Infect Dis Clin North Am. 2008 Jun;22(2):289-300.
Lyme arthritis: pathogenesis, clinical presentation, and management.
Puius YA, Kalish RA.
Division of Infectious Diseases, Roger Williams Medical Center, 825 Chalkstone
Avenue, Providence, RI 02908-4735, USA.
Arthritis is one of the most prominent features of Lyme disease, the tick-borne illness caused by Borrelia burgdorferi. Although the pathogenesis of Lyme arthritis is complex and still under study, the clinical presentation and natural history have been established by long-term observation of untreated and treated patients.
This review addresses the clinical presentation of Lyme arthritis as a mono- or oligoarticular relapsing/remitting arthritis primarily affecting the large joints and describes presentations in which arthralgias rather than arthritis are seen. Strategies for diagnosis and treatment are discussed, and methods are reviewed for addressing treatment- refractory Lyme arthritis and arthralgias that may occur after treatment of Lyme disease (sometimes as a component of what is known as the post-Lyme disease syndrome).
PMID: 18452802 [PubMed - in process]
Muutamia aiheesta tehtyjä tutkimuksia:
1. Quinn SJ, Boucher BJ. Reversible sensorineural hearing loss in Lyme disease. Journal of Laryngology & Otology 1997; 111(6): 562-4.
2. Goldfarb D, Sataloff RT. Lyme disease: a review for the otolaryngologist. Ears Nose and Throat. Journal 1994; 73 (11): 824-9.
3. Ishizaki H, Pyykko I, Nozue M. Neuroborreliosis in the etiology of vestibular neuronitis. Acta Oto-Laryngologica ? Supplement 1993; 503: 67-9.
4. Riechelmann H, Hauser R, Vogt A, Mann W. The Borrelia titer in ENT diseases. Laryngo-Rhino-Otologie 1990; 69(2): 65-9.
5. Hanner P, Rosenhall U, Edstrom, Kaijser B. Hearing impairment in patients with antibody production against Borrelia. Lancet 1989; 1(8628): 13-5.
"Kaikkien Parsons-Turnerin oireyhtymää sairastavien kohdalla tulee rutiininomaisesti ottaa huomioon borrelioosin mahdollisuus."
"Neljällä henkilöllä esiintyi hartiakipua ja hartialihasten heikkoutta. Oiretta kutsutaan hartiapunoksen neuralgiaksi, pleksusneuriitiksi, neuralgiseksi amyotrofiaksi tai Parsonage-Turnerin syndroomaksi. Oireiden aiheuttajaksi paljastui borreliabakteeri. Kaikkien serologiset testit olivat positiiviset ja kahden selkäydinneste oli positiivinen. Kaksi potilaista oli täysin oireeton antibioottihoitojen jälkeen 6 kuukauden seurannassa. Kaikkien Parsons-Turnerin oireyhtymää sairastavien kohdalla tulee rutiininomaisesti ottaa huomioon borrelioosin mahdollisuus." (Ranska)
Suom. huom. Suomalainen tarkkaan dokumentoitu pleksusneuriitti potilastapaus.
http://www.ebm-guidelines.com/terveyspo ... o96877.htm
Potilaan kohdalla ei huomioitu borreliabakteerin mahdollisuutta. Antibioottihoitojen sijaan oiretta hoidettiin esim. kortisonilla jne. "Potilaallemme ei tehty laajoja serologisia selvityksiä virus- ja bakteerivasta-aineista."
Artriittipotilaan hartiapunoksen neuropatia
Taina Heinonen, Irma Soini, Timo Nyrke, Marja Mikkelsson ja Markku Hakala
Artikkeliin liittyvät kuvat ja taulukot löytyvät viereisestä Pdf-versiosta.
Oireet, taudinkulku ja ennuste
Neuralginen amyotrofia on neuropatia, joka yleensä vaurioittaa hartiapunosta ja siten häiritsee olkanivelen ja yläraajan toimintaa. Neuralgisessa amyotrofiassa yksittäiset olkapunoksesta lähtevät hermohaarat vaurioituvat, ja niiden hermottamat lihakset halvaantuvat. Muutokset näkyvät alkuvaiheessa olkapään magneettikuvissa näiden lihasten turvotuksena ja ENMG:ssä denervaatiolöydöksinä. Kuvaamme potilaan, jolla on sekä artriitti että neuralginen amyotrofia. Esittelemme potilaan kliiniset, magneettikuvaus- ja ENMG-löydökset. Tapaus osoittaa, että artriittipotilaan olkanivelen oireet ja toimintahäiriö voivat olla myös neurologista alkuperää.
Bakteereista kampylobakteeri, yersinia, salmonella ja klamydia ovat tavallisia reaktiivisen artriitin aiheuttajia. Bulgen ym. 1979 kuvasivat miespotilaan, joka sai yersiniainfektion jälkeen sekä reaktiivisen artriitin että neuralgisen amyotrofian. Potilaallamme ei ollut yersiniavasta-aineita. Viruksista esimerkiksi vihurirokkovirus, Epstein-Barrin virus ja Coxsackie B -virus voivat aiheuttaa postinfektiivisen artriitin. Parvovirus B19 aiheuttaa erythema infectiosumin eli parvorokon. Parvovirus aiheuttaa myös postinfektiivistä artriittia (Reid ym. 1985). Sen aiheuttama artriitti on tyypillisempi naisilla. Edeltävään infektioon ei aikuisilla yleensä liity iho-oireita, ja infektio saattaa niveloireita lukuun ottamatta olla muuten oireeton. Niveloireet voivat alkaa jo itse infektion aikana, ja tyypillisesti ne ovat symmetriset ja alkavat käsistä tai polvista. Niveloireisto alkaa yleensä helpottaa parissa viikossa, mutta joillakin potilailla oireet jatkuvat vuosia. Infektio voidaan todeta vasta-ainetutkimuksin. IgM-luokan parvovirusvasta-aineet häviävät yleensä noin kolmessa kuukaudessa.
Englanninkielisestä kirjallisuudesta löytyy neljä tapausselostusta, joissa naisen parvovirusinfektioon on liittynyt neuralginen amyotrofia. Yksi englanninkielinen tapausselostus on nuorehkosta naispotilaasta, jolla parvovirusinfektioon liittyi sekä artriitti että neuralginen amyotrofia (Puéchal ym. 1998), ja yksi saksankielinen naisesta, jolla erythema infectiosumia komplisoivat sekä artriitti että hartiapunoksen neuriitti siirottavine lapaluineen (Zander ym. 2001).
Potilaallemme ei tehty laajoja serologisia selvityksiä virus- ja bakteerivasta-aineista. Potilas tuli sairaalaamme runsaan kahden vuoden kuluttua niveloireiden alusta, joten odotettavaa oli, että enää ei todettu IgM-luokan parvovirusvasta-aineita. Emme siis tiedä, onko potilaalla esiintynyt oireiden alkuvaiheessa IgM-luokan parvovirusvasta-aineita. Löydös sitoisi tämän viruksen varmasti oireisiin. Pidämme mahdollisena, että parvovirus on oireiden syy. Potilaamme kyllä poikkeaa aiemmin kuvatuista siinä, että muille neuralginen amyotrofia on ilmaantunut hyvin pian parvovirusinfektion jälkeen. Potilaallamme oli niveloireita jo runsaan kahden vuoden ajan ennen neurologisten oireiden alkua.
Potilaamme on ammatiltaan sihteeri, eikä olkapäitten toimintahäiriö tee hänestä työkyvytöntä. Pahimman neuropaattisen kivun aikaan hän oli muutaman viikon työkyvytön. Potilaan neuralgisen amyotrofian hoito on ollut oireenmukaista, ja hän on saanut fysioterapeuttista ohjausta. Neuralgisessa amyotrofiassa ei ole tehty kontrolloituja lääketutkimuksia, joten luotettavaa tietoa eri hoitomuotojen tehosta ei ole. Jos potilaamme oireista olisi seurannut toimintakyvyn vaikeampi heikkeneminen, olisi tullut harkittavaksi hoitokokeilu laskimoon annettavalla immunoglobuliinilla.
Tapausselostuksien määrän perusteella kyseessä näyttää olevan hyvin harvinainen tautiyhdistelmä tai sitten näitä tapauksia ei tunnisteta. Niveltulehdustapauksissa voi käydä niin, että olkapään seudun lihasheikkouden neurologinen alkuperä jää huomaamatta ja heikkoutta pidetään seurauksena nivelen tulehduksesta, kivusta ja toimintahäiriöstä tai kiertäjäkalvosimen sairauksista.
Revue du Rhumatisme
Copyright © 2008 Elsevier Masson SAS All rights reserved.
Joint Bone Spine Joint Bone Spine
Revue du Rhumatisme (International edition)
Sous presse. In press. Epreuves corrigées par l'auteur. Disponible en ligne depuis le mercredi 14 janvier 2009
Tests corrected by the author. Available online since Wednesday 14 January 2009
Parsonage-Turner syndrome revealing Lyme borreliosis.Wendling D, Sevrin P, Bouchaud-Chabot A, Chabroux A, Toussirot E, Bardin T, Michel F.
Service de Rhumatologie, CHU Jean Minjoz, et EA 3186 <<Agents Pathogènes et Inflammation>> Université de Franche-Comté, Boulevard Fleming, 25030 Besançon, France.
Parsonage-Turner syndrome, also known as acute brachial neuritis or neuralgic amyotrophy, can be caused by various infectious agents. We report on four patients who experienced Parsonage-Turner syndrome as the first manifestation of Lyme disease. The clinical picture was typical, with acute shoulder pain followed rapidly by weakness and wasting of the shoulder girdle muscles. Electrophysiological testing showed denervation. A single patient reported erythema chronicum migrans after a tick bite. Examination of the cerebrospinal fluid showed lymphocytosis and protein elevation in 3 patients. Serological tests for Lyme disease were positive in the serum in all 4 patients and in the cerebrospinal fluid in 2 patients. Antibiotic therapy ensured a favorable outcome in all 4 cases. Two patients achieved a full recovery within 6 months. Parsonage-Turner syndrome should be added to the list of manifestations of neuroborreliosis. Serological tests for Lyme disease should be performed routinely in patients with Parsonage-Turner syndrome.
PMID: 19147387 [PubMed - as supplied by publisher]
Lyme Disease Is Now Linked To Stroke in 20-Year-Old
August 17, 1990
LEAD: Two neurologists have reported that a 20-year-old man suffered a stroke as a result of meningitis brought on by Lyme disease. Eleven similar cases have been documented in Europe, they say.
Two neurologists have reported that a 20-year-old man suffered a stroke as a result of meningitis brought on by Lyme disease. Eleven similar cases have been documented in Europe, they say.
In a report published yesterday in Stroke, a journal of the American Heart Association, the two neurologists at the Walter Reed Army Medical Center in Washington recommend that victims of inexplicable strokes be tested for Lyme disease.
''This is not the first time stroke has been linked to Lyme disease,'' said Dr. Eugene F. May, who, with Dr. Bahman Jabbari, wrote the report. ''But it is not a widely known syndrome.''
Lyme disease is caused by a tick- transmitted bacteria, called Borrelia burgdorferi. Its early symptoms are a skin rash, headaches and fever, but if untreated the disease can cause arthritis as well as heart and neurological damage. It is rarely fatal.
Link Is Long Suspected
Neurologists say a link between Lyme disease and stroke has long been suspected. ''Everybody has been looking for this for years,'' said Dr. John J. Halperin of the State University of New York at Stony Brook. ''This is probably the best documentation we've had so far.''
Dr. Andrew Pachner, a neurologist at Georgetown University Medical Center in Washington, said he had treated patients for strokes that he believes resulted from meningitis after the patients were afflicted with Lyme disease. ''It's probably more common than we think,'' he said.
In their report, Dr. May and Dr. Jabbari described the case of a 20-year-old soldier stationed in West Germany who began having recurring headaches in January 1989. He suffered a mild stroke in March and another in April.
Tests showed he had meningitis, an inflamation of the membrane that surrounds the brain and spinal cord, as a result of Lyme disease.
Meningitis is a known complication of the disease. Doctors could not identify any other possible cause of the strokes, and concluded that Lyme disease and the meningitis caused the strokes.
The soldier was treated with antibiotics and has regained much of the function lost in the strokes.
Similar Cases in Europe
The neurologists said medical journals had reported 11 similar cases, all in Europe, involving people 20 to 74 years of age.
Dr. May said the report should not cause alarm. ''The chance of any one person who has Lyme disease of developing a stroke because of it is extremely low,'' he said.
The researchers speculate that only certain strains of the bacteria lead to stroke, particularly those found in Europe. Variant strains have been associated with different complications of Lyme disease, which may explain why arthritis is a more common complication in North America while neurological complications are more common in Europe.
Patellar Tendon Rupture as a Manifestation of Lyme Disease
Nirav K. Pandya, MD, Miltiadis Zgonis, MD, Jaimo Ahn, MD, PhD, and Craig Israelite, MD
A 50-year-old woman with a known history of Lyme disease presented to our institution with 4 days of fevers, right knee swelling, and pain. Five years earlier, she had been diagnosed with Lyme disease after presenting to an emergency department with rapid-onset chills, generalized myalgias, lethargy, and an erythema migrans rash?but no joint symptoms.
