BORRELIOOSI/SILMÄSAIRAUDET

Asiantuntijana Soile Juvonen TTT

Valvojat: Bb, Tiina, viltsu, Sailairina

BORRELIOOSI/SILMÄSAIRAUDET

ViestiKirjoittaja soijuv » Ma Syys 20, 2010 10:56

Borrelia-bakteeri/silmäsairaudet

Tutkimusaineiston koonnut: Soile Juvonen TTT

Borrelia-bakteeri voi aiheuttaa silmiin erilaisia tulehdustiloja ja muutoksia. Aiheesta löytyy lisää tutkimuksia sivujemme ?Tutkimustietoa Borrelioosista/Borrelioosin oireet? -osiosta
http://p1.foorumi.info/lymeborrelioosi/ ... c.php?t=17

Allaolevissa kuvissa nähdään borrelia-bakteerin aiheuttama silmien suonikalvontulehdus, atrofia, pigmentin epiteelin hyperplasia, verkkokalvotulehdus, epänormaalit sarveiskalvon hermot.

1. Lyme Disease: The disease may occur also as multifocal choroiditis The yellowish lesions have blurred boundaries and do not involve the retina.
Author(s): Naumann, G.O.H. Schönherr, Ulrich, Erlangen, GermanyICD10-Code:H32.8
Kuva: http://www.atlasophthalmology.com/atlas ... &locale=cn

2. Angiogrammi: Lyme Disease (Borreliosis), AngiogramComment to photo:The early angiogram (left) shows many more non-staining defects than the late phase (right). These are active infiltrates that are not yet clinically visible. (Unfortunately, only fundus photos of the left eye are available.)
Kuva: http://www.atlasophthalmology.com/atlas ... &locale=cn

3. Lyme Disease (Borreliosis)Comment to photo:Focal atrophy in the foveal area with pigment epithelial hyperplasia in a patient who had lyme disease. (This is a rare manifestation that reminds one of age-related maculopathy).Author(s): Naumann, G.O.H. Schönherr, Ulrich., Erlangen, GermanyICD10-Code:H32.8
Kuva: http://www.atlasophthalmology.com/atlas ... &locale=cn

4. Diagnosis:Lyme Disease (Borreliosis) Choroidal AtrophyComment to photo:The choroid developed diffuse atrophy after antibiotic treatment of a diffuse choroiditis. In the macula are a few hyperpigmentations.Author(s): Naumann, G.O.H. Schönherr, Ulrich., Erlangen, GermanyICD10-Code:H32.0
Kuva: http://www.atlasophthalmology.com/atlas ... &locale=cn

5.Spirokeetat tulevat hyvin näkyviin hopeavärjäyksessä.Diagnosis:Lyme Disease (Borreliosis), Borrelia burgdorferi. Comment to photo:With a silver stain the spirochetes become well visible
http://www.atlasophthalmology.com/atlas ... &locale=cn
6. Lyme Disease (Borreliosis), ChorioretinitisComment to photo:Multiple partially confluent choriretinal infiltrates. Very few cells in the vitreous. Typical IGM and IGG titers.
Kuva: http://www.atlasophthalmology.com/atlas ... &locale=cn

7.Lyme Disease (Borreliosis), Choroiditis,Comment to photo:This disease is caused by a spirochete (Borrelia burgdorferi) and transmitted by ticks. It has many similarities to syphilis. Here we see at the posterior pole a diffuse choroiditis and infiltration of the RPE layer leaving the inner retina intact. Fluid may accumulate under the retina.Author(s): Naumann, G.O.H. Schönherr, Ulrich, , Erlangen, GermanyICD10-Code:H32.8
Kuva: http://www.atlasophthalmology.com/atlas ... &locale=cn

8.Lyme Disease (Borreliosis), PapillitisComment to photo:Optic neuritis occurs as part of the picture of Lyme disease.Author(s): Naumann, G.O.H., Schönherr, Ulrich Erlangen, Germany
Kuva: http://www.atlasophthalmology.com/atlas ... &locale=cn

9. . Abnormal corneal nerves in a patient with Lyme disease.
Ricaud X, Rozenbaum JP, Landowski S, Baudouin C, Labbé A
Eye (Lond) 2011 08 19
Viimeksi muokannut soijuv päivämäärä Pe Elo 26, 2011 10:41, muokattu yhteensä 1 kerran
soijuv
 
