Currently worldwide lyme disease has become a major public health problem, due to the annual increase in cases, which in the United States amounts to about 380,000, new cases annually, 2 times more than breast cancer and 6 times more than aids, and beyond this, the lack of modernization of the disease codes at the software or digital level, them do not appear currently and they need to be recognized so that patients to be and treated in time. The events that I present below they are highly related to this lack of “CODIFICATION” of the Lyme disease and its different ways of manifesting itself clinically:

Difficulty to make the diagnosis:
  It is well known that some test, to diagnose the disease, result in “NEGATIVE” due to the ability of the causative agent, the spirochaete borrelia to “hide (Biofilm) before the diagnostic tests” Many patients with symptoms of different diseases such as meningitis, arthritis, and recurrent fever, in late stages it is discovered that they are lyme “positive” after having multiple tests for the diagnosis, losing a valuable time to initiate an adequate treatment, and the worse thing is that the chronic development of these symptoms, impar the quality of life of patients who are unattended because they do not have a specific diagnosis.

Resistance to conventional treatment:
  Another aspect to consider is that borrelia and its species over time have developed a “great resistance” to conventional therapy with the usual antibiotic treatments: minocycline, doxicycline, amoxicillin, cefuroxime, and many others, leading patients to the despair at the occurrence of the codification of the symptoms. LYME disease has four stages classically known: Initial (I), Secondary (II), Late (III) Chronic (IV).

The lack of modernization of the codes for the Lyme disease:
  In this modern and globalized world, digitalization and information technology have become essential elements and everything or almost everything has a code, even diseases at the software level, and in the case of lyme disease these must be updated, and this is done based on the evidence reports, studies and publications of the different manifestations of the disease.

  Then you will be asking why the Lyme disease needs the update of its codes? If you enter in the World Health Organization (WHO) and look for lyme disease, you will only find two(2) mentions in the subject ZOONOSES, transmission by ticks: lyme disease and recurrent fever (borreliosis), and the latest relevant reports in terms of studies of the disease by WHO date from the years 1993 and 1995:
• WHO Workshop on Diagnosis and Surveillance of Lyme Borreliosis. Warsaw, Poland, 20 - 22 June 1995, Ref.: WHO / CDS / VPH / 95.141:
• The countries involved were: Austria, Bulgaria, Czech Republic, Denmark, Yugoslavia, France, Hungary, Ireland, Japan, Holland, Poland, Russia, Sweden, Switzerland, United Kingdom and the United States.
• Report of a WHO Workshop on Lyme Borreliosis. Piestany, Slovak Republic, 6 October 1993, Ref: WHO / CDS / VPH /93.132:

  The countries involved: Germany, Slovakia and the United States. If you read those reports you will notice that they are totally out of date regarding the reality of Lyme disease today.

And I will always give you the answer.
  I will place here more than 276 bibliography references classified based on the different manifestations of lyme disease or lyme borreliosis that are sufficient to recognize that beyond “Lyme Disease” and recurrent fever (Borreliosis) there are other manifestations of the borreliosis that should be codified, digitalized, to give a total coverage to the disease and search of its clinical manifestations.

  This “Absence” of codes causes that many patients carrying lyme are not treated adequately, because they do not “Appear in the system” with their respective consequences.
  Here I ask the innocent question, what happens is “Unknown” or “Intentioned”? Because to recognize all these IMPLIED CODES means more public spending by the State and the insurance companies.

1) Congenital Lyme Disease: Potential infection of the foetus with possibility of death^[1-15]:
• Lyme borreliosis in pregnant women.
• Erlichiosis and Borreliosis in Pregnant Women.
• The Infectious Origins of Stillbirth.
• Intrauterine Transmission of Borrelia Burgdorferi in dogs.

2) Lyme Disease: Primary Infection^[16-20]:
• Newborn dead woman pregnant with Lyme disease.
• Lyme borreliosis, implication for the foetus.
• Fetal borreliosis, texemia of pregnancy and fetal death.
• Eritema migrans in pregnancy.
• Fetal maternal transmission of lyme disease.
• Borrelia burdogferi in newborn.

A.) Primary infection and erythema migrans.
- Primary and secondary erythema migrans.
B.) Primary seronegative infection^[21-26].
- Negative antigens against borrelia burdogferi in cerebrospinal fluid in neurologic lyme disease.
- Seronegative Lyme disease.
- Seronegative chronic relapsing neuroborreliosis.

3.) Lyme disease, persistent infection in secondary and late stage^[27-30].
- Persistent infection with antibiotics doxycyline and amoxicillin.
- Isolation of borrelia burdogferi from ocular iris.
- Survival of borrelia burdogferi after therapy with antibiotic.

4.) Lyme disease, persistent infection in secondary and late stage^[31-40]:
A.) Cutaneous Manifestations:
- Borrelial Lymphocytoma (BL).
- Acrodermatitis atrophicans^[41-45].
- Annulare granuloma^[46-48].
- Morphea^[49-51].
- Localized scleroderma^[52-54].
- Lichen sclerosus and atrophicus^[55-57].

