"Borrelioosi on monimutkainen sairaus joka voi aiheuttaa oireita missä tahansa elimessä. Yleisimmät oireet alussa: fatiikki, kivut, kuume, vilutus, niskajäykkyys, anoreksia, päänsärky, hengenahdistus, kognitiiviset häiriöt, mielialanvaihtelu jne. Mikäli sairautta ei hoideta ajoissa, tauti saattaa edetä keskushermostoon aiheuttaen MS-, aivokalvontulehdus-, aivokasvain-, Alzheimer-, Parkinson-, ALS-, psyykkisten sairauksien tai autismin kaltaisia oireita. Punkinpureman välityksellä voi saada lukuisia taudinaiheuttajia samanaikaisesti.
Tauti on vaikeasti diagnosoitavissa koska bakteerin aiheuttamat oireet muistuttavat useiden eri sairauksien oireita. Siksi sairastunut tapaa alle kahden vuoden sisällä keskimäärin 5 lääkäriä. Laboratoriotestit eivät ole koskaan ensisijaisessa asemassa borrelioosidiagnoosia tehtäessä niiden epäluotettavuuden vuoksi.
Hoito: Akuutissa vaiheessa 3 - 4 viikon antibioottihoito saattaa olla riittävä. Kroonisen borrelioosin hoito: mikään yksittäinen antibiootti tai yhdistelmäantibiootti ei poista infektiota täydellisesti. Lyhyitä antibioottihoitoja annettaessa epäonnistuneita hoitoja/taudin uusiutumista esiintyy 24 - 50 %:ssa tapauksia. Hoidon pituudesta esiintyy kahdenlaisen koulukunnan näkemyksiä. Joidenkin mukaan yli kuukauden mittaisia hoitoja ei tule käyttää ilman objektiivista näyttöä infektiosta. Toisten lääkärien mukaan objektiivinen näyttö eli laboratoriotestit ovat tällä hetkellä niin epäluotettavia että ne eivät kykene luotettavasti löytämään taudinaiheuttajaa. Siksi he hoitavat sairastuneita kunnes oireet ovat poissa. Hoitovaihtoehdoista, niiden hyödyistä ja haitoista tulee keskustella potilaan kanssa. Sen jälkeen potilas itse viime kädessä päättää mitä hoitoja hän on valmis käyttämään. ..."
http://www.personalconsult.com/articles ... fcare.html
Lyme Disease: Two Standards of Care
By Lorraine Johnson, JD, MBA
Executive Director, CALDA
Lyme disease: Lyme disease, which is caused by the bacterial spirochete Borrelia burgdorferi, is a public health threat of major proportions. The majority of Lyme disease cases result from bites by infected nymphal ticks that may be as small as the period at the end of this sentence. Only 14-35% of patients recall a tick bite. In addition to transmission of Lyme disease by ticks, some studies have a) provided evidence of gestational transmission, b)suggested transmission by other insects and blood transfusions, and c) hypothesized transmission by intimate human contact[1, 3-6]
Coinfections: Ticks have been called "sewers of infection." They feed primarily on birds, rodents, and deer and can transmit to humans many of the diseases carried by these animals. Hence, patients with Lyme disease may be infected with multiple pathogens. The most widely known co-infections acquired from ticks are babesia, bartonella, ehrlichia and Mycoplasma fermentans. Not all pathogens have been identified.[8-10] Patients with coinfections may have more severe symptoms and an extended course of illness.
Prevalence According to the Centers for Disease Control and Prevention (CDC), only one in ten cases of Lyme disease which meet the CDC surveillance criteria is reported, which means that the 23,763 cases national reported in 2002 reflect 237,630 actual cases which meet the CDC criteria. The annual incidence of Lyme disease, which accounts for 95% of vector-borne illnesses in the United States, has increased almost 50-fold since the national surveillance began in 1982.[1, 12] In 2002, Lyme disease increased 40% over the prior year. Lyme disease is hyperendemic along the East Coast, in the upper Midwest, and on the Pacific coast. Lyme infected ticks may be transported from Lyme-endemic areas into non-endemic areas along the "flyways" of migratory birds. Children under 15 years of age account for 25% of reported cases. Many children with Lyme disease experience a dramatic drop in IQ, a decline in grade point average, and require home instruction.