Viestit: 3010
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Ti Loka 19, 2010 14:57

Bb aiheuttaa mm erilaisia silmätulehduksia (2010)

Ocular Signs of Lyme Disease
http://www.livestrong.com/article/71899 ... e-disease/

Lyme disease is a tick-borne disease that can cause symptoms in many body systems, including the eyes, well after the initial tick bite occurs. Ocular problems are uncommon side effects of Lyme disease that can occur in the early or late phase of the disease and can take many different forms. Treating Lyme disease with antibiotics along with treating specific eye complications is essential to prevent recurrent eye problems.
Conjunctivitis

Conjunctivitis, or redness and discharge due to inflammation of the conjunctiva, can occur in the early phase of Lyme disease. The conjunctiva, or lining of the eyeball and lower eyelid, looks pinkish, with tiny reddened blood vessels visible. Pus may be present, according to the Illinois Eye and Ear Infirmary. This type of conjuncitvitis is not contagious and clears up on its own.
Tarjouksia Helsingistä www.CityDeal.fi/Helsinki
Huipputarjouksia käsittämättömän edullisesti. Iske kiinni!
Sponsored Links
Uveitis

An inflammation of the uvea, the middle part of the eye, is called uveitis. The uvea is made up of the iris, the colored part of the eye; the ciliary body, which makes the fluid that fills the eye; and the choroid, the layer beneath the retina. According to Allen Ho, M.D., Lyme disease can cause intermediate uveitis, also known as pars planitis, which affects the area behind the iris. According to the Merck Manual, pars planitis is often painless; the main symptoms are increased floaters--dark dots or lines that move around--and vision loss. The main treatment used for uveitis is steroid eye drops, which reduce inflammation. Treatment can take several months, because steroids need to be slowly reduced or a rebound effects will occur. Drops that dilate the pupil may be used to keep the iris from sticking to the lens, which can happen if the iris becomes scarred, according to Dr. Ho. This can cause permanent vision loss.
Optic Neuritis

The optic nerve carries impulses from the retina to the brain. Optic neuritis is an inflammation of the fibers that cover the optic nerve. According to the Mayo Clinic, Lyme disease can cause optic neuritis. Symptoms of the disease are pain in the eye, inability to see color and vision loss.Steroids are given both intravenously and as eye drops to treat optic nerve neuritis, according to the Mayo Clinic.
Keratitis

Keratitis, or inflammation of the cornea, can be a sign of Lyme disease, according to the Merck Manual. Keratitis may cause pain in the eye, light sensitivity, tearing and blurred vision. The eye may appear opacified, or covered with a white haze. Prednisone, a steroid, is given as eye drops, or by mouth for two to six months in deeper infections.
Retinal Vasculitis

Inflammation of the blood vessels of the retina, also known as retinal vascultis, can occur as a complication of Lyme disease, according to K. Durrani, M.D. The most common symptoms of retinal vasculitis are painless, gradual vision loss. According to Durrani, treatment depends on the presentation of the disease but usually includes high-dose steroids and may include ocular injection of steroids. Laser may be used if many small hemorrhages occur in the eye.
Branch Retinal Vein Occlusion

Lyme disease is occasionally associated with Branch Retinal Vein Occlusion (BRVO), a blockage in the veins of the retina. BRVO can cause vision loss in the area where the blockage is located, according to VitreoRetinal Surgery. There's no pain associated with a BRVO, but vision loss occurs if the blockage causes swelling in the macula. Treatment is laser if the blockage is away from the macula, or intravitreal injection of steroids if swelling occurs in the macula.


Read more: http://www.livestrong.com/article/71899 ... z12nyO283b
soijuv
 
Viestit: 3010
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Ma Tammi 24, 2011 11:58

Borrelia-bakteerin oireena voi ilmetä silmäluomien roikkumista, sidekalvontulehdus, valoarkuutta. (2011)


Clin Pediatr (Phila). 2011 Jan 10; [Epub ahead of print]
Lyme Disease Presenting as Ptosis, Conjunctivitis, and Photophobia.

