VIRHEDIAGNOOSIT

Asiantuntijana Soile Juvonen TTT

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VIRHEDIAGNOOSIT

ViestiKirjoittaja soijuv » To Tammi 22, 2009 20:14

Borrelioosin virhediagnosointi

"Borrelioosia sairastavat tapaavat usein lukuisia lääkäreitä eivätkä välttämättä senkään jälkeen saa oikeata diagnoosia. Borreliabakteerin aiheuttamat oireet sekoitetaan esim. MS-, ALS- ja Parkinsonin tautiin, lupukseen, reumaan, fibromyalgiaan, krooniseen fatiikkiin, erilaisiin lihassairauksiin ja psyykkisiin sairauksiin jne. Kyseiset oireet saattavat kuitenkin olla borreliabakteerin aiheuttamia/laukaisemia. Borrelioosi kuuluu kymmenen yleisimmän sairauden joukkoon, jota lääkärit eivät osaa diagnosoida oikein. Muita yleisesti virheellisesti diagnosoituja sairauksia ovat keliakia, uniapnea, kilpirauhasen vajaatoiminta, aneurysma, lupus, hepatiitti C, klamydia jne."

(Suom. huom. mielenkiintoista on, että borrelioosia sairastavilla tavataan toisinaan lisäinfektiona mm. edellämainittuja oireita/taudinaiheuttajia).


http://www.wrongdiagnosis.com/l/lyme_di ... isdiag.htm "10 Diseases Doctors Miss"

http://www.wrongdiagnosis.com/intro/overview.htm Overview of Misdiagnosis.


Yleiskatsaus virhediagnosoinnista.

"Vastasairastuneen tulee selvittää ensimmäiseksi onko hänen saamansa diagnoosi oikea. On tärkeää arvioida diagnoosia ja sen oikeellisuutta. Toisaalta ei tule myöskään uskotella että diagnoosi on varmuudella väärä. Joka tapauksessa diagnoosin oikeellisuus tulee vahvistaa hakemalla asiasta toinen mielipide, konsultoida alan asiantuntijoita, teettää lisätutkimuksia ja etsiä tietoa asiasta.

Virhediagnooseja sattuu yleisesti - ne ovat yksi yleisimmistä lääketieteellisistä virheistä. Tutkimuksien mukaan virhediagnoosin mahdollisuus vaihtelee 8 - 40%. Virhediagnoosin syynä voi olla lääkäri, erikoisasiantuntija, laboratoriotutkimukset ja joissakin tapauksessa sairastunut henkilö itse. Diagnoosi voi olla kokonaan tai osittain väärä tai sen kohdalla ei ole huomioitu muita siihen liittyviä seikkoja, lääkitystä, komplikaatioita jne. Joitakin sairauksia ylidiagnosoidaan ja joitakin selkeästi alidiagnosoidaan tai jätetään huomioimatta."

Esimerkkejä borrelioosiin liittyvistä virhediagnooseista:

1. Kaksi naista sairastui krooniseen borrelioosiin koska lääkärit eivät osanneet diagnosoida heidän oireitaan oikein. Toinen nainen yritti 13 vuoden ajan löytää syytä oireisiinsa; päänsärkyä, kovia kipuja rystysissä ja leuassa. Vuosien virheellinen diagnosointi aiheutti borrelioosin kroonistumisen. Nainen kärsii nyt kovista olkapää-, nivel- ja lantiokivuista. Toisessa tapauksessa kahdeksan lääkäriä ilmoitti naiselle ettei hänellä ole borrelioosia. Naisella diagnosoitiin lopulta borrelioosi.


Medical News Summary: Two women develop chronic Lyme disease because doctors were unable to diagnose their condition 27 August 2004
Source: Easton Courier Author: Deanna Holgerson

Medical News Summary (summary of medical news story as reported by Easton Courier): A woman spent 13 years trying to find the cause of her symptoms ? headaches, severe jaw pain and knuckle pain. Years of misdiagnosis led to chronic Lyme disease with symptoms such as intense shoulder, joint and hip pain. Lyme disease is treatable if diagnosed early. Another woman was told by 8 doctors that she didn?t have Lyme disease but was eventually diagnosed by a physician who specializes in Lyme disease.

URL: http://www.zwire.com/site/news.cfm?BRD= ... =461&rfi=9

Related Disease Topics: Lyme disease
Related Symptom Topics: Headaches, joint pain, hip pain, shoulder pain, knuckle pain

2. Borrelioosin virheellinen diagnosointi saattaa johtaa vakaviin terveydellisiin seurauksiin. Borrelioosin varhaisvaiheen nuhankaltaiset oireet jäävät usein vähäiselle huomiolle ja saattavat johtaa virhediagnoosiin. Vuosien ajan kahden New Lennoxlaisen naisen ilmoitettiin sairastavan ALS-tautia borrelioosin sijaan. Russell Johnston sairastui borrelioosiin v. 1998 ja hänen sairautensa ilmeni reumankaltaisin oirein - mm. hänen polviniveleensä jouduttiin laittamaan proteesi.


Medical News Summary: Easily curable Lyme disease leads to serious consequences when misdiagnosed 2 May 2004
Source: Daily Southtown Author: Jennifer Martike

Medical News Summary (summary of medical news story as reported by Daily Southtown): Early symptoms of this disease are flu like and are therefore often misdiagnosed. Two New Lennox residents were diagnosed as having Lou Gehrig?s disease for several years. Russel Johnston contracted Lyme disease in 1998 and the infection resulted in rheumatoid arthritis. He subsequently had knee replacement surgery. Early detection of Lyme disease is easily cured by antibiotics.

URL: http://www.dailysouthtown.com/southtown ... 7seyt1.htm

Related Disease Topics: Lyme disease, Flu, Lou Gehrig?s disease, Flu-like symptoms, Rheumatoid arthritis
Related Symptom Topics: Flu-like symptoms

3. ALS-tauti vai borrelioosi? 39-vuotias mies oli 8 kk aiemmin täysin terve. Nyt hän on niin huonossa kunnossa, ettei kykene kävelemään, puhumaan eikä huolehtimaan itsestään. Häneltä menee kuukausittain tuhansia dollareita hoitokuluihin. Valitettavasti lääkärit eivät osanneet päättää, onko sairaus ALS vai borrelioosi. Mies löysi Internetistä samankaltaisen ALS/borrelioositapauksen kuin hänen omansa. Kyseisellä miehellä diagnosoitiin borrelioosi ja hän kuntoutui hoitojen jälkeen täydellisesti. Borrelioosi diagnosoidaan usein virheellisesti erilaisiksi lihassairauksiksi, fibromyalgiaksi, MS-taudiksi, krooniseski fatiikiksi. Muita oireita ovat esim. nivelkivut, mielialahäiriöt, kasvohalvaus, voimakas uupumus, tuntohäiriöt, rintakehäkivut, selän jäykkyys jne.


Medical News Summary: Lou Gerhig's disease or Lyme disease? 10 July 2005
Source: The Herald-Dispatch Author: Jean Tarbett

Medical News Summary (summary of medical news story as reported by The Herald-Dispatch): A 39 year old man, who 8 months ago was in peak physical condition is now so weak he cannot walk, talk or take care of himself, and spends thousands of dollars each month to treat his condition. Unfortunately his diagnosis is baffling doctors, with a dual diagnosis of amyotrophic lateral sclerosis (ALS or Lou Gerhig's disease) and Lyme disease. The neuromuscular disease, ALS, first caused him to feel lethargic and have hot flushes, then it attacked his motor function limb by limb, with paralysis starting in the hand, later including foot drop, general loss of function and upper torso pain. An MRI of his spine revelled spinal scarring, causing back stiffness. Through internet research, the man discovered another gent with a similar story who was diagnosed with Lyme disease, was being treated for the condition, and had subsequently recovered all of his muscle function. ALS is not treatable, by Lyme disease is. Lyme disease is a bacterial disease transmitted by the bite of a tick. However, Lyme disease is commonly misdiagnosed as other diseases, and vice versa, e.g. fibromuscular disease, fibromyalgia, multiple sclerosis, and chronic fatigue syndrome. Other symptoms of Lyme disease include joint pain, mental dysfunction, paralysis of the facial muscles, extreme tiredness, and flu-type symptoms. Methods to avoid tick bites are to wear appropriate clothing when outdoors, avoid potential tick infested areas, use insect repellents. If bitten, remove the tick with tweezers directly near the head, wash the site thoroughly with disinfectant and preserve the tick in case of future illness.
URL: http://www.herald-dispatch.com/2005/July/10/LNspot.htm
Related Disease Topics: Amyotrophic lateral sclerosis, ALS, Lou Gerhig's disease, Lyme disease, Neuromuscular disease, Fibromuscular disease, Fibromyalgia, Multiple sclerosis, Chronic fatigue syndrome

Related Symptom Topics: Lethargy, hot flushes, hand paralysis, foot drop, loss of function, upper torso pain, back stiffness, joint pain, mental dysfunction, paralysis of the facial muscles, extreme tiredness, flu-type symptoms

4. Virhediagnoosin seurauksena mies sai vakavat neurologiset vauriot. Vaimon mukaan vuosikausia jatkunut virheellinen diagnosointi ja sitä seurannut virheellinen hoito aiheuttivat hänen miehelleen vakavia neurologisia vaurioita. Mies sai punkin pureman jälkeen keuhkokuumeen. Tämän jälkeen hänen selkäytimeensä alkoi kasvaa rustokalvoa jonka seurauksena mies ei kykene enää kävelemään. Borreliabakteerin katsotaan aiheuttavan rustokalvon kasvun sekä miehen muutkin oireet kuten näönmenetyksen ja muistihäiriöt. Hoitamaton borrelioosi voi johtaa vaikeaan fatiikkiin, lihas-/nivelkipuihin, kasvohalvaukseen, sydämen vaurioihin, psyykkisiin ongelmiin, vatsavaivoihin, neurologisiin ongelmiin, sokeuteen, kuurouteen ja jopa kuolemaan.

Medical News Summary: Misdiagnosed Lyme disease leaves man with severe neurological damage Date: 16 May 2005
Source: Scranton Times Tribune Author: Joe Sylvester

Medical News Summary (summary of medical news story as reported by Scranton Times Tribune): A woman claims that years of misdiagnosis and improper treatment led to her husband suffering severe effects from Lyme disease. Lyme disease is a blood-borne disorder spread by tick bites. She claims her husband suffered a bout of pneumonia after suffering a tick bite. The man has a painful spinal cord growth called perichordoma which has made him wheelchair dependent. Lyme disease is blamed for this growth as well as his neurological damage, loss of vision and memory loss. Lyme disease is easily treated with antibiotics if caught in the early stages but untreated can lead to extreme fatigue, joint or muscle pain, facial paralysis, heart damage, psychological disturbances, stomach problems, neurological disorders, blindness, deafness and possible even death. The condition is often misdiagnosed to the symptoms mimicking other conditions such as multiple sclerosis, amyotrophic lateral sclerosis, seizure and arthritis. The Lyme disease foundation claims that 37,865 cases of Lyme disease have been reported in Pennsylvania since 1980.