She had been treated with a full course (3 weeks) of oral doxycycline antibiotic therapy and had had no posttreatment sequelae.
Approximately 13 months before the current presentation, the patient had been involved in a motor vehicle accident in which she was a restrained driver. She suffered a right inferior pole patella fracture with disruption of the extensor mechanism. At our institution then, the patient underwent an uneventful inferior pole patellectomy with reattachment of the patellar tendon (Figures 1, 2). She was kept immobilized for 1 month and then over 2 months performed gentle range-of-motion (ROM) exercises followed by strengthening exercises. She did quite well and by time of discharge from our care had regained full strength and ROM.
Approximately 4 days before the current presentation, the patient experienced low-grade fevers, myalgias, and fatigue. Then she noticed right knee swelling and pain. She denied any specific traumatic event, joint pain, or weakness leading up to the swelling and pain, as well as insect bites, tick exposure, swelling in other joints, recent increase in activity, and development of cutaneous lesions.
Physical examination revealed a moderate-sized effusion on the right knee. The scar from the prior surgery was intact. There was a significant extensor lag, to approximately 40° to 45°, but from 45° to 90° the patient was able to actively extend the knee against mild resistance. She was unable to perform a straight-leg raise. She was otherwise neurovascularly intact...
This case report in fact exemplifies another possible manifestation of late-phase Lyme disease. It is essential that clinicians realize this possible connection between Lyme disease and patellar tendon rupture so that they can adequately treat the underlying disease process with antibiotics (rather than simply correct the rupture itself) when faced with a patient presenting to clinic with a history of Lyme disease, constitutional symptoms, knee effusion, and an examination suggestive of patellar tendon disruption.
In addition, if the clinician encounters a midsubstance tear in the operating room (away from the area of most biomechanical stress3), suspicion for an inflammatory condition such as Lyme disease leading to the rupture should also be heightened. This is particularly important, as failure to treat Lyme arthritis can lead to prolonged synovitis, cartilage loss, bone cysts, and chronic pain.24,25 Lyme disease should be in the clinician?s differential for patients presenting nontraumatically with patellar tendon disruptions, particularly when a history of exposure has been documented.
Suom. huom. Millä menetelmällä poissulkivat borreliabakteerin mahdollisuuuden verrokkiryhmällä? Sellaista testiä ei ole vielä tällä hetkellä olemassa.
By Megan Rauscher
NEW YORK (Reuters Health) - Depression and the chronic pain syndrome fibromyalgia are common in patients who suffer from chronic Lyme disease and seem to correlate with poor functional outcomes, results of a study indicate.
The term chronic Lyme disease describes patients with persistent Lyme disease despite prior treatment with a conventional 2- to 4-week course of antibiotics.
Dr. Afton L. Hassett from the University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick and colleagues studied 159 patients seen at an academic Lyme disease referral center.
They evaluated the prevalence and role of psychiatric "co-morbid" illness and psychological factors in 77 patients with chronic Lyme disease and 82 (comparison) patients without chronic Lyme disease. The comparison patients either recovered from Lyme disease or had Lyme-like symptoms explained by other conditions.
Ann Dermatol Venereol. 2008 Dec;135(12):852-4. Epub 2008 Oct 26.
[Borrelial erythema of the face.]
[Article in French]
de Heller-Milev M, Peter O, Panizzon RG, Laffitte E.
Service de dermatologie et venerologie, centre hospitalier universitaire Vaudois (CHUV), Lausanne, Suisse.
Borrelial infection is characterized by various skin manifestations that are usually classified into three main types: chronic migratory erythema, borrelial lymphocytoma and acrodermatitis chronica atrophicans. We report an unusual case of borrelial cutaneous infection presenting as a mediofacial erythema that cannot be included in any of these three categories.
A 51-year-old woman presented with infiltrated erythema of the middle of the face extending to the neck and chin. Medical history and physical examination revealed no signs of rosaceae. Infection with Borrelia was suspected on skin biopsy examination, which showed an inflammatory dermal infiltrate containing numerous plasma cells. The diagnosis of B.afzelii infection was confirmed by serology and polymerase chain reaction on the skin biopsy, both of which were positive for B.afzelii.
Borrelial erythema of the face may represent a special form of cutaneous borrelial infection, which must be considered in the differential diagnosis of facial erythema, especially in areas of endemic borreliosis.
PMID: 19084697 [PubMed - in process]
Arthritis Rheum. 2008 Nov 26;59(12):1742-1749 [Epub ahead of print]
Role of psychiatric comorbidity in chronic Lyme disease.
Hassett AL, Radvanski DC, Buyske S, Savage SV, Gara M, Escobar JI, Sigal LH.
University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick.
OBJECTIVE: To evaluate the prevalence and role of psychiatric comorbidity and other psychological factors in patients with chronic Lyme disease (CLD).
METHODS: We assessed 159 patients drawn from a cohort of 240 patients evaluated at an academic Lyme disease referral center. Patients were screened for common axis I psychiatric disorders (e.g., depressive and anxiety disorders); structured clinical interviews confirmed diagnoses. Axis II personality disorders, functional status, and traits like negative and positive affect and pain catastrophizing were also evaluated. A physician blind to psychiatric assessment results performed a medical evaluation. Two groups of CLD patients (those with post-Lyme disease syndrome and those with medically unexplained symptoms attributed to Lyme disease but without Borrelia burgdorferi infection) were compared with 2 groups of patients without CLD (patients recovered from Lyme disease and those with an identifiable medical condition explaining symptoms attributed to Lyme disease).
RESULTS: After adjusting for age and sex, axis I psychiatric disorders were more common in CLD patients than in comparison patients (P = 0.02, odds ratio 2.64, 95% confidence interval 1.30-5.35), but personality disorders were not. Patients with CLD had higher negative affect, lower positive affect, and a greater tendency to catastrophize pain (P < 0.001) than comparison patients. All psychological factors except personality disorders were related to level of functioning. A predictive model based on these psychological variables was confirmed. Fibromyalgia was diagnosed in 46.8% of CLD patients.
CONCLUSION: Psychiatric comorbidity and other psychological factors distinguished CLD patients from other patients commonly seen in Lyme disease referral centers, and were related to poor functional outcomes.
PMID: 19035409 [PubMed - as supplied by publisher]
Myöhempiä ilmenemismuotoja ovat lymfosytooma joka esiintyy useimmiten korvalehdessä tai rinnassa ja acrodermatitis chronica jota esiintyy lähinnä taudin myöhäisvaiheessa. Acrodermatitis diagnosoidaan usein virheellisesti verisuoniperäiseksi sairaudeksi. Erythema-vaiheessa vääriä negatiivisa testituloksia esiintyy yleisesti. Myöhemmissä vaiheissa testit ovat luotettavampia. (Itävalta)
Am J Clin Dermatol. 2008;9(6):355-68.
Skin manifestations of lyme borreliosis: diagnosis and management.
Mullegger RR, Glatz M.
Department of Dermatology, Central Hospital Wiener Neustadt, Wiener Neustadt, Austria.
Lyme borreliosis is a multisystem infectious disease caused by tick-transmitted spirochetes of the Borrelia burgdorferi sensu lato complex. The three characteristic cutaneous manifestations are erythema migrans, borrelial lymphocytoma, and acrodermatitis chronica atrophicans.
Erythema migrans occurs in acute Lyme borreliosis, lymphocytoma is a subacute lesion, and acrodermatitis is the typical manifestation of late Lyme borreliosis. Clinical appearances of erythema migrans and lymphocytoma (when located on the ear or breast) are characteristic, whereas acrodermatitis is often confused with vascular conditions.
The diagnosis of erythema migrans is made clinically. Serologic analyses often yield false-negative results and are not required for the diagnosis. However, serologic proof of the diagnosis in lymphocytoma (approximately 90% positive) and acrodermatitis (100% positive) is mandatory.
Histopathologic examination often adds substantial information in patients with skin manifestations of Lyme borreliosis and is recommended in clinically (and serologically) undecided cases of erythema migrans or lymphocytoma and is obligatory in acrodermatitis.
Polymerase chain reaction for Borrelia-specific DNA (rather than culture of the spirochete) and immunohistochemical investigations (lymphocytoma) are sometimes necessary adjuncts for the diagnosis.
Antibacterial treatment is necessary in all patients to eliminate thespirochete, cure current disease, and prevent late sequelae. Oral doxycycline, also effective against coinfection with Anaplasma phagocytophilum, is the mainstay of therapy of cutaneous manifestations of Lyme borreliosis. Other first-line antibacterials are amoxicillin and cefuroxime axetil.
Erythema migrans is treated for 2 weeks, lymphocytoma for 3-4 weeks, and acrodermatitis for at least 4 weeks.
PMID: 18973402 [PubMed - in process]
2. Skandinaviassa lasten neuroborrelioosin oireena on useimmiten lievä aivokalvontulehdus tai kasvohermohalvaus.
Chronic and recurrent meningitis -- Ginsberg and Kidd 8 (6): 348 -- Practical Neurology
Practical Neurology 2008;8:348-361; doi:10.1136/jnnp.2008.157396
Copyright © 2008 by the BMJ Publishing Group Ltd.
Chronic and recurrent meningitis
L Ginsberg, D Kidd
Consultant Neurologists, Department of Neurology, Royal Free Hospital, London, UK
Dr L Ginsberg, Department of Neurology, Royal Free Hospital, Pond Street, London NW3 2QG, UK; firstname.lastname@example.org
Chronic meningitis is defined as the persistence of clinical symptoms and signs of meningitis, with or without abnormal cerebrospinal fluid, for more than four weeks. In as many as one third of cases, no cause is found. In the remainder, infective, neoplastic and so-called aseptic disorders may be identified. Important infective causes include partially treated bacterial (pyogenic), tuberculous, syphilitic, Lyme and fungal meningitis. Sarcoidosis, Behçet?s disease, vasculitis and drugs are major non-infective, non-malignant causes. The definitive diagnosis of the cause of chronic meningitis may be made only after extensive investigation. This review describes the clinical features and causes of chronic and recurrent meningitis, and provides an algorithm for investigation and treatment. ...[End of Extract] [PDF of this article]
Scand J Infect Dis. 2008 Dec 8;:1-7 [Epub ahead of print]
Clinical characteristics of childhood Lyme neuroborreliosis in an endemic area
of northern Europe.
Oymar K, Tveitnes D.
From the Department of Paediatrics, Stavanger University Hospital, Stavanger.
Neuroborreliosis may be caused by different species of Borrelia burgdorferi (BB) and the clinical presentation of neuroborreliosis in children may differ between geographical areas due to occurrence of different BB genospecies. The aim of this study was to evaluate the clinical characteristics in children with neuroborreliosis in an endemic area of Scandinavia. During 1996-2006, children with suspected neuroborreliosis referred to Stavanger University Hospital were investigated by a standard procedure including a lumbar puncture. A total of 143 children were diagnosed with neuroborreliosis, and all cases were diagnosed from April to December. The most common clinical presentations were symptoms of mild meningitis (75%) and/or facial nerve palsy (69%). Radicular pain was present in only 10 children. In all but 5 children, laboratory signs of meningitis were present. Erythema migrans preceded the neurological symptoms in only 27% of the children.
In conclusion, we have found that in an endemic area of northern Europe, meningitis is present in the majority of children with neuroborreliosis, and that symptoms of a mild meningitis or facial nerve palsy are the most common presentations.
PMID: 19065451 [PubMed - as supplied by publisher]
Suom.huom. Kyseinen ihomuutos ja siitä tehty tutkimus saattaa olla merkityksellinen, sillä näyttää siltä että ihomuutoksesta kärsivät eivät välttämättä saa oikeaa diagnoosia ja hoitoa.
"Törmäsin" sattumalta esim. seuraavaan nettikeskusteluun:
http://keskustelu.suomi24.fi/terveys_sh ... 0010536217
Granuloma annulare - a manifestation of infection with Borrelia?
Ziemer M, Grabner T, Eisendle K, Baltaci M, Zelger B.
Department of Dermatology and Venereology, Friedrich-Schiller-University, Jena,
Among the theories of origin of granuloma annulare (GA) are those of infection. Reports gave raise to the assumption that there is evidence for Borrelia as the causing agent.
Methods: To assess the evidence for infection with Borrelia in GA, tissue sections were stained with a polyclonal Borrelia antibody. With focus-floating microscopy (FFM), slides were scanned at a 200- to 400-fold magnification. Part of the material was also investigated with a Borrelia-specific polymerase chain reaction (PCR).
Results: A total of 157 biopsies of GA have been investigated. Using FFM, Borrelia were detected in 127 cases of GA (80.9%). Borrelia were more prominent in localized (85.2%) than in diffuse GA (62.1%). In 27 cases of GA analysed by PCR, Borrelia-specific DNA could be detected in only one case (3.7%), but was positive in 21 cases by FFM (77.8%). About 93.3% of 15 control cases of borreliosis were positive with FFM and 46.7% with PCR, while all controls other than borreliosis remained negative for spirochetes.
FFM is a reliable method to show Borrelia in tissue sections of GA, which is more sensitive than PCR. This underlines the possibility that Borrelia are involved specifically in the aetiology and pathogenesis of GA.