Goldberg S, Katz BZ.

http://eutils.ncbi.nlm.nih.gov/entrez/e ... md=prlinks
PMID: 21224251 [PubMed - as supplied by publisher]
soijuv
 
Viestit: 3010
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Ti Maalis 22, 2011 12:56

Borrelia-bakteerin aiheuttamia silmäsairauksia:


Atlas Of Ophthalmology - Disorders of the eye caused by borrelia (Lyme) infection

http://www.atlasophthalmology.com/atlas ... &locale=cn
_____________________________________________________
Optician Online : Lyme disease

View PDF: http://www.opticianonline.net/assets/ge ... temID=2495
______________________________________________________
[Ocular manifestations of Lyme disease]

Med Mal Infect. 2007 Jul-Aug;37(7-8):518-22. Epub 2007 Mar 21.

http://www.ncbi.nlm.nih.gov/pubmed/17376626
______________________________________________________
Ocular Signs of Lyme Disease

http://www.livestrong.com/article/71899 ... e-disease/
______________________________________________________
Long-term follow-up of chronic Lyme neuroretinitis.

http://www.ncbi.nlm.nih.gov/pubmed/9002133
______________________________________________________
Neuroretinitis.

http://www.ncbi.nlm.nih.gov/pubmed/11198149
soijuv
 
Viestit: 3010
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Elo 26, 2011 10:01

Borrelia-bakteeri aiheutti suonikalvon tulehduksen ja verkkokalvon irtoamisen. 69-vuotiaalle miehelle annettiin suunkautta amoksisilliinia (500mg x 3) sekä suonensisäisesti keftriaksonia 2g/vrk kuukauden ajan. Kahden viikon kuluttua hoidoista verkkokalvo oli parantunut. Löydös vahvistaa kyseessä olleen käynnissä olevan infektion eikä autoimmuunireaktion. (2011)

RETINAL Cases & Brief Reports:
POST AUTHOR CORRECTIONS, 09 August 2011
doi: 10.1097/ICB.0b013e3182247783
Case Report: PDF Only
Lyme Disease Resolution of a serous retinal detachment and chorioretinal folds after antibiotic therapy
Grinager, Hans S MD; Krason, David A MD; Olsen, Timothy W MD
Abstract
Background: Ocular manifestations of Lyme disease are uncommon. There has not been a documented case of serous retinal detachment and chorioretinal folds because of Lyme disease that have resolved after only antibiotic treatment.
Methods (Case Report): A 69-year-old white man with a history of recent tick bites presented with a gradual decrease in visual acuity in the left eye. Initial visual acuity was 3/200 in the left eye. Examination revealed an inferior, serous, macula-off retinal detachment. Chorioretinal folds were also noted. Lyme screening antibody test (enzyme-linked immunosorbent assay) was positive and a confirmatory Western blot was immunoglobulin M negative and immunoglobulin G positive.
Results: Oral amoxicillin (500 mg 3 times daily for 2 weeks) was given followed by intravenous ceftriaxone (2 g daily for 4 weeks). After two weeks of ceftriaxone, fundus examination and ultrasonography showed complete reattachment of the macula and periphery, and only mild residual chorioretinal folds remained on fluorescein angiogram.
Conclusion: We suggest that Borrelia burgdorferi infection led to choroidal inflammation with secondary chorioretinal folds and a serous retinal detachment, which resolved with antibiotic therapy alone. This supports the suspicion of an intraocular infection, perhaps involving the choroid, as opposed to a secondary autoimmune reaction.
(C) 2011 Ophthalmic Communications Society, Inc.
soijuv
 
Viestit: 3010
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Su Loka 09, 2011 20:20

Borrelia-bakteeri tulee ottaa huomioon silmätulehduksissa. 90-vuotiaalla naisella oli ollut puoli vuotta aiemmin punkinpurema. Borreliatestit olivat silloin negatiiviset. Nyt positiiviset. (2011)

Lyme-Associated Orbital Inflammation Presenting as Painless Subacute Unilateral Ptosis.

Xu L, Winn BJ, Odel JG

J Neuroophthalmol 2011 09 27

ABSTRACT: A 90-year-old woman presented with subacute painless left ptosis. Examination of the left eye revealed ptosis with loss of the superior eyelid sulcus, 2 mm of proptosis, mild tenderness with retropulsion, and optic disc edema. Levator function and extraocular movements were normal, and there was no relative afferent pupillary defect. MRI demonstrated thickening of the extraocular muscles in the left orbit with lacrimal gland enlargement and mild enhancement of the optic nerve sheath. Serology revealed a positive enzyme-linked immunosorbent assay for Lyme antibodies and a positive Western blot of Lyme IgG titer. The patient recalled a tick bite 6 months earlier, at which time Lyme serologies were negative. After 3 weeks of intravenous ceftriaxone, she had a significant improvement and a full recovery by 3 months. Lyme disease should be included in the differential diagnosis of orbital inflammation, especially in Lyme-endemic areas.
soijuv
 