URL: http://www.zwire.com/site/news.cfm?news ... 6046&rfi=6

Related Disease Topics: Pneumonia, Lyme disease, Multiple sclerosis, Amyotrophic lateral sclerosis, Seizure, Arthritis, Perichordoma, Neurological damage (see Cognitive impairment), Vision loss, Memory loss

Related Symptom Topics: Extreme fatigue, joint or muscle pain, facial paralysis, heart damage, psychological disturbances, stomach problems, neurological disorders, blindness, deafness, spinal cord growth

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42-vuotias mies oli metsävaelluksella heinäkuussa viikon ajan. Palattuaan kotiin hän sai nuhankaltaisia oireita ja voimakasta uupumusta. Ei kuumetta eikä ihomuutosta. Kaksi päivää myöhemmin hänellä ilmeni voimakasta lihasheikkoutta. Hänet vietiin ensiapuun jossa häneltä läydettiin punkki hiusrajasta. Diagnoosi? Borrelioosi, babesioosi, Guillan-Barre, TP, Colorado-kuume?

Kaikki testit olivat negatiivisia mukaanlukien borrelioositesti. Miehellä epäiltiin Guillan-Barre -syndroomaa. Potilas kuitenkin alkoi paranemaan kun punkki poistettiin joten diagnoosi viittasi paremminkin punkin syljen toksiinien aiheuttamaan halvaukseen (TP = Tick paralysis).

TP:n aiheuttamat oireet alkavat, kun neurotoksiinien määrä on saavuttanut huippunsa, noin 5 -6 päivää punkin kiinnittymisestä ihoon. Oireina esiintyy levottomuutta, uupumusta, pahoinvointia, tuntohäiriöitä, mahdollisesti ataksiaa. Seuraavien päivien aikana saattaa esiintyä halvauksia ja alaraajojen heikkoutta, refleksien heikkoutta, pään alueen hermosto-oireita jne. Sairastuneet kuolevat kun hengityksestä vastaavat lihakset halvaantuvat.

Tilaa hoidetaan poistamalla punkki välittömästi. Koko keho, myös nenän limakalvot, genitaalialue, korvakäytävät, pää, kaula jne. on tarkastettava. Oireet, erityisesti pohjoisamerikkalaisten punkkien aiheuttamat, yleensä paranevat nopeasti punkin/punkkien poiston jälkeen. Joidenkin punkkien erittämä neurotoksiini, esim. australialaisten, on kuitenkin niin voimakasta että oireet jatkuvat poiston jälkenkin. Punkit välittävät joka tapauksessa useita taudinaiheuttajia jotka saattavat aiheuttaa jatkossakin ongelmia. Asiasta on tiedotettava sairastuneelle.


NOTE: To view the article with Web enhancements, go to:
http://www.medscape.com/viewarticle/589591
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A Case of Ascending Paralysis: the Signs and Symptoms of Tick Paralysis
Menyoli Malafa, MSII; Veronica Tucci, JD, MS IV; Albert Vincent, PhD; Sajeel Chowdhary, MD

American Academy of Emergency Medicine. 2009;16(1):22,26,27. ©2009 American Academy of Emergency Medicine
Posted 03/26/2009

Summary and Case
Summary
Tick paralysis (TP), a response to the neurotoxic effects of the salivary secretions produced by attached hard ticks (Ixodidae), is a syndrome that mimics a large number of better known neurological disorders. TP is a sporadic, seasonal, rural disorder in which acute ataxia often develops five to six days following a history of walking in grass or low brush, followed by ascending flaccid paralysis. Recognition and timely removal of the tick usually leads to complete resolution of symptoms, whereas continued feeding can lead to respiratory arrest and death. Follow-up includes species determination and patient surveillance for tick-borne infectious disease.

Case
A 42 year-old man was hiking in Colorado for one week in July. Upon returning to his home in Tampa, Florida, he felt flu-like symptoms and fatigue but no fever or rash was noted. Two days later, he developed global muscle weakness and presented to the emergency room. Upon physical exam, a tick was found under the hair of the right occipital area.

Question: The patient likely has which of the following diagnoses:

a) Lyme Disease
b) Guillain-Barre Syndrome (GBS)
c) Colorado Tick Fever
d) Tick Paralysis
e) Babesiosis

Further Case History and Discussion
Further Case History
The patient underwent extensive workup. All laboratory testing including CBC, CMP and Lyme titers were within normal limits. Neurology was consulted given the concern of possible Guillan-Barre Syndrome (GBS). After the tick was removed, the patient improved, indicating a diagnosis of tick paralysis (TP).

Discussion
TP is a worldwide disease, occurring in Australia, Europe, South Africa and throughout North America. In the United States, most cases occur in the Rocky Mountain states and the Pacific Northwest, including Washington, Montana, Oregon, Idaho, Wyoming, Nevada, Utah, Colorado and the northern parts of Arizona, New Mexico and California. However, cases have also been reported in central, southern and eastern states, including Texas, Oklahoma, Mississippi, Florida, Georgia, North Carolina, South Carolina, Virginia, Washington, D.C., Pennsylvania and New York. In Canada, most cases are encountered in the western part of the country, primarily southern British Columbia.[1,2]

More than 60 species of ticks are known to cause paralysis, but only a handful are responsible for most cases. In North America, the disease is associated primarily with six species: Dermacentor andersoni (?Rocky Mountain wood tick'), D. variabilis (?American dog tick'), Amblyomma americanum (?Lone Star tick'), A. maculatum (Gulf Coast tick), Ixodes scapularis (formerly I. dammini, ?Blacklegged tick') and I. pacificus (?Western Black-legged tick'). Peak incidence occurs between April and June when nymphs and mature adults abound in low vegetation and climb upward, questing for their next host by extending their anterior pairs of legs.[1,3,4] Paralysis is a response to a neurotoxin secreted by the salivary glands of the arachnid.[1,5] The biochemistry and pharmacology of the specific paralysis- inducing toxins produced in North American ticks are yet to be fully elucidated, but current evidence points to a mechanism by which the toxins inhibit presynaptic acetylcholine release at the neuromuscular junction.[1,3,6] TP presents more often and more severely in children, suggesting a concentration-dependent relationship between toxin levels and symptom expression.[1,4]

Signs and symptoms of TP begin about five to six days after the parasite has attached, when neurotoxin is secreted at its peak levels. These prodromal symptoms include restlessness, irritability, fatigue, nausea, paresthesias and possibly ataxia. Over the next 24-48 hours, the patient develops ascending symmetrical flaccid paralysis and weakness in the lower extremities. Over the course of the next day or two, paralysis and weakness may ascend to involve the trunk, axial and upper limb muscles. Cranial nerves may also become involved in an ascending pattern, resulting in bulbar, facial and/or extraocular paralysis. Patients demonstrate diminished or absent deep tendon and superficial reflexes while, aside from occasional paresthesias, their sensory exam remains normal. Pain and fever are absent. Death ensues following paralysis of the respiratory muscles.[1,5,7,8,9]

Atypical presentations reflect variations in the site of tick attachment. There may be ataxia and associated cerebellar deficits without accompanying muscle weakness. The disorder may also present as an isolated facial paralysis without trunk or limb involvement. Another group of atypical presentations is unilateral paralysis and/or weakness, including isolated unilateral facial paralysis.[1,8]

Tick paralysis is treated by removal of the tick. Although the site of attachment is most often the head and neck region, the entire body should be scrutinized, including ear canals, nostrils and genitalia. Multiple ticks should be suspected, and all must be removed.[1,4,7,10] Applications of petroleum jelly, nail polish, alcohol, a needle and heat are inappropriate. These measures may result in infection and cause the parasite to salivate or regurgitate more of its bodily fluids.

The tick should be grasped with blunt, angled forceps as close as possible to the skin and to the embedded mouthparts (hypostome). Wearing protective gloves, slowly pull the organism straight outward with a gentle and steady traction, without twisting its body. Do not burst the tick. The hypostome is usually deeply and firmly embedded and should be removed surgically should it come detached. Antiseptic solution is then applied to the wound, and the recovered tick and severed mouthparts may be preserved in 75% ethanol for identification. The patient should be instructed to return in the event of additional illness and educated on protective measures against ticks.

The symptoms of TP, at least those caused by North American species, typically resolve rapidly following removal of all ticks from the patient. Improvement in the condition of the patient subsequent to tick removal is confirmatory for the diagnosis. Species found in some other parts of the world, notably Ixodes holocyclus of Australia, produce a very potent neurotoxin and symptoms may not subside as quickly, even worsening after removal.[5] The prognosis depends on clinical presentation prior to removal. If all ticks were removed prior to the onset of bulbar weakness, the patient often makes a full recovery within the first 24 hours. However, if onset of bulbar symptoms occurs during continued feeding, the likelihood of fatal respiratory paralysis increases to 10%. Therefore, prompt of diagnosis and tick removal are paramount.[1,5,7,8]

Because ticks are both vectors and reservoirs for various infectious diseases, it is important to educate the patient about this added risk for possible concurrent illnesses. Table 1 displays the geographical location and infectious diseases associated with North American tick species which are also known to cause TP.[1,8,11,12]

The list of differential diagnoses for ascending flaccid paralysis and acute ataxia is extensive: 1) neuropathies such as Guillain-Barre syndrome, diptheric polyneuropathy, porphyrias and meningoradiculopathies, 2) neuromuscular junction disorders such as botulism and myasthenia gravis, 3) myopathies due to electrolyte imbalance such as hypokalemia, hypophosphatemia, hypomagnesemia, 4) heavy metal intoxication, 5) spinal cord disease and 6) various CNS disorders such as rabies and poliomyelitis.[1,5,8,13] In addition to the previously described symptoms of TP and the recent history of exposure to rural tick-inhabited areas, there are other distinguishing clinical features of tick paralysis. Neurophysiological studies reveal diminished compound muscle action potential (CMAP) amplitudes, normal nerve conduction velocities and normal response to repetitive stimulation. There are normal CSF findings and but an absence of response to cholinergic drugs. Table 2 compares several of the major differential diagnoses with hallmarks of TP.[1,5,6,13]

It is important for clinicians to include TP in the differential diagnosis of ascending, flaccid paralysis with ataxia. The disease should be strongly suspected when confronted by a bilateral ascending paralysis following a one week history of hiking in tick-infested grasslands or brush during the spring or summer. The entire skin should be scrutinized for embedded hard ticks, and all must be promptly extracted by the appropriate technique to avoid potential respiratory failure. Recovered specimens should be preserved in 75% ethanol for identification*. The patient should be instructed to return in the event of additional illness that may indicate a tick-borne infectious disease.

*Species indentification is offered by co-author
Albert L. Vincent Ph.D., Epidemiology Program
Hillsborough County Health Department
1105 E. Kennedy Blvd, Tampa, Fl 33602
Tel: (813) 307-8015 ext. 2910
Fax: (813) 276-2981 attn: Dr. Vincent
albert_vincent@doh.state.fl.us


Table 1.

Tick Species Geographical Location Infectious Diseases
D. andersoni Rocky Mountain states, western Canada Tularemia, Rocky Mountain spotted fever, Colorado tick fever
D. variabilis Eastern 2/3 of U.S., southern Canada Tularemia, Rocky Mountain spotted fever, Ehrlichiosis
A. americanum South central and south eastern U.S. Tularemia, Ehrlichiosis, Lyme disease
I. scapularis North central and north eastern U.S. Lyme disease, Babesiosis
I. pacificus Pacific coast from California to British Columbia Lyme disease, Babesiosis


Table 2.