PMID: 18616764 [PubMed - as supplied by publisher]
Acta Dermatovenerol Alp Panonica Adriat. 2008 Dec;17(4):171-6. Granuloma annulare displaying pseudorosettes in Borelia infection. Fernandez-Flores A, Ruzic-Sabljic E. S. Patologia Celular, Clinica Ponferrada, Avenida Galicia 1, 24400 Ponferrada,Spain. email@example.com.
Aims: In 2003, pseudorosettes were described as highly suspicious of infectionby Borrelia burgdorferi sensu lato in the appropriate clinical context.Nevertheless, such a pattern has been described in the literature in othernon-infectious conditions. On the other hand, granuloma annulare (GA) has beenrecently closely associated with infection by Borrelia. We investigated howfrequently pseudorosettes can be detected in common GA cases confirmed forBorrelia by PCR.
Methods and results: We studied 13 biopsies of non-interstitialGA and 2 biopsies of interstitial GA from patients without clinical suspicion ofborrelial infection. We also performed immunohistochemical studies in all thebiopsies, using the CD-68 antibody. Molecular studies with PCR were performedwith beta-globin PCR (human DNA). Borrelial DNA was confirmed by amplifying theOspA gene and intergenic rrf-rrl region. We found histiocytic pseudorosettes in13 biopsies (86.66%). Human DNA was successfully amplified from 8 of 13paraffin-embedded skin samples. From these we amplified borrelial DNA in 5 of 8samples. Out of the 8 cases in which human DNA was amplified, a correlationbetween pseudorosettes and the molecular tests (Borrelia DNA) was confirmed in 5instances.
Conclusions: a) Pseudorosettes are not an unusual finding in commongranuloma annulare; b) Borrelia is present in (most) cases of granulomaannulare; and c) Pseudorosettes seem to be a good morphological sign predictiveof infection with Borrelia in granuloma annulare. PMID: 19104742 [PubMed - in process]
a Neurol Belg. 2008 Sep;108(3):103-6.
Acute ischaemic pontine stroke revealing lyme neuroborreliosis in a young adult.
Van Snick S, Duprez TP, Kabamba B, Van De Wyngaert FA, Sindic CJ. Service de Neurologie, Universite catholique de Louvain, Brussels, Belgium.
We report the case of a 23-year-old male patient who suddenly developed righthemiparesis, cerebellar ataxia, dysarthria, and bilateral dysmetria. Brainmagnetic resonance (MR) examination demonstrated hyperacute ischaemic lesionswithin the pons. CSF analysis revealed a high protein content, lymphocyticpleocytosis, and oligoclonal IgG bands not present in the serum. Elevated IgMand IgG anti-Borrelia burgdorferi antibodies were shown in both serum and CSFsamples, associated with an intrathecal synthesis of these antibodies. IschaemicCNS lesions have been rarely observed as the first manifestation of Lymeneuroborreliosis. The putative mechanism for parenchymal ischaemia is the localextension of inflammatory changes from meninges to the wall of penetratingarterioles.
PMID: 19115674 [PubMed - in process]
J Am Acad Dermatol. 2008 Nov 18; [Epub ahead of print]
"Borrelia-associated early-onset morphea": A particular type of scleroderma inchildhood and adolescence with high titer antinuclear antibodies? Results of acohort analysis and presentation of three cases.
Prinz JC, Kutasi Z, Weisenseel P, Poto L, Battyani Z, Ruzicka T. Department of Dermatology, University of Munich, Germany.
BACKGROUND: Morphea is an inflammatory autoimmune skin sclerosis of unknownetiology. A causative role of Borrelia burgdorferi infection has beencontroversially discussed, but no conclusive solution has yet been achieved.
OBJECTIVE: Intrigued by 3 young patients with severe Borrelia-associated morpheaand high-titer antinuclear antibodies, we retrospectively examined therelationship between Borrelia exposure, serologic autoimmune phenomena and ageat disease onset in morphea patients.
METHODS: In 90 morphea patients thepresence of Borrelia-specific serum antibodies was correlated to the age atdisease onset and the presence and titers of antinuclear antibodies. Patientswith active Borrelia infection or high-titer antinuclear antibodies due tosystemic sclerosis or lupus erythematosus served as controls. RESULTS: We observed a statistically highly significant association between morphea, serologic evidence of Borrelia infection, and high-titer antinuclear antibodies when disease onset was in childhood or adolescence.
LIMITATIONS: Because pathogenic Borrelia species may vary in different geographic regions the relevance of Borrelia infection in morphea induction may show regional variations. CONCLUSION: B burgdorferi infection may be relevant for theinduction of a distinct autoimmune type of scleroderma; it may be called"Borrelia-associated early onset morphea" and is characterized by thecombination of disease onset at younger age, infection with B burgdorferi, andevident autoimmune phenomena as reflected by high-titer antinuclear antibodies.As exemplified by the case reports, it may take a particularly severe course andrequire treatment of both infection and skin inflammation.
PMID: 19022534 [PubMed - as supplied by publisher]
http://actionlyme.50megs.com/neuroborre ... ession.htm
http://www.mentalhealthandillness.com/A ... isease.htm
Clinical Psychology Forum 194 ? February 2009 Why psychologists need to know about Lyme disease Sarah L. Marzillier People with undiagnosed Lyme disease may present with chronic fatigue, mentalhealth problems, neuropsychological impairments and autistic spectrum disorders.This article considers the evidence across each of these areas, before discussing how psychologists can recognise and support people with Lyme disease.
Wien Med Wochenschr. 2009 Jan;159(1-2):58-61.
Normal pressure hydrocephalus or neuroborreliosis?
Aboul-Enein F, Kristoferitsch W. Department of Neurology, Sozialmedizinisches Zentrum Ost, Donauspital, Vienna,Austria, firstname.lastname@example.org.
BACKGROUND: An 80-year-old woman presented with progressive cognitive declineand with a 6-month history of gait ataxia. Brain MRI depicted enlargedventricles and periventricular lesions. Clinical improvement after CSF spinaltap test suggested a normal pressure hydrocephalus syndrome. But CSF pleocytosiswith activated lymphocytes and plasma cells and intrathecal Borrelia burgdorferispecific antibody production led to the diagnosis of active Lymeneuroborreliosis. Clinical symptoms of NPH resolved after a course ofceftriaxone.
METHODS: Neurological examination, MMSE, brain MRI, lumbarpuncture, spinal tap test.
RESULTS: Dementia due Borrelia burgdorferi infectionwith chronic meningitis was reversible after treatment with iv.2 g ceftriaxoneper day for 4 weeks.
CONCLUSIONS: Rare but treatable dementias must be diagnosedpromptly to slow down or even reverse cognitive decline. PMID: 19225737 [PubMed - as supplied by publisher]
Borrelioosidiagnoosi tehdään kliinisin perustein vaikka serologiset testit olisivatkin negatiiviset. 69-vuotiaalla naisella ilmeni Hornerin syndrooma ja kuumetta. Antibioottihoito aloitettiin ja oireet paranivat. Serologiset testit olivat positiiviset vasta 4 viikkoa myöhemmin.
The Journal of the American Board of Family Medicine 22 (2): 219-222 (2009)
Unusual Presentation of Lyme Disease: Horner Syndrome with Negative Serology
Candis Morrison, PhD, CRNP, Ari Seifter and John N. Aucott, MD
From the Department of Medicine, Division of General Internal Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland
Correspondence: Corresponding author: John N. Aucott, MD, Johns Hopkins at Greenspring Station, 10755 Falls Road, Suite 200, Lutherville, Maryland 21093 (E-mail: email@example.com )
Early disseminated Lyme disease can be difficult to diagnose because of atypical symptoms and physical findings. A clinical diagnosis must be made in the absence of confirmatory serologic testing to allow timely therapy. We report a case of a 69-year-old woman who presents with fever, Horner syndrome, and a 12-cm oval-shaped erythematous macular rash with multiple vesiculopustular eruptions. The patient recovered after appropriate intravenous antibiotics, but serologic testing only confirmed the diagnosis 4 weeks later. This case also describes an unusual complication involving the neurologic system. We illustrate the clinical presentation and review the medical literature. Lyme disease should always be considered in patients from endemic regions with viral-like symptoms or a new rash.
Infectious Diseases in Clinical Practice:
November 2004 - Volume 12 - Issue 6 - pp 356-357
Case Reports and Reviews: Case Report
Ocular Flutter: A Presenting Diagnostic Feature of Lyme Disease
Touray, Musa; Saiah, Lila; Ombelli, Julien; Sovilla, Jean-Yves; Wyss, Pierre
Abstract: Several historical and physical examination findings of Lyme disease are yet to be elucidated. In this article, we report that ocular flutter, a saccadic horizontal eye movement, is a diagnostic feature of acute disseminated stage of Lyme disease.
Borreliabakteerin aiheuttamien sydäntulehdusten todellista määrää ei tiedetä sillä monilla sairastuneista ei esiinny selkeitä kliinisiä oireita. Bakteeria tulee kuitenkin epäillä, erityisesti miehillä, silloin kun henkilöllä esiintyy rintakipua, sydänentsyymien kohoamista ja ST-T - muutoksia EKG:ssä."
Int J Cardiol. 2009 Mar 27. [Epub ahead of print]
Lyme carditis: Epidemiology, pathophysiology, and clinical features in endemic areas.
Rostoff P, Gajos G, Konduracka E, Gackowski A, Nessler J, Piwowarska W.
Department of Coronary Disease, Institute of Cardiology, Jagiellonian University Medical College, John Paul II Hospital, Krakow, Poland.
PMID: 19328565 [PubMed - as supplied by publisher]
Lyme borreliosis (Lyme disease, LB) is the most prevalent arthropod-borne zoonosis in the Northern hemisphere ,  and . This multisystem infectious disease with a wide spectrum of clinical symptoms is caused by a phylogenetically-distinct group of spirochetes, known as Borrelia burgdorferi sensu lato (Borrelia afzelii, B. garinii, and B. burgdorferi sensu stricto), and classified in the family Spirochaetaceae ,  and . All three genospecies are endemic in Europe, whereas only B. burgdorferi sensu stricto occurs in North America ,  and .
These genetically unique bacteria with characteristic genome, consisting of a linear chromosome, and linear and circular plasmids, are transmitted to humans by ixodid ticks, Ixodes ricinus in Europe, Ixodes persulcatus in Asia, and by Ixodes scapularis and Ixodes pacificus in North America ,  and . In Europe, Ixodes ricinus is also the main vector for other tick-borne diseases, including tick-borne encephalitis, babesiosis, human granulocytic anaplasmosis, and human rickettsioses , ,  and .
The role of other borrelial species (B. lusitaniae, B. valaisiana, B. bissettii, B. spielmanii, and B. genospecies A14S) and co-pathogens (Anaplasma phagocytophilum, Ehrlichia spp., Rickettsia spp., and Babesia spp.) in the pathogenesis of LB remains unclear and is currently under investigation , ,  and .
From the epidemiological point of view, it is very important that some tick species (e.g. Ixodes uriae) can transmit LB spirochetes, particularly B. garinii, among songbirds and seabirds, and thus significantly participate in transcontinental/global spreading of Lyme borreliosis .
Importantly, besides ticks, many arthropods (mosquitoes, horseflies, Stomoxydae flies, lice, fleas, and mites) can be infected by LB spirochetes  M. Derdáková and D. Lencáková, Association of genetic variability within the Borrelia burgdorferi sensu lato with the ecology, epidemiology of Lyme borreliosis in Europe, Ann Agric Environ Med 12 (2005), pp. 165?172. View Record in Scopus | Cited By in Scopus (13). However, as yet, no study has confirmed their competence as vectors for transmission of B. burgdorferi sensu lato to humans .
NOTEWORTHY: According to the IDSA guidelines, all symptomatic patients with Lyme carditis, particularly those with syncope, dyspnea or chest pain, as well as those with second- or third-degree atrioventricular block and patients with first-degree atrioventricular block with the prolonged PR interval (≥ 300 ms) should be hospitalized and continuously monitored .
In conclusion, Lyme borreliosis is the most common tick-borne infectious disease in the Northern hemisphere. The incidence of LB in endemic regions is remarkably underestimated. The true prevalence of Lyme carditis is unknown, because most of these cases are clinically asymptomatic. Lyme carditis should be considered in the differential diagnosis of acute chest pain, elevated levels of cardiac enzymes and troponin I, and diffuse ST-T changes, particularly in males living in endemic areas for Lyme disease and exposed to tick bites.
April 2009, Vol. 3, No. 2, Pages 125-140
Preventable cases of autism: relationship between chronic infectious diseases and neurological outcome
Robert C Bransfield?
