tick testing at the Connecticut Veterinary Medical Diagnostic Laboratory to innovative research like Dr. Groshong’s at the Spirochete Research Lab. UConn’s faculty, postdoctoral fellows, and students are conducting research to find solutions to the major health challenges we face today.”
Groshong plans to build on this research through a project that will explore possible ways to target this system for the development of therapeutics and to evaluate if a limited peptide environment, such as the mammal, promotes the formation of antibiotic-tolerant persister cells. This research will be funded through a Blackman Fellowship from the Global Lyme Alliance.
According to Groshong, there is still a long way to go before this research could translate into a new treatment option, but she’s hopeful about what this discovery means for the study of Lyme disease.
“Right now, our options for treating and preventing this infection are limited and not specific to the bacteria,” says Groshong. “Our goal is to conduct research that could lead to better understanding of how these bacteria cause disease, as well as novel and targeted approaches to new therapies.”
Other UConn Health authors include Abhishek Dey, Irina Bezsonova, Melissa J. Caimano, and Justin D. Radolf.
Source: UConn Health
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**Comment**
This research presents patients with some definite hope for novel treatment.
One word; however, about the elephant in the room that needs to be addressed. Researchers keep saying that the way to acquire Bb is through a black-legged tick.
Period. End of story.
What about other ticks, other insects? What about sexual transmission, congenital transmission & via breast milk? What about through bodily fluids? There is evidence for all of these modes of transmission yet…..
the elephant keeps standing, unnoticed in the middle of the room.
People would rather blame “climate change,” to obtain hefty grants to provide them with monetary support for the next few years rather than truly help sick and dying patients who need these questions answered. These are practical questions that affect our day to day decisions as humans.
According tick expert, John Scott, who has volunteered some 30,000-plus hours as a citizen scientist and was awarded a Sovereign’s Medal for Volunteers in recognition of 27 years of research and advocacy on Lyme disease and tick populations in Canada,
“Climate change has nothing to do with tick movement. Blacklegged ticks are ecoadaptive, and tolerate wide temperature fluctuations. On hot summer days, these ticks descend into the cool, moist leaf litter and rehydrate. In winter, they descend into the leaf litter, and are comfortable under an insulating blanket of snow. Ticks have antifreeze-like compounds in their bodies, and can tolerate a wide range of temperatures. For instance, at Kenora, Ontario, the air temperature peaks at 36°C and dips to –44°C, and blacklegged ticks survive successfully……ticks are marvellous eco-adaptors. They will be the last species on the planet.” https://madisonarealymesupportgroup.com/2017/08/14/canadian-tick-expert-climate-change-is-not-behind-lyme-disease/
He also states:
“Any research on ticks and climate change is inconclusive––in essence, there is no validity. The long-range, futuristic projections and statistical models are bogus science because blacklegged ticks have already been found in northern Canada. In fact, we documented blacklegged ticks on migratory songbirds in northern Alberta dating back to 1998. Any allocation of government funding for ticks and climate change research is a complete waste of taxpayers’ money. It will not help Lyme disease patients one iota.” https://madisonarealymesupportgroup.com/2017/08/14/canadian-tick-expert-climate-change-is-not-behind-lyme-disease/
The following article explains that Borrelia Miyamotoi is not new to California. First considered nonpathogenic, it wasn’t even reported until 2011 in Russia. http://www.nejm.org/doi/full/10.1056/NEJMc1215469 Diagnosis relies on PCR testing during acute infection and two-tiered testing for Lyme will not pick it up. It is not a reportable illness so prevalence is pure conjecture. Dr. Horowitz states clinicians should be vigilant for clinical pictures that look like viral infections such as high fever, headache, and muscle and joint pain. In publications, only 16% of patients presenting with BMD were seropositive for IgG and/or IgM antibody to B. miyamotoi rGlpQ, so PCR should also be considered in patients with a history of tick bites and appropriate clinical manifestations.
This is also an important reminder that new strains and species are being discovered continually, so nothing about Tick Borne Illness should be set in stone and open minds are a must.
LYME SCI: B. miyamotoi has been in California ticks for a long time
Like forensic detectives, using a bank of frozen blood serum from the 1980s, tick researchers from both the west and east coasts set out to determine how prevalent Borrelia miyamotoi infection is in California. What they discovered should set off more than a few alarms.
B. miyamotoi is a spiral-shaped bacterium in the same genus as Borrelia burgdorferi, the agent of Lyme disease. But it is most closely related to the group of relapsing fever Borrelia spirochetes. It has recently been recognized as causing a form of borreliosis that is similar to Lyme disease—Borrelia miyamotoi disease (BMD).
B. miyamotoi is transmitted by the same hard-bodied ticks that carry Lyme disease—the blacklegged or deer tick (Ixodes scapularis) and the western blacklegged tick (Ixodes pacificus).
The symptoms of BMD are similar to Lyme disease but generally more severe, with the addition of a relapsing fever, and the absence of a typical bull’s-eye rash. Because BMD is not a reportable disease in the US, there is very little information about its symptoms or prevalence.
For this study, the researchers were given access to a biobank of 101 blood samples collected from a rural community in Mendocino County, California, after an outbreak of Lyme disease in the late 1980s. The area has since been the focus of many tick studies and is known for high prevalence of ticks that carry both BMD and Lyme disease.
