Monthly Archives: juli 2013

Rickettsiahelvetet

Ser att det är många som googlar på rickettsia och hittar hit, så tänkte att jag skulle skriva lite om mina erfarenheter av den infektionen, ifall andra känner igen sig, så kanske ni kan få rätt hjälp innan det går så långt som det gjorde för mig.

Medan jag ”bara” hade borrelia och ett par andra coinfections (vilket redan det var illa nog), så gick det på något sätt att samexistera med alla bakterier i kroppen, även om borrelian gjorde mig väldigt sjuk i skov och de övriga infektionerna tryckte ner immunförsvaret. Det funkade i c:a 24 år. När rickettsian kom med i bilden gick inte det längre, den höll till sist på att ta kål på mig förra hösten, nu kom det inte längre skov som gjorde mig sämre, jag var konstant mycket sjuk.

Det började med ett fästingbett förra sommaren, som först fick en ”borreliaring” men efter ett tag blev blålila och oregelbundet med en svart sak i mitten, tänkte först att det var en bit av fästingen som satt kvar, men det är tydligen ett typiskt sår av rickettsia helveticabakterien, har fått flera sådana bett efteråt (rickettsia finns i var femte fästing i Sverige).

Trodde till en början att det var påfyllning av borrelia, det trodde de först även på vårdcentralen dit jag gick akut, och jag fick då en penicillinkur, som tyvärr gjorde det ännu värre. Båda benen fylldes av stora blå knölar dagen efter att jag slutade med penicillinkuren. Då gavs ingen mer behandling där.

Fick efter bettet en ny sorts intensiv spränghuvudvärk som inte gick över med några huvudvärkstabletter, huvudet kändes som en varböld, även illamående, stel nacke, ledvärk, yrsel och influensasymtom. Hade då feberfrossa ofta (får det fortfarande ibland, men i vanliga fall numera är det låg feber hela tiden). Hade sannolikt hjärnhinneinflammation när de symtomen var som allra värst under ett par månader i början.

Var konstant extremt trött, som om jag inte hade sovit alls. Och det blev svårt att andas, det kändes som att jag höll på att kvävas, som att nån som väger 200 kg satt på bröstkorgen så det inte gick att få in luft.

Fick efter några månaders kamp mot de nya bakterierna en åttaveckors-”förkylning” som till slut orsakade en rethosta som inte gick över av hostmediciner, ens med morfin i. Höll på att hosta upp lungorna till slut. Hjärtat pumpade också hårt och mycket snabbt i viloläge som att det fick lov att kämpa för livet, och ibland var slagen matta och oregelbundna som om det höll på att ge upp, det gjorde ont kring det, högg som av knivar, särskilt om jag försökte böja mig framåt eller röra på mig, att ligga på vänster sida och sova blev också omöjligt, vet inte om det berodde på lungan på den sidan eller på hjärtat.

Hade fruktansvärt ont i ryggen redan innan bettet (diskbråck sen ett år tillbaka), men det blev värre efter det, kunde varken sitta eller ligga utan svår värk, senare började ena benet domna bort tillfälligt, så att känseln försvann, och blodet liksom rusade ner under foten i andra benet och det brände. Fick även ryckningar i ögonlocken och i benen. 

Fick snart kondition som en 90-åring trots att utgångsläget var bra, har alltid rört mycket på mig, cyklat, promenerat, men det gick till slut inte att ta sig upp för en pytteliten backe längre utan att det kändes som att ha sprungit ett maratonlopp.

Till slut gav det sig på minnet, framför allt närminnet, som när det var som värst hade kortare varaktighet än fem sekunder, så att jag glömde vad jag just hade gjort, det var ganska hopplöst att försöka göra något, det var svårt att tänka, att få ihop meningar, hitta välbekanta ord, jag kunde inte längre formulera mig skriftligt, och det var omöjligt att lära sig något nytt. Men jag försökte se humorn i det. Livet blev ju extra spännande när man inte längre hade nån koll, man blev överraskad hela tiden, som när ”nån” hade satt på spisen på högsta läget med en stekpanna med smör eller olja i, men utan något som stektes, eller när plattorna stod på hela dagarna ibland utan stekpannor ens, eller när man öppnade mikron och hittade saker som legat där länge, eller om maten blev kvarglömd utanför kylskåpet hela natten. Kallade det för ”lymezheimer”, för det var som att ha fått Alzheimer. Levde i en tät hjärndimma som kändes som att ha bomull i huvudet som hindrade tankarna, gjorde dem sega som sirap.

Var helt utan behandling i fyra månader efter penicillinkuren, och blev bara sämre och sämre. Till slut förstod jag att detta inte skulle gå över av sig självt utan behandling, jag kände ju att det gick åt helt fel håll, det kändes som att jag var på väg att dö, som att kroppen inte klarade av mer. Började då desperat ta antibiotika för att försöka överleva, hade ett gammalt recept som jag inte hade tagit ut (det visade sig senare att det var fel sort, men i rätt antibiotikafamilj). Visste inte exakt vad det var jag behandlade, visste bara att det måste vara en infektion, och att jag aldrig nånsin hade varit sjukare.

En mycket intelligent nykläckt läkare på vårdcentralen hade dessförinnan just kommit fram till diagnosen: ”ångest” utifrån alla dessa symtom, han förklarade mig ”fysiskt frisk” och bemötte mig otroligt hånfullt efter sitt konstaterande. Väldigt smart och trevlig grabb som kan räkna med en stor fet anmälan så snart jag orkar ta itu med det.

Ett tag senare fick jag äntligen en remiss till infektionskliniken (en sådan skulle ha skickats redan i början av förra hösten, men den glömdes bort), där jag efter mycket tjat fick igenom några test för olika fästingsjukdomar, bl.a. just rickettsia, som det alltså visade sig vara.  Då hade det gått ett halvår sen bettet och jag hade behandlat mig själv i två månader, och sett dramatiska förbättringar av symtomen, både de nya från rickettsian och glädjande nog även symtom av borrelian som hade hängt med väldigt länge. Ryggsmärtan försvann också! Tyvärr kom mycket tillbaka när jag slutade med behandlingen. Fick en kortare kur via infektionskliniken med rätt sorts antibioktika mot slutet av året, förbättrades då igen, och blev sämre när den var slut. Då friskförklarades jag, trots kvarvarande symtom och ett nytt test som även det var positivt.