Associate Director of Psychiatry Riverview Medical Center, 225 Hwy, 35 Red Bank, NJ 07701, USA. firstname.lastname@example.org
?Author for correspondence
There is evidence that chronic infections and the immune reactions associated with them may contribute to causing autism spectrum disorders. These infections include Babesia, Bartonella, Borrelia burgdorferi, Ehrlichia, Human herpesvirus-6, Chlamydia pneumoniae and Mycoplasma (in particular Mycoplasma fermentans). Maternal immune reactions to infections appear to adversely affect fetal brain development and possible pathophysiological mechanisms include both inflammatory cytokines, such as IL-6, and maternal autoantibodies to fetal neural tissue of the same kilodalton mass as those seen with B. burgdorferi and some other chronic infections. The timing of the infection and immune response is critical in determining the pathophysiology. It is advisable to evaluate women who are pregnant or planning on becoming pregnant for chronic infections, especially if they demonstrate symptoms of an infection or a systemic illness with persistent inflammatory symptoms. The mother and the newborn should be treated when indicated.
AJNR Am J Neuroradiol. 2009 Apr 3; [Epub ahead of print]
Lyme Neuroborreliosis: Manifestations of a Rapidly Emerging Zoonosis.
Hildenbrand P, Craven DE, Jones R, Nemeskal P.
Departments of Radiology, Infectious Disease, Neurology, and Mediicine, Lahey Clinic Medical Center, Burlington, Mass; Tufts University School of Medicine,Boston, Mass; and Harvard Medical School, Boston, Mass.
SUMMARY: Lyme disease has a worldwide distribution and is the most common vector-borne disease in the United States. Incidence, clinical manifestations, and presentations vary by geography, season, and recreational habits. Lyme neuroborreliosis (LNB) is neurologic involvement secondary to systemic infection by the spirochete Borrelia burgdorferi in the United States and by Borrelia garinii or Borrelia afzelii species in Europe. Enhanced awareness of the clinical presentation of Lyme disease allows inclusion of LNB in the imaging differential diagnosis of facial neuritis, multiple enhancing cranial nerves, enhancing noncompressive radiculitis, and pediatric leptomeningitis with white matter hyperintensities on MR imaging. The MR imaging white matter appearance of successfully treated LNB and multiple sclerosis display sufficient similarity to suggest a common autoimmune pathogenesis for both. This review highlights differences in the epidemiology, clinical manifestations, diagnosis, and management of Lyme disease in the United States, Europe, and Asia, with an emphasis on neurologic manifestations and neuroimaging.
PMID: 19346313 [PubMed - as supplied by publisher]
Ps. Lymfosytoomaa esiintyy tyypillisesti korvalehdessä, nännien alueella ja seuraavan lähteen mukaan esim. lasten kiveksissä.
http://www.terveyskirjasto.fi/terveyski ... i=ima00349
Br J Dermatol. 2009 Mar 19; [Epub ahead of print]
Species of Borrelia burgdorferi complex that cause borrelial lymphocytoma in France.
Lenormand C, Jaulhac B, De Martino S, Barthel C, Lipsker D. Clinique Dermatologique, Universite Louis Pasteur, 67091 Strasbourg, France.
Only about 30 cases of borrelial lymphocytoma (BL) withidentification of the causative species of Borrelia have been published to date,mainly from Eastern or Central European countries.
To identify thespecies of B. burgdorferi complex responsible for BL in France. Methods Ninepatients with BL acquired in France and for whom skin samples were sent to thenational reference centre laboratory between 1994 and 2007 were included in thisretrospective study. Direct detection of Borrelia in skin samples was made bypolymerase chain reaction targeting the fla gene. Culture was performed whentechnically possible, and identification of each species was made byhybridization of a fragment of the fla gene with a panel of species-specificoligonucleotides.
Borrelia afzelii was identified in three cases, B.garinii and B. burgdorferi sensu stricto in one case each. Culture was positivein only one case (B. garinii).
Borrelia afzelii seems to be thepredominant species of Borrelia responsible for BL in France, as alreadyreported in other European countries.
PMID: 19302068 [PubMed - as supplied by publisher]
Borreliabakteerin osuudesta autismiin löytyy oma sivusto osoitteessa
G Ital Dermatol Venereol. 2009 Apr;144(2):157-71. The expanding spectrum of cutaneous borreliosis. Eisendle K, Zelger B. Department of Dermatology and Venerology, Innsbruck Medical University,Innsbruck, Austria Klaus.email@example.com.
The known spectrum of skin manifestations in cutaneous Lyme disease iscontinuously expanding and can not be regarded as completed.
Besides theclassical manifestations of cutaneous borreliosis like erythema (chronicum)migrans, borrelial lymphocytoma and acrodermatitis chronica atrophicans evidenceis growing that at least in part also other skin manifestations, especiallymorphea, lichen sclerosus and cases of cutaneous B-cell lymphoma are causallyrelated to infections with Borrelia. Also granuloma annulare and interstitialgranulomatous dermatitis might be partly caused by Borrelia burgdorferi orsimilar strains.
There are also single reports of other skin manifestations tobe associated with borrelial infections like cutaneous sarcoidosis, necrobiosislipoidica and necrobiotic xanthogranuloma. In addition, as the modern chameleonof dermatology, cutaneous borreliosis, especially borrelial lymphocytoma, mimicsother skin conditions, as has been shown for erythema anulare centrifugum orlymphocytic infiltration (Jessner Kanof) of the skin.
PMID: 19357623 [PubMed - in process]
Serologisissa vasta-aine testeissä - ELISA ja immunoblottaus (Western Blot) - IgG oli koholla, IgM normaali, runsaasti koholla olevia eri proteiineja. Löydös viittasi joko aiempiin oireettomiin infektioihin, myöhäisempään tai akuuttiin infektioon jossa IgM ei ole vielä ehtinyt kohota." (Saksa 2009)
Bilateral Facial Palsy in Neuroborreliosis Archives of Neurology, 04/16/09
Hagemann G, Aroyo IM. Department of Neurology, Friedrich-Schiller-University, Erlanger Alle 101, 07740 Jena, Germany. firstname.lastname@example.org
A 54-year-old forest worker experienced bilateral facial weakness. A few days later, he presented with an almost complete facial palsy without any disturbances of taste, hearing, or sensation. He had a marked Bell phenomenon (Figure). He was diagnosed some years before with Lyme disease without any clinical symptoms and was treated with oral antibiotics. Meanwhile, he received some new tick bites. A lumbar puncture revealed a lymphocyte count of 77/microL and an elevated protein level of 2.5 g/L. Serological testing revealed positive IgG results, a negative IgM borreliosis titer on an enzyme-linked immunosorbent assay, and multiple bands on Western blotting, suggestive of either remnants of an earlier asymptomatic contact with borrelia or a late or very recent infection with still-absent IgM antibodies.
Psychiatr Clin North Am. 1998 Sep;21(3):693-703, viii.Related Articles, L
The underdiagnosis of neuropsychiatric Lyme disease in children and adults.
Fallon BA, Kochevar JM, Gaito A, Nields JA.
Department of Psychiatry, Columbia University Medical Center, New York, New York, USA.
Lyme Disease has been called "The New Great Imitator," a replacement for that old "great imitator" neurosyphilis. This article reviews the numerous psychiatric and neurologic presentations found in adults and children. It then reviews the features of Lyme Disease, which makes it almost uniquely hard to diagnose, including the complexity and unreliability of serologic tests. Clinical examples follow that illustrate those presentations of this disease that mimic attention deficit hyperactivity disorder (ADHD), depression, and multiple sclerosis.
Research Support, Non-U.S. Gov't
PMID: 9774805 [PubMed - indexed for MEDLINE]
Suom.huom. Esim. MS-taudissa tapahtuu aivojen valkean aineen vaurioitumista. Yhteys borreliabakteeriin on osoitettu useissa tutkimuksissa. Muutkin taudinaiheuttajat voivat todennäköisesti aiheuttaa vastaavanlaista tuhoa keskushermostossa.
Neurology. 2009 May 19;72(20):1786-7.
Antibiotic responsive demyelinating neuropathy related to Lyme disease.
Muley SA, Parry GJ. Department of Neurology, University of Minnesota, Minneapolis, 55455, USA.email@example.com PMID: 19451535 [PubMed - in process]
Intracranial aneurysms in three patients with disseminated Lyme borreliosis: cause or chance association
METHODS: Three patients with Borrelia burgdorferi infection and intracranial aneurysms are described.
RESULTS: All three patients had neurological symptoms. Perivascular and vasculitic lymphocytic inflammation were detected in the brain biopsy specimen of one patient. The aneurysm was located in the internal carotid arteries in two patients and in the basilar artery in one patient. The aneurysm ruptured in two patients.
CONCLUSIONS: Cerebral lymphocytic vasculitis and intracranial aneurysms may be associated with B burgdorferi infection. It is suggested that inflammatory changes caused by B burgdorferi in vessel walls may be a pathogenetic mechanism for the formation of aneurysms.
Oksi J, Kalimo H, Marttila RJ, Marjamäki M, Sonninen P, Nikoskelainen J, and Viljanen MK
Journal of Neurology, Neurosurgery, and Psychiatry 1998;64:636-642
J Cutan Pathol. 2009 Mar 11; [Epub ahead of print] High prevalence of 'Borrelia-like' organisms in skin biopsies of sarcoidosispatients from Western Austria. Derler AM, Eisendle K, Baltaci M, Obermoser G, Zelger B. Department of Dermatology and Venereology, Innsbruck Medical University,Innsbruck, Austria. Background: Sarcoidosis is a multisystem granulomatous disorder of unknownaetiology with frequent skin involvement. Objective: To investigate thefrequency of 'Borrelia-like' organisms in cutaneous sarcoidosis (CS) byfocus-floating microscopy (FFM). Methods: Retrospective analysis of 38 CSspecimens by immunohistochemistry with polyclonal anti-Borrelia antibody andassessment by FFM. Results: Specimens of 34.2% CS were positive for'Borrelia-like' organisms by FFM. Usually single spirochetes, rarely pairs orsmall clusters of bacteria were observed between collagen bundles or at theperiphery of granulomas. Polymerase chain reaction (PCR) was performed inaddition in 11 cases and was negative in all biopsies. Samples of erythemamigrans served as positive controls: 92.3% of 39 samples were positive by FFM,but only 46.6% gave positive results by PCR. Of 61 negative controls only onespecimen was falsely positive by immunohistochemistry. Conclusion: Detection of'Borrelia-like' organisms by FFM in tissue sections of CS underlines thepossibility that such microorganism may be involved in the pathogenesis of somecases of CS. Derler AM, Eisendle K, Baltaci M, Obermoser G, Zelger B. Highprevalence of 'Borrelia-like' organisms in skin biopsies of sarcoidosis patientsfrom Western Austria. PMID: 19469874 [PubMed - as supplied by publisher]
Borrelial fasciitis: as yet insufficient proof for a distinct entity.
Houtman PM, Jansen TL, Weel J, Grond JK.
Department of Rheumatology, Medical Centre Leeuwarden, PO Box 888, 8934 AD,
Leeuwarden, The Netherlands, firstname.lastname@example.org.
The clinical picture of diffuse fasciitis is described in three male patients,
living in a highly Borreliosis endemic region. We discuss the likelihood of a
causal relationship with a Borrelia infection.
PMID: 19506881 [PubMed - as supplied by publisher]
Kardiol Pol. 2009 May;67(5):516-20. [May Lyme borreliosis lead to heart transplantation? - a case report.] [Article in Polish] Maroszynska-Dmoch E, Wozakowska-Kaplon B. I Oddzial Kardiologii, Swietokrzyskie Centrum Kardiologii, ul. Grunwaldzka 45,25-736 Kielce, tel.: +48 41 367 13 01, e-mail: email@example.com.
A case of a 65-year-old man, who used to work as a forester for many years, withend-stage dilated cardiomyopathy and subsequent heart transplantation isdescribed. Eight years later the diagnosis of Lyme borreliosis was established,which was the likely cause of cardiac disease in this patient. Publication Types:English Abstract PMID: 19521937 [PubMed - in process]
Possible role of glial cells in the onset and progression of Lyme neuroborreliosis
Geeta Ramesh , Juan T Borda , Amy Gill , Erin P Ribka , Lisa A Morici , Peter Mottram , Dale S Martin , Mary B Jacobs , Peter J Didier and Mario T Philipp
Journal of Neuroinflammation 2009, 6:23doi:10.1186/1742-2094-6-23
Published: 25 August 2009
Borreliabakteeri kykenee aiheuttamaan erilaisia neurologisia tulehduksia kuten aivokalvontulehduksen, neuropatian, radikuloneuropatian, enkefalomyeliitin jne. Yhtenä syynä näyttäisi olevan glia-solujen reaktio bakteeria kohtaan ja sitä seuraava tulehdus.