Viestit: 3010
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Pe Loka 14, 2011 21:36

Borrelioosi/silmäsairaudet

Borreliabakteeri kykenee aiheuttamaan silmän eri osissa tulehduksia, valoherkkyyttä, kipua jne. Bakteerin aiheuttamat näköhermon vauriot saattavat johtua tulehduksesta tai kohonneesta kallonsisäisestä paineesta. Silmäsairauksia voi esiintyä sairauden kaikissa vaiheissa, mutta ne ovat yleisempiä myöhäisvaiheessa. Antibioottihoito auttaa joissakin tapauksissa, mutta ei aina.

Suomalaisten tutkijoiden mukaan borrelioosia/silmäoireita sairastavilta tulee ottaa vasta-ainetesti ELISAn lisäksi immunoblottaus ja PCR. Positiivinen PCR näytää olevan yhteydessä negatiiviseen vasta-ainetestiin. Lisäksi osalla sairastuneista ELISA oli negatiivinen mutta immunoblottaus positiivinen. (Graefes Arch Clin Exp Ophthalmol. 1999 Mar; 237(3): 225-30 The laboratory diagnosis of ocular Lyme borreliosis. Mikkilä ym.)


Ophthalmology. 2000 Mar;107(3):581-7

The expanding clinical spectrum of ocular lyme borreliosis.
Mikkila HO,
Seppala IJ,
Viljanen MK,
Peltomaa MP,
Karma A.
Department of Ophthalmology, Helsinki University Central Hospital, Finland.

OBJECTIVE: To delineate the clinical manifestations of ocular Lyme borreliosis, while concentrating on new symptoms and findings and the phase of appearance of ophthalmologic disorders. DESIGN: Observational case series. PARTICIPANTS: Ten patients with Lyme borreliosis-associated ophthalmologic findings previously reported from the Helsinki University Central Hospital in addition to 10 new cases that have since been diagnosed. INTERVENTION/TESTING: The patients underwent medical and ophthalmologic evaluation. The diagnosis of Lyme borreliosis was based on medical history, clinical ocular and systemic findings, determinations of antibodies to Borrelia burgdorferi by enzyme-linked immunosorbent assay and immunoblot analysis, the detection of DNA of B. burgdorferi by polymerase chain reaction, and exclusion of other infectious and inflammatory causes. MAIN OUTCOME MEASURES: Ocular complaints, presenting ophthalmologic findings, and the stage of Lyme borreliosis were recorded. RESULTS: Four patients presented with a neuro-ophthalmologic disorder, five had external ocular inflammation, 10 patients had uveitis, and one had branch retinal vein occlusion. One patient developed episcleritis and one patient developed abducens palsy within 2 months of the infection incident. In the remaining 14 patients in whom the time of infection was traced, the ocular manifestations appeared in the late stage of Lyme borreliosis. Two patients with a neuro-ophthalmologic disorder and one with external ocular inflammation experienced severe photophobia, whereas the main reported symptom of the patients with uveitis was decreased visual acuity. Four patients with external ocular disease and one with a neuro-ophthalmologic disorder experienced severe periodic ocular or facial pain. Retinal vasculitis developed in seven patients with uveitis.

CONCLUSIONS: Lyme borreliosis can cause a variety of ocular manifestations, which develop mainly in the late stage of the disease. Photophobia and severe periodic ocular pain can be characteristic symptoms of Lyme borreliosis. In the differential diagnosis of retinal vasculitis, Lyme borreliosis should be taken into account, especially in endemic areas.

PMID: 10711899 [PubMed - indexed for MEDLINE]



Ophthalmology. 2001 Nov;108(11):2071-5. Links

Occurrence of uveitis in recently diagnosed juvenile chronic arthritis: a prospective study.
Kotaniemi K,
Kautiainen H,
Karma A,
Aho K.
Rheumatism Foundation Hospital, Heinola, Finland.