B.) Other Cutaneous manifestations^[58-62]:
- Benign lymphocytic infiltration of jessner kanof.
- Infantile acrodermatitis of gianotti-crosti.
- Atypical erythema multiforme.
- Urticarial vasculitis.

5.) Lyme disease of skin and mucous membranes^[63-65]:
- Association of Lyme disease with morgellons disease.
- Difusse alopecia^[66-69].
- Scleroderma in cup de sabre.
- Pseudopelade of brocq.

6.) Lyme disease and other lesions^[70-72]:
- Anetoderma.
- Primary and secondary erythema migrans in children.

7.) Lyme disease late stage: meningitis, oculopathy, iridocyclitis, iritis, uveitis^[73-83].
A.) Lyme Meningitis.
B.) Lyme Oculopathy.
C.) Lyme Iridocyclitis, Iritis and Uveitis.

8.) Lyme disease secondary and late stage: Nephritis, Hepatitis, Lymphadenopathy, Myositis and Other^[84-107].
A.) Lyme Nephritis.
B.) Lyme Hepatitis.
C.) Lyme Lymphadenopathy.
D.) Lyme Myositis.
E.) Other Conditions:

- Perplexing Symptoms.
- Pancytopenia.
- Eye Symptoms.

9.) Lyme disease late stage and cardiovascular disease^[108-128].
A.) Aortic Aneurysm.
B.) Aneurysm of Coronary Arteries.
C.) Late Endocarditis.
D.) Carditis.
E.) Atrioventricular Block.

10.) Lyme disease late stage, neuro-borreliosis, neuritis or neuropathy, meningovascular, nb with cerebral infarcts, lyme Parkinsonism, lyme encephalitis^[129-182].
A.) Neuro Borreliosis (NB) Late Symptoms.
B.) Neuritis or Late Neuropathy.
C.) Neuro Borreliosis (NB) Meningovascular with Cerebral Infarcts.
D.) Intracraneal Aneurysm.
E.) Parkinsonism.
F.) Late Encephalitis.
G.) Stroke due to Neuro borreliosis.
H.) Neuro Borreliosis (NB) Unspecific Symptoms:

- Late Lyme disease (Neuro Borreliosis: Comparison and Evidence of the Spirochetes and late Neurosyphilis.
- Evidence between the infection of spirochetes and Alzheimer’s disease.

11.) Lyme Disease: Neuro borreliosis, Late Lyme Meningoencephalitis or Meningomyeloencephalitis^[183-212].

12.) Lyme Disease Late Stage: Atrophic form of Meningoencephalitis with Dementia, Subacute presenile dementia and neuropsychiatric manifestations^[213-243].

13.) Lyme Disease: Late Stage: Bone, Joint and Musculoskeletal Manifestations^[244-252].

14.) Lyme Disease, Late Stage: Oculopathy, Liver, Kidney and respiratory manifestations^[253-267].
A.) Oculopathy.
B.) Liver and other visceras.
C.) Kidney and ureter.
D.) Bronchia and Lungs.

15.) Lyme Disease, Latent Stage, Unspecified^[268-281].
A.) Infection of the Central Nervous System.
B.) Simple Herpes Type 1.
C.) Diseases by Spirochetes of the Central Nervous System.

  This classification that you have just read is a summary of the 276 bibliographic references that I describe below which you can find in the best scientific databases such as Pubmed, Medscape, Lilacs etc, if you have some doubt copy and paste of any of them, put it in your browser and you will get the exact information on the mentioned databases.

Figure 1:

Conclusion

  As you can see, there are enough evidences, to update the codes of Lyme disease in all the databases systems of the planet, to give a total coverage to the diagnosis and treatment of this disease that in my particular way of seeing is becoming the new plague of the 21^st century. But this does not end here, suddenly you think that some details are missing, some or several questions, which I will explain in the next edition:
Lyme’s Disease, Syphilis and Leprosy, the missing link.
Do not miss it!!!