Resten av storyn är för lång för att få med här…

Har fortfarande symtom kvar efter c:a tio månaders behandling med olika sorters antibiotika, rickettsiabakterierna syns i blodet även i senaste testet, men det är ju inte bara de som finns där, utan de samexisterar med flera andra infektioner, det är förmodligen därför det är så otroligt svårt att bli av med dem. Det som är kvar är febern, huvudvärken (som brukar hålla i sig i upp till tre veckor när den börjar), extrem trötthet och en del kognitiva svårigheter, främst med minnet. Lungkapaciteten har också försämrats, permanent verkar det som. Har även fått tinnitus. Och några röda märken på huden (gamla bettställen) blossar upp av värme och blir till knallröda stora märken. Borreliaskoven har återkommit med full styrka. Och jag har även fått nya bett, varav det senaste liknar rickettsiabettet, och har lett till nya symtom som liknar de jag hade förra sommaren, känns som en mildare variant av hjärnhinneinflammation.

Fick veta sen att om jag hade fått rätt behandling inom 4-5 dagar från första rickettsiabettet så hade jag sannolikt blivit frisk från det på en gång utan komplikationer. Men den officiella behandlingen från vårdens sida sattes alltså inte in förrän ett halvår efter bettet. På tok för sent, och även för kortvarig.

Varning för svenska mygg!

Inte bara fästingar är otäcka smittbärande kryp…

”Den som smittats av av den myggburna sjukdomen harpest blir snabbt dålig och får hög feber. Men det stannar inte där. Det tydligaste symtomet är ett otäckt sår på bettstället: som en krater med upphöjda kanter och en varfylld grop i mitten.

– Det ser riktigt äckligt ut, säger Jan Lundström, myggforskare vid Uppsala universitet.”

”Ytterligare ett symtom är svullna lymfkörtlar, som kan drabba den smittade i exempelvis armhålorna eller på halsen.

– Bölderna är blåröda och kan bli stora som en mansnäve. Det är väldigt svåra att bli av med, man måste äta speciell antibiotika under en lång tid.”

”En annan smitta som sprids via myggor i Sverige är Ockelbosjukan. Från den första augusti förekommer den i hela landet, undantaget fjällkedjan, och drabbar upp emot 50 svenskar varje år.”

”– Man får röda utslag över hela kroppen, utom i ansiktet. Det ser väldigt otäckt ut, säger Jan Lundström.

Sedan blir det ännu värre och man kan få svårt att röra sig, med stela, ömma leder. För de flesta håller besvären i sig ett par veckor, andra blir aldrig av med dem.

– 25 procent av patienterna fortsätter att ha ledproblem, vissa resten av livet.”

http://www.aftonbladet.se/nyheter/article17208959.ab

Samordna vården för kronisk borrelia

http://www.expressen.se/debatt/samordna-varden-for-kronisk-borrelia/

Vi upplever att borreliasjuka smutskastas och ifrågasätts. Kronisk borrelia är inte ”en påhittad sjukdom som sprids via internet”. 273 studier (peer reviewed) visar på ett högst verkligt problem. Vi önskar att debatten inriktas på att driva utvecklingen framåt. Vi vill inte ha något borreliakrig. Att med öppet sinne försöka förstå varandra borde inte vara så svårt.

Vi efterlyser samarbete mellan olika specialistläkare på sjukhusen för en samlad bedömning. Det vi behöver är inte symtomlindring utan möjligheten att bli helt friska. Vi är många som kan stå till förfogande för forskningen, med borrelia och olika kombinationer av co infections kvar i kroppen efter behandling. Ni kan bidra med er kunskap och forskarresurser för bättre diagnostik och behandling.

Vi kan bidra till att förbättra vården, samt tipsa om forskning och behandlingar. Men vi har inte hela lösningen. Enbart antibiotika hjälper inte alla, en del förblir sjuka. Beror det på immunförsvaret? Eller rentav på genförändringar? Vi behöver tillsammans finna vad som är orsaken till persisterande borrelia.

Vid en ny landstingstyrd specialistklinik i Sverige, som enbart tar emot patienter som har drabbats av fästingsjukdomar, skulle läkare och forskare kunna vidareutbilda sig och få en mer samlad syn på problematiken. Vi behöver er hjälp för att kunna bli friska.

 

Video

Alzheimer = långt gången borrelia?

”Det finns en mycket stor korrelation mellan Alzheimers och Borrelia. Dr. Allan MacDonald 2, har i vävnadsprov hos 7 av 10 av dem som dog av Alzheimers, funnit en produkt av Flagelin epitop, specifik för Borrelia burgdorferi, inkilad inne i kromosom nr 11. Spiroketer tycks alltså ha nästlat sig in i hjärncellerna hos de patienter som dog av Alzheimers.

Vid studier som har gjorts uppskattar man att Borrelios är en stark bidragande orsak till 50 % av våra kroniska lidanden. År 1995 erhöll Dr. Mattman positiva odlingar av Borrelia burgdorferi hos 43 av 47 personer med kroniska sjukdomar. Bara en person av 23 i kontrollgruppen var positiv.”

http://www.2000taletsvetenskap.nu/special/borrelia/borrelia_lena_dicksson.htm

CFS/ME – och kronisk borrelia – orsakat av tusentals mikrober i samverkan?

Vi fick en så intressant länk i en kommentar att den förtjänar ett eget inlägg.

Tack till våra kommenterande läsare som ofta förser oss med spännande material som kan öppna upp nya vinklingar!

Borrelia som inte går över har för många drabbade lett till en (riktig eller oriktig) ME/CFS-diagnos. Vilket i och för sig inte innebär nån större skillnad i praktiken, då den inte heller behandlas nämnvärt.

En forskare i Uppsala har för något år sen påvisat skillnader i likvor mellan ME/borrelia men frågan är om inte dessa diagnoser överlappar på flera sätt, eller kan tänkas ha liknande bakgrundsorsaker, men eventuellt med olika patogenmixvariationer i botten. Symtomen är slående lika, hur som helst.