Lyme neuroborreliosis (LNB) may present as meningitis, cranial neuropathy, acute radiculoneuropathy or, rarely, as encephalomyelitis. We hypothesized that glia, upon exposure to Borrelia burgdorferi, the Lyme disease agent, produce inflammatory mediators that promote the acute cellular infiltration of early LNB. This inflammatory context could potentiate glial and neuronal apoptosis. Methods: We inoculated live B. burgdorferi into the cisterna magna of rhesus macaques and examined the inflammatory changes induced in the central nervous system (CNS), and dorsal root nerves and ganglia (DRG). Results: ELISA of the cerebrospinal fluid (CSF) showed elevated IL-6, IL-8, CCL2, and CXCL13 as early as one week post-inoculation, accompanied by primarily lymphocytic and monocytic pleocytosis. In contrast, onset of the acquired immune response, evidenced by anti-B. burgdorferi C6 serum antibodies, was first detectable after 3 weeks post-inoculation. CSF cell pellets and CNS tissues were culture-positive for B. burgdorferi. Histopathology revealed signs of acute LNB: severe multifocal leptomeningitis, radiculitis, and DRG inflammatory lesions. Immunofluorescence staining and confocal microscopy detected B. burgdorferi antigen in the CNS and DRG. IL-6 was observed in astrocytes and neurons in the spinal cord, and in neurons in the DRG of infected animals. CCL2 and CXCL13 were found in microglia as well as in endothelial cells, macrophages and T cells. Importantly, the DRG of infected animals showed significant satellite cell and neuronal apoptosis. Conclusions: Our results support the notion that innate responses of glia to B. burgdorferi initiate/mediate the inflammation seen in acute LNB, and show that neuronal apoptosis occurs in this context.
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.
soijuv kirjoitti:Tutkimuksen mukaan 75 %:lla borrelioosia sairastavista esiintyy epänormaali EEG-löydös. "Neurofeedback"-terapialla aivokäyrät saatiin useissa tapauksissa paranemaan. (Suom. huom. Olisi mielenkiintoista tietää kuinka monelle on tehty EEG tutkimus ja kuinka monelta on löytynyt poikkeavuuksia.)
Neurofeedback Training May Help Normalize Some Abnormal Brain Wave Patterns
October 12, 2006 1:47 p.m. EST
Linda Young - All Headline News Staff Writer
Salt Lake City, Utah (AHN) - A new study reveals that neurofeedback training may help normalize abnormal brain waves caused by some medical conditions.
The study was published in the latest edition of Biofeedback a journal published by the Association for Applied Psychophysiology and Biofeedback.
According to Newswise, individuals with Lyme disease, systematic lupus, erythematosus, migraines, irritable bowel syndrome, and cardiopulmonary bypass surgery patients typically have disturbed electroencephalography patterns.
Other conditions that may produce abnormal EEG patterns are fibromyalgia, chronic fatigue and exposure to toxic substances or large doses of radiation.
The study found that 75 percent of patients with Lyme disease had abnormal EEG patterns. After neurofeedback treatment that declined to 54 percent of those treated.
The report stated that these results could be used as baseline to help therapists treat patients with abnormal brain wave patterns.
The study focused on children with migraines. The study was done by D. Corydon Hammond, Ph.D., University of Utah School of Medicine.
Borrelian aiheuttama lymfosytooma pikku pojan scrotumin ihossa. Histopatologia oli tyypillinen, borreliavasta-aineet olivat voimakkaasti kohonneet. Antibioottihoidon jälkeen ihomuutos hävisi.
Kuva: http://www.terveyskirjasto.fi/terveyski ... i=ima00349
http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed
Crit Care Nurs Clin North Am. 2007 Mar;19(1):39-42.
Spirochete infections: lyme disease and southern tick-associated rash illness.
* Overstreet M.
Vanderbilt University, School of Nursing, 303 Godchaux Hall, 461 21st Avenue South, Nashville, TN 37241, USA.
This article describes the etiology, symptoms and stages, pathophysiology, diagnosis, treatment, and prevention of Lyme disease and a cluster of similar symptoms called "Southern tick-associated rash illness." It is important for the critical care nurse to be alert to the possibility of these infections because some of the symptoms can have devastating effects on the heart and meninges. In some cases Lyme disease may be a comorbidity, not the primary reason a patient is admitted to an ICU. The cause of the symptoms must be recognized for effective treatment to be initiated.
PMID: 17338948 [PubMed - in process]
J Dent Child (Chic). 2009 May-Aug;76(2):165-9. Limited opening secondary to Lyme disease in an 8-year-old child. Lee DH, Chu PK, King B, Rosenberg D. Little Smiles of Orange County, USA.
In the United States, Lyme disease is the most common vector-born disease. Itoften presents with a wide variety of symptoms that may delay its diagnosis andpresent challenging patient management issues. The purpose of this report was todiscuss the case of an 8-year, 6-month-old Hispanic male who presented to ahospital emergency room with restricted mandibular opening and was diagnosed with Lyme disease after an initial period of uncertainty regarding thediagnosis. http://eutils.ncbi.nlm.nih.gov/entrez/e ... rlinksPMID: 19619432 [PubMed - in process]
Tuesday, March 10, 2009
Rhesus monkeys with Lyme spirochetes in the brain
Lyme disease has been mentioned in the news a lot lately. First it was a pet chimp mauling his neighbor last month in a Connecticut town. Many news accounts of the assault reported that Travis the chimp suffered from Lyme disease and had been given tea laced with Xanax to calm his erratic behavior prior to the attack. Investigators may never figure out what provoked Travis to attack Charla Nash. Was Lyme disease a factor? Maybe (although if I had to guess, it had more to do with a wild animal being kept as a pet, living where it didn't belong).
This past weekend a human reportedly suffering from long-term Lyme disease gunned down a pastor and injured several parishioners in an Illinois church. As with any topic having to do with chronic Lyme disease, experts disagree on whether Lyme disease can trigger aggression (but I'm pretty sure what the shooter's defense attorney believes). One prominent researcher even questions whether the alleged shooter truly had Lyme disease.
A blogger on Forbes.com doubts whether chimps could be stricken with Lyme disease. In reality, seeing a chimp with Lyme disease should not surprise us at all since another nonhuman primate, the rhesus monkey, has been used for years to study neuroborreliosis, the form of Lyme disease caused by infection of the nervous system. Neuroborreliosis is observed in up to 15% of untreated Lyme disease patients. I will present two studies in which scientists examined infection of the central nervous system of rhesus monkeys by the Lyme disease spirochete, Borrelia burgdorferi.
In a 2000 study by Cadavid and colleagues, the investigators found small numbers of spirochetes in the meninges and spinal cord nerve roots of rhesus monkeys four months following laboratory infection with B. burgdorferi by needle inoculation into the skin (see figure below). In humans, the inflammatory response to the spirochetes in the meninges and nerve roots can cause meningitis (headache, stiff neck, and sensitivity to light) and radiculoneuritis (shooting pains and abnormal skin sensations), respectively.
Figure 2b from Cadavid et al., 2000. A single B. burgdorferi cell in the anterior nerve root stained by immunohistochemistry with anti-B. burgdorferi antibodies.
The investigators found no convincing evidence for the presence of B. burgdorferi in the brain parenchyma of the infected rhesus monkeys. B. burgdorferi was not found in the brain by microscopy. On the other hand, B. burgdorferi DNA was detected in brain tissue by polymerase chain reaction (PCR). This result may suggest that the spirochete is present in the brain at low levels, although the authors believed that spirochetes in the meninges surrounding the brain was the real source of the DNA. It's also possible that the N40 B. burgdorferi strain used by the authors was incapable of invading the brain of rhesus monkeys and that another strain if injected into the skin would have found its way to the brain.
Two conditions associated with neuroborreliosis disrupt brain function in humans. The first is Lyme encephalopathy, which can cause fatigue and problems with concentration and memory. Brain activity is clearly affected in patients with Lyme encephalopathy, yet the underlying pathogenic mechanism remains an enigma. Many patients with this potentially disabling condition do not exhibit the classic signs of central nervous system inflammation such as the presence of white blood cells in their cerebral spinal fluid (CSF), production of antibodies against the infective agent in the CSF, or abnormal brain MRIs. Some neuroborreliosis experts have proposed that these cases of Lyme encephalopathy are a result of "toxic-metabolic" effects of infection elsewhere in the body (such as Lyme arthritis in the joints) spilling into the brain. Nevertheless, a low-level infection of the brain by B. burgdorferi cannot be ruled out. More obvious brain involvement is observed in neuroborreliosis patients with encephalitis, in whom brain lesions are detected by MRI, accompanied by white blood cells and production of anti-B. burgdorferi antibodies in the CSF. Symptoms include slight weakness or paralysis affecting one side of the body, spastic muscles, inability to feel sensations, and bladder dysfunction. In rare cases, patients may experience strokes or seizures. Patients with encephalitis are likely to have spirochetes in their brain, usually near blood vessels.
Lyme disease may also be associated with psychiatric illness, particularly depression. Rare cases of panic attacks, bipolar disorder, mania, obsessive-compulsive disorder, dementia, and violent outbursts have also been reported. .
A recent study by Mario Philipp's group in Tulane, published recently in The American Journal of Pathology, described the potential effects of B. burgdorferi on brain cell activity of rhesus monkeys. Spirochetes injected into the skin with a needle or by tick bite are unable to make it into the brain of rhesus monkeys, as I explained above. Therefore, the investigators injected live B. burgdorferi spirochetes directly into the right side of the brains of rhesus monkeys. After two weeks, they found that an average of ~10% of oligodendrocytes at the injection sites had undergone death by apoptosis, as detected by fluorescent TUNEL staining (see figure below). In contrast, fewer than 2% of oligodendrocytes underwent apoptosis when sites in the left side of the brain of the same animals were injected with saline. Oligodendrocytes produce the myelin sheaths that surround the axons of neurons and promote transmission of electric impulses; one would expect the loss of oligodendrocytes to affect neuron function.
The in vivo results corroborated ex vivo experiments in which brain slices from rhesus monkeys were incubated with B. burgdorferi for up to eight hours. In the ex vivo experiments, apoptosis of both oligodendrocytes and neurons were detected by fluorescent TUNEL staining and with antibody against activated caspase 3, a more specific marker of apoptosis. The authors speculated that neurons undergoing apoptosis in vivo were removed by phagocytes and therefore went undetected in the brain injection experiment. The other major brain cell types, microglial cells and astrocytes, were spared from apoptotic death both ex vivo and in vivo.
Figure 4A from Ramesh et al., 2008. Oligodendrocytes are stained red with antibody to S-100. Nuclei of cells undergoing DNA fragmentation, a consequence of apoptosis, are TUNEL stained green. When the images are merged, the nuclei of oligodendrocytes undergoing apoptosis become yellow. B. burgdorferi, which are stained in blue, do not appear to be in physical contact with the oligodendrocytes.
Figure 4B from Ramesh et al., 2008. Percentage of oligodendrocytes undergoing apoptosis from 3 sites of spirochete (A-C) and saline (D-F) injections (click on image for larger view).
The Tulane group also detected myriad cytokines and chemokines such as IL-6, IL-1ß, and CXCL13 being produced in the B. burgdorferi-treated brain slices by immunofluorescence antibody staining and DNA microarray analysis. The authors concluded that B. burgdorferi invasion of the brain elicits production of a brew of inflammatory mediators that promote apoptotic death of oligodendrocytes and neurons. It may be true that brain invasion by B. burgdorferi in cases of human neuroborreliosis leads to production of these cytokines and chemokines, as IL-6, IL-1ß, and CXCL13 have been detected in the CSF of neuroborreliosis patients in earlier studies. However, the apoptotic cells observed by the Tulane group may be the unnatural consequence of small areas of the brain being exposed to extremely large numbers of spirochetes. Each site was injected with 5,000 spirochetes, a number far greater than the rare spirochetes observed by microscopy in the brains of neuroborreliosis patients. For the ex vivo experiments, a 2-mm section of brain was incubated with 20 million spirochetes, again a large burden of bacteria. More convincing would be finding apoptosis of oligodendrocytes and neurons in brain tissues in patients with Lyme encephalitis. Clearly more studies are needed to understand the events that really occur when B. burgdorferi invades the brain.
Ramesh, G., Borda, J., Dufour, J., Kaushal, D., Ramamoorthy, R., Lackner, A., & Philipp, M. (2008). Interaction of the Lyme Disease Spirochete Borrelia burgdorferi with Brain Parenchyma Elicits Inflammatory Mediators from Glial Cells as Well as Glial and Neuronal Apoptosis American Journal Of Pathology, 173 (5), 1415-1427 DOI: 10.2353/ajpath.2008.080483
Diego Cadavid, Tim O'Neill, Henry Schaefer, and Andrew R. Pachner (2000). Localization of Borrelia burgdorferi in the Nervous System and Other Organs in a Nonhuman Primate Model of Lyme Disease Laboratory Investigation, 80 (7), 1043-1054
Posted by Microbe Fan at 3/10/2009 11:57:00 PM
Labels: animal model, Borrelia, chronic Lyme disease, Lyme disease, neuroborreliosis
Perinnölliset geenivirheet altistavat munuaistaudeille ja silmänpohjan ikärappeumalle
?Borrelia-bakteerien hyväksikäyttämän faktori H:n geenissä esiintyvä vaihtelu altistaa silmänpohjan ikärappeumalle ja vaikealla munuaistaudille?, sanoi Helsingin yliopiston professori Seppo Meri Suomen Akatemian Tiedeaamiaisella keskiviikkona. Faktori H on erityisen tärkeä elimistön puolutusjärjestelmään kuuluvan komplementin suojaproteiini, joka estää hyökkäyksiä omia kudoksiammekin kohtaan. Sitä tuottavat monet ihmisen solut eri kudoksissa.