GBS Botulism MG Poliomyelitis Spinal Cord Compression
Ascending paralysis X (descending) X x
Symmetrical weakness X
Diminished/absent DTR's X
Normal sensory exam X X
Bulbar involvement X X X
No bladder/bowel dysfunction X X X
Normal CSF X* X X
Diminished CMAP amplitudes
Normal nerve conduction velocity X*
Normal response to repetitive stimulation X X (muscle show more fatigability)
No response to acetyl cholinesterase inhibitors X
Rapid disease progression (hours to days) X (days to weeks) X (symptoms tend to fluctuate)
Symptom improvement following tick removal X X X X X
Other distinguishing disease features History of recent illness/infection Toxin detection AchR antibody detection, positive Tensilon test History of fever, virus detection, virus antibody detection Positive MRI, Babinski sign

*may be normal early on in disease course


References
Cunha BA, editor. Tickborne Infectious Diseases Diagnosis and Management. New York: M. Dekker; 2000.
Meier J, White J. Handbook of Clinical Toxicology of Animal Venoms and Poisons. STATE: CRC Press; 1995.
CDC. Tick paralysis - Washington. Morbidity and Mortality Weekly Report 1996; 45(16): 325-6.
Schmitt N, Bowmer EJ, Gregson JD. Tick paralysis in British Columbia. Can Med Assoc J 1969 Mar 1; 100(9): 417-21.
Meriggioli MN, Howard JF, Howard Jr. JF, Harper CM, Harper Jr. CM. Neuromuscular Junction Disorders: Diagnosis and Treatment. STATE: Informa Health Care; 2003.
Grattan-Smith PJ, Morris JG, Johnston HM, Yiannikas C, Malik R, Russel R, Ouvrier RA. Clinical and neurophysiological features of tick paralysis. Brain 1997 Nov;120(Pt 11):1975-87.
CDC. Tick paralysis - Colorado. Morbidity and Mortality Weekly Report 2006 Sep 1; 55(34): 933-5.
Knoop KJ, Stack LB, Storrow AB. Atlas of Emergency Medicine. STATE: McGraw-Hill Professional; 2002.
Biller J. Practical Neurology. STATE: Lippincott Williams and Wilkins; 2002.
Gammons M, Salam G. Tick removal. Am Fam Physician 2002 Aug 15; 66(4): 646.
Winn WC, Kineman EW, Allen SD, Janda WM, Schreckenberger PC,Procop GW, Woods GL. Koneman´s Color Atlas and Textbook of Diagnostic Microbiology. STATE: Lippincott Williams and Wilkins; 2005.
Sonenshine DE, Mather TN. Ecological Dynamics of Tick-borne Zoonoses. STATE: Oxford University Press US; 1994.
Greenberg BM. Clinical cases in neurology from John Hopkins. Case 2: acute ascending paralysis in a 4-year-old body. MedGenMed 2003 Apr 9; 5(2): 36.

Menyoli Malafa, MSII

Veronica Tucci, JD, MS IV, University of South Florida College of Medicine

Albert Vincent, PhD, Assistant Professor of Medicine, Division of Infectious Diseases and International Medicine, Department of Internal Medicine, College of Medicine, University of South Florida

Sajeel Chowdhary, MD, Assistant Professor, Department of Oncological Sciences, Division of Neuro-Oncology, H Lee Moffitt Cancer Center, University of South Florida College of Medicine
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Borreliabakteerin aiheuttama halvaus saatetaan diagnosoida väärin muiksi neurologisiksi sairauksiksi kuten Guillain-Barre -syndrooma ja botulismi. Neurologiset oireet alkavat yleensä 4 - 7 päivää punkin puremasta. Oireina esiintyy esim. alaraajojen heikkoutta ja pistelyä. Osa tapauksista saattaa johtaa kuolemaan hengityslihashermojen vaurion vuoksi. Päivittäisessä punkkitarkastuksessa tulee tutkia erityisesti pää, selkä ja kaula.

http://www.medscape.com/viewarticle/544057?src=mp


NEW YORK (Reuters Health) Aug 31 - Tick paralysis, which manifests as acute, ascending, flaccid paralysis, may be confused with other neurologic disorders, such as Guillain-Barre syndrome or botulism, according to a report in the Morbidity and Mortality Weekly Report for September 1.

Symptoms usually begin within 4 to 7 days of the tick feeding. Sensory loss is rare, and there is no associated pain. If the tick is not identified and removed, a 10% mortality rate results from respiratory paralysis.

Over a period of 6 days in May of this year, the Colorado Department of Public Health and Environment received accounts of four cases of tick paralysis, Dr. W. J. Pape and associates report. The four individuals all resided in or had recently visited within 20 miles of each other in the mountains of north central Colorado.

The patients were a 6-year-old girl, a 78-year-old woman, and two men, ages 58 and 86. Initial symptoms included difficulty walking because of bilateral lower extremity weakness and tingling sensations.

The tick causing the disease was embedded in the skin on the patients' neck or back and removed within a day or two of the their admission to a hospital. Once the tick was removed, symptoms improved within a few days, although the three adult patients reported residual weakness several weeks later.

Clinicians need to consider tick paralysis in the differential diagnosis of ascending paralysis, the authors of the report advise, and to check patients with these symptoms for the presence of a tick, especially among individuals living in tick-endemic areas in the western part of North America.

"Ticks should be removed by grasping the tick close to the patient's skin with forceps and pulling with a steady, even pressure," Dr. Pape and colleagues write.

The article recommends that people who live in tick-endemic areas should routinely check their bodies for ticks, especially on the head, neck and back. Insect repellents applied to the skin and permethrin-containing acaricides should be sprayed on clothing to prevent bites.

Mor Mortal Wkly Rep CDC Surveill Summ 2006;55:933-935.
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MS-taudin diagnostiikkaan ei ole olemassa spesifiä testiä. Virhediagnoosien määrä on melko suuri. Arvioiden mukaan jopa yksi kahdestakymmenestä. Erilaiset tulehdukselliset tilat kuten verisuonitulehdus, ja mikrobeista borreliabakteeri voivat aiheuttaa MS-oireita.

Neurol Sci. 2001 Nov;22 Suppl 2:S98-102. Links
The differential diagnosis of multiple sclerosis: classification and clinical features of relapsing and progressive neurological syndromes.
Trojano M, Paolicelli D.
Department of Neurological and Psychiatric Sciences, University of Bari, Italy.

In the absence of pathognomonic clinical features or a definitive laboratory test, multiple sclerosis (MS) remains ultimately a diagnosis of exclusion. Accurate diagnosis is increasingly important with available disease modifying therapy. Unfortunately the rate of misdiagnosis remains around 5%-10%, indicating that 1 in 20 patients thought to have MS has, instead, a condition resembling MS. In this review we describe conditions that may be confused with MS because they can present as lesions disseminated in time, space, or both.

Conditions often confused with MS may be inflammatory (systemic lupus erythematosus, Sjögren's syndrome, vasculitis, sarcoidosis, Behçet's disease), infectious (Lyme disease, syphilis, progressive multifocal leukoencephalopathy, HTLV-1 infection, herpes zoster), genetic (lysosomal disorders, adrenoleukodystrophy, mitochondrial disorders, CADASIL), metabolic (vitamin B12 deficiency), neoplastic (CNS lymphoma) and spinal (degenerative and vascular malformations) diseases. The key to the accurate diagnosis of MS is vigilance for atypical features, suggesting the possibility of an alternative diagnosis.

PMID: 11794488 [PubMed - indexed for MEDLIN
Viimeksi muokannut soijuv päivämäärä Ke Huhti 18, 2012 20:17, muokattu yhteensä 6 kertaa
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Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » La Tammi 24, 2009 19:28

Tutkimuksia borreliabakteerin osallisuudesta Alzheimerin tautiin. Viimeisenä suomalainen tutkimus jossa todettiin hermosolujen viestintäreitti, joka johtaa hermosolujen kuolemaan. Yhdessä potilaskertomuksessa tri A. McDonald löysi dementiaan kuolleen miehen aivoista borreliabakteereita. Yksi bakteereista oli juuri tunkeutumassa hermosolun sisälle. Kertomus löytyy osoitteesta http://www.canlyme.com/jim_foris.html


1. Miklossy J, Khalili K, Gern L, Ericson RL, Darekar P, Bolle L, Hurlimann J, Paster BJ.
Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer disease.
J Alzheimers Dis. 2004 Dec;6(6):639-49; discussion 673-81.
PMID: 15665404 [PubMed - indexed for MEDLINE]

2: Kuntzer T, Bogousslavsky J, Miklossy J, Steck AJ, Janzer R, Regli F.
Borrelia rhombencephalomyelopathy.
Arch Neurol. 1991 Aug;48(8 ):832-6.
PMID: 1898257 [PubMed - indexed for MEDLINE]

3: Miklossy J, Kuntzer T, Bogousslavsky J, Regli F, Janzer RC. Meningovascular form of neuroborreliosis: similarities between neuropathological findings in a case of Lyme disease and those occurring in tertiary neurosyphilis.
Acta Neuropathol (Berl). 1990;80(5):568-72.
PMID: 2251916 [PubMed - indexed for MEDLINE]

4. Further ultrastructural evidence that spirochaetes may play a role in the aetiology of Alzheimer's disease.

Miklossy J, Kasas S, Janzer RC, Ardizzoni F, Van der Loos H.
University Institute of Pathology, Division of Neuropathology, Lausanne, Switzerland.Neuroreport. 1994 Jun 2;5(10):1201-4.

Recently it was reported that, at autopsy, in neuropathologically confirmed cases of Alzheimer's disease spirochaetes were found in blood and cerebrospinal fluid using dark-field microscopy. Moreover, the spirochaetes were isolated and cultured from brain tissue. We now show, using scanning electron microscopy and atomic force microscopy that the helically shaped microorganisms isolated and cultured from the Alzheimer brains possess axial filaments. This indicates that these microorganisms taxonomically indeed belong to the order Spirochaetales. A morphometric analysis reinforces this notion.

PMID: 7919164 [PubMed - indexed for MEDLINE]


Medical News 8.3.2007 http://www.medicalnewstoday.com/youropi ... onid=14575

MacDonald in 1986 and 1987 and 1989 published evidence for Borrelia in Alzheimer's disease Autopsy tissue as follows:
1. Borrelia spirochetes present in Autopsy Alzheimer's disease tissue using Monoclonal murine antibodies to H5332 and H9724 epitopes of Borrelia burgdorferi.
2. Borrelia burgdorferi was isolated from in vitro cultures of Autopsy Alzheimer's Disease tissue - with immunoreactivity to Monoclonhal Antibody H5332, which is specific for B. burgdorferi.

Plaques of Alzheimer?s disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete

Alan B. MacDonald *

St. Catherine of Siena Medical Center, Department of Pathology, 50 Rte 25 A, Smithtown, NY 11787, USA

Received 20 February 2006; accepted 23 February 2006

http://www.e-clipx.ch/lyme/documents/Al ... _May_3.pdf

Summary Here is hypothesized a truly revolutionary notion that rounded cystic forms of Borrelia burgdorferi are the root cause of the rounded structures called plaques in the Alzheimer brain. Rounded ??plaques? in high density in brain tissue are emblematic of Alzheimer?s disease (AD). Plaques may be conceptualized as rounded ??pock mark-like?? areas of brain tissue injury. In this century, in brain tissue of AD, plaques are Amyloid Plaques according to the most up to date textbooks. In the last century, however, Dr. Alois Alzheimer did not require amyloid as the pathogenesis for either the disease or for the origin of its plaques. Surely, amyloid is an event in AD, but it may not be the primal cause of AD. Indeed in plaques, amyloid is regularly represented by the ??congophilic core?? structure which is so named because the waxy amyloid material binds the congo red stain and is congophilic. However an accepted subset of plaques in AD is devoid of a congophilic amyloid core region (these plaques ??cotton wool?? type plaques, lack a central congophilic core structure).