OBJECTIVE: To examine the occurrence and characteristics of uveitis in patients with recently diagnosed juvenile chronic arthritis (JCA). DESIGN: A prospective observational case series. PARTICIPANTS/METHODS: The study covered the new cases detected with JCA (426 children), all of whom were referred to an ophthalmologic consultation during 1989 to 1996 at the Pediatric Department of the Rheumatism Foundation Hospital, Heinola, Finland. MAIN OUTCOME MEASURES: The children with JCA were followed by ophthalmologic and pediatric examinations two to four times a year. The type and course of arthritis and presentation and characteristics of uveitis were examined prospectively. RESULTS: Uveitis was detected in 104 of 426 children (24%). Two thirds of all patients and the same proportion of those with uveitis were girls. Proportionally, uveitis was found to be as common among children with oligoarthritis (27%) as among those with seronegative polyarthritis (25%). Antinuclear antibodies (ANA) were detected significantly more frequently in patients with uveitis (66%) than among those without uveitis (37%) (P < 0.001). The uveitis was asymptomatic in 99 cases; only 5 children had episodes of acute anterior symptomatic uveitis. Uveitis was found before or within 3 months from the onset of recent arthritis in 51 of 104 children (49%) and later on in 53 of 104 children (51%). The mean age at diagnosis of uveitis was 5.9 years (range, 1.1-17.7; median, 4.9 years). The mean period from the diagnosis of JCA to the diagnosis of uveitis was 1.1 years (range, -2.4-6.5; median, 0.3 years). The mean age at diagnosis of JCA was 4.8 years (range, 0.6-15; median, 3.2 years) among those with uveitis and 7.3 years (range, 0.9-16; median, 6.7 years) among those who did not have it (P < 0.001). Uveitis was ongoing in 63 children at the end of the follow-up period. The mean follow-up time was 4.5 years (range, 0-9.7) for all children and 5.6 years (range, 1.3-9.6) for those with uveitis. In most instances, the visual prognosis was good. In 25 of 104 patients (24%) one or more complications of uveitis were found, but in only three children did the visual acuity decrease to 20/60 or less, and none became blind. All the other patients had visual acuity > or = 20/40.

CONCLUSIONS: In this patient group, uveitis in JCA frequently appeared very early after the onset of arthritis. The uveitis was significantly more common in patients with an early onset of arthritis combined with ANA positivity. The proportion of children with uveitis was as large in those with polyarthritis as in those with oligoarthritis, with no predilection to girls.

PMID: 11713082 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=11713082

Pediatrics. 2001 Aug;108(2):477-81

Optic neuropathy in children with Lyme disease.
Rothermel H,
Hedges TR 3rd,
Steere AC.
Division of Rheumatology/Immunology, Tufts University School of Medicine, New England Medical Center, Boston, MA 02111, USA.

Involvement of the optic nerve, either because of inflammation or increased intracranial pressure, is a rare manifestation of Lyme disease. Of the 4 children reported here with optic nerve abnormalities, 2 had decreased vision months after disease onset attributable to optic neuritis, and 1 had headache and diplopia early in the infection because of increased intracranial pressure associated with Lyme meningitis. In these 3 children, optic nerve involvement responded well to intravenous ceftriaxone therapy. The fourth child had headache and visual loss attributable to increased intracranial pressure and perhaps also to optic neuritis. Despite treatment with ceftriaxone and steroids, he had persistent increased intracranial pressure leading to permanent bilateral blindness. Clinicians should be aware that neuro-ophthalmologic involvement of Lyme disease may have significant consequences. If increased intracranial pressure persists despite antibiotic therapy, measures must be taken quickly to reduce the pressure.

PMID: 11483820 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=11483820

Eur J Ophthalmol. 2001 Apr-Jun;11(2):203-6. Links

Optic nerve lesion following neuroborreliosis: a case report.
Burkhard C,
Gleichmann M,
Wilhelm H.
Ahaus Eye Hospital, Germany. carsten@dr-burkhard.de

PURPOSE: Neuroborreliosis may cause various neuro-ophthalmological complications. We describe a case with a bilateral optic neuropathy. CASE REPORT: A 58-year-old female developed facial paresis six weeks after an insect bite. One week later she developed bilateral optic disc swelling with haemorrhages and nerve fibre bundle defects in the lower visual field of the left eye. In CSF and serum, raised IgM and IgG titres to Borrelia burgdorferi were found. Systemic antibiotic treatment led to improvement of the vision and facial paresis, but not all visual field defects resolved, probably due to ischemic lesions of the optic disc. DISCUSSION/CONCLUSIONS: In optic nerve lesions due to neuroborreliosis it is difficult to distinguish between inflammatory and ischemic lesions. This patient demonstrated features of an ischemic optic nerve lesion.