References

1) Bale, J.F. Jr., Murph, J.R. Congenital infections and the nervous system. (1992) Pediatr Clin North Am 39(4): 669–690.
Pubmed | Crossref | Others
2) Brzostek, T. Human granulocytic ehrlichiosis co-incident with Lyme borreliosis in pregnant woman--a case study. Przegl Epidemiol (2004) 58(2): 289–294.
Pubmed | Crossref | Others
3) Gardner, T. Lyme disease. In: Remington JS, Klein JO, eds. Infectious Diseases of the Fetus and Newborn. (1995) 5th ed. Philadelphia: Saunders 447–528.
Pubmed | Crossref | Others
4) Goldenberg, R.L., Thompson, C. The infectious origins of stillbirth. (2003) Am J Obstet Gynecol. 189(3): 861–873.
Pubmed | Crossref | Others
5) Gustafson, J.M., Burgess, E.C., Wachal, M.D., et al. Intrauterine transmission of Borrelia burgdorferi in dogs. (1993) Am J Vet Res 54(6): 882–890.
Pubmed | Crossref | Others
6) MacDonald, A.B., Benach, J.L., Burgdorfer, W. Stillbirth following maternal Lyme disease. (1987) N Y State J Med 87(11): 615–616.
Pubmed | Crossref | Others
7) MacDonald, A.B. Gestational Lyme borreliosis. Implications for the fetus. (1989) Rheum Dis Clin North Am 15(4): 657–677.
Pubmed | Crossref | Others
8) Macdonald, A.B. Human fetal borreliosis, toxemia of pregnancy, and fetal death. Zentralblatt für Bakteriologie, Mikrobiologie und Hygiene. Series A: Medical Microbiology, Infectious Diseases, Virology, Parasitology (1986) 263(1-2): 189–200.
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9) Maraspin, V., Cimperman, J., Lotric-Furlan, S., et al. Erythema migrans in pregnancy. (2000) Wien klin Wochenschr 111: 933–940.
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10) Markowitz, L.E., Steere, A.C., Benach, J.L., et al. Lyme disease during pregnancy. (1986) JAMA: J Am Med Asso 255(24): 3394.
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11.) Schlesinger, P.A., Duray, P.H., Burke, B.A., et al. Maternal-fetal transmission of the Lyme disease Spirochete, Borrelia burgdorferi. (1985) Ann Inter Med 103(1): 67.
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12) Silver, R.M., Yang, L., Daynes, R.A., et al. Fetal outcome in Murine Lyme disease. (1995) Infect Immu 63(1): 66–72.
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13) Strobino, B.A., Williams, C.L., Abid, S., et al. Lyme disease and pregnancy outcome: A prospective s of two thousand prenatal patients. (1993) Am J Obstet Gynecol 169(2): 367–374.
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14) Weber, K., Bratzke, H.J., Neubert, U., et al. Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy. (1988) Pediatr Infect Dis J 7(4): 286–288.
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15) Christova, I., Komitova, R. Clinical and epidemiological features of Lyme borreliosis in Bulgaria. (2004) Wien Klin Wochenschr 116(1-2): 42-46.
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16) Hercogová, J., Tománková, M., Barták, P. Contributions to the treatment of dermatologic manifestations of Lyme borreliosis. (1992) Cutis 49(6): 409-411.
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17) Lipsker, D., Hansmann, Y., Limbach, F., et al. Disease expression of Lyme borreliosis in north-eastern France. (2001) Eur J Clin Microbiol Infect Dis 20(4): 225-230.
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18) Melski, J.W., Reed, K.D., Mitchell, P.D., et al. Primary and secondary erythema migrans in central Wisconsin. (1993) Arch Dermatol 129(6): 709-716.
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19) Schmid, G.P. Epidemiology and clinical similarities of human spirochetal diseases. (1989) Rev Infect Dis 6: S1460-S1469.
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20) Coyle, P.K., Deng, Z., Schutzer. S.E., et al. Detection of Borrelia burgdorferi antigens in cerebrospinal fluid. (1993) Neurology 43(6): 1093-1098.
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21) Coyle, P.K., Schutzer, S.E., Deng, Z., et al. Detection of Borrelia burgdorferi-specific antigen in antibody-negative cerebrospinal fluid in neurologic Lyme disease. (1995) Neurology 45(11): 2010–2015.
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22) Dattwyler, R.J., Volkman, D.J., Luft, B.J., et al. Seronegative Lyme disease. Dissociation of T- and B-Lymphocyte Responses to Borrelia burgdorferi. (1988) N Engl J Med 319: 1441-1446.
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23) Holak, H., Holak, N., Huzarska, M., et al. Tick inoculation in an eyelid region: report on five cases with one complication of the orbital myositis associated with Lyme borreliosis. (2006) Klin Oczna 108(4-6): 220-224.
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24) Karma, A., Seppälä, I., Mikkilä, H., et al. Diagnosis and clinical characteristics of ocular Lyme borreliosis. (1995) Am J Ophthalmol 119(2): 127-135.
Pubmed | Crossref | Others
25) Lawrence, C., Lipton, R.B., Lowy, F.D., et al. Seronegative Chronic Relapsing Neuroborreliosis. (1995) Eur Neurol 35: 113-117.
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26) Feng, J., Wang, T., Shi, W., et al. Identification of novel activity against Borrelia burgdorferi persisters using an FDA approved drug library. (2014) Emerg Microbes Infect 3(7): e49.
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27) Oksi, J., Marjamaki, M., Nikoskelainen, J., et al. Borrelia burgdorferi detected by culture and PCR in clinical relapse of disseminated Lyme borreliosis. (1999) Ann Med 31(3): 225–232.
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28) Preac-Mursic, V., Pfister, H.W, Spiegel, H., et al. First Isolation of Borrelia burgdorferi from an Iris Biopsy. (1993) J Clin Neuro-ophthalmol 13: 155-161.
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29) Preac-Mursic, V., Weber, K., Pfister, H.W., et al. Survival of Borrelia burgdorferi in Antibiotically Treated Patients with Lyme borreliosis. (1989) Infec 17: 355-359.
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30) Schmidli, J., Hunziker, T., Moesli, P., et al. Cultivation of Borrelia burgdorferi from joint fluid three months after treatment of facial palsy due to Lyme borreliosis. (1988) J Infect Dis 158(4): 905–906.
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31) Arne