Furthermore, there is ??plaque diversity?? in Alzheimer?s; small, medium and large plaques parallel variable cystic diameters for Borrelia burgdorferi. Perturbations of AD plaque structure (i.e. young plaques devoid of a central core and older plaques with or without a central core structure) offer room for an alternate pathway for explanation of ontogeny of the plaque structures. If amyloid is not required to initiate all of the possible plaques in Alzheimer?s, is it
possible that amyloid just a by product of a more fundamental primal path to dementia? If a byproduct status is assigned to amyloid in the realm of plaque formation, then is amyloid also an epiphenomenon rather than a primary pathogenesis for Alzheimer?s disease. In the ??anatomy is destiny?? model, cysts of borrelia are always round. Why then not accept roundness as a fundamental ??structure determines function?? argument for the answer to the mystery of why Alzheimer plaques are always round? Parataxis causality, a concept borrowed from philosophy, is the error that comes from linking two events, which occur contemporaneously or in close proximity to one another with a cause and effect relationship.

Parataxis tells us that what appears to be cause and effect in the couplet ??amyloid plaque?? merely by a proximity relationship may be ??spurious causality?? which is a cognitive dead end.

_c 2006 Elsevier Ltd. All rights reserved.


Turun yliopiston tutkijat löysivät hermosolujen kuolemaan johtavan viestintäketjun

ANNE SAVOLAINEN

Turun yliopiston Biotekniikan keskuksen työryhmät ovat akatemiatutkija Michael Courtneyn ja dosentti Eleanor Coffeyn johdolla onnistuneet kuvaamaan molekyylitasolla uuden hermosolujen viestintäreitin, joka johtaa hermosolujen kuolemaan. Hermosolujen kuolemalla on tärkeä rooli aivojen rappeumasairauksissa, kuten Alzheimerin taudissa, epilepsiassa ja aivohalvauksessa.

- Solujen viestintäketjuja on tutkittu tarkkaan esimerkiksi syöpätutkimuksessa, mutta samankaltaisten viestiketjujen löytyminen hermosolujen yhteydessä oli suuri yllätys, Michael Courtney kertoo.

Tämä tarkoittaa sitä, että on olemassa runsaasti syöpäsolujen viestiketjuja koskevaa tutkimuskirjallisuutta, jota voidaan soveltaa hermosolujen viestiketjujen tutkimuksessa.

Monissa neurologisissa sairauksissa ja sairaskohtauksissa hermosolut aktivoituvat epätavallisen voimakkaasti, mikä johtaa hermosolujen kuolemaan. Rho-proteiinin, joka on jo pitkään yhdistetty syövän syntyyn, on nyt julkaistussa tutkimuksessa havaittu olevan tärkeässä roolissa myös hermosolujen tuhoutumisessa.


Lääkehoito vielä kaukana

Tutkimustulos tarjoaa mahdollisuuden kehittää lääke vakavien neurologisten sairauksien hoitoon.

- Lääketutkimuksessa ongelmaksi voi muodostua lääkkeiden sivuvaikutukset, mutta viestiketjun proteiinien tarkempi tutkimus edesauttaa oikeanlaisen lääkkeen kehittämistä, Eleanor Coffey pohtii.

Tutkimuksen kohteena oleva Rho-proteiini kuuluu proteiiniperheeseen, jonka jäsenten väliset viestiketjut liittyvät solujen tuhoutumiseen.

Tutkimuksessa osoitettiin, että Rho-proteiini aktivoituu solunsisäisen kalsiumin välityksellä, mikä johtaa solujen kuolemaan. Kun Rho-proteiinin aktiivisuus estetään geneettisen muokkaamisen avulla, solut pysyvät elossa.

- On olemassa erilaisia sairauksia, joissa hermosolujen viestintäreitin tutkimus on oleellista. Alzheimerin taudissa ongelmat ovat suurempia, ja ratkaisu ajallisesti kauempana. Esimerkiksi aivohalvaustapauksissa meillä on yhteistyökumppani, joka on tehnyt kliinisiä lääketestejä jo useiden vuosien ajan. Sillä saralla hoitoa voi löytyä vuosien päästä, Michael Courtney kertoo tutkimuksesta, jonka tuloksista tämän hetkiset potilaat eivät välttämättä vielä hyödy.

Tutkijat toivovat kuitenkin, että tutkimustulosta voidaan hyödyntää suunniteltaessa kohteita hermosolujen kuolemalta suojaaville lääkeaineille.

TS 20.3.2007
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ViestiKirjoittaja soijuv » Su Tammi 25, 2009 10:46

36-vuotias mies sairastui borrelioosiin ja ehrlichioosiin; kuume, kova päänsärky, valonarkuus, heikotus, ärtyneisyys, kipuja eri puolilla kehoa, yöhikoilu jne. Hänellä todettiin borrelioosi ja ehrlichioosi. Testeissä hänellä ilmeni väärät positiiviset reuma- ja mononukleoosi -testitulokset.

Koko artikkeli http://tinyurl.com/yt7sqa

Borreliosis And Human Granulocytic Anaplasmosis Coinfection WithPositive Rheumatoid Factor And Monospot Test:Case-Report Mohammad Sami Walid, MD, PhDResearch FellowMedical Center of Central Georgia Mohammed Ajjan, M.D.Internal MedicineMedical Center of Central Georgia Nalini Patel, M.D.Infectious DiseasesMedical Center of Central Georgia

Abstract
We are reporting a case of co-infection with B.burgdorferi andA.phagocytophila with unusual clinical and lab results.

A 36-year-old Caucasian man from Warner Robins, GA, an engineer,presented with a two-week history of febrile illness up to 103 F,severe headaches, fear of light, body aches, irritability, weaknessand night sweats. This started two weeks after a 5-days trip to PanamaCity, Florida, where he had to work outdoors. Physical exam yielded nospecific signs. Ultrasound showed hepatomegaly. Laboratory studiesrevealed elevated liver enzymes, B.burgdorferi IgM 3.7 index,A.phagocytophila IgM ≥1:1280, rheumatoid factor, atypical lymphocytesand positive monospot test. Patients who have been diagnosed with one tick-borne infection are atan increased risk and should be tested for other related infections.Rheumatoid factor and monospot test may be falsely positive in suchcases. free full text url:http://tinyurl.com/yt7sqa
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ViestiKirjoittaja soijuv » Su Tammi 25, 2009 10:47

Seuraavissa tutkimuksissa todetaan borreliabakteerin saattavan aiheuttaa esim. erilaisia neurologisia oireita joita tavataan eri neurologisissa sairauksissa kuten MS, Parkinson, dementia, ALS jne. Esim. puolalaisen tutkimuksen mukaan borreliabakteeri saattaa olla useissa tapauksissa MS-taudin aiheuttaja. Tutkimus suoritettiin vuosien 1997 - 2000 välisenä aikana. Tutkimukseen osallistui 769 henkilöä.

Chmielewska-Badora J, Cisak E, Dutkiewicz J.
Lyme borreliosis and multiple sclerosis: any connection? A seroepidemic study.
Department of Occupational Biohazards, Institute of Agricultural Medicine, Jaczewskiego 2, 20-090 Lublin, Poland.


A total of 769 adult neurological patients hospitalised in clinics and hospitals situated in the Lublin region (eastern Poland) were examined during the years 1997-2000 with ELISA test for the presence of anti-Borrelia burgdorferi sensu lato antibodies. A statististically significant (p=0.0422) relationship was found between the clinically confirmed diagnosis of multiple sclerosis and the positive serologic reaction with Borrelia antigen. Ten out 26 patients with multiple sclerosis (38.5%) showed positive serologic reaction to Borrelia, whereas among the total number of examined neurological patients the frequency of positive findings was twice as low (19.4%). The result suggests that multiple sclerosis may be often associated with Borrelia infection

J Neurol Neurosurg Psychiatry 1997;63:257-258 ( August )
Letters to the editor
Generalised motor neuron disease as an unusual manifestation of Borrelia burgdorferi infection


Lyme borreliosis is a well known multisystem disease caused by the spirochete Borrelia burgdorferi and can produce a wide array of neurological abnormalities in humans. The most frequent are meningitis, cranial neuritis, and painful radiculoneuritis.1 Other clinical manifestations include chronic encephalomyelitis, spastic paraplegia, and axonal polyneuropathy. Our report concerns what we think to be the first case of a patient with upper and lower motor neuron disease and Borrelia burgdorferi infection of the CNS. A causal relation is strongly supported by an evaluation of the Borrelia burgdorferi specific antibody index and the patient's favourable response to medical treatment.


Oksi J; Kalimo H; Marttila RJ; Marjamaki M; et al. ,Inflammatory brain changes in Lyme borreliosis: A report on three patients and review of literature.
Brain, 119 ( Pt 6):2143-54. 1996.
?Chronic CNS involvement of LNB [Lyme neuroborreliosis] may mimic diseases such as neurosyphilis, meningoencephalitis of viral, fungal or ?The occurrence of severe encephalitis resulting in dementia in two of these patients... enlarges the known spectrum of neurologic abnormalities due to infection with B. burgdorferi.?
mycobacterial origin, multiple sclerosis, brain tumor, autoimmune disease, stroke or Alzheimer's disease.?


Reik L; Burgdorfer W; Donaldson JO, Neurologic abnormalities in Lyme disease without erythema chronicum migrans.: American Journal of Medicine, 81:73. 1986.
?The occurrence of severe encephalitis resulting in dementia in two of these patients... enlarges the known spectrum of neurologic abnormalities due to infection with B. burgdorferi.?
Pachner AR. Borrelia burgdorferi in the nervous system: the new "great imitator". Annals of the New York Academy of Sciences, 539:56-64. 1988
?Six patients had relapsing-remitting episodes of focal CNS disease, sometimes mimicking multiple sclerosis?
Trock DH; Craft JE; Rahn DW, Clinical manifestations of Lyme disease in the United States. Connecticut Medicine, 53(6). 1989.
?Later neurologic sequelae, such as demyelinating conditions... occur less commonly and may not become evident until several years after acute infection. ...MRI scanning of the brain may reveal demyelinating lesions...?
Hansel Y, Ackerl M, Stanek G., ALS-like sequelae in chronic neuroborreliosis
Wien Med Wochenschr. 1995;145(7-8 ):186-8. German.
?CSF investigation in a 61-year old female patient with clinical picture of motoneuron disease gave evidence for chronic infection with Borrelia burgdorferi. Improvement of clinical and CSF findings could be observed after antibiotic therapy. The diagnosis of amyotrophic lateral sclerosis which was initially suspected had to be revised and the disorder was interpreted as chronic neuroborreliosis.?
Hemmer B, Glocker FX, Kaiser R, Lucking CH, Deuschl G.
Generalised motor neuron disease as an unusual manifestation of Borrelia burgdorferi infection; J Neurol Neurosurg Psychiatry 1997;63:257-258
Fredrikson S, Link H. ,CNS-borreliosis selectively affecting central motor neurons. Acta Neurol Scand 1988;78:181-184
?A patient is described having Borrelia burgdorferi spirochetal infection clinically affecting central motor neurons selectively and without any sensory impairment.?