PMID: 11456029 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=11456029

Ophthalmology. 2002 Jan;109(1):143-5

Posterior scleritis associated with Borrelia burgdorferi (Lyme disease) infection.
Krist D,
Wenkel H.
Department of Ophthalmology, University Erlangen-Nurnberg, Schwabachanlage 6, D-91054 Erlangen, Germany.

OBJECTIVE: To report on the clinical findings in a patient with posterior scleritis associated with infection with Borrelia burgdorferi. DESIGN: Interventional case report. PARTICIPANT: A 39-year-old male ranger who experienced posterior scleritis after several tick bites with erythema migrans. TESTING: Extensive ophthalmic and systemic workup, including serologic testing and imaging techniques. RESULTS: Sonography and contrast-enhanced computed tomography showed a large scleral mass (16 x 12 x 13 mm) in a patient with painful proptosis in the left eye with episcleral vascular dilation, reduction in bulbar motility, and chorioretinal folds in the upper temporal quadrant. Treatment with high-dose corticosteroids resulted in rapid regression of clinical symptoms and of the scleral mass. Intensive workup revealed immunoglobulin M antibodies (enzyme-linked immunoassay, Western immunoblot) and a positive lymphocyte transformation assay against B. burgdorferi. No other cause for posterior scleritis could be identified. CONCLUSIONS: Posterior scleritis should be added to the list of ocular manifestations associated with Lyme disease. Because corticosteroids alone resulted in rapid improvement of clinical symptoms, the scleritis might be mediated by autoimmunologic mechanisms.

PMID: 11772594 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=11772594



J Neurol. 2002 Aug;249(8 ):1119-20. Links

Internuclear ophthalmoplegia as the first sign of neuroborreliosis.
Hardon WJ,
Bernsen HJ,
van Nouhuys-Leenders J,
Mulder B.
PMID: 12420716 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum



Przegl Epidemiol. 2002;56 Suppl 1:85-90. Links

[Ophthalmic manifestations in Lyme borreliosis]
[Article in Polish]

Zagorski Z,
Biziorek B,
Haszcz D.
Katedra i I Klinika Okulistyki Akademii Medycznej w Lublinie.

We reviewed ophthalmic manifestations in Lyme borreliosis, concentrating on clinical and laboratory diagnosis, differential diagnosis and treatment options. Ocular involvement may occur in every stage of the disease. Conjunctivitis and episcleritis are the most frequent manifestations of the early stage. Neuro-ophthalmic disorders and uveitis occur in the second stage whereas keratitis, chronic intraocular inflammation and orbital myositis have been reported in the third stage of borreliosis.

PMID: 12194235 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum





AJNR Am J Neuroradiol. 2002 Apr;23(4):657-9

Orbital Lyme disease: MR imaging before and after treatment: case report.
Fatterpekar GM,
Gottesman RI,
Sacher M,
Som PM.
Department of Radiology, Mount Sinai School of Medicine, New York University, NY 10029, USA.

Lyme disease is a multi-system organ disease caused by Borrelia burgdorferi. Although ocular manifestations have been reported, these remain a rare feature of the disease. To our knowledge, the radiology literature has not documented orbital Lyme disease both before and after treatment. We present the MR imaging findings of florid Lyme disease affecting the extraocular muscles in a 46-year-old man. A follow-up MR imaging study performed 6 months after a course of antibiotic therapy revealed complete resolution of the myositic changes.

PMID: 11950661 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum



Rev Neurol (Paris). 2005 May;161(5):599-601. Links

[Rapid onset of visual recovery following acute visual loss due to leber's hereditary optic neuropathy]
[Article in French]

Kawasaki A,
Borruat FX.
Unite de Neuro-Ophtalmologie, Hopital Ophtalmique Jules-Gonin, Lausanne, Suisse. aki.kawasaki@ophtal.vd.ch