Common Symptoms: Lyme disease is a complex, multi-system disease that has now been shown to involve nearly every organ and organ system in both sexes. The most common symptoms in patients with early Lyme are fatigue, arthralgia , fever or chills; stiff neck and anorexia. Erythema migrans, the characteristic rash that is an initial indicator of Lyme disease, is present in fewer than 50% of Lyme disease patients.[17, 18] Other common symptoms include headache, shortness of breath, cognitive impairment, and mood disorders.
Disease Progression: If it is not detected and treated early on, Lyme disease may involve the central nervous system, mimicking diseases such as multiple sclerosis (MS), neurosyphilis, meningitis, brain tumor, Alzheimer's disease, Parkinson's disease, amyotropic lateral sclerosis (ALS), autism, or psychiatric illness.[19, 20] Untreated or inadequately treated Lyme disease patients become increasingly disabled over time. Patients with persistent Lyme disease suffer physical disability equivalent to that of congestive heart failure. Although it is commonly believed that Lyme disease does not result in death, at least 22 research studies have documented deaths associated with Lyme disease.[18, 20, 23, 24]
Clinical Diagnosis: Because Lyme disease mimics so many other conditions, it can be difficult to diagnose. The average patient with persistent Lyme disease sees five doctors over a 21-month period to obtain an accurate diagnosis. Lab tests should never be the primary basis for making a Lyme disease diagnosis. Because the commercially available lab tests used to diagnose Lyme disease are flawed, the CDC, FDA and NIAID have all stressed that Lyme disease is a clinical diagnosis (based primarily on clinical presentation and supportive history, such as exposure to environments where ticks occur) and cautioned against over-reliance on lab tests.[1, 25, 26]. The two most commonly used lab tests, the ELISA and Western blot, miss between 20-50% of patients with Lyme disease. ELISA tests miss roughly 50% of those with Lyme disease. Although the Western blot is recognized by the NIAID as the most useful antibody test currently available for Lyme disease, it may miss 20-30% of the cases that are seronegative.[29-31] However, many insurers and HMOs deny treatment and reimbursement to patients with negative tests regardless of the clinical diagnosis.
Misuse of CDC Surveillance Definition for Diagnosis and Insurance Reimbursement. According to the CDC, surveillance case definitions are created for the purpose of standardization, not patient care This is because physicians should appropriately err on the side of over-diagnosis (so they do not miss a case), while surveillance case definitions appropriately err on the side of specificity, (so they do not inadvertently capture other illnesses). For purposes of surveillance only, the CDC has adopted a restricted definition of Lyme disease which includes two-tiered testing (positive ELISA followed by positive Western blot) and a narrow definition of antibody bands necessary for a positive Western blot. As noted above, the ELISA alone misses approximately 50% of confirmed Lyme cases and combining it with a Western blot that misses 20-30% of confirmed Lyme cases is a recipe for disaster in terms of diagnosis and treatment. Preliminary results on a CALDA survey indicate that more than 50% of patients with persistent Lyme disease were initially misdiagnosed for an average of 3.18 years due to misuse of the CDC surveillance criteria. According to the CDC, surveillance criteria should not be used as the sole criteria to establish a clinical diagnosis, the appropriate standard of care, or insurance reimbursement. However, many HMOs and insurers misuse the CDC surveillance case definition and apply it to diagnostic and insurance reimbursement determinations.
Treatment: The central difficulties in the diagnosis and treatment of Lyme disease stem from the lack of sufficiently sensitive and reliable biological markers of the disease. Without such markers, it is difficult to determine who has the disease, the effectiveness of a course of treatment, and the end point of treatment. When diagnosed and treated early, antibiotic treatment for 3-4 weeks may be effective. IV antibiotics are indicated where there is meningitis, carditis, later-stage neurologic Lyme disease, and complicated Lyme disease arthritis.
Treatment of Persistent Lyme disease: Patients who are not diagnosed and treated promptly are more difficult to treat. No single antibiotic or combination of antibiotics completely eradicates the infection which may include coinfections; and treatment failures or relapses (ranging from 24-50%) are reported with all short term treatment regimens.[35-37]. Two schools of thought regarding treatment of these patients exist. Some terminate treatment after 30 days unless objective evidence of continued infection can be demonstrated on the theory that the on-going symptoms reflect an autoimmune condition, while others, recognizing the shortcomings of the currently available lab tests, continue treatment until the patient's symptoms resolve. Where treatment options exist, physicians are required to discuss material options with the patient (regardless of their cost or the extent to which the treatment options are covered by health insurance).[38, 39] Treatment choice involve trade-offs between the risks and benefits of the different treatment alternatives that only patients--who know the kinds of risks they are willing to run and the types of quality of life outcomes that matter to them--are uniquely suited to make. However, many HMOs and insurers have adopted the short- term treatment protocols and deny treatment and insurance reimbursement to those who remain ill.