Halperin JJ, Kaplan GP, et al. Immunologic reactivity against Borrelia burgdorferi in patients with motor neuron disease. Arch. Neurol 1990; 47: 586-594
?Cerebrospinal fluid was examined in 24 ALS patients--3 (all with severe bulbar involvement) appeared to have intrathecal synthesis of anti- B burgdorferi antibody.?


Smith L. Improvement of patient with amyotrophic lateral sclerosis given ceftriaxone. Lancet 1992; 339:1417

Fredrikson S, Link H. ,CNS-borreliosis selectively affecting central motor neurons. Acta Neurol Scand 1988;78:181-184
Johnson R, et al., Borrelia burgdoferi antibodies and amyotrophic lateral sclerosis The Lancet. August 8, 1987.
Case studies are discussed whereby persons who tested positive for Lyme on antibody tests ALSo showed classic ALS symptoms including denervation, atrophy, weakness, bulbar involvement, dysarthria, ataxia and so on. The end of the article states that any person with ALS should be given the opportunity for a Lyme diagnosis based on these compelling studies.

David S. Cassarino, MD, PhD,a Martha M. Quezado, MD,a Nitya R. Ghatak, MD,a and Paul H. Duray, MDa
Lyme-Associated Parkinsonism: A Neuropathologic Case Study and Review of the Literature, Archives of Pathology and Laboratory Medicine: Vol. 127, No. 9, pp. 1204-1206.
From the Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Md (Drs Cassarino, Quezado, and Duray); and the Departments of Pathology and Neuropathology, Virginia Commonwealth University, Richmond (Dr Ghatak)


Accepted April 11, 2003


Neurological complications of Lyme disease include meningitis, encephalitis, dementia, and, rarely, parkinsonism. We present a case of striatonigral degeneration, a form of multiple system atrophy, in Lyme- associated parkinsonism. A 63-year-old man presented with erythema migrans rash, joint pains, and tremors. Serum and cerebrospinal fluid antibodies and polymerase chain reaction for Borrelia burgdorferi were positive. Clinical parkinsonism was diagnosed by several neurologists. Despite treatment, the patient continued to decline, with progressive disability, cognitive dysfunction, rigidity, and pulmonary failure. At autopsy, the brain showed mild basal ganglia atrophy and substantia nigra depigmentation, with extensive striatal and substantia nigral neuronal loss and astrogliosis. No Lewy bodies were identified; however, ubiquitin-positive glial cytoplasmic inclusions were identified in striatal and nigral oligodendroglia. There were no perivascular or meningeal infiltrates, the classic findings of neuroborreliosis. To our knowledge, this is the first report of striatonigral degeneration in a patient with B burgdorferi infection of the central nervous system and clinical Lyme-associated parkinsonism.
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ViestiKirjoittaja soijuv » Su Tammi 25, 2009 16:38

Borrelioosi vaikuttaa useisiin eri elimiin. Ihossa bakteeri aiheuttaa tyypillisimmillään ihomuutoksen joka tunnetaan nimeltä erythema migrans. 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 negatiivisia testituloksia esiintyy yleisesti. Myöhemmisä 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 the spirochete, 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]
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ViestiKirjoittaja soijuv » Ke Syys 02, 2009 16:29

Tutkimus v. 2009. 165 potilasta, tutkimus suoritettiin v. 2002 -2007. 61 %:lla oli diagnosoitu varhaisvaiheen borrelioosi. 13 %:lle ei ollut ilmaantunut ihomuutosta. Heistä suurin osa (54 %) oli diagnosoitu virheellisesti. Niistäkin, joilla ihomuutos oli esiintynyt, se oli 23 %:lla jätetty huomioimatta. Virhediagnoosin saaneista 41 % oli saanut borrelioosin hoitoon sopimattomia antibiootteja.

This article is available from: http://www.biomedcentral.com/1471-2334/9/79

© 2009 Aucott et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Diagnostic challenges of early Lyme disease: Lessons from a community case series

John Aucott*1, Candis Morrison?2, Beatriz Munoz?3, Peter C Rowe?4,
Alison Schwarzwalder?2 and Sheila K West?3
Address: 1Department of Medicine, Johns Hopkins School of Medicine, Baltimore,
Maryland, USA, 2Lyme Disease Research Foundation of
Maryland, Lutherville, Maryland, USA, 3Dana Center for Preventive Ophthalmology,
Johns Hopkins School of Medicine, Baltimore, Maryland,
USA and 4Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore,
Maryland, USA

* Corresponding author ?Equal contributors

Abstract
Background: Lyme disease, the most common vector-borne infection in North America, is increasingly reported. When the characteristic rash, erythema migrans, is not recognized and treated, delayed manifestations of disseminated infection may occur. The accuracy of diagnosis and treatment of early Lyme disease in the community is unknown.

Methods: A retrospective, consecutive case series of 165 patients presenting for possible early Lyme disease between August 1, 2002 and August 1, 2007 to a community-based Lyme referral practice in Maryland. All patients had acute symptoms of less than or equal to 12 weeks duration.

Patients were categorized according to the Centers for Disease Control and Prevention criteria and data were collected on presenting history, physical findings, laboratory serology, prior diagnoses and prior treatments.

Results: The majority (61%) of patients in this case series were diagnosed with early Lyme disease. Of those diagnosed with early Lyme disease, 13% did not present with erythema migrans; of those not presenting with a rash, 54% had been previously misdiagnosed. Among those with a rash, the diagnosis of erythema migrans was initially missed in 23% of patients whose rash was subsequently confirmed. Of all patients previously misdiagnosed, 41% had received initial antibiotics likely to be ineffective against Lyme disease.


Conclusion: For community physicians practicing in high-risk geographic areas, the diagnosis of Lyme disease remains a challenge. Failure to recognize erythema migrans or alternatively, viral-like presentations without a rash, can lead to missed or delayed diagnosis of Lyme disease, ineffective antibiotic treatment, and the potential for late manifestations.
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ViestiKirjoittaja soijuv » Ke Tammi 27, 2010 14:04

Mercury News 2010:

Kuukausi sitten Bart Fenoliolle kerrottiin hänen sairastavan ALS-tautia ja että hänellä oli n. kaksi kuukautta elinaikaa. Vaimoa kehotettiin viemään puoliso kotiin ja aloittamaan saattohoidot. Fenolio osoitti kuitenkin lääkäreiden olleen väärässä. Hän aloitti antibioottihoidot borrelioosiin ja voi nyt päivä päivältä paremmin.

Tri Stricker kertoo tapaavansa jatkuvasti borrelioosia sairastavia jotka ovat saaneet vääriä Parkinson-, krooninen väsymysoireyhtymä- jne. diagnooseja.Yhtenä päivänä vastaanotolleni tuli nainen jolla oli outoja oireita. Hän oli käynyt Mayo-klinikalla jossa hänelle oli tehty useita testejä. Lääkärit eivät osanneet sanoa muuta kuin että naisella on fibromyalgia. Tri Stricker ihmettelee että lääkärit eivät ollett lainkaan huomioineet sitä tosiasiaa että nainen oli elänyt elämänsä Cape Codissa jossa borreliabakteereja kantavia punkkeja esiintyy paljon. "Miten ihmeessä lääkärit jättivät huomioimatta niin tärkeän yksityiskohdan", Stricker ihmettelee.

Fenolio, 69, tietää tarkkaan miten hän sai borrelioosin. Kuusi vuotta sitten hän oli täysin terve. Hän sai punkinpureman ollessaan koiransa kanssa lammen rannalla. Pureman ympärille tuli ihomuutos. Hän näytti sitä lääkärille mutta koska borrelioositesti oli negatiivinen, asia unohdettiin.

Kolme vuotta myöhemmin hän alkoi oireilla ja neurologi kertoi syynä olevan ALS-taudin.

Fenolion poika kuitenkin muisti isällä olleen aikoinaan punkinpureman. He lähettivät borrelianäytteen laboratorioon. Se oli positiivinen. Borrelioosiin erikoistunut lääkäri kirjoitti Fenoliolle pitkän antibioottilääkityksen.

Taistelu ei kuitenkaan ollut ohi. Vaikka Fenolio alkoi tulla antibioottihoidolla parempaan kuntoon kotikunnan lääkärit halusivat lopettaa hoidon Tähän oli syynä se, että IDSA, eli Amerikkalaisten infektiolääkärien yhdistys, on sitä mieltä että kroonista borrelioosia ei ole eikä pitkistä antibioottihoidoista ole hyötyä.

Fenolioiden mukaan antibiooteista on ollut selkeä apu. Bart Fenolio on tullut päivä päivältä parempaan kuntoon. Hän on tällä hetkellä vielä hoitolaitoksessa mutta vaimo on toiveikas että hän on parissa kuukaudessa tarpeeksi hyvässä kunnossa tullakseen kotiin.

Vaimo toivoo ettei kukaan muu joutuisi käymään läpi samaa painajaista kuin he ovat joutuneet. "Mikäli minun kerrottaisiin sairastavan ALS-tautia haluaisin totisesti että minulle tehtäisiin ensin borrelioositesti."


http://www.mercurynews.com/columns/ci_1 ... ck_check=1
Fisher: Learning about Lyme disease the hard way

By Patty Fisher

pfisher@mercurynews.com
Posted: 01/21/2010 05:41:13 PM PST
Updated: 01/22/2010 11:34:54 AM PST

Click photo to enlarge
Bart Fenolio with his wife, Heidi, at A Grace Sub-Acute Care... (Nhat V. Meyer, Mercury News)

A month ago, Bart Fenolio was told he had Lou Gehrig's disease and had two months to live. Doctors advised his wife, Heidi, to take him home and call a hospice.

But Fenolio is proving the doctors wrong. Instead of getting worse, he's growing stronger each day, thanks to antibiotics. That's because he doesn't have Lou Gehrig's disease, which isn't curable. He has Lyme disease, which is.

Lyme disease, a bacterial illness spread by ticks, is a poorly understood and strangely controversial illness that has been sweeping the country since it was discovered in Connecticut in the 1970s. While still rare in California, there were 28,921 confirmed cases and 6,277 probable cases in the United States in 2008, nearly twice as many as in 1994.

But Lyme experts suspect there could be 10 times that many. That's because when not treated immediately, Lyme can hide in the body for years and then attack, masquerading as anything from heart disease to arthritis to lupus. Folks might not even know they'd been bitten. And the tests for Lyme disease are notoriously unreliable.

Dr. Raphael Stricker, a Lyme disease expert in San Francisco, regularly sees patients who have been misdiagnosed with chronic fatigue syndrome or Parkinson's disease.

"I saw a new patient the other day who had weird symptoms and had gone to the Mayo Clinic for a complete work-up," Stricker told me. "All they could come up with was fibromyalgia," a syndrome characterized by chronic pain, fatigue and depression. Stricker learned that the woman had grown up on Cape Cod, where Lyme-carrying ticks are common.

"How could you miss that little tidbit of her history?" he wondered.

Bitten in Morgan Hill

Fenolio, 69, knows just how he contracted the disease. Six years ago a healthy and hearty Fenolio was playing with his dog Cody near a percolation pond in Morgan Hill and was bitten by a tick. When a circular rash appeared around the bite, he went to the doctor. A Lyme test came back negative, and he forgot all about it.

Three years later he retired from the tropical fish store ?Dolphin Pet Village ? he and his sister owned in Campbell. He and his wife moved to San Diego to be near their grandchildren and to enjoy playing lots of golf.

But his golf game slowly deteriorated. He couldn't seem to grip the club. Then, during a vacation in Hawaii, he was too weak to climb out of the pool. His doctor told him he was just getting old. His wife wasn't buying it.