Three quarters of the people in the study reported frequent tick bites in the one to two years prior to the blood draw. Later, a confirmatory blood test showed that 79% had antibodies to tick saliva—a rate nearly three times that of residents of Block Island, Rhode Island (29%), where Lyme disease is highly endemic.
For the BMD screening, researchers used two different methods to look for evidence of prior exposure to B. miyamotoi—a two-step glycerophosphodiester phosphodiesterase enzyme-linked immunosorbent (rGlpQ) assay and a whole-cell lysate (WCL) assay.
Twenty-six of the 101 samples were reactive for BMD. [Note: the B. miyamotoi GlpQ assay is not affected by Lyme disease infection because B. burgdorferi does not produce GlpQ antigen.]
The samples were also tested for Borrelia hermsii and Borrelia burgdorferi, to examine the possibility of cross-reactivity and/or dual infection.
The researchers feel there is probable cause of BMD infection for several reasons:
Studies showing 0.5% to 15% of Ixodes pacificus ticks carry B. miyamotoi infection in Northern California, B. miyamotoi is passed from parent to offspring (transovarial transmission), increasing risk of infection from nymphal ticks, and mild climates allow for nearly year-round activity of ticks in California.
“No human cases of B. miyamotoi previously have been reported from the western United States even though I. pacificus ticks in northern California have a spirochete-infection prevalence similar to or exceeding that of I. scapularis ticks in the Northeast and upper Midwest,” according to the authors.
The authors go on to warn, “Healthcare professionals in the far-western United States should be aware that B. miyamotoi disease may occur throughout the geographic distribution of I. pacificus and that improved relapsing fever group spirochete antibody assays are urgently needed.”
In summary, while B. miyamotoi is considered an “emerging” infectious disease, it is not new to California. The fact that there are no previously reported cases is because 1) until recently there have been no commercially available tests and 2) since BMD is not a reportable disease, nobody collects such information.
This study highlights the pressing need to develop better diagnostic tests capable of detecting all tick-borne diseases–and to collect the results of those tests in a way that’s accessible to the public.
LymeSci is written by Lonnie Marcum, a Licensed Physical Therapist and mother of a daughter with Lyme. Follow her on Twitter: @LonnieRhea Email her at: lmarcum@lymedisease.org .
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**Comment**
Interestingly, the CDC states that PCR and antibody-based testing for Bm are under development and not widely available but can be ordered from a few CLIA-approved labs.
Now that’s sweet isn’t it? Up until now the CDC has vilified all CLIA approved labs – especially for Lyme testing.
Dr. Cameron points out the hypocrisy marvelously here: http://danielcameronmd.com/fda-test-borrelia-miyamotoi/ Researchers have had to diagnose B. miyamotoi based on blood smear, direct detection of spirochetes in cerebrospinal fluid and follow-up polymerase chain reaction (PCR) and molecular detection of B. miyamotoi DNA in acute whole blood from patients. These are all non FDA-approved tests. So, where would these patients be if the FDA insisted on only its tests being utilized?
The incidence of tick-borne zoonoses such as Lyme disease has steadily increased in the southeastern United States. Southeastern states accounted for 1500 of over 28,000 confirmed cases of Lyme disease reported in the United States during 2015. Borrelia burgdorferi, the etiologic agent of Lyme disease, is maintained in small mammal reservoirs and vectored to new hosts by ixodid ticks.
This study examined ecological relationships of the B. burgdorferi/vector/reservoir system in order to understand the dynamics of Lyme disease risk in Kentucky. Small mammals were captured using live traps from November 2014 to October 2015.Ticks were removed and blood and tissue collected from small mammals were screened for B. burgdorferi DNA by PCR with primers specific to the OspA gene.
Prevalence of B. burgdorferi(21.8%) in Kentucky small mammals was comparable to the lowest recorded prevalence in regions where Lyme disease is endemic. Moreover, infestation of small mammals by Ixodes scapularis, the primary vector of B. burgdorferi, was rare, while Dermacentor variabilis comprised the majority of ticks collected.
These findings provide ecological insight into the relative paucity of Lyme disease in Kentucky.
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**Comment**
The conclusion of this study is all wrong. Bb was found Kentucky mammals. That in itself is important. Also, the fact the preponderance of ticks were dermacentor variabilis (wood tick or American dog tick) which supposedly has not been proven to be a competent vector of Bb as supposedly it doesn’t efficiently pass Bb from inside the tick to humans or other hosts), it does transmit Tularemia and Rocky Mountain Spotted Fever.
Regardless of whether the wood tick can transmit Bb or not, they do transmit pathogens. The fact that nearly 22% of small Kentucky mammals have Bb due to the black legged deer tick and most of the ticks they picked up were wood ticks, those deer ticks were particularly infected.
“That’s a spider bite,” a local pediatrician told her. “We don’t have Lyme in Oklahoma.”
The doctor was wrong. Had my friend taken his advice, her daughter would not have been diagnosed in a timely fashion and she would likely have developed symptoms over the next few months or years. She probably would have become severely debilitated, and the infections might have crossed the blood-brain barrier and become chronic.
Madison Area Lyme Support Group 