For further information, please visit the national Lyme Disease Association's (LDA) website at www.LymeDiseaseAssociation.org. The president of the LDA can be reached at Lymeliter@aol.com.
1. Center for Disease Control, Recommendations for the use of Lyme disease vaccine. MMWR. 48(RR-7). www.cdc.gov/mmwr/PDF/RR/RR4807.pdf.
2. Nadelman, R.B. and G.P. Wormser, Erythema migrans and early Lyme disease. Am J Med, 1995. 98(4A): p. 15S-23S; discussion 23S-24S. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=7726187.
3. Harvey, W.T. and P. Salvato, 'Lyme disease': ancient engine of an unrecognized borreliosis pandemic? Med Hypotheses, 2003. 60(5): p. 742-59. .
4. Stricker, R., D. Moore, and E. Winger, Clinical and immunologic evidence for transmission of Lyme disease through intimate human contact. abstract submitted.
5. Nadelman, R.B., et al., Survival of Borrelia burgdorferi in human blood stored under blood banking conditions. Transfusion, 1990. 30(4): p. 298-301. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2349627.
6. MacDonald, A.B., Gestational Lyme borreliosis. Implications for the fetus. Rheum Dis Clin North Am, 1989. 15(4): p. 657-77. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2685924.
7. Schouls, L.M., et al., Detection and identification of Ehrlichia, Borrelia burgdorferi sensu lato, and Bartonella species in Dutch Ixodes ricinus ticks. J Clin Microbiol, 1999. 37(7): p. 2215-22. http://www.ncbi.nlm.nih.gov/entrez/quer ... s=10364588.
8. Schabereiter-Gurtner, C., W. Lubitz, and S. Rolleke, Application of broad-range 16S rRNA PCR amplification and DGGE fingerprinting for detection of tick-infecting bacteria. J Microbiol Methods, 2003. 52(2): p. 251-60. http://www.ncbi.nlm.nih.gov/entrez/quer ... s=12459246.
9. Eskow, E., et al., Evidence for disseminated Mycoplasma fermentans in New Jersey residents with antecedent tick attachment and subsequent musculoskeletal symptoms. J of Clin Rheum, 2003. 9(2): p. 77-87.
10. Eskow, E., R.V. Rao, and E. Mordechai, Concurrent infection of the central nervous system by Borrelia burgdorferi and Bartonella henselae: evidence for a novel tick-borne disease complex. Arch Neurol, 2001. 58(9): p. 1357-63. http://www.ncbi.nlm.nih.gov/entrez/quer ... s=11559306.
11. Krause, P.J., et al., Concurrent Lyme disease and babesiosis. Evidence for increased severity and duration of illness. Jama, 1996. 275(21): p. 1657-60. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=8637139.
12. US Department of Labor (OSHA), Lyme Disease. Hazard Information Bulletin (April 2000). http://www.osha.gov/dts/hib/hib_data/hib20000420.pdf.
13. Centers for Disease Control, Lyme Disease --- United States, 2001--2002. MMWR, 2004. 53(17): p. 365-69. www.cdc.gov/mmwr/preview/mmwrhtml/mm5317a4.htm.
14. American Lyme Disease Association, Latest Statistics 2004 Tick Activity Forecast. www.aldf.com/LateBreakingNews.asp.
15. Duray, P.H., Clinical pathologic correlations of Lyme disease. Rev Infect Dis, 1989. 11 Suppl 6: p. S1487-93. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2814170.
16. Nadelman, R.B., et al., The clinical spectrum of early Lyme borreliosis in patients with culture-confirmed erythema migrans. Am J Med, 1996. 100(5): p. 502-8. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=8644761.
17. Burrascano, J.J., Diagnostic hints and treatment guidelines for Lyme and other tick-borne illnesses. 2002. www.ilads.org/burrascano_1102.htm.
18. Vanderhoof, I.T. and K.M. Vanderhoof-Forschner, Lyme Disease: The Cost to Society. Contingencies, 1993. Jan-Feb: p. 42-48.
19. Fallon, B.A. and J.A. Nields, Lyme disease: a neuropsychiatric illness. Am J Psychiatry, 1994. 151(11): p. 1571-83. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=7943444.