”Chronic fatigue syndrome/Myalgic Encephalomyelitis has long been associated with the presence of infectious agents, but no single pathogen has been reliably identified in all patients with the disease. Recent studies using metagenomic techniques have demonstrated the presence of thousands of microbes in the human body that were previously undetected and unknown to science. More importantly, such species interact together by sharing genes and genetic function within communities. It follows that searching for a singular pathogen may greatly underestimate the microbial complexity potentially driving a complex disease like CFS/ME. Intracellular microbes alter the expression of human genes in order to facilitate their survival.

We have put forth a model describing how multiple species – bacterial, viral and fungal – can cumulatively dysregulate expression by the VDR nuclear receptor in order to survive and thus drive a disease process. Based on this model, we have developed an immunostimulatory therapy that is showing promise inducing both subjective and objective improvement in patients suffering from CFS/ME.”

I flera av trådarna har frågan om D-vitamin kommit upp, bl.a. hur man ska tolka ett förhöjt D 1,25-test. Här är en möjlig förklaring: 

”The primary ligand activating the VDR is 1,25-dihydroxyvitamin-D (1,25-D). VDR dysregulation reduces expression of CYP24A1, an enzyme primarily responsible for the breakdown of 1,25-D. The dysregulation of this pathway allows 1,25-D levels to rise. It is standard practice for clinicians and researchers to test only levels of the precursor 25-hydroxyvitamin-D (25-D) in patients with CFS/ME. We have found that if 1,25-D is also tested, observed levels are often elevated above normal range. Indeed, elevated levels of 1,25-D can serve as a fairly reliable marker of disease progression. We have shown that in a Canadian cohort of patients with CFS/fibromyalgia, 38 of 43 subjects had levels of 1,25-D above 110 pmol/L. We have previously proposed a model describing how these elevated levels of 1,25-D can displace the native ligands of other nuclear receptors including the glucocorticoid receptor, the androgen receptor and the thyroid receptor. This can lead to a host of endocrine problems, including those commonly found in CFS/ME such as adrenal, thyroid, and sex hormone imbalances. The subsequent dysregulation also generates further immune dysfunction since, like the VDR, each of these receptors controls the expression of several important families of antimicrobials.

Brahmachary et al. have shown that the Androgen Receptor, the Glucocorticoid Receptor, and the Vitamin D Receptor, are respectively in control of 17, 20, and 16 families of the AMPs analyzed by the team. This means that direct and flow-on effects of VDR dysregulation may well disable the bulk of the body’s AMPs, leading to profound suppression of the innate immune system’s ability to respond to intracellular attack.”

Att i ett sånt läge ytterligare öka på D 1,25-nivån med tillskott av D-vitamin verkar inte vara en särskilt bra idé. Eller vad säger ni läsare som är läkare?

Läs hela studien här: http://autoimmunityresearch.org/preprints/2013-Lindseth-ImmunologicResearch.pdf

MS är det Borrelia, TWAR (Chlamydia pneumoniae) som egentligen ligger bakom det?

Ja frågan är berättigad eftersom borrelia har visat sig ge likadana symtom och lesioner i hjärnan som vid MS.

http://www.ncbi.nlm.nih.gov/pubmed/15617845

http://owndoc.com/lyme/multiple-sclerosis-is-lyme-disease-anatomy-of-a-cover-up/
”Perhaps the biggest ongoing medical scandal of the past hundred years is the fact that it has been known since 1911 that Multiple Sclerosis is caused by a bacterium, and that the Big-Pharma-controlled medical-industrial complex covered this up in order to make money selling symptom relievers to MS patients.”
”But were those 15 researchers who said they found living Lyme bacteria (spirochetes) in the brains of a great majority of Multiple sclerosis patients all lying?”

Jag fick själv en massa neurologiska problem och fick höra att jag har lesioner och är på väg att utveckla MS. Lite av mina problem var Sluddrande tal, dålig finmotorik, signalfel båsmuskel osv.
Nu efter många månaders antibiotika så sluddrar jag inte längre, kan kissa utan kateter, bättre finmotorik i händer osv,,

http://www.abc.net.au/catalyst/stories/3572695.htm

http://www.davidwheldon.co.uk/ms-treatment.html
After much controversy a considerable body of evidence now demonstrates a firm causal connection between chronic infection with the primary respiratory pathogen Chlamydophila (Chlamydia) pneumoniae and at least some variants of the neurological disease Multiple Sclerosis. These web-pages review the evidence. References are cited.”

http://www.lymepa.org/Chronic_Lyme_borreliosis_at_the_root_of_Multiple_Sclerosis_and_a_possible_cure_with_antibiotics.pdf

Kolla dessa kartor om var majoriteten av MS dödsfall finns i USA och jämför med Kartan gällande dödsfall i Borrelia/Lyme.
Fundera sen om det inte finns ett samband, ett starkt sådant?
http://www.esri.com/news/arcwatch/1007/spatial-patterns.html

BeFunky_spatial1-lg.jpg BeFunky_spatial3-lg.jpg

273 ”peer reviewed studies” bekräftar kronisk borrelia

 

Persistence of Lyme Disease

 

The following references for persistence of Lyme disease (Lyme borreliosis) are listed alphabetically and chronologically:

 