INTRODUCTION: Leber's hereditary optic neuropathy (LHON) is a maternally inherited disorder affecting the optic nerves in which the typical clinical presentation is subacute, painless, sequential visual loss in young adult males. Patients with LHON who have atypical clinical features may be initially misdiagnosed. OBSERVATION: An 8-year-old boy developed an acute severe bilateral optic neuropathy associated with pain and mild optic disc edema. Molecular genetic testing of his mitochondrial DNA revealed two point mutations, T14484C and G15257A. His vision began to improve within one month of onset of visual loss and eventually recovered to 20/15 in both eyes. Four years previously, his oldest sister had acutely lost vision in both eyes at age 12 years. Her young age, female gender, the bilateral visual loss associated with pain, optic disc edema, absent family history of visual loss and negative workup were felt to be most consistent with a clinical diagnosis of idiopathic optic neuritis of childhood. Her visual recovery which began within two months of visual loss further supported the diagnosis. She was retrospectively re-diagnosed with LHON after her younger brother was genetically confirmed. CONCLUSION: We describe two siblings with LHON whose time course from onset of visual loss to onset of visual recovery was unusually rapid. Because of other atypical features for LHON such as their young age at presentation, bilateral simultaneous visual loss and associated periorbital pain, their clinical profile appeared more typical of a demyelinating disease such as childhood optic neuritis. The first affected sibling (sister) was initially misdiagnosed. This report emphasizes that the clinical spectrum of LHON is variable and thus, LHON should be considered in any patient with an acute bilateral optic neuropathy, even in the absence of a positive family history. Correct diagnosis of this maternally inherited disorder is important for assessment of visual prognosis and appropriate genetic counseling.

PMID: 16106816 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=16106816



Acta Clin Belg. 2005 Sep-Oct;60(5):270-5. Links

An eye on inflammatory eye disease.
Kestelyn PG.
Afdeling Oogheelkunde, Universitair Ziekenhuis, Gent. philippe.kestelyn@ugent.be

The purpose of this article is to outline the interaction between ophthalmologists and internists in the management of uveitis. Two issues will be addressed: 1) which strategies should the internist follow when asked to investigate a case of uveitis; and 2) in which systemic diseases should the internist order an ocular examination to rule out intraocular inflammation. The modern approach to the diagnosis of uveitis is based on the naming-meshing system popularized by Smith and Nozik. After a short history (ocular complaints, general health) an ophthalmic examination is carried out to determine the anatomic structures involved. Based on the results a uveitis is classified as anterior uveitis, intermediate uveitis, posterior uveitis, or panuveitis. Associated factors (eg, unilateral versus bilateral, acute versus chronic, granulomatous versus nongranulomatous, etc.) are also assessed. Based on this information the type of uveitis will be named (eg, acute, nongranulomatous, unilateral, anterior uveitis) and matched (meshing) to a potential list of etiologies (eg, viral iritis, HLA-B 27 associated iritis). Targeted questioning and selected medical and laboratory investigations based on the shortlist will then identify a possible cause for a particular patient's uveitis. In other words the ophthalmologist should never ask the internist to run the full battery of tests in a patient with uveitis. He rather should indicate which type of uveitis is present and what are the most likely diagnoses to be excluded. Many systemic diseases cause diffuse inflammation and are associated with uveitis. These include tuberculosis, spirochaetal diseases such as Lyme disease and syphilis, sarcoidosis, Behcet syndrome, juvenile idiopathic arthritis, and HIV infection amongst many others. Routine ophthalmic examination in patients with systemic disease may be indicated for diverse reasons: to prevent profound damage due to asymptomatic uveitis in JIA; to detect diagnostic clues in patients with febris e causa ignota; or to rule out opportunistic infections in HIV positive patients. It is clear that the information gained from routine examination in systemic disease will be greatly dependent on the prevalence of ocular involvement in a particular disease.

PMID: 16398326 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum



Rev Prat. 2005 Mar 15;55(5):471-7. Links

[Lyme borreliosis]
[Article in French]

De Martino S,
Jaulhac B.
Laboratoire de bacteriologie, Hopitaux universitaires de Strasbourg, 3, rue Koeberle, 67000 Strasbourg.

Lyme borreliosis is a bacterial tick borne infection due to Borrelia burgdorferi sensu lato. In 50% of the cases, the disease begins by a centrifuge erythema migrans localized around the tick bite. Neurological, articular and rarely cardiac, ocular or cutaneous manifestation may be observed as secondary manifestations. They sign the dissemination, the proliferation of Borrelia burgdorferisensu lato and the development of the immune response. In the absence of erythema migrans, secondary clinical manifestations may be difficult to diagnose. Direct detection of Borrelia burgdorferi sensu lato by culture is fastidious, time consuming and of a low sensitivity. Molecular methods (polymerase chain reaction) are very specific but limited by a low bacterial burden in the tissues. Serological testing interpretation is tricky but guides the diagnosis at the disseminate phase. Curative antibiotherapy is efficient, especially at the initial phase of infection. The two main elements for prophylaxis are individual protection from tick bites and a rapid and complete tick extraction. Antibioprophylaxy of tick bites is not recommended and a strict clinical surveillance must be done.