"I said, 'This is not old age. My husband is disintegrating before my eyes, and something's going on.' "

Their Kaiser Permanente internist referred them to a neurologist, who diagnosed Lou Gehrig's disease. Then Fenolio's son remembered the tick bite.

Fighting for treatment

A laboratory that specializes in Lyme tests confirmed his suspicion, and a Lyme specialist in Redwood City prescribed a long-term course of antibiotics. But the ordeal wasn't over. Although Fenolio began to improve on antibiotics, his wife told me, Kaiser doctors wanted to discontinue them.

That's because the Infectious Disease Society of America still recommends against extended treatment using antibiotics, and it casts doubt on whether chronic Lyme disease exists at all, despite thousands of documented cases. Because of the IDSA's position, health insurers generally refuse to cover long-term antibiotics. In most states, though not in California, doctors can lose their licenses just for treating chronic Lyme.

Dr. Sara Cody of the Santa Clara County Health Department cautioned that Lyme disease is rare here, and Fenolio's case doesn't prove that there's rampant misdiagnosis going on.

"What he is experiencing is tragic but not common," she said.

Dr. Jonathan Blum, an infectious disease specialist at Kaiser Permanente Santa Clara, wouldn't discuss Fenolio's case. He confirmed that Kaiser follows the IDSA protocols.

Tri Jonathan Blum on Kaiser-alueen infektiolääkäri. Hän vahvistaa alueella noudatettavan IDSA:n näkemyksiä. Hänen mielestään pitkillä antibiooottihoidoilla on vakavia sivuvaikutuksia eikä niitä tule käyttää ellei niistä ole osoitettavissa selkeää hyötyä.


"Long-term antibiotics can cause significant side effects," he said, "and should be used only if they are going to help the patient."

Fenolio's family is convinced that the antibiotics are helping. Today he is in a San Jose nursing home, improving each day. He knows there will be setbacks, but his wife hopes he'll be strong enough to go home in a couple of months.

"I just wouldn't want anyone else to go through this nightmare," she said. "If I had one of those diseases and was told there was no cure, I would definitely want to be tested for Lyme."

Contact Patty Fisher at pfisher@mercurynews.com or 408-920-5852.

# Named for the Connecticut town where it was identified in the 1970s, Lyme disease is carried by ticks, specifically deer ticks and Western black legged ticks.
# To prevent infection, wear long sleeves and trousers when hiking and do frequent tick checks.
# If you are bitten, remove the tick and see a doctor.

# For more about Lyme disease or to find a Lyme disease specialist, go to the International Lyme And Associated Diseases Society at www.ilads.org, or the California Lyme Disease Association at www.lymedisease.org
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Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Kesä 11, 2010 11:54


Tri Jon Sterngold:

"Borreliabakteeri on ainutlaatuinen bakteerien joukossa esim DNA rakenteensa vuoksi. Lukuisat DNA:t mahdollistavat bakteerin selviämisen elimistössä ja pakenemisen immuunipuolustuksen tuhoamisyrityksiltä. Bakteeri kykenee esim. muuntamaan pintaproteiinejaan. Bakteeri kykenee muuntamaan myös muotoaan korkkiruuvimaisetsa muodosta kystamuotoon. Kystamuodossa bakteeri on erittäin vastustuskykyinen.

Antibioottihoidon teho riippuu bakteerin aktiivisuustasosta; miten nopeasti bakteeri kasvaa ja lisääntyy. Useimmat bakteerit (useimmat virtsatieinfektiot, keuhkokuume jne) lisääntyvät alle 24 tunnissa. Tällaisissa infektioissa ihminen saa yleensä nopeasti avun antibiooteista. Borreliabakteerin lisääntymissykli on jopa yhdeksän kuukauden mittainen. Passiivisessa tilassa olevaa bakteeria on erittäin vaikea saada tuhotuksi hoidoilla.

Sen lisäksi joidenkin tutkimusten mukaan borreliabakteeri muodostaa muiden taudinaiheuttajien kanssa myös ns. biofilmi-yhteisöjä.

Mikroskoopissa tämä nähdään bakteerien kerääntymisenä geelimäisiin 'kasoihin'. Tällöin ne ovat suojassa immuunipuolustukselta ja antibiooteilta. Tässä 'bunkkerissa' niistä kuitenkin vapautuu (aineenvaihdunnallisen kierron aikana) esim. hermostolle myrkyllisiä aineita. Kyseessä on taistelu elintilasta. Bakteerit voivat tarpeidensa mukaisesti esim. heikentää ihmisen puolustujärjestelmiä tai muuttaa muita elintomintoja. Niiden tarkoituksena ei ole tuhota isäntäelimistöä vaikka sitäkin joskus tapahtuu.

Aivo-, hermo-, sydän-, verisuoni-, tukikudos-, nivel- jne. tulehdusten lisäksi borreliabakteeri pystyy aiheuttamaan ns. autoimmuunisairauksia kuten ALS, lupus, MS jne. Kyseisiä oireita pidetään parantumattomina mutta monissa tapauksissa pitkillä, korkea-annoksisilla antibioottihoidoilla taudit on saatu jopa parannettua.

Borrelioositestit ovat ongelmallisia. Yleensä testeissä mitataan elimistön kykyä muodostaa vasta-aineita borreliabakteeria kohtaan. MUTTA bakteeri kykenee piiloutumaan, muuntumaan, heikentämään elimistön kykyä muodostaa vasta-aineita. SIKSI testitulokset voivat olla täysin negatiiviset vaikkka henkilö sairastaa borrelioosia. Näemme usein, että esim. vuoden antibioottihoitojen jälkeen immmuunipuolustus viimein kykenee havaitsemaan joitakin bakteerin jäänteitä ja testitulokset muuttuvat positiivisiksi. Potilaalla on kuitenkin ongelmia mikäli häntä hoitava lääkäri luottaa ainoastaan negatiivisiin testituloksiin. Tällöin hän ei saa asianmukaista hoitoa ja kärsimykset jatkuvat.

Tässä vaiheessa erottuvat sellaiset lääkärit, jotka ymmärtävät testeihin liittyvät ongelmat ja hoitoihin liittyvät haasteet niistä lääkäreistä, jotka eivät osaa tai eivät halua ymmärtää bakteeriin/tautiin liittyviä ongemia. Ongelman laajuus ja syvyys on erittäin suuri tänä päivänä."

http://www.willitsnews.com/ci_13453460
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » La Loka 02, 2010 09:13

Tutkimuksessa selvitettiin Borrelioosia sairastavien/ sairastaneiden naisten ja miesten välisiä diagnostisia eroja. Tapaukset olivat jo aiemmin varmennettuja borrelioositapauksia.
Eroja löytyi vasta-ainetesti ELISAN:n, IgG:n kohdalla. Tutkimuksen mukaan 50%:lla miehistä ja n.70%:lla naisista borrelioositesti oli virheellisesti negatiivinen.

Merkittävää oli että testi oli virheellisesti negatiivinen suuressa osassa tapauksia.



http://www.prohealth.com/library/showar ... ibid=15636

Sex differences in the clinical and serologic presentation of early Lyme disease: Results from a retrospective review ? Source: Gender Medicine, Aug 2010
by Alison Schwrzwalder, et al.
September 29, 2010

[Note: To read the full text PDF of this article click HERE ]

Background: Lyme disease is the most common vector-borne disease in the United States, and the number of reported cases has more than doubled between 1992 and 2008.

Few studies have explicitly examined sex-based differences in the clinical presentation of or serologic response to early Lyme disease. It is unknown whether the sex-based variability observed in other infectious diseases is relevant to this clinical setting.

Objective: This study retrospectively examined clinical and serologic differences by sex among a community case series of patients with a current or past episode of confirmed early Lyme disease.

Methods: This was a retrospective, consecutive case series of adult patients in Maryland enrolled from August 2002 to August 2007 meeting criteria for a current or past episode of confirmed early Lyme disease.

Clinical variables and patients' self-report surrounding illness onset were abstracted through chart review. All serologic tests drawn within 3 months of illness onset were interpreted using Centers for Disease Control and Prevention criteria.

Results: In a total of 125 patients, there were no significant differences in clinical presentation by sex.

The initial self-misdiagnosis rates for men and women were 10% and 18%, respectively (P = NS).

Among the 62 patients with a serologic test as part of their clinical evaluation:

? 50% of men had a positive, 2-tier result

? Compared with 32% of women (P = NS).


Among the 41 patients with a positive ELISA, median ELISA values (3.4 vs 2.0; P = 0.03) and median number of immunoglobulin G (IgG) bands (4 vs 2; P = 0.03) were significantly higher among men.

Conclusions: In this small, retrospective sample, we found evidence for sex-based differences in the magnitude of ELISA and IgG serologic response to early Lyme disease.

Such differences could have implications for appropriate diagnosis, treatment, and disease classification.

Larger, prospective studies are needed to replicate the results found in this study and to examine their relationship to sex-based immunologic variability.

Source: Gender Medicine, Aug 2010;7(4):320-9. PMID: 20869632, by Schwarzwalder A, Schneider MF, Lydecker A, Aucott JN.The Lyme Disease Research Foundation of Maryland, Lutherville, Maryland, USA.
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Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Ti Huhti 10, 2012 15:58

http://www.nationallymereport.com/symptoms/300_medical_conditions.htm

Tri Katrina Tangin mukaan borrelia-bakteeri huijaa monia lääkäreitä sillä sen aiheuttamat oireet ovat samanlaiset kuin monissa muissa tunnetuissa taudeissa.
ALDAn tekemän tutkimuksen mukaan esim. suuri osa kroonista väsymysoireyhtymää sairastavista sairastaa Borrelioosia. Eräässä tutkimusessa selvitettiin 31:n CFS potilaan oireiden syytä. 29:llä todettiin Borrelioosi.

Amerikan psykiatrien liiton entinen puheenjohtaja, tri Paul Fink, kertoo borrelia-bakteerin kykenevän aiheuttamaan jokaisen tunnetun psykiatrisen oireiston, esim. epäsosiaalinen käytös, paniikkikohtaukset, tarkkaavaisuushäiriöt, anorexia, autismi, Asperger jne. Borrelia-bakteerin osuus oireisiin jätetään kuitenkin useimmiten huomioimatta. Allolevassa listassa on esitetty tutkimuksissa esiintulleita virhediagnooseja.

300 Medical Conditions Related to Lyme Borreliosis


Questions? Comments? Write: National Lyme Report Editor Derek Clontz. He reads and answers all e-mails, usually within minutes and always within one business day.

A Disease Frequently Misdiagnosed

Katrina Tang, M.D., HMD, founder and Director of Research at the Sierra Integrative Medicine Clinic in Reno, Nevada, states that Lyme disease eludes many doctors because of its ability to mimic many other diseases.

According to an informal study conducted by the American Lyme disease Alliance (ALDA),most patients diagnosed with Chronic Fatigue Syndrome (CFS) are actually suffering from Lyme disease. In a study of 31 patients diagnosed with CFS, 28 patients, or 90.3%, were found to be ill as a result of Lyme.