  1. Aalto A, Sjowall J, Davidsson L, Forsberg P, Smedby O. Brain magnetic resonance imaging does not contribute to the diagnosis of chronic neuroborreliosis. Acta Radiol 2007; 48: 755-762. [white matter hyperintensities or basal ganglia lesions].
  2. AbeleDC and Anders KH. The many faces and phases of borreliosis. J Am Acad Dermotol 1990; 23:401-410. [chronic Lyme borreliosis].
  3. Aberer E and Klade H. Cutaneous manifestations of Lyme borreliosis. Infection 1991; 19: 284-286. [chronic Lyme borreliosis].
  4. Aberer E, Breier F, Stanek G, and Schmidt B.  Success and failure in the treatment of acrodermatitis chronica atrophicans skin rash. Infection 1996; 24: 85-87.
  5. Aberer E, Kersten A, Klade H, Poitschek C, Jurecka W. Heterogeneity of Borrelia burgdorferi in the skin. Am J Dermatopathol 1996; 18(6): 571-519.
  6. Akin E, McHugh Gl, Flavell RA, Fikrig E, Steere AC. The immunoglobulin (IgG) antibody response to OspA and OspB correlates with severe and prolonged Lyme arthritis and the IgG response to P35 with mild and brief arthritis. Infect Immun 1999; 67: 173-181.
  7. Albert S, Schulze J, Riegel H, Brade V. Lyme arthritis in a 12-year-old patient after a latency period of 5 years. Infection 1999; 27(4-5): 286-288.
  8. Al-Robaiy S, Dihazi H, Kacza J, et al. Metamorphosis of Borrelia burgdorferi organisms―RNA, lipid and protein composition in context with the spirochete’s shape. J Basic Microbiol 2010, 50 Suppl 1, S5-17.
  9. Appel MJG, Allan S, Jacobson RH, Lauderdale TL, Chang YF, Shin SJ, Thomford JW, Todhunter RJ, and Summers BA. Experimental Lyme disease in dogs produces arthritis and persistent infection. J Inf Dis 1993; 167: 651-664.
  10. Åsbrink E, Hovmark A. Successful cultivation of spirochetes from skin lesions of patients with erythema chronicum migrans, Afzelius and acrodermatis chronica atrophicans. Acta Pathol Microbiol Immunol Sect B 1985; 93: 161-163.
  11. Åsbrink E, Hovmark A, and Olsson I. Clinical manifestations of acrodermatitis chronica atrophicans in 50 Swedish patients. Zentralbl Bakteriol Mikrobiol Hyg A 1986; 26: 253-261. [chronic Lyme borreliosis].
  12. Asch ES, Bujak DI, Weiss M, Peterson MGE, and Weinstein A. Lyme Disease: an infectious and postinfectious syndrome. J Rheumatol 1994; 21 (3): 451-461.
  13. Bankhead T and Chaconas G. The role of VlsE antigenic variation in the Lyme disease spirochete: persistence through a mechanism that differs from other pathogens. Molecular Microbiology 2007; 65: 1547-1558.
  14. Barthold SW, Persing DH, Armstrong AL, and Peeples RA. Kinetics of Borrelia burgdorferi dissemination and evolution of disease following intradermal inoculation of mice. Am J Pathol 1991; 139: 263-273. [in mice]
  15. Barthold SW, deSouza MS, Janotka JL, Smith AL, and Persing DH. Chronic Lyme borreliosis in laboratory mouse. Am J Pathol 1993; 143: 951-971. [in mice]
  16. Barthold S. Lyme Borreliosis. Chapter 14, In Persistent Bacterial Infections. Edited by J.P. Nataro, M.J. Blaser, and S. Cunningham-Rundles, pp 281-304. ASM Press, Washington, D.C.
  17. Barthold SW, Hodzic E, Imai DM, Feng S, Yang X, and Luft BJ. Ineffectiveness of tigecycline against persistent Borrelia burgdorferi. Antimicrob Agents Chemother 2010; 54(2): 643-651. [Persistence is listed for many reservoir-competent hosts: mice, rats, Peromyscus leucopus, hamsters, gerbils, rabbits, dogs, nonhuman primates, and humans]
  18. Battafarano DF, Combs JA, Enzenauer RJ, Fitzpatrick JE. Chronic septic arthritis caused by Borrelia burgdorferi. Clin Orthop 1993; 297: 238-241. [Patients with chronic septic Lyme arthritis of the knee for seven years, despite multiple antibiotic trials and synovectomies. Bb documented in synovium and synovial fluid.]
  19. Bayer ME, Zhang L, Bayer MH. Borrelia burgdorferi DNA in the urine of treated patients with chronic Lyme disease symptoms. A PCR study of 97 cases. Infection 1996; 24: 347-353. [97 patients who had been treated with antibiotics for extended periods of time and had symptoms of chronic Lyme were PCR-positive.]
  20. Benjamin J and J Luft. Chronic Lyme disease; an evolving syndrome. 9th Annual International Scientific Conference on Lyme Disease & Other Tick-Borne Disorders. 1996.
  21. Berglund J, Stjernberg L, Ornstein K, Tykesson-Joelsson K, Walter H. 5-y follow-up study of patients with neuroborreliosis. Scand. J. Infect. Dis. 2002; 34(6): 421-425.
  22. Bloom BJ, Wyckoff PM, Meissner HC, and Steere AC. Neurocognitive abnormalities in children after classic manifestations of Lyme disease. Pediatric Infect. Dis. J. 1998; 17(3): 189-196.
  23. Bradley JF, Johnson RC, Goodman JL.  The persistence of spirochetal nucleic acids in active Lyme arthritis. Ann Intern Med 1994; 120: 487.
  24. Bransfield R, Brand S, and Sherr V. Treatment of patients with persistent symptoms and a history of Lyme disease. N Engl Med 2001; 345: 1424-5.
  25. Breier F, Khanakah G, Stanek G, Aberer E, Schmidt B, and Tappeiner G.  Isolation and polymerase chain reaction typing of Borrelia afzelii from a skin lesion in a seronegative patient with generalized ulcerating bullous lichen sclerosus et atrophicus. Br J Dermatol 2001; 144: 387-392. [Borrelia afzelii, ulcerating lichen sclerosus et atrophicus]. [Despite treatment with four courses of ceftriaxone, “[s’pirochetes were isolated from skin cultures obtained from enlarging LSA lesion…[S]erology …was repeatedly negative.]
  26. Bockenstedt LK, J Mao, E Hodzic, SW Barthold, and D Fish. Detection of attenuated, noninfectious spirochetes in Borrelia burgdorferi-infected mice after antibiotic treatment. J Infect Dis 2002; 186: 1430-1437. [in mice]
  27. Brorson O and Brorson S-H. Transformation of cystic forms of Borrelia burgdorferi to normal mobile spirochetes. Infection. 1997; 25: 240-246. [change in physical characteristics; change of spirochetes to other pleomorphic forms, i.e., cell wall deficient forms, namely cysts.]
  28. Brorson O and Brorson S. In vitro conversion of Borrelia burgdorferi to cystic forms in spinal fluid, and transformation to mobile spirochetes by incubation in BSK-H medium. Infection. 1998; 26: 144-150. [change in physical characteristics; change of spirochetes to other pleomorphic forms, i.e., cell wall deficient forms, namely cysts.]
  29. Brorson O and Brorson S-H. An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to tinidazole. International Microbiol 2004; 7: 139-142.
  30. Brown JP, Zachary JF, Teuscher C, Weis JJ, and Wooten M. Dual role of interleukin-10 in murine Lyme disease: regulation of arthritis severity and host defense. Infect Immun 1999; 67: 5142-5150. [suppression of harmful immune responses: defense stratagem of B. burgdorferi]
  31. Burrascano J.  Failure of aggressive antibiotic therapy to protect the placenta from invasion by B. burgdorferi in a pregnant patient with Lyme borreliosis.  6th Annual International Science Conference on Lyme Disease and other Tick-borne Diseases.1993.
  32. Cabello FC, Godfrey HP, and Newman SA. Hidden in plain sight: Borrelia burgdorferi and the extracellular matrix. Trends in Microbiology 2007; 15: 350-354. [sequestration]
  33. Cadavid D, O’Neill T, Schaefer H, and Pachner AR. Localization of Borrelia burgdorferi in the nervous system and organs in a nonhuman primate model of Lyme disease. Lab Invest 2000; 80: 1043-1054.
  34. Cadavid D, Y Bai, E Hodzic, K Narayan, SW Barthold, and Pachner AR. Cardiac involvement in non-human primates infected with the Lyme disease spirochete Borrelia burgdorferi. Lab Invest 2004; 84: 1439-1450. [in monkeys]
  35. Cameron D, Gaito A, Harris N et al. Evidence-based guidelines for the management of Lyme disease. Expert Rev Anti-Infect. Ther 2004; 2 (Suppl. 1), S1-S13.
  36. Cameron D. Results from Lyme disease treatment trial. Columbia University/LDA Conference, Lyme & Other Tick-Borne Diseases: Emerging Tick-Borne Diseases. October 28, 2005; Philadelphia, Pennsylvania.
  37. Cameron DJ. Generalizability in two clinic trials of Lyme disease. Perspectives and Innovation 2006; 3(12). [http://dx.doi.org/10.1186/1742-5573-3-12].
  38. Cameron D. Severity of Lyme disease with persistent symptoms. Insights from a double-blind placebo-controlled clinical trial. Minerva Med 2008; 99: 489-496.
  39. Cameron DJ. Insufficient evidence to deny antibiotic treatment to chronic Lyme disease patients. Med Hypotheses (2009), doi:10.1016i/j.mehy.2009.01.017
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Compiled by: John D. Scott, Research Division                                                                               April 2013