Silmänpohjan ikärappeuma (makuladegeneraatio) on hyvin yleinen tauti, johon ei ole olemassa kunnollista hoitoa. Henkilöillä, joilla on poikkevat geenit, tauti on noin 10 kertaa yleisempi kuin muilla. Tauti kehittyy tavallisimmin eläkeiässä ja haittaa muun muassa lukemista, autolla ajoa ja TV:n katselua. ?On mahdollista, joskaan ei vielä suoraan tutkittua, että sama geneettinen vaihtelu voi vaikuttaa alttiuteen saada Borrelia-infektio?, sanoo Meri.
Meren mukaan faktori H:ssa esiintyvät synnynnäiset mutaatiot aiheuttavat myös vaikean munuaistaudin, hemolyyttisureemisen syndrooman (HUS-tauti). Tässä taudissa komplementti tuhoaa potilaiden verisuonten seinämien soluja ja verisoluja aiheuttaen anemiaa ja munuaisten vaurioitumisen. Tautiin ei toistaiseksi ole muuta hoitoa kuin yhdistetty munuaisen ja maksan siirto, joka Suomessa on tehty onnistuneesti jo kolmelle potilaalle.
- professori, ylilääkäri Seppo Meri, p. (09) 191 26758, seppo.meri(at)helsinki.fi
Suomen Akatemian viestintä
tiedottaja Outi Jalonen
p. (09) 7748 8327, 040 359 2936
outi.jalonen (at) aka.fi
Suicidal Thoughts and Rage: What are Causing Your Symptoms of Side Effects
September 4, 2009
Suicidal thoughts and Rage are often symptoms of conditions like clinical depression, and bipolar disorder. Since everyone handles depression differently, the symptoms of this disease manifest in different ways. Extreme anger is a common ? but often ignored ? symptom of depression, especially in men.
Rage and suicidal thoughts can also be related to diseases like Lyme disease, or could be side effects associated with certain medications, such as Chantix and Welbutrin. Below is a list of diseases and conditions associated with symptoms like Suicidal Thoughts and Rage, as well as a list of medications related to similar side effects.
We are not medical professionals, and these are not comprehensive lists. Please contact your doctor if you are experiencing any of the following symptoms or side effects, or similar health issues.
Suicidal Thoughts and Rage are Symptoms of
Depression: Clinical depression, or major depressive disorder, can easily lead to suicidal thoughts and for some can cause rage. The symptoms of depression can be misleading to doctors and patients alike because so many things can be at the root of the problem including nutritional imbalance, hormonal imbalance, environmental toxins, and side effects from medications.
Bipolar Disorder: Bipolar disorder, also called manic-depression, is a form of depression with a very high suicide rate. It is characterized by extreme mood swings which include rage. Rage is an aspect of bipolar disorder that is often overlooked and many people are not aware that it is something to expect with the condition.
Traumatic Brain Injury: Traumatic brain injury (TBI) effects each victim differently. When there is no loss of consciousness and/or no blow to the head, it often goes undetected or undiagnosed. Mood swing, depression, suicidal thoughts, and episodes of extreme rage are common after TBI and the symptoms can be life-long. To complicate matters further TBI can cause epilepsy. When we think of seizures, we typically think of convulsions, but a seizure is really electrical misfiring in the brain and does not always cause convulsions. Seizures can be mistaken for outbursts of rage.
Lyme Disease: Lyme disease is carried by some ticks and can be transmitted to humans by a tick bite. It is an inflammatory disease that can affect different areas of the body and has widely varying symptoms. Rage is such a common complication of Lyme disease that it is simply referred to as ?Lyme rage.? Suicidal thoughts are not uncommon in people with Lyme disease and can be a result of the disease in action or due to excruciating symptoms from which there is no relief.
Suicidal Thoughts and Rage Are Side Effects Associated With
Chantix: Chantix is a smoking cessation drug. Instead of delivering nicotine, as many smoking cessation aids do, it attaches to the receptors in the brain that nicotine normally attaches to, blocking the nicotine out.
Zyban and Wellbutrin: Bupropion, sold as Zyban and Wellbutrin, is used as a smoking cessation aid and an antidepressant. It is a norepinephrine and dopamine reuptake inhibitor and, like Chantix, blocks the reception of nicotine.
Zoloft: Zoloft is an antidepressant also sold under the brand name Lustral and generically as sertraline hydrochloride. It is a selective serotonin reuptake inhibitor (SSRI).
Neurontin: Neurontin is used to treat nerve pain in people with herpes or shingles and to treat epilepsy. It affects the chemical and nerves in the body, but exactly how it works is not yet known.
Cymbalta: Cymbalta is used to treat depression, anxiety, fibromyalgia, and pain caused by diabetic neuropathy. It was tested as a treatment for stress urinary incontinence, but failed due to suicides and liver toxicity.
Schweiz Arch Tierheilkd. 2009 Oct;151(10):479-83. [The dilemma with Lyme borreliosis in the dog with particular consideration of"Lyme nephritis"] [Article in German] Gerber B, Eichenberger S, Haug K, Wittenbrink M. Klinik fur Kleintiermedizin der Universitat Zurich.
Lyme borreliosis is the most commonly reported tick-transmitted infectiousdisease in the northern hemisphere in humans. Certain diseases are associatedwith Lyme borreliosis in the dog as well, but only intermittent lameness witharticular swelling, lymphadenomegaly, fever, and anorexia were experimentallydocumented. Lyme borreliosis is considered an over diagnosed disease. The term"Lyme nephritis" was introduced for dogs with characteristic renal lesions andtypical clinical signs, in which antibodies against Borrelia burgdorferi werefound. Different studies have been aimed at showing a relation between renaldisease and B. burgdorferi infection; however, this was not possible until now.Reasons for the uncertainty of the effects of B. burgdorferi in the dog are thehigh prevalence of circulating antibodies, the unspecific clinical picture andthe inaccuracy of serologic tests. Publication
http://eutils.ncbi.nlm.nih.gov/entrez/e ... rlinksPMID: 19780008 [PubMed - in process]
J Laryngol Otol. 2009 Sep 10;:1-3 [Epub ahead of print] Recurrent laryngeal nerve paralysis due to subclinical Lyme borreliosis. Karosi T, Racz T, Szekanecz E, Toth A, Sziklai I. Department of Otolaryngology Head and Neck Surgery, University Medical School of Debrecen, Debrecen, Hungary.
Objective:We report an extremely rare case of recurrent laryngeal nerveparalysis due to subclinical Lyme borreliosis. Method:Case report presenting a 15-year-old girl referred with hoarseness and soft voice. Results:Right-sidedrecurrent laryngeal nerve paralysis was observed using videolaryngoscopy.Imaging was used to exclude intracranial, cervical and intrathoracicembryological lesions, vascular malformations and tumours. Laboratory andelectrophysiological investigations were used to exclude inflammatory andparaneoplastic processes, endocrinopathy and metabolic disorders. Serologicaltesting was positive for Lyme disease. Parenteral ceftriaxone therapy wascommenced. The patient's nerve paralysis showed complete recovery on the seventh day of antibiotic treatment; this was confirmed byvideolaryngoscopy.
Conclusion:Recurrent laryngeal nerve paralysis is an extremelyrare complication of neuroborreliosis associated with Lyme disease. In patientswith recurrent laryngeal nerve paralysis in whom the clinical history isuncertain and the usual diagnostic methods give negative results, screening with anti-borrelia immunoglobulin M is suggested.
http://eutils.ncbi.nlm.nih.gov/entrez/e ... rlinksPMID: 19740453 [PubMed - as supplied by publisher]
Autoimmunity. 2009 Aug;42(5):432-8.
The infectious etiology of vasculitis.
Lidar M, Lipschitz N, Langevitz P, Shoenfeld Y. Center for Autoimmune Diseases, Rheumatology Unit, Sheba Medical Center (SMC),Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv,Israel.
Infectious agents have been implicated in the etiopathogenesis of variousvasculitides via numerous and overlapping mechanisms including direct microbialinvasion of endothelial cells, immune complex mediated vessel wall damage andstimulation of autoreactive B and/or T cells through molecular mimicry andsuperantigens. While the causative role of hepatitis B virus in polyarteritisnodosa and hepatitis C virus in mixed cryoglobulinemia is clearly established,evidence for the association of other infectious agents with vasculitis,including human immunodeficiency virus, parvovirus B19, cytomegalovirus,varicella zoster virus, Staphylococcus aureus, rickettsiaceae, Treponemapallidum and Borrelia burgdorferi, among numerous others, is accumulating. Thespectrum of association of infectious agents; bacteria, viruses and parasites,with systemic vasculitides, will be reviewed herewith. http://eutils.ncbi.nlm.nih.gov/entrez/e ... rlinksPMID: 19811260 [PubMed - in process]
2. Silmien värinä ensimmäinen oire borrelioosista. (Tanska)
3. Halvauksellinen karsastus borrelioosia sairastavien silmissä.
4. Punkit välittävät ihmiseen useita bakteereja ja viruksia. Näillä kaikilla saattaa olla haitallinen vaikutus ihmisen aivotoimintaan. Henkilöillä saattaa esiintyä huomattavia persoonallisuuden häiriöitä ilman että he ovat tietoisia niiden aiheuttajasta. Useiden oireiden ilmetessä sairastuneet saattavat itsekin epäillä olevansa "luulotautisia" tai "turhasta valittajia".
Huolellinen tutkimus on kuitenkin usein osoittanut oireiden johtuvan neuroborrelioosista. Kroonisen borrelioosin ensimmäiset oireet ovat usein psyykkisiä esim. ärtyneisyys, ahdistus, masennus jne. Oireet hävisivät useimmiten riittävän pitkän antibioottihoidon aikana.
1. Clin Infect Dis. 2009 Feb 1; [Epub ahead of print] Five Cases of Paralytic Strabismus as a Rare Feature of Lyme Disease. Sauer A, Hansmann Y, Jaulhac B, Bourcier T, Speeg-Schatz C. Departments of 1Ophthalmology, 2Infectious Disease, Pole Specialty MedecineOphthalmology Hygiene, and 3Bacteriology, Hopitaux Universitaires de Strasbourg,Strasbourg, France. Lyme borreliosis is the most common human tick-borne disease in the NorthernHemisphere. The prevalence of Lyme borreliosis is estimated to be 20-100 casesper 100,000 persons in the United States and 100-155 cases per 100,000 personsin Europe [ 1 , 2 ]. It is caused by the spirochete Borrelia burgdorferi sensulato [ 2 , 3 ]. The course of clinical manifestations is thought to occur in 3stages: early, disseminated, and chronic [ 2 , 4 ]. Lyme borreliosis can cause avariety of ocular manifestations, and the frequency of these manifestationsamong cases of Lyme disease involving systemic manifestations is approximately1% [ 5 ]. PMID: 19193112 [PubMed - as supplied by publisher]
2. Neurology. 2009 Jan 20;72(3):291. Ocular flutter as the first manifestation of Lyme disease. Gyllenborg J, Milea D. Department of Neurology, Glostrup Hospital, University of Copenhagen, 57, NordreRingvej, DK-2600 Glostrup, Denmark. firstname.lastname@example.org Publication Types:Case Reports PMID: 19153379 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/quer ... &DB=pubmed
Klin Oczna. 2006;108(4-6):220-4.
3. Tick inoculation in an eyelid region: report on five cases with one complication of the orbital myositis associated with Lyme borreliosis.
* Holak H,
* Holak N,
* Huzarska M,
* Holak S.
Kliniki Okulistycznej w Centrum Medycznym im R. Virchowa w Salzgitter. email@example.com
PURPOSE: To determine the frequency and dependence of Lyme borreliosis after tick infestation in the eyelid region.
MATERIAL AND METHODS: Five patients after tick inoculation were investigated by immunofluorescence assays for IgM and IgG system). Ophthalmologic evaluation of myositis was supported with MRI, laboratory, and internal clinical investigations. RESULTS: Four children showed negative Borrelia serology after a bite from a tick. In one case the left abducens nerve palsy was found, which was diagnosed in MRI as a thickened left lateral rectus muscle. The diagnosis of myositis with positive Borrelia burgdorferi serology was consistent with Lyme borreliosis. Other laboratory examinations were negative. The symptoms were reduced after treatment with ceftriaxon. CONCLUSIONS: Lyme borreliosis was found in one in five patients after tick infestation in the eyelid region. Antibiotic prophylaxis against Lyme borreliosis with ampicillin is recommended for children after a tick bite.
PMID: 17020000 [PubMed - in process]
4. First Symptoms Of Chronic Lyme Disease Often Are Psychiatric In Nature
By Virginia T. Sherr, MD
Poster presented at the Lyme Disease Foundation's
14th International Scientific Conference on Lyme Disease, 2001
http://www.thehumansideoflyme.net/viewa ... php?aid=36
Objectives: Five patients who sought help for major personality changes and who later reported physical symptoms were selected from an adult psychiatry private practice near Philadelphia in PA, USA, evaluated via Western Blot antibody tests and, in two cases, PCR blood tests for possible borrelia DNA. No patient was previously suspected of having Lyme disease but while in psychotherapy each described symptoms compatible with chronic LD. All had recent onset of cognitive deficits, and new episodic irritability. Neither joint swelling nor other "typical" Lyme symptoms were prominent at the time of initial work up for Lyme disease (LD) and other tick-borne diseases (TBDs). Patients were tested to ascertain if TBDs could be causing or complicating their mental/emotional symptoms and, if so, would antibiotic treatment help. No patient was aware of having had a tick bite or bull's eye rash.