20. Oksi, J., et al., Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature. Brain, 1996. 119 ( Pt 6): p. 2143-54. .
21. Shadick, N.A., et al., The long-term clinical outcomes of Lyme disease. A population-based retrospective cohort study. Ann Intern Med, 1994. 121(8 ): p. 560-7. .
22. Klempner, M.S., et al., Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. N Engl J Med, 2001. 345(2): p. 85-92. .
23. Rubel, J., Lyme disease symptoms and characteristics: a compilation of peer reviewed literature reports (compilation of 19 Lyme related deaths). 2003. www.lymeinfo.net/LDSymptoms.pdf.
24. Sigler, S., et al., Respiratory failure due to Lyme meningoradiculitis. Am J Med, 1997. 103(6): p. 544-7. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=9428840.
25. National Institute of Allergies and Infectious Diseases, N.I.o.H., Diagnosis of Lyme Disease. www.niaid.nih.gov/dmid/lyme/diagnosis.htm.
26. Federal Drug Administration, Lyme disease test kits: potential for misdiagnosis. FDA Medical Bulletin, 1999, Summer, Final Issue. www.fda.gov/medbull/summer99/Lyme.html.
27. Ekerfelt, C., et al., Lyme borreliosis in Sweden--diagnostic performance of five commercial Borrelia serology kits using sera from well-defined patient groups. Apmis, 2004. 112(1): p. 74-8. http://www.ncbi.nlm.nih.gov/entrez/quer ... s=14961978.
28. National Institute of Allergies and Infectious Diseases (National Institute of Health), NIAID, Profile, Fiscal Year 2001. p. 68-69. http://www.niaid.nih.gov/publications/N ... le2001.pdf.
29. Aguero-Rosenfeld, M.E., et al., Evolution of the serologic response to Borrelia burgdorferi in treated patients with culture-confirmed erythema migrans. J Clin Microbiol, 1996. 34(1): p. 1-9. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=8748261.
30. Aguero-Rosenfeld, M.E., et al., Serodiagnosis in early Lyme disease. J Clin Microbiol, 1993. 31(12): p. 3090-5. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=8308100.
31. Donta, S.T., Tetracycline therapy for chronic Lyme disease. Clin Infect Dis, 1997. 25 Suppl 1: p. S52-6. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=9233665.
32. Mead, P., Statement by Paul Mead, M.D., M.P.H., Medical Epidemiologist, Division of Vector-Borne Infectious Diseases, National Center for Infectious Diseases, Center for Disease Control and Prevention, U.S. Department of Health and Human Services on Hearing: CDC's Lyme Disease Prevention and Control Activities before the Connecticut Department of Public Health and the Connecticut Attorney General's Office on January 29, 2004. www.hhs.gov/asl/testify/t040129.html.
33. Center for Disease Control, Case definition for infectious conditions under public health surveillance (Lyme disease surveillance case definition) http://www.cdc.gov/ncidod/dvbid/lyme/casedef2.htm. MMWR, 1997. 46(RR10): p. 1-3, 15-16. www.cdc.gov/mmwr/preview/mmwrhtml/ooo47449.htm.
34. Center for Disease Control (Division of Vector-Borne Infectious Diseases), Questions and answers about Lyme disease. www.cdc.gov/ncidod/dvbid/lyme/qa.htm.
35. Hunfeld, K.P., et al., Standardised in vitro susceptibility testing of Borrelia burgdorferi against well-known and newly developed antimicrobial agents--possible implications for new therapeutic approaches to Lyme disease. Int J Med Microbiol, 2002. 291 Suppl 33: p. 125-37. http://www.ncbi.nlm.nih.gov/entrez/quer ... s=12141737.
36. Johnson, L.B. and R.B. Stricker, Treatment of Lyme disease--a medicolegal assessment. Expert Rev Anti-infect Ther, 2004. 2(4): p. 533-57. http://www.ncbi.nlm.nih.gov/entrez/quer ... s=15482219.
37. Coyle, P.K., Neurologic complications of Lyme disease. Rheum Dis Clin North Am, 1993. 19(4): p. 993-1009. http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=8265833.
38. American Medical Association, Code of Medical Ethics. http://www.ama-assn.org/apps/pf_new/pf_ ... t_p=&nth=1&.
39. Mathis v. Morrissey, 13 Cal. Rptr. 2d 819 (1992).