         Lyme Disease Association of Ontario     

IDSA vs ILADS – why there is a chronic Lyme conflict

We are very happy for this guest posting by Lisa Hilton, USA!

While you’re reading this fascinating background to the chronic Lyme conflict, we want you to ponder some questions and answer to them in the comments if you have any thoughts:

How come IDSA is still trusted after these reveals (see below)? 

Why does the CDC use the IDSA guidelines? 

Why does the rest of the world follow the IDSA guidelines?

*******

The Two Lyme Camps
First there is the IDSA side. The IDSA, (Infectious Disease Society of America) states that it is easy to diagnose, simple to treat, and easy to recover from. They recommend anything from two pills of doxycycline to take care of a lyme infection to three weeks of oral doxycycline.Note: While IDSA is a private professional organization, it has government preference over the other nonprofit organization, ILADS. The CDC’s website links to IDSA’s guidelines instead of ILADS’ guidelines.Since the CDC subscribes to the IDSA’s guidelines, doctors fear medical board investigations and censure if they treat outside of those guidelines. This limits the doctors as to how they can treat us. It takes away their being able to make their own judgement calls. For example, if their patient takes all three weeks of doxycycline, and is still showing symptoms, the doctor can be under scrutiny from the medical board if they should decide to give them another prescription. The insurance company will want to know why the doctor is prescribing more meds and they will refuse to pay anymore of the patients bills stating that they have already taken the full treatment and should be cured now according to the IDSA guidelines.Consider this: *The IDSA’s guidelines state: ”Clinical findings are sufficient for the diagnosis of erythema migrans, but clinical findings alone are not sufficient” to diagnosis other signs of Lyme. Patients without an EM rash (bull’s eye rash) must have 2 positive Lyme tests ”using the 2-tier testing algorithm recommended by the CDC.”

Then consider this:
*CDC’s surveillance definition, which states: ”This surveillance case definition was developed for national reporting of Lyme disease; it is not intended to be used in clinical diagnosis.”

Further consider

* The CDC reports that only 68% of Lyme patients meeting its surveillance definition have EM rashes.

* Its two-tier test requires positive ELISA and western blot tests for a diagnosis. The CDC relied on studies showing that this two-tier approach had sensitivities of 33% and 57% for early-and late-stage Lyme respectively. This leaves 22% of patients untreated with early-stage Lyme and 43% untreated of late-stage Lyme, since standard EM rashes disappear in early-stage Lyme.

* The IDSA guidelines recommend only up to 28 days of antibiotics, even for late-stage neurological Lyme. They say: ”There is no convincing biologic evidence for the existence of symptomatic chronic B. burgdorferi infection among patients after receipt of recommended treatment. Antibiotic therapy has not proven to be useful and is not recommended for patients with chronic Lyme for more then 6 months with subjective symptoms after administration of recommended 10-to 28-day treatment.

Yet, the same IDSA panelists said elsewhere that Lyme’s successful yield rate for blood cultures is below 10%. So why do the IDSA guidelines call these cultures the ”gold standard?”

* The guidelines rejected a study that used a new method to culture the bacterium in 97% of 47 guideline-treated patients because the germ was found with microscopes, not DNA tests, and because two other studies with 22 guideline-treated patients couldn’t culture it.