Rationale: Ticks infect humans with viruses, smaller parasites grid bacteria, some or all of which eventually may exert noxious influences on the victim's neural/cognitive systems. Patients may have resultant personality changes but no awareness of causative underlying infections. When multi-system symptoms appear and if the nature of their illness is unrecognized, patients may describe themselves to psychiatrists as "hypochondriacs" or "complainers". Careful testing of such patients in endemic areas often reveals clear evidence of neuro-Lyme disease (spirochetal neuroborreliosis).
Method: Five outpatients, who originally considered themselves well physically but who had manifested notable personality changes, eventually began to describe symptoms of chronic Lyme disease. Four tested positive by the Center for Disease Control Western Blot IgG antibody criteria of 5 or more positive bands and 1 tested positive by IGeneX Ref. Lab WB criteria. The latter patient's test had 4 CDC positive IgG LD bands plus a positive band #34. The two PCR-tested cases were positive for the DNA of the causative spirochete.
Results: When these neuro-Lyme patients were treated with appropriate antimicrobial medications for extended periods of time, most physical symptoms were reversed completely in every case. One patient was restored psychologically without the use of any psychotropic medication; the others retained lesser, residual emotional/mental symptoms, requiring intermittent or regular use of psychotropic drugs. Major cognitive symptoms slowly resolved with antibiotics. Modafinil or methylphenidate helped by relieving mental fog/excessive sleepiness; zolpidem or mirtazapine ended the insomnia.
Conclusions: Greater understanding of the diverse effects of disseminated spirochetal disease should prove helpful to physicians in their evaluation of anxious, irritable, depressed patients whose brain function and cognitive abilities may be distorted by microbes. Achieving such diagnostic skills allows psychiatrists to test, then to arrange for and support appropriate medical referrals for on-going antimicrobial treatment of these widely epidemic, personality-altering, tick-borne infections. Sophisticated history taking and lab testing are recommended. It is important to note that some patients with or without PCR positive tick-borne diseases will test sero-negative on early examinations but usually will convert to positive WB testing as antimicrobial treatment progresses over time and they are able to make appropriate antibodies.
Borrelia burgdorferi, a great chameleon: know it to recognize it!
Iolanda Santino ? Paola Comite ? Giuseppe Maria Gandolfo
Received: 11 December 2008 / Accepted: 13 October 2009
Borrelia burgdorferi is a spirochaete that can penetrate the blood?brain barrier in early infection and can cause endothelial damage other than central nervous system lesions. We describe a clinical case of neuroborreliosis that occurred in the absence of classical erythema migrans or arthralgia. Magnetic resonance imaging findings compatible with simil-vasculitis and demyelinating lesions associated with the presence of anti-B. burgdorferi antibodies in the plasma or cerebrospinal liquid is an indication for antimicrobial treatment against B. burgdorferi. An early diagnosis and a prompt establishment of an adequate antibiotic treatment is needed for a successful recovery.
Keywords Neuroborreliosis Multiple sclerosis Vasculitis Borrelia burgdorferi
Lyme borreliosis (LB) is a well recognized multisystem disorder caused by spirochaetes belonging to the genospecies complex Borrelia burgdorferi sensu lato. Borrelia is transmitted to humans by the bite of infected ticks belonging to the genus Ixodes spp. .
The infection begins as a cutaneous lesion followed, weeks or months later, by arthritic, cardiac or neurological manifestations . Neurologic disorders may occur in early disseminated or late chronic Lyme borreliosis. In particular, persisting borreliosis often affects the central nervous system with demyelinating lesions which may be misdiagnosed as multiple sclerosis (MS).
In addition, Lyme disease can cause a variety of neuro-ophthalmologic manifestations [2, 3].
LB is the most common tick-borne infection in Europe and it is also present in Italy where it is endemic in some regions of the northern part of the country, although is known to occur also in other Italian regions. In Latium, clinical cases of Lyme disease in humans have been reported and Borrelia species have been identified in ticks [4?8].
In this report, we describe a clinical case of neuroborreliosis that occurred in the absence of classical erythema migrans or arthralgia. The diagnosis of Borrelia infections was achieved through a meticulous evaluation of the clinical, radiological and laboratory data.
The patient was a 33-year-old male living in the centre of Italy. He presented a central scotoma in right eye in May. On ophthalmologic examination, visual acuity was decreased to 4/10 in the right eye and 10/10 in the left. No fundus? alteration was observed, except a light papilloedema. The neurological examination showed no alteration. Neither extra signs nor symptoms were found. The motor and somatosensory evoked potentials were normal. The visual evoked potentials were lightly decreased.
I. Santino (&)
Department of Public Health Sciences, Sapienza University of Rome, P.le Aldo Moro, 5, 00185 Rome, Italy
P. Comite G. M. Gandolfo
Department of Experimental Medicine and Pathology, Sapienza University of Rome, P.le Aldo Moro, 5, 00185 Rome, Italy 123
Blood count, serum inflammatory markers, thyroid profile, autoimmunity screening (ANA, ENA, anti-DNA, C3, C4, circulating immunocomplexes), thrombophilia screening (antithrombin, protein C and protein S, factor V Leiden, homocysteine, lupus anticoagulant, anti-cardiolipin, anti-beta2 glycoprotein) were within normal limits. IgG and IgM anti-B. burgdorferi antibodies were found in blood. The differential diagnosis included TPHA test for Treponema pallidum, Parvovirus B, EBV, CMV, HIV, hepatitis viruses were negative. No fever was present.
In addition, examination of the cerebrospinal fluid (CSF) showed the presence of white blood cells with lymphocytic predominance without any malignant cells. CSF glucose levels were normal, CSF total proteins were increased and no oligoclonal IgGs were observed.
Eventual presence of demyelinating lesions or neoplasms affecting the nervous system was investigated by magnetic resonance imaging (MRI) scan of the brain and cervical spine with and without contrast.
Bilateral multifocal cerebral lesions, apparently consistent with a possible simil-vasculitic involvement of cerebral parenchyma were observed in the brain. Moreover, an area of altered signal intensity was described in supraventricular area. Altered signal intensity was observed in T2-weighted sequence at C3?C5. No enhancement of the cerebral and spinal lesions occurred upon injection of mean of contrast.
An electrocardiogram (ECG) was performed and it was normal. The patient did not have a prior history of infection or vaccination, neither any evidence of typical signs and symptoms of acute disseminated encephalomyelitis . None of the diagnostic criteria of fibromyalgia was present . There was also no history, symptoms or imaging findings to suggest a granulomatous-type process like neurosarcoidosis.
The initial diagnosis was then monolateral optic neuritis with demyelinating lesions.
Upon corticosteroid therapy (5 days intravenous methylprednisolone, 1 g/daily) neuritis symptoms disappeared with recovery of the visual acuity on the right eye (10/10 in the right eye and 10/10 in the left).
We decided to make another serum sample to assess the further evaluation of antibodies titre to B. burgdorferi and for the detection of Borrelia antigens by Western Blot. At this stage, the presence of IgG and IgM antibodies to B. burgdorferi was investigated using a commercially available immunoenzymatic assay (ELISA) (recomWell IgM/IgG, Mikrogen, Neuried, Germany) and Western blot (ViraBlot IgM/IgG, Viramed Biotech AG) tests according to the manufacturer?s instructions. ELISA tests were considered negative, positive or borderline when values were lower than 20, higher than 24 or between 20 and 24 U/ml, respectively as suggested by the manufacturer. Western Blot IgM test was considered positive for the presence of 2/ 3 significant bands: 24 kDa (OspC), 39 kDa (BmpA), and 41 kDa (Fla). Western Blot IgG test was considered positive for the presence of 5/10 significant bands: 18, 21 kDa (OspC), 28, 30, 39 kDa (BmpA), 41 kDa (Fla), 45, 58 kDa (not GroEL), 66, and 93 kDa.
Elisa test showed evidence of specific IgM and IgG antibodies to B. burgdorferi. Western blot analysis showed four bands (60, 58, 41, 24 kDa) for IgM and six (60, 58, 41, 30, 24, 18 kDa) for IgG.
Finally, the serum of the patient was further analysed with the technique of polymerase chain reaction (PCR) developed in our laboratory  that has confirmed the positivity to B. burgdorferi s.l.
Based on clinical picture and microbiological data, an active Borrelia infection with involvement of the nervous system, i.e. neuroborreliosis, was identified. This patient fulfilled the European clinical case definitions for Lyme borreliosis .
Accordingly an antibiotic therapy was started with i.v. ceftriaxone for 3 weeks. Two months after treatment, another sample of serum showed a decrease of IgM and IgG by Elisa (a reduction from 72 to 14 ng/ml). Eight months after the initial treatment there was no evidence of IgM and a mild improvement of IgG. MRI with and without contrast were performed to monitor the potential evolution of demyelinating lesions at 3, 6, 12, 24, 36 months. No evidence of progression was found.
In the subsequent 3 years the patient has been well, he regularly underwent clinical and instrumental checkup and there were no recurrence of visual or other symptoms.
Lyme disease is known to cause intermittent neurologic events, include Bell?s palsy , nonspecific symptoms of numbness, fatigue, amnesia, headache, stroke-like syndromes, central nervous system vasculitis , encephalitis, myelitis, neuritis , nervous tumour-like lesions .
Most importantly, in this case report, demyelinating disease which mimics multiple sclerosis can also occur .
Essentially, Lyme disease is characterized from a phenotypic variability depending on stage. The prevalence has a seasonal incidence and disease manifestations are influenced by genetic diversity and differential distribution of spirochaete species. Arthritis appears to be more frequent in America, while encephalomyelitis occurs more often in Europe . Furthermore, encephalomyelitis or myelitis is a relatively common complication in adults, rarely seen in children, while facial palsy is the most common paediatric neurological manifestation .
Because of limitations of laboratory tests the diagnosis is essentially clinical and one must be mindful that the laboratory testing is recommended if there is a clear evidence of the characteristic symptoms and signs of this disease. Nevertheless, the laboratory data and a correct interpretation of them are supportive to the clinical diagnosis.
The characteristic erythema migrans rash, the host reaction to the bite and the hallmark of the disease, is not often present .
Several studies have revealed than less than 50% of the patients recalled a tick bite [20, 21].
In addition, in some cases, especially those with involvement of central nervous system, signs and symptoms overlapping with several pathological conditions can occur and an accurate differential diagnosis must be done.
Although already shown as an emerging problem, Borrelia infection is often misdiagnosed: only one out of ten cases of Lyme disease is reported to the Control Disease Center (CDC).
In our case, according to criteria of International Lyme and Associated Diseases Society, we have searched for Lyme disease in a patient living in a area where the Borrelia is present [4?6], with systemic signs and symptoms compatible with Borrelia infection and that, subsequently, has shown the seropositivity, the seroconversion on paired sera, the antigen and DNA recovery, and finally the response to prescribed treatment. They are sufficient data to consider the diagnosis compatible with a ??borreliosis?? .
In the case we report hereby, the laboratory analysis has a crucial role in confirming the diagnosis of Lyme disease. In fact, in primary and in secondary stage, especially in the case of neuroborreliosis, the antibody profile of the patient is often unclear and hard to distinguish from the profile of a healthy subject previously exposed to Borrelia. Additionally, the laboratory test might be untruthfully negative (the so-called ??seronegative Lyme disease??), as it might the case for those clinical reports of patients with equivocal serology tests and neurological symptoms and MRI findings consistent with MS, treated successfully with antibiotic therapy .
However, in our case the strong positivity of IgM and IgG in the serum associated to other reported clinical and instrumental data of the patient suggested the final diagnosis.
Spinal taps are not routinely recommended, as a negative tap does not rule out Lyme. Especially, not all patients with neuroborreliosis have CSF abnormalities. Most patients with neuroborreliosis have specific antibodies in serum and testing for CSF antibodies is usually not necessary . Specific antibodies in the CSF are present in 40?85% of cases. Furthermore, in neuroborreliosis the oligoclonal bands may be present, but they are not typically expressed [24, 25].
Although the mechanism underlying the involvement of nervous system in Lyme disease remains unclear, it is speculated that it may be a direct or an indirect action of the spirochaete on neural cell, which may explain development of vasculitis associated with opthalmo-neuropathy .
Most likely B. burgdorferi can act as a trigger for T-cell mediated autoimmune reactions within the CNS, exhibiting a molecular mimicry with human nervous tissue, especially for myelinated fibres of human peripheral nerve, on nerve cells and axons of the central nervous system, as well as on certain epithelial cells, joint synovial and heart muscle cells .
In conclusion, our report confirms that in daily clinical neurological practice Borrelia microbiological investigation is a crucial step for identification of neuroborreliosis and for optimal therapy. The successful follow-up after 3 years demonstrates the importance of systematic investigation of these bacteria in several neurological conditions to promptly establish an adequate antibiotic treatment. In particular it is recommended to investigate possible exposure to Lyme disease even when classical symptoms could be missing.