Dr. Paul Fink, past president of the American Psychiatric Association, has acknowledged that Lyme disease can contribute to every psychiatric disorder in the Diagnostic Symptoms Manual IV (DSM-IV). This manual is used to diagnose psychiatric conditions such as attention deficit disorder (ADD), antisocial personality, panic attacks, anorexia nervosa, autism and Aspergers syndrome (a form of autism) to name a few.
List of Conditions

Lyme Borreliosis causes, mimics, is manifested as, is misdiagnosed as or is a contributing factor to many conditions. The following list of over 300 conditions was compiled by means of a non exhaustive search of published scientific literature and includes:

A

Abdominal pseudo-eventration
Acrodermatitis chronica atrophicans (ACA)
Acute Acral Ischemia
Acute conduction disorders
Acute coronary syndrome
Acute exogenous psychosis
Acute meningitis
Acute myelo-meningo-radiculitis
Acute peripheral facial palsy
Acute perimyocarditis
Acute pyogenic arthritis
Acute reversible diffuse conduction system disease
Acute transitory auriculoventricular block
Acute transverse myelitis
Acute urinary retention
Acquired Immune Deficiency Syndrome (AIDS)
Algodystrophy
Allergic conditions
Allergic conjunctivitis
Alopecia
Alzheimer?s Disease
Amyotrophic lateral sclerosis (ALS - Lou Gehrig's Disease)
Amyotrophy
Anamnesis
Anetoderma
Anorexia nervosa
Antepartum fever
Anxiety
Arrhythmia
Arthralgia
Arthritis
Asymmetrical hearing loss
Atraumatic spontaneous hemarthrosis
Atrioventricular block
Attention Deficit Disorder (ADD)
Attention Deficit Hyperactivity Disorder (ADHD)

B

Bannwarth?s Syndrome
Behcet's disease
Bell?s Palsy
Benign cutaneous lymphocytoma
Benign lymphocytic infiltration (Jessner-Kanof)
Bilateral carpal tunnel syndrome
Bilateral facial nerve palsy
Bilateral follicular conjunctivitis
Bilateral keratitis
Bilateral papilloedema
Biphasic meningoencephalitis
Bipolar Disorder
Brain Tumor
Brown recluse spider bite
Brown-Sequard syndrome

C

Cardiac Disease
Cardiomegaly
Cardiomyopathy
Carditis
Carpal tunnel syndrome
Catatonic syndrome
Cauda equina syndrome
Central vestibular syndrome
Cerebellitis
Cerebral atrophy
Cerebro-vascular disease
Cervical facet syndrome
Cheilitis granulomatosa
Chiasmal optic neuritis
Chorea
Choriocapillaritis
Chronic encephalomyelitis
Chronic Fatigue Syndrome
Chronic muscle weakness
Chronic urticaria
Cerebellar ataxia
Cogan?s syndrome
Collagenosis
Complete flaccid paraplegia
Complex Regional Pain Syndrome (CRPS)
Concomitant neuroretinitis
Conduction disorder
Conus medullaris syndrome
Coronary aneurysm
Cortical blindness
Coxitis
Cranial Neuritis
Cranial polyneuritis
Craniopharyngioma
Cutaneous B-cell lymphoma

D

Dementia
Demyelinating disorders
Depression
Dermatomyositis
Diaphragmatic paralysis
Diffuse fasciitis
Dilated cardiomyopathy
Diplopia
Discopathy
Disseminated choroiditis
Dorsal epiduritis

E

Encephalitis
Encephalomyelitis
Encephalopathy
Endogenous paranoid-hallucinatory syndrome
Eosinophilia
Eosinophilic fasciitis (Shulman syndrome)
Epilepsy
Epileptic crises
Episcleritis
Epstein Barr
Erythema chronicum migrans
Exanthema (local and generalized)
Extrapyramidal disorders


F

Facial diplegia
Fascicular tachycardia
Fatal adult respiratory distress syndrome
Fetal death
Fever
Fibromyalgia
Fibrositis
Focal nodular myositis
Frontotemporal atrophy

G

Generalised motor neuron disease
Geniculate neuralgia
Giant cell arteritis
Gonarthritis
Granuloma annulare
Guillain-Barré Syndrome

H

HLA-B27 negative sacroiliitis
Headaches (severe)
Hearing loss
Heart block
Hemiparesis
Hemophagocytic syndrome
Hepatic disorders
Hepatitis
Herniated discs
Holmes-Adie syndrome
Horner's syndrome
Human necrotizing splenitis
Hydrocephalus
Hyperacusis
Hyperbilirubinemia
Hypothyroidism

I

Idiopathic atrophoderma of Pasini and Pierini (IAPP)
Idiopathic facial paralysis
Infarction pain
Impaired Brainstem response
Infantile sclero-atrophic lichen
Infectious Mononucleosis
Infiltrating lymphadenosis benigna cutis
Inflammatory cerebrospinal fluid syndrome
Influenza
Internuclear ophthalmoplegia
Interstitial granulomatous dermatitis
Intracerebral haemorrhage
Intracranial aneurysm
Intracranial hypertension
Intracranial mass lesions
Intrauterine growth retardation
Iritis
Irritable Bowel Syndrome
Isolated acute myocarditis
Isolated lymphadenopathy
Isolated neuritis of the sciatic nerve
Isolated oculomotor nerve paralysis
Isolated posterior cord syndrome

J

Jaundice
Juvenile Rheumatoid Arthritis


K

Keratitis
Keratoconus

L

Left sided sudden hemiparesis
Lichen sclerosus
Livedo racemosa
Lofgren's syndrome
Lupus
Lymphadenosis benigna cutis
Lymphocytoma cutis
Lymphoma
Lumboradicular syndrome

M

Melkersson-Rosenthal syndrome
Memory impairment
Meningeal lymphoma
Meningitis
Meningoencephalomyelitis
Meningoencephalomyeloradiculoneuritis
Meningoradiculitis
Migraines
Mono-arthritis
Monolateral chorioretinitis
Morgagni-Adams-Stokes syndrome (MAS)
Morning glory syndrome
Morphea
Motor neuron syndrome
Multiple mononeuropathy
Multiple Sclerosis
Myelopathy
Myofascial pain syndrome
Myositis

N

Neonatal respiratory distress
Neuromyotonia
Nodular panniculitis
Normal-pressure hydrocephalus (NPH)
Oculomotor paralysis
Oligoarthritis
Opsoclonus-myoclonus syndrome
Nodular fasciitis
Non-Hodgkin?s lymphoma


O

Obsessive-compulsive disorder
Optic atrophy
Optic disk edema
Organic mood syndrome
Optic nerve lesion
Otoneurological Disorders

P

Panuveitis
Papillitis
Paralysis of abdominal muscles
Paraneoplastic polyneuropathy
Paranoia
Parkinsonism
Parotitis
Pars plana vitrectopy
Parsonage and Turner syndrome
Peripheral facial palsy
Peripheral neuropathy
Peripheral vascular disorder
Pericarditis
Perimyocarditis
Persistent atrioventricular block
Pigment epitheliitis
Polymyalgia rheumatica
Polyneuritis cranialis
Polyneuropathy
Polysymptomatic autoimmune disorder
Porphyrinuria
Posterior scleritis
Primary lymphoma of the nervous system
Presenile dementia
Progressive cerebral infarction
Progressive facial hemiatrophy (Parry-Romberg syndrome)
Progressive stroke
Progressive supranuclear paralysis
Prolonged pyrexia
Propriospinal myoclonus
Pseudo tumor Cerebrae
Pseudolymphoma
Pseudoneoplastic weight loss
Psychosomatic disorders


R

Radiculoneuritis
Ramsay Hunt syndrome (pleocytosis)
Raynaud's syndrome
Recurrent paralysis
Reflex sympathetic dystrophy
Reiter's Syndrome
Respiratory failure
Restless legs syndrome
Retinal pigment epithelium detachment
Retinal vasculitis
Reversible dementia
Rheumatic Fever
Rheumatoid Arthritis
Rhombencephalitis


S

Sacro-iliitis infection
SAPHO syndrome
Sarcoidosis
Schizophrenia
Schoenlein-Henoch purpura
Scleroderma
Secondary syphilis
Seizure Disorders
Sensorineural Hearing Loss
Septal panniculitis
Septic arthritis
Seventh nerve paralysis
Sick sinus syndrome
Spontaneous brain hemorrhage
Stevens-Johnson syndrome
Stiff-man syndrome
Still's disease
Stroke
Subacute Bacterial Endocarditis
Subacute multiple-site osteomyelitis
Subacute organic psychosyndrome
Subacute multiple-site osteomyelitis
Subacute presenile dementia
Subarachnoid hemorrhage
Sudden deafness
Sudden hemiparesis
Sudden infant death syndrome (SIDS)
Sudeck's atrophy
Synovitis
Syphilis
Symmetric Polyarthritis


T

Temporal arteritis
Temporomandibular joint syndrome
Thrombocytopenic purpura
Thyroiditis
Tourette's syndrome
Transient Ischemic Attack
Transient left ventricular dysfunction
Trigeminal Neuralgia


U

Unilateral interstitial keratitis
Unilateral papillitis
Urticaria
Uveitis


V

Vasculitic neuropathy
Vasculitic mononeuritis multiplex
Vasculitis
Ventricular asystole
Vertigo
Vestibular neuronitis
Vitreous clouding.
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Ti Huhti 10, 2012 16:23

12 Borreliatapausta joissa potilailla esiintyi erilaisia neurologisia oireita kuten Parkinson, meningoradikuliitti, meningomyeliitti, kasvohermohalvaus, polyneuriitti jne. Vain 3 muisti punkinpureman ja ainoastaan yhdellä oli ollut ihomuutos. Useimmilla esiintyi kovaa kipua. Kipu hellitti suonensisäisellä antibioottihoidolla. Parkinson ja hydrokefalus oireet eivät parantuneet antibiooteilla vaan vaativat lisähoitoja.


Rev Neurol (Paris). 1989;145(5):362-8.
[Neurologic forms of Lyme disease. 12 cases].
[Article in French]
Viader F, Poncelet AM, Chapon F, Thenint JP, Dupuy B, Morin P, Lechevalier B.
Source

Service de Neurologie Dejerine, CHU de Caen.

Abstract


Twelve cases of Lyme's disease with neurological complications are reported. Seven patients had meningoradiculitis of the Garin-Bujadoux-Bannwarth type, with facial palsy in 2 cases. In 1 case the radiculitis involved only the cauda equina. Two more patients had meningomyelitis. Of the remaining 3, 1 had subacute inflammatory polyneuritis with albumino-cytologic dissociation, 1 had probable dorsal epiduritis, and the last one developed parkinsonism and communicating hydrocephalus after an otherwise classical meningoradiculitis. Three patients recalled a tick bite but only one a cutaneous eruption. No arthritis or cardiac involvement were observed. In 2 cases the CSF contained pseudo-neoplastic cells. Severe pain was a prominent feature in most cases. Pain consistently and rapidly improved on high-dose intravenous penicillin, while other signs or symptoms (e.g. paresthesias or fatigue) often lasted several months. Parkinsonism and hydrocephalus were not influenced by penicillin, and both required specific therapy. Isolated neurological (both central and peripheral) involvement is not unusual in Lyme's disease and may give rise to a wide range of signs and symptoms. This diagnosis is to be considered even when other features of Borrelia burgdorferi infection are lacking.