* The IDSA’s guidelines will not say ”Chronic Lyme,” instead they state that chronically ill patients suffer from post-Lyme syndrome. This is defined as ”unexplained chronic subjective symptoms following treatment with recommended antibiotic regimens.” It is their way of denying persistant infection and making it seem there is another reason for ongoing symptoms.

In 2006, an antitrust investigation was initiated by Connecticut Attorney General Richard Blumenthal. Here are some of the reasons for the investigation.

1. Lyme Guidelines suggest relying upon inaccurate testing to diagnoses Lyme. Many doctors believe that they should diagnose Lyme based clinically (based upon symptoms).

2. The IDSA says its guidelines are voluntary, but the truth is, major insurers use them to deny coverage for long-term antibiotic treatment, limiting patients in getting the appropriate long term treatment they need. We are in an insurance-dominated environment, and insurance companies and hospitals use economic profiling to pressure their doctors to conform to cost parameters and restrictive guidelines when providing treatment.

The Conclusion of the Antitrust Investigation:

In May 2008, Blumenthal concluded the investigation and announced the flaws he discovered in the Lyme Disease guidelines’ development.

1. The investigation revealed panelists’ connections to insurance and vaccine companies in violation of antitrust principles, failure to review potential conflicts of interest such as financial interests in drug companies, Lyme disease diagnostic tests, patents and consulting arrangements with insurance companies. He found there was bias in the selection committee, and exclusion of dissenting panelists.

2. The attorney found misrepresentation of the guideline authors’ views as independent, and misrepresentation of the guidelines as voluntary. There were what they called ”improper links” between the IDSA’s and the American Academy of Neurology’s (AAN) Lyme panels. The two panels shared key members, and were working on both sets of guidelines at the same time, which is a violation of IDSA’s conflicts of interest policy. When the IDSA learned of the improper links, it aggressively sought AAN’s endorsement.” The investigation showed that their guidelines used ”strikingly similar language” to conclude that chronic Lyme didn’t exist and defined symptoms persisting after treatment as ”Post-Lyme Syndrome” also in the same way as the IDSA. Then the IDSA portrayed the AAN’s guidelines as independent corroboration and tried using them to defeat legislation supporting long-term Lyme treatment.

3. Failure to significantly evaluate contradictory evidence. Doctors were pressured to conform to the beliefs that Lyme was not chronic.

The guidelines reported conflicts of interests for five IDSA panelists:

1. Dr. Gary Wormser, the panel chair, received funds ”from Baxter and Immunetics, and is one of the founders of Diaspex. Eventually discovered also was that Wormser disclosed he was receiving grants related to Lyme disease from Bio-Rad, Biopeptides, Merck and AstraZeneca, owning equity in Abbott, and being retained in some medical-malpractice cases involving Lyme disease.”

2. R. J. Dattwyler, is a speaker for Pfizer and a part owner of Biopeptides. Later is was discovered that Dattwyler disclosed he had a financial connection to Baxter and serving as an expert witness in medical malpractice actions

3. J. J. Halperin, an expert witness on behalf of Lymerix (GlaxoSmithKline) the failed Lyme vaccine.

4. Allen C. Steere is a consultant for Baxter and P. J. Krause. This is a developer of a diagnostic procedure for a coinfection of Lyme. Later disclosed was that Steere has a financial connection to GlaxoSmithKline and Viramed.

5. Dattwyler elsewhere disclosed a financial connection to Baxter and serving as an expert witness in medical malpractice actions, and Steere disclosed a financial connection to GlaxoSmithKline and Viramed. (51) A sixth panelist, Eugene Shapiro, elsewhere admitted to receiving grants for Lyme vaccines, testifying in Lyme-related medical malpractice actions, and reviewing Lyme disability claims for Metropolitan Life Insurance Company.

Later discovered also was that another panelist, Eugene Shapiro, admitted to receiving grants for Lyme vaccines, testifying in Lyme-related medical malpractice actions, and reviewing Lyme disability claims for Metropolitan Life Insurance Company.

And this is the panel we rely on to help us who are suffering with Lyme get the care we need?

Final Outcome

The attorney general’s antitrust action resulted in a settlement, which required that the guidelines be reviewed by a completely new panel that is free of conflicts of interest and represents a range of views.

New Issues

Many Lyme patients were not happy with the resulting review panel because its chair was a former IDSA president. The new panel elected totally excluded any candidates who supported long-term treatment. Lyme advocates felt like the new panel just ended up being ”more of the same.” The final blow came when the new review panel’s final report decided that even though they thought the guidelines should be updated to give doctors discretion in diagnosing patients who have a high probability of Lyme but only equivocal tests, but that antibiotics are still not recommended to treat patients beyond a short 28-day treatment. Still no long term treatment was thought to be necessary.

The attorney general also found that the IDSA failed to follow its own procedures for appointing panelists. The IDSA’s procedures say that guideline panels should have a wide range of experts, therefor hearing all sides of different views. They also are strongly encouraged to include members of relevant professional societies and to work toward consensus. But the attorney general found that the 2006 Lyme panel’s chairman had handpicked a like-minded panel without the IDSA oversight committee’s approval. When a dissenting member of IDSA’s 2000 Lyme guidelines panel had different opinions and argued that chronic Lyme exists, the panel pressured him to conform, and removed him when he refused. When scientists with differing views on chronic Lyme sought to join the 2006 panel, IDSA told them that it was fully staffed, although later they hired more like minded panelists.

Again, like the 2000 panel, the 2006 Lyme panel was clearly biased. They then proceeded to write the guidelines in a flawed manner. Here is the attorneys’ findings.

* The IDSA left out any research that didn’t fit into their definition of Lyme and refused to even consider information regarding the existence of Chronic Lyme.