1. Steere A (2001) Lyme disease. N Engl J Med 345:115
2. Mikkila¨ EO, Seppa¨la¨ IJT, Viljanen MK, Peltomaa MP, Karma A (2000) The expanding clinical spectrum of ocular Lyme borreliosis. Ophthalmology 107:581?587
3. Stricker RB, Lautin A (2003) Lyme disease and optic neuritis: long-term follow-up of seropositive patients. Neurology 61:1162
4. Santino I, Sessa R, Di Pietro M, del Piano M (2000) Lyme borreliosis in Central Italy. Microbiologica 23:261?269
5. Santino I, Grillo R, Nicoletti M, Santapaola D, Speziale D, Sessa R, Fadda G, del Piano M (2002) Prevalence of IgG antibodies against Borrelia burgdorferi s.l. and Ehrlichia phagocytophila in sera of patients presenting symptoms of Lyme disease in a central region of Italy. Int J Immunopathol Pharmacol 15(3):239?242
6. Santino I, del Piano M, Sessa R, Favia G, Iori A (2002) Detection of four Borrelia burgdorferi genospecies and first report of human granulocytic ehrlichiosis agent in Ixodes ricinus ticks collected in central Italy. Epidemiol Infect 129:93?97
7. Santino I, Cammarata E, Franco S, Galdiero F, Oliva B, Sessa R, Cipriani P, Tempera G, del Piano M (2004) Multicentric study of seroprevalence of Borrelia burgdorferi and Anaplasma phagocytophila in high-risk groups in regions of central and southern Italy. Int J Immunopathol Pharmacol 17:219?224
8. Santino I, Berlutti F, Pantanella F, Sessa R, del Piano M (2008) Detection of Borrelia burgdorferi sensu lato DNA by polymerase chain reaction in serum of patients with clinical symptoms of Lyme borreliosis. FEMS Microbiol Lett 283:30?35
9. Young NP, Weinshenker BG, Lucchinetti CF (2008) Acute disseminated encephalomyelitis: current understanding and controversies. Semin Neurol 28:84?94
10. Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, Tugwell P, Campbell SM, Abeles M, Clark P et al (1990) The American College of Rheumatology 1990 criteria for the classification of fibromyalgia. Report of the Multicenter Criteria Committe. Arthritis Rheum 33(2):160?172
11. Stanek G, O?Connel S, Cimmino M, Aberer E, Kristoferitsch W, Granstro¨m M et al (1996) European Union concerted action on risk assessment in Lyme borreliosis: clinical case definitions for Lyme borreliosis. Wien Klein Wochenschr 108:741?747
12. Arias G, Nogue´s J, Man?o´s M, Amilibia E, Dicenta M (1998) Bilateral facial nerve palsy: four case reports. J Otorhinolaryngol Relat Spec 60:227?229
13. Schmitt AB, Ku¨ker W, Nacimiento W (1999) Neuroborreliosis with extensive cerebral vasculitis and multiple cerebral infarcts. Nervenarzt 70:167?171
14. Todorovic L, Ibisevic M, Alajbegovic A, Suljic-Mehmedika E, Jurisic V (2008) Bilateral retrobulbar optic neuritis as first signs of Lyme disease. Med Arh 62:117?118
15. Latsch K, Tappe D, Warmuth-Metz M, Hebestreit H (2006) Central nervous system borreliosis mimicking a pontine tumour. J Med Microbiol 55:1597?1599
16. Agosta F, Rocca MA, Benedetti B, Capra R, Cordioli C, Filippi M (2006) MR imaging assessment of brain and cervical cord damage in patients with neuroborreliosis. Am J Neuroradiol 27:892?894
17. Aguero-Rosenfeld ME, Wang G, Schwartz I, Wormser GP (2005) Diagnosis of lyme borreliosis. Clin Microbiol Rev 18:484?509
18. Rothermel H, Thomas R, Hedges III, Steere AC (2001) Optic Neuropathy in Children with Lyme disease. Pediatrics 108:477?481
19. van Dam AP, Kuiper H, Vos K, Widjojokusumo A, de Jongh BM, Spanjaard L, Ramselaar AC, Kramer MD, Dankert J (1993) Different genospecies of Borrelia burgdorferi are associated with distinct clinical manifestations of Lyme borreliosis. Clin Infect Dis 17:708?717
20. Lovett JK, Evans PH, O?Connell S, Gutowski NJ (2008) Neuroborreliosis in the South West of England. Epidemiol Infect 136:1707?1711
21. Pachner AR, Steiner I (2007) Lyme neuroborreliosis: infection, immunity and inflammation. Lancet Neurol 6:544?552
22. Burrascano JJ (2005) Guidelines for the management of Lyme disease. International Lyme and Associated Disease Society
23. Vianello M, Marchiori G, Giometto B (2008) Multiple cranial nerve involvement in Bannwarth?s syndrome. Neurol Sci 29:109?112
24. Scheld WM, Whitley RJ, Marra CM (eds) (2004) Infections of the central nervous system, 3rd edn. Lippincott Williams and Wilkins, Philadelphia
25. Halperin JJ, Shapiro ED, Logigian E, Belman AL, Dotevall L, Wormser GP, Krupp L, Gronseth G, Bever CT Jr (2007) Practice parameter: treatment of nervous system Lyme disease (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 69(1):91?102
26. Kursawe H (2002) Diagnosis and therapy of neuroborreliosis. On the hunt for the ??great imitator??. MMW Fortschr Med 144(22):33?36
27. Aberer E, Brunner C, Suchanek G, Klade H, Barbour A, Stanek G, Lassmann H (1989) Molecular mimicry and Lyme borreliosis: a shared antigenic determinant between Borrelia burgdorferi and human tissue. Ann Neurol 26:732?737
Neurobiol Dis. 2009 Nov 25; [Epub ahead of print]
Inflammation and Central Nervous System Lyme Disease.
Fallon BA, Levin ES, Schweitzer PJ, Hardesty D.
Department of Psychiatry, Columbia University; New York State Psychiatric Institute, Columbia University.
Lyme disease, caused by the bacterium Borrelia burgdorferi, can cause multi-systemic signs and symptoms, including peripheral and central nervous system disease. This review examines the evidence for and mechanisms of inflammation in neurologic Lyme disease, with a specific focus on the central nervous system, drawing upon human studies and controlled research with experimentally infected rhesus monkeys. Directions for future human research are suggested that may help to clarify the role of inflammation as a mediator of the chronic persistent symptoms experienced by some patients despite antibiotic treatment for neurologic Lyme disease.
http://eutils.ncbi.nlm.nih.gov/entrez/e ... md=prlinks
PMID: 19944760 [PubMed - as supplied by publisher]
Inflammation and Central Nervous System Lyme Disease
Brian A. Fallon, Elizabeth S. Levin, Pernilla J. Schweitzer and David
Neurobiology of Disease, Article in press, accepted manuscript,
available online 26 November 2009.
Lyme disease, caused by the bacterium Borrelia burgdorferi, can cause
multi-systemic signs and symptoms, including peripheral and central
nervous system disease. This review examines the evidence for and
mechanisms of inflammation in neurologic Lyme disease, with a specific
focus on the central nervous system, drawing upon human studies and
controlled research with experimentally infected rhesus monkeys.
Directions for future human research are suggested that may help to
clarify the role of inflammation as a mediator of the chronic persistent
symptoms experienced by some patients despite antibiotic treatment for
neurologic Lyme disease
J Laryngol Otol.:1-3. [Epub ahead of print]
A non-traumatic, blue-purple auricle: case report.
Sewnaik A, Kamarashev J, Peters NS, van Rijswijk JB.
Department of Otorhinolaryngology, Head and Neck Surgery, Erasmus
Medical Center Rotterdam, The Netherlands.
Objective:We report a typical case of earlobe lymphocytoma.
Method:A case report and literature review are presented.
Results:A 10-year-old girl presented with a blue-coloured earlobe. A
diagnosis of Lyme disease was confirmed by serological tests. Lyme
borreliosis is the most common tick-borne disease in the northern
hemisphere. It is caused by the spirochete Borrelia burgdorferi sensu
lato. The patient was successfully treated with antibiotics.
Conclusion:The diagnostic process and ENT symptomatology of Lyme disease
and borrelial lymphocytoma are summarised and discussed.
PMID: 20003592 [PubMed - as supplied by publisher]
Hypercoagulation, or thrombophilia, may be defined as reduced capillary blood flow or a greater tendency than normal for blood to coagulate, or clot. Of approximately 900 borreliosis patients that I have tested, 90 percent have hypercoagulation. Comparatively, only five percent of the general healthy population has hypercoagulation.
Two major aspects of hypercoagulation are infections and hereditary or genetic abnormalities. Chronic infections such as borreliosis, Epstein-Barr virus, cytomegalovirus, human herpes virus 6 and mycoplasma have all been associated with hypercoagulation. These infections appear to be the driving force behind the greater tendency to form blood clots. Infections may elevate levels of fibrinogen, fibrin, thrombin/antithrombin complexes, fragment 1+2, and Factor II (prothrombin) activity which may decrease capillary blood flow..
When you get a cut, the fibrinogen in your blood converts into fibrin, which in turn forms a mesh to create a blood clot to help stop the bleeding. Antithrombin binds to thrombin to form a complex to prevent thrombin from causing blood to clot. Antithrombin protects against too much clotting, when it binds thrombin.
When thrombin is forming a clot it produces fragment 1+2. Prothrombin (Factor II) converts into thrombin, which causes blood to clot. When these coagulation components are high, it indicates that the blood has a greater tendency to clot., and may inhibit blood circulation in capillaries.
Inherited or genetic disorders may also predispose to blood clotting. Some of these hereditary defects include antithrombin activity deficiency, protein C activity deficiency, protein S activity deficiency, Factor II gene mutation, APC resistance (Activated Protein C resistance is also called Factor V Leiden deficiency), elevated lipoprotein(a) or Lp(a), elevated PAI-1 (Plasminogen Activator Inhibiter-1), and elevated homocysteine. Hereditary hypercoagulation test panels are abnormal in 66 percent of borreliosis patients, as opposed to about 25 percent of the general healthy population.
Treatment for hypercoagulation caused by infections is heparin, which is a blood thinner. Typically, heparin is given subcutaneously (under the skin) by injection twice a day in low doses for not more than nine months. It can also be compounded into a troche that dissolves in the mouth, but that is usually more expensive and is often less effective than injections.
Symptoms that improve with heparin are pain, fatigue, cognitive problems and neurological problems. About 80 percent of borreliosis patients feel better with heparin, and it has been a safe treatment so far. One patient did develop bleeding from the rectum, but then a colonoscopy revealed a colon cancer that had not yet spread to the local lymph nodes. In other words, the heparin unmasked a hidden malignancy, so in this case the side effect was a blessing.
Heparin is not only a blood thinner, it is also anti-inflammatory, antiviral, antibacterial, and may even be anti-cancer (unproven). Therapy with heparin usually lowers the level of the coagulation components fibrinogen, fibrin, thrombin/antithrombin complexes, fragment 1+2 and Factor II activity. This is desirable, because elevated levels of these coagulation components can cause decreased capillary blood flow, if they are high enough. Capillaries are microscopic blood vessels that are about eight microns wide. A normal red blood cell, which travels through the capillaries, is about seven microns wide. When elevation of coagulation components occur, they could conceivably attach to the inside surface (endothelial surface) of capillaries, thereby narrowing them. For example, fibrinogen attached to the inside surface could make it harder for a seven-micron-wide red blood cell to squeeze through the narrowed capillary. Reduced blood flow in capillaries would in turn reduce oxygen and nutrients, and reduce removal of toxins from tissues. It stands to reason that if heparin could improve blood flow, antibiotics and hormones would be more effective because they could pass through capillaries easier.
Life is in the blood. Less blood flow means less ?life,? and possibly more symptoms and diseases -- perhaps even death.
Hypercoagulation is associated with other chronic diseases, not just borreliosis. It is my opinion that how hypercoagulation is treated will become a paradigm shift in medicine, once further research has been accomplished.
Clinical Pediatrics, Vol. 49, No. 1, 82-85 (2010)
Asymptomatic, Transient Complete Heart Block in a Pediatric Patient with Lyme Disease
Alan K. Heckler, DO
National Capitol Military Children's Center, Walter Reed Army Medical Center, Washington, DC, firstname.lastname@example.org
Daniel Shmorhun, MD
National Capitol Military Children's Center, Walter Reed Army Medical Center, Washington, DC
Lyme Disease, caused by the spirochete Borrellia burgdorferi, is the most common vector-borne disease in the United States. Clinically, it primarily affects the skin, joints, nervous system, and heart. Lyme carditis occurs in 4 % - 10 % of adults with Lyme disease. Transient variable-level atrioventricular blocks, occurring in 77 % of adults with Lyme carditis, are the most common cardiac manifestation. Up to 50 % of Lyme carditis patients may develop complete heart block. The incidence of Lyme carditis in the pediatric population is not well established. We present a pediatric patient with a transient asymptomatic complete heart block resulting from Lyme carditis, an under-recognized complication of Lyme disease in the pediatric population.
Key Words: Lyme disease ? Lyme carditis ? complete heart block ? third degree heart block ? pediatric patient
This version was published on January 1, 2010