PMID:
2662339
[PubMed - indexed for MEDLINE]
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Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

Re: VIRHEDIAGNOOSIT

ViestiKirjoittaja soijuv » Ke Joulu 26, 2012 14:03

"Nuorella miehellä esiintyi erilaisia oireita; päänsärky, uneliaisuus, painonlasku. Neurologit ja psykiatrit eivät löytäneet laajoista tutkimuksista huolimatta mitään syytä oireisiin, ei myöskään magneettikuva (MRI). Siksi potilaan oireiden ajateltiin olevan psykosomaattisia. Potilaan oireet kuitenkin pahenivat edelleen ja paino jatkoi alenemistaan. Sairaalahoitoon. Edelleenkään missään tutkimuksissa ei löytynyt mitään poikkeavaa. Koska mies oli ollut metsässä tehtiin borreliatestit. Miehen todettiin sairastavan akuuttia neuroborrelioosia. Hoidoksi suonensisäistä keftriaksonia ja oireet hävisivät. Kliinikoiden tulee huomioida borreliabakteerin mahdollisuus myös silloin kun oireet ovat epätyypillisiä."

Misleading presentation of acute Lyme neuroborreliosis.

Authors: Winter EM, Rothbarth PH and Delfos NM

Citation: BMJ Case Rep 2012; 2012

Location: Department of Internal Medicine, Leiden University Medical Center, Leiden, Netherlands.

DOI: 10.1136/bcr-2012-006840


A young man presented with recent-onset non-specific symptoms like headache, sleepiness and weight loss, interfering with normal daily life. Physical and biochemical irregularities were absent. Because extensive examination by neurologist and psychiatrist including brain imaging did not reveal any clues, the complaints were initially considered psychosomatic. As the symptoms deteriorated with ongoing weight loss, the patient was re-admitted to the hospital. Again, extensive additional investigation did not reveal any abnormalities. Because of previous exposition to the woods Lyme serology was determined. Surprisingly, it appeared to be a remarkable presentation of acute Lyme neuroborreliosis which was successfully treated with ceftriaxon. Clinicians must be aware of the fact that this severe illness can present without any typical symptoms.
10.1136/bcr-2012-006840
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

Re: VIRHEDIAGNOOSIT

ViestiKirjoittaja soijuv » Pe Maalis 08, 2013 12:24

Kreikka 2013. 7-vuotias lapsi sai autoimmuunitaudin kaltaisia oireita; ihottumaa, kuumeilua, yöhikoilua ja nivelkipuja. Useat tulehdustekjät olivat koholla, maksassa ja pernassa muutoksia, suurentuneita imusolmukkeita, silmätulehdus (uveiitti) jne. Tytön epäiltiin sairastavan sarkoidoosia. Myöhemmissä tutkimuksissa tytön oreiden todettiin kuitenkin johtuvan bartonella-bakteerin aiheuttamasta infektiosta. Antibioottihoito: gentamysiini + siprofloksasiini.

Case Rep Pediatr. 2013;2013:726826. doi: 10.1155/2013/726826. Epub 2013 Jan 17.
Bartonella henselae Infection: An Uncommon Mimicker of Autoimmune Disease.


Maritsi DN, Zarganis D, Metaxa Z, Papaioannou G, Vartzelis G.
Source
Second Department of Academic Pediatrics, Athens Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece ; Department of Paediatrics, MITERA Childrens' Hospital, 15237 Athens, Greece.

Abstract
We present a case of a seven-year-old immunocompetent female patient who developed systemic symptoms mimicking an autoimmune rather than an infectious disease. The patient presented with rash, biquotidian fever, night sweats, and arthralgias. There was no antecedent history of cat contact. Investigations showed increased inflammatory markers, leukocytosis, thrombocytosis, hypercalcemia, and raised angiotensin-converting enzyme. Interferon-gamma releasing assay for tuberculosis infection was negative. Abdominal imaging demonstrated multifocal lesions of the liver and spleen (later proved to be granulomata), chest X-ray showed enlarged hilar lymph nodes, and ophthalmology review revealed uveitis. Clinical, laboratory, and imaging features pointed towards sarcoidosis. Subsequently, raised titers (IgM 1 : 32, IgG 1 : 256) against Bartonella confirmed the diagnosis of B. henselae infection. She was treated with gentamycin followed by ciprofloxacin; repeat investigations showed complete resolution of findings. The presence of hepatic and splenic lesions in children with bartonellosis is well documented. Our case, however, exhibited certain unusual findings such as the coexistence of acute ocular and systemic involvement in an immunocompetent host. Serological testing is an inexpensive and effective way to diagnose bartonellosis in immunocompetent patients; we suggest that bartonella serology is included in the baseline tests performed on children with prolonged fever even in the absence of contact with cats in countries where bartonellosis is prevalent.
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

Re: VIRHEDIAGNOOSIT

ViestiKirjoittaja soijuv » Ke Maalis 13, 2013 18:53

Virheelliseen diagnoosiin voidaan päätyä myös virheellisen negatiivisen testituloksen johdosta. Virheellinen testitulos voi johtua mm siitä syystä että testissä käytetyt antigeenit eivät havaitse bakteerin alalajia esim. B.miyamotoita. Esim. USA:ssa löydetään yhä enenevässä määrin Euroopassa esiintyviä B.gariniita ja afzeliita mutta borreliatesteissä käytetään siellä antigeeninä ainoastaan B.burgdorferi B31. Se saattaa selittää osaltaan lukuisat virheelliset negatiiviset testitulokset.

Reconciliation of Published Facts with the Presence of Garinii type Borrelia on the North American Continent:

The presence of Garinii in the blood of USA patients ( N=5 patients) from the Advanced Labs paper by
Dr Eva Sapi, the additional patient with blood culture positive Afzelii, and two patients with
Kurtenbachii all reinforced the breakthrough idea that European Type Borrelia are now most likely
in the USA population - either by virtue of Travel to Europe on Vacation, or even because of exposure
to European ticks during military service [ the USA has a sizable ground force in Germany}

These Garinii " European strains" are also prominent in Mexican Lyme and are the exclusive agents
in Brazilian Lyme.
So we need to recalibrate our thinking about what strains might be in any individual's blood
from any continent.
Garinii will not be deteted in ELISA or WB manufactured from B31 USA borrelia burgdorferi.
So an an unknown % of "seronegative" patients may be " B31 diagnositic kit" negative but
seropositive with kits developed from "european" strains.

Further muddying the waters is the identification of Miyamotoi in Northeastern USA with a well
documented case of human disease now recorded. Miyamotoi test kits are not standardized
and are not commercially available. So here is another scenario for so called False negative but
in the body positive Borrelia infection of either the pure miyamotoi type or of the mixed
miyamotoi/burgdorferi type.

Further complicating the Serology unanswered questions :: the 92 genotypes {pyrG DNA sequencing} of
Burgdorferi type borrelia
now known to exist in the USA as subtypes of BB sensu stricto. The best genotyped among these are what
I refer to as the Schutzer "13 Strains" and among these is stran Bb ss Sz7.
One of the 92 isolates from Advanced labs was Sz7 Bb ss.
--------------------------
Whole-genome sequences of thirteen isolates of Borrelia burgdorferi.
http://www.ncbi.nlm.nih.gov/pubmed/20935092by SE Schutzer - 2011 - Cited by 20 - Related articles
Oct 8, 2010 – Schutzer SE, Fraser-Liggett CM, Casjens SR, Qiu WG, Dunn JJ, Mongodin EF, Luft BJ. ... The first complete genome sequence of B. burgdorferi strain 31, ... we determined the whole-genome sequences of 13 additional B.

Sapi,E., et al ,"Improved Culture conditions for the Growth and Detection of Borrelia from Human Serum",
International Journal of Medical Sciences, 2013, 10(4) 362-376, doi: 10.7150/ijms.5698
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

Re: VIRHEDIAGNOOSIT

ViestiKirjoittaja soijuv » Ke Maalis 13, 2013 20:04

Useita ihomuutoksia (2-3) siitä huolimatta 50% seronegatiivisia, ihosta otettu PCR kuitenkin positiivinen.

The Many Faces of Solitary and Multiple Erythema Migrans Acta Dermato-Venereologica

Accepted Nov 5, 2012; Epub ahead of print Feb 28, 2013

Acta Derm Venereol 2013; 93: XX–XX.

Pernilla Eriksson1, Marika T. Schröder1, Kirsi Niiranen1, Antti Nevanlinna2, Jaana Panelius1 and Annamari Ranki1

1Department of Dermatology and Allergology, Helsinki University Central Hospital, and 2Center for Information Technology, University of Helsinki, Helsinki, Finland


DOI: 10.2340/00015555-1549
Abstract:

Case definitions for European Lyme disease have been published. However, multiple erythema migrans may pose a diagnostic challenge. Therefore, we retrospectively reviewed the clinical and serological findings and response to therapy in a cohort of consecutive 54 patients with PCR-confirmed erythema migrans, referred to a university dermatology clinic. The proportion of patients with multiple erythema migrans lesions (usually 2 or 3) was almost equal (46%) to the proportion of patients with single erythema migrans lesions (54%). All patients, except for 2 multiple erythema migrans patients with a concomitant autoimmune disease, completely responded to treatment. In conclusion, multiple erythema migrans may be more common than anticipated, and since only 50% of the patients were seropositive when seeking medi-cal help, PCR testing of skin lesions is helpful to confirm the diagnosis in clinically atypical cases.

Full text and photos here:
http://www.medicaljournals.se/acta/cont ... &preview=1
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16

Re: VIRHEDIAGNOOSIT

ViestiKirjoittaja soijuv » Pe Joulu 20, 2013 11:14

Slovakia 2010.
32 potilasta. Kaikilla ELISA negatiiivinen mutta Western blot positiivinen. Kaikilta kroonisia oireita sairastavista tulee ottaa Wb vaikka ELISA on olut negatiivinen. Negatiivinen vasta-ainetulos on tutkijoiden mukaan todennäköisesti immuunipuutoksesta johtuvaa.

Suom. huom. Suomessa tehdään ensin vain ELISA. Mikäli se on negatiivinen jatkotutkimusta ei tehdä.
Useimmilla Suomessa negatiivisen testituloksen saaneista, Saksan testit ovat olleet positiiviset ja sen lisäksi immuunipuolustuksesta kertova CD 57 erittäin alhainen.


Bratisl Lek Listy. 2010;111(3):153-5.

Our experience with examination of antibodies against antigens of Borrelia burgdorferi in patients with suspected lyme disease.
Durovska J, Bazovska S, Ondrisova M, Pancak J.
1st Department of Neurology, Faculty of Medicine, Comenius University, Bratislava, Slovakia. durovska@borelioza.sk

Abstract
BACKGROUND: Lyme borreliosis is a multisystemic disease which affects several organs such as skin, nervous system, joints and the heart. The presented study focused on patients with persisting symptoms of the disease, which could be in correlation with Lyme disease but antiborrelial antibodies were not confirmed by screening tests.

MATERIAL AND METHODS: 32 patients with anamnestic data and suspected clinical signs of lyme borreliosis were tested for the presence of antiborrelia antibodies by using ELISA and westernblot analysis and the state of cellular and humoral immunity.

RESULTS: All patients had specific antiborrelial antibodies confirmed by using the westernblot in spite of negative ELISA.

Immunological investigations revealed a deficiency of cellular immunity in all patients and in a part of them (15.6%) a deficiency of humoral immunity was also found. The presence of different types of autoantibodies was detected in 17 (53.1%) patients.

CONCLUSION: In patients with persisting difficulties that could be associated with Lyme disease, it is necessary to use the westernblot test which could prove the presence of specific antibodies. It is probably due to the very low production of specific antibodies caused also by the status of immune deficiency detected in all our patients (Tab. 1, Ref. 11).
soijuv
 
Viestit: 3097
Liittynyt: Ke Tammi 21, 2009 14:16


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