ILADS

International Lyme And Associated Diseases Society

Their description from ILADSILADS is a nonprofit, international, multidisciplinary medical society, dedicated to the diagnosis and appropriate treatment of Lyme and its associated diseases. ILADS promotes understanding of Lyme and its associated diseases through research and education and strongly supports physicians and other health care professionals dedicated to advancing the standard of care for Lyme and its associated diseases.The ILADS guidelines are what most Lyme doctors go by. They promote long term treatment, and diagnosis which can be based on clinical diagnosis.Which, doesn’t this make sense? If you were being treated for strep throat and at the end of your antibiotic treatment you found you still had a sore throat, would your doctor not prolong your prescription of anitobiotics? Would he not try a new one? Would he tell you it’s cured, or it’s all in your head and you are not really sick?ILADS has a list of research that backs up their claims that Lyme Disease is a chronic condition caused by a persistant infection. To See Research Click Here.

Vi inbjuder till en seriös dialog med läkare och forskare

Vi önskar att debatten kring borrelia var inriktad på att driva utvecklingen framåt. Nu smutskastas och idiotförklaras det åt båda håll vilket inte är vad vi önskar. Att seriöst och med ett öppet sinne försöka förstå varann även om man har olika åsikter och erfarenheter i borreliafrågan borde inte vara så svårt.

Vi är inga “motståndare” utan endast sjuka människor som önskar förståelse och att det blir bättre för oss och andra framtida drabbade.

Vi kan bidra med våra erfarenheter av vården och olika aspekter ur patientens synvinkel om hur det skulle kunna bli bättre, efter att ha snurrat runt i vården under många år.

Vi kan bidra med den kunskap vi har samlat på oss under lång tid genom den info vi har tagit del av från många olika håll, både vad gäller forskning och erfarenheter av behandling som har fungerat för många patienter, och vi vet också vad som inte hjälper. Men vi har inte hela lösningen.

Enbart antibiotika hjälper inte alla, ens under lång tid, en del blir helt friska av det, många blir mycket bättre (tyvärr med stor risk för recidiv), men några förblir sjuka trots behandling. Det behövs uppenbarligen något mer för att bakterierna ska försvinna helt ur kroppen, åtminstone om människor och apor har ungefär samma biologiska funktioner:  http://www.plosone.org/article/info:doi/10.1371/journal.pone.0029914

Frågan är vad?

Handlar det om samverkan med immunförsvaret att borrelian i vissa fall blir en svårare, långvarig infektion? Borde det inte forskas mer om de genförändringar som har visats göra vissa mer mottagliga för dessa infektioner och som även gör det svårare att bli av med dem? Se fakta om HLA-DR4-genen en bit ner i detta inlägg, och läs gärna även om MTHFR-genen på annat håll, det finns mycket material online om den: https://borreliablogg.wordpress.com/2013/07/05/kronisk-borrelia-somatiseringssyndrom/

HLA-DR4 skulle kunna vara själva orsaken till kronisk borrelia, och i så fall behöver man forska fram något som blockerar immunsvaret.

 Ja frågorna är många och vi önskar få er hjälp för att att lösa dem!

Vi är många som kan stå till förfogande för forskningen, som har konstaterats ha borrelia och olika coinfections, vilket kanske kan vara intressant, eftersom det har betydelse för behandlingen.

Ni kan bidra med er allmänläkar- och specialistkunskap, samt med era forskarresurser för att utveckla bättre metoder för diagnos och behandling. Ni kan välja att forska på sånt som verkligen behöver undersökas bättre, på sätt som kan leda till tillförlitliga resultat. STING-studien skulle t.ex. ha kunnat ge väldigt intressanta resultat om man hade inkluderat de värst fästingdrabbade områdena.  https://borreliablogg.wordpress.com/2013/07/18/sting-en-studie-utan-sting-i/

Vi efterlyser ett samarbete mellan specialistläkare inom olika avdelningar på sjukhusen för en samlad bedömning av symtomen. Vi består inte bara av ett speedat hjärta eller neurologiska besvär, bilden är ofta väldigt omfattande och bedöms bäst som helhet, inte uppsplittrad. Det vi behöver är inte tillfällig symtomlindring av det ena eller det andra utan möjligheten att bli helt friska från infektionen.

Det skulle kanske rentav behövas en landstingstyrd specialistklinik i Sverige som enbart tar emot patienter som har drabbats av fästinginfektioner. Då skulle läkare och forskare kunna utbilda sig och få en mer samlad syn på problematiken runt fästingsjukdomar.

Här är en fiktiv patient som ni som är läkare gärna får öva era talanger på:

https://borreliablogg.wordpress.com/2013/07/17/vem-kan-hjalpa-mats/

Hämta särskilt inspiration från läkaren Göran som vi tycker svarade föredömligt i det inlägget, såna läkare vill vi gärna möta, som gör en grundlig utredning, som är kunniga, och nogranna. Som inte sätter en diagnos i förväg utan verkligen går in med ett öppet sinne, empati och ser hela patienten.

Det vi vet med säkerhet är att vi behöver er hjälp!!!

****************

Det följande är en kort sammanfattning av vad vi VILL, inte bara i Sverige, utan i hela världen.

Worldwide Patients are raising awareness and protesting to highlight the need for:

1. Recognition that Lyme disease/borreliosis, and other tick-borne infections, such as Babesia, Bartonella, Rickettsia, Ehrlichia, are serious, and sometimes fatal illnesses.

2. Awareness of the fact that the transmission of tick-borne pathogens, such as borrelia, babesia, rickettsia, via blood transfusion is of global concern.

3. Agreement that Lyme disease/borreliosis should be listed as a notifiable infection. Notifiable status will aid in ensuring that the incidence and spread of this disease are monitored, a necessary precursor to determining the human suffering and socioeconomic impact of the disease.

4. Education of the healthcare sector regarding the accurate diagnosis of Lyme, which in some cases may be limited to clinical presentation due to limitations of serological testing.

* Education should ensure all doctors are familiar with the CDC caution pertaining to criteria for blood tests for Lyme: “This surveillance case definition was developed for national reporting of Lyme disease; it is NOT appropriate for clinical diagnosis… Surveillance case definitions are created for the purpose of standardization, not patient care.”

* Education that Lyme should be included as a differential diagnosis when considering other illnesses that are also reliant on subjective clinical presentation, or have no known cause. This includes, but is not limited to: Motor Neurone Disease (MND) also known as Lou Gehrig’s disease or Amyotrophic lateral sclerosis (ALS); Multiple Sclerosis; Alzheimer’s; Parkinson’s disease; Sarcoidosis.

5. Education of the healthcare sector regarding affordable and effective treatment of both acute and chronic Lyme and other tick-borne infections. This includes the need to update the outdated treatment guidelines of the Infectious Diseases Society of America (IDSA) and to take into account the treatment methods of other Societies such as: The International Lyme and Associated Diseases Society (ILADS) and the German Borreliosis Society (Deutsche Borreliose-Gesellschaft: DBG)

6. Funding for research into tick-borne diseases. Including: Funding for medical research into accurate Lyme testing and treatment, Funding for research into vectors and reservoir hosts to determine what diseases they may carry and transmit.

STING – en studie utan sting i

SvD sänder idag ett webbtvinslag, en intervju med Barbro Hedin Skogman, barnläkare i Falun, som berättar om att risken skulle vara liten för att smittas av ett fästingbett. Samtidigt gör man reklam för STING-studien:

http://www.svd.se/nyheter/inrikes/liten-risk-att-smittas-efter-fastingbett_8353780.svd

Om studien:

”STING-studien” är en studie som pågår i Sverige, Norge och på Åland. Man samlar in fästingar som bitit människa och tar blodprov på de personer som blivit fästingbitna. Syftet är bla att undersöka hur stor risk det är att smittas av olika fästingburna infektioner vid fästingbett i olika delar av Skandinavien. Målet är att samla in 10 000 fästingar och blodprov, så studien kommer att pågå till minst 2015.” http://www.stingstudien.se/

“Trots att var fjärde fästing bär på borrelia så verkar risken för en borreliaöverföring från fästing till människa vara låg. Endast 3% av de 1550 fästingbitna personerna visade tecken på en pågående infektion.” http://www.stingstudien.se/?page_id=261

Vi har tittat närmare på studien, och kan direkt konstatera att: det allra största problemet med den är att man väljer att inte samla in fästingar från flera av de värst drabbade områdena i landet. Stora delar av Västkusten samt hela Mälardalen med Stockholms skärgård och Uppsala är väldigt fästingtäta och många blir sjuka av bett där. Inga orter i Mälardalen deltar i studien! Vattenregioner är särskilt hårt drabbade. De finns knappt med på STING-kartan.

Varför utelämnar man de orter som sannolikt skulle öka infektionsfrekvensen dramatiskt? Det kan väl inte vara så att man vill få fram ett så lågt (men dessvärre missvisande) resultat som möjligt för att försöka visa att fästingbett är harmlösa, att det är svårt att bli biten av fästingar och ännu svårare att bli sjuk av borrelia, och att det är lätt att bota med en veckas penicillin om det ändå händer? Det är ju den melodin som forskare utomlands försöker trumma in hos sina åhörare, med misslyckat resultat, då väldigt många tyvärr insjuknar varje år, och motbevisar detta IRL.

http://www.stingstudien.se/?page_id=9 (karta över vårdcentralerna som ingår)

Vill man undersöka även TBE på ett rättvisande sätt så måste förstås de områden där TBE är vanligast inkluderas:

“Områden där TBE förekommer är Östersjökusten, utmed Mälarens mellersta och östra delar i Stockholms, Södermanlands och Uppsala län. Personer har även smittats med TBE längs Öster­sjö­kusten i Östergötlands och Kalmars län längs Vätterns kuster, samt vid södra delen av Vänern.

Ett fåtal personer brukar smittas på Västkusten. Enstaka fall har konstaterats längs Blekingekusten och i Skånes sydöstra hörn.

I Europa förekommer TBE på Åland, på Bornholm samt i Baltikum och delar av Central- och Östeuropa.” http://www.fasting.nu/riskomraden_tbe.html

Ytterligare problem med studien:

Vilka tester används för att konstatera infektion? Är det ELISA som används normalt i Sverige så har den i studier visat fel i upp till 75% av konstaterade fall. Är det så, så blir ju utfallet i deras beräkningar helt fel.

Hur korrelerar de låga siffrorna från STING-studien med att antalet drabbade av borrelia är så högt? Antalet konstaterat drabbade, mätt med undermåliga svenska tester, är över 10 000 st årligen, varav mörkertalet beräknas vara stort.
http://www.sahlgrenska.gu.se/aktuellt/nyheter/Nyheter+Detalj/nordiskt-samarbete-efter-kraftig-okning-av-fastingburna-infektioner-.cid1108094

En annan fråga är varför olika studier visar så olika resultat. Är det så att vissa studier är beställda för att ge ett oriktigt, lägre resultat för att minska oro, tryck på vård osv? Denna studie visar t.ex. att allt fler fästingar bär på borrelia, vilket rimligtvis borde öka risken att bli smittad:
http://sverigesradio.se/sida/artikel.aspx?programid=91&artikel=5564266

Man bör även beakta att de som får konstaterat borrelia i under 50% av fallen vet om att de har haft en fästing på sig. Studien undersöker enbart de fästingar som lämnas in, och de patienter som således vet om att de har plockat bort en fästing.

En av punkterna som skulle undersökas var: “I vilken utsträckning utvecklar människan antikroppar mot dessa mikroorganismer i de fall hon får respektive inte får symptom på sjukdomen (subklinisk).”
Det skulle vara intressanta fakta men i den preliminära sammanfattningen av studieresultatet framkommer inte några siffror på det, utan enbart uppgifter vad gäller TBE.

Har de ansvariga för studien dessutom glömt att väga in att risken att drabbas av ytterligare infektioner av ett fästingbett är betydligt större om man har immunbrister, redan är sjuk?

Varför passar de inte på att kolla förekomsten av samtliga coinfections, eller ännu hellre, samtliga 17 patogener som hittills har hittats hos fästingar i Sverige? Man nöjer sig med borrelia, anaplasma och TBE, medan t.ex. rickettsia finns hos var femte fästing:

http://www.aftonbladet.se/halsa/article15460540.ab

Det finns som synes ganska många frågetecken kring hur STING-studien utförs, vi hoppas att de ansvariga vill kommentera här och reda ut dem!

Elisa och Besell