PMID: 15895947 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum



J Fr Ophtalmol..

2005 Feb;28(2):218-23

[Lyme disease from an ophthalmological point of view]
[Article in French]

Kadz B,
Putteman A,
Verougstraete C,
Caspers L.
Service d'Ophtalmologie, CHU Saint Pierre, Universite Libre de Bruxelles, Rue Haute 322, 1000 Bruxelles, Belgique. barbaraopht@hotmail.com

The first case of Lyme disease was described more than 25 years ago in the city of Lyme, Connecticut (USA) and although the responsible pathogenic organism is known (Borrelia Burgdorferi) as well as its vector (a tick from the Ixode genus), it is still underdiagnosed and often poorly known by practitioners. The symptomatology is classically divided into three phases depending on the time between the tick bite and the first symptoms. However, in a number of cases this clinical division of the disease is not easily applied. We describe three cases of atypical ocular manifestations to illustrate this problem. Recently developed laboratory tests help confirm the diagnosis but should not be used without a good knowledge of the disease. This study aims to emphasize the difficulty of diagnosis and the importance of appropriate treatment and to avoid potentially permanent complications.

PMID: 15851957 [PubMed - indexed for MEDLINE

http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum



Arch Soc Esp Oftalmol. 2003 Jan;78(1):51-4. Links

[Diplopia as the first manifestation of Lyme disease]
[Article in Spanish]

Asensio Sanchez VM,
Corral Azor A,
Bartolome Aragon A,
De Paz Garcia M.
Hospital General del INSALUD, Medina del Campo, Valladolid, Espana.

CASE REPORT: We report a case of Lyme disease with diplopia as the first manifestation, without systemic symptoms in contrast with other cases of this disease. The serodiagnosis was confirmed by ELISA analysis and evaluation of cerebrospinal fluid (CSF) antibodies. Symptoms readily vanished after the introduction of antibiotherapy. DISCUSSION: Lyme disease is an infectious multi-systemic disorder caused by Borrelia burgdorferi. Neuro-ophthalmological manifestations occur during the second stage of the illness in extremely variable clinical forms.

PMID: 12571776 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=12571776



Ophthalmology. 2004 May;111(5):1023-8

Orbital myositis associated with Borrelia burgdorferi (Lyme disease) infection.
Carvounis PE,
Mehta AP,
Geist CE.
Department of Ophthalmology, The George Washington University, Washington, DC 20037, USA.

OBJECTIVE: To report on the clinical findings in a patient with isolated left inferior rectus myositis associated with serologically confirmed Borrelia burgdorferi infection. DESIGN: Interventional case report. TESTING: Comprehensive clinical, laboratory, and imaging evaluation. RESULTS: Contrast-enhanced computed tomography showed a swollen inferior rectus muscle with infraorbital soft tissue swelling in a patient with diplopia and prior symptoms consistent with manifestations of Lyme disease. Positive serum and cerebrospinal fluid antibodies to B. burgdorferi by enzyme-linked immunoassay were confirmed by Western blot, and the cerebrospinal fluid/serum antibody ratio was elevated. No alternative cause for orbital myositis was found, and treatment with antibiotics resulted in a complete recovery. CONCLUSIONS: Orbital myositis should be added to the expanding list of ophthalmic manifestations of Lyme disease. Correct diagnosis and appropriate antibiotic therapy may reduce the likelihood of further neurologic or ophthalmologic sequelae.

PMID: 15121383 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=15121383



Lijec Vjesn. 2004 May-Jun;126(5-6):124-8. Links

[Ocular manifestations of Lyme borreliosis in northwest Croatia]
[Article in Croatian]

Golubic D,
Vinkovic T,
Turk D,
Hranilovic J,
Slugan I.
Zupanijska bolnica Cakovec, Djelatnost za infektologiju.

Ocular manifestations in patients with Lyme borreliosis in northwest Croatia that occurred during the period between 1992 and 2001 were retrospectively analysed. The diagnosis of Lyme borreliosis was based on medical history, clinical manifestations, epidemiological data about tick contact, determinations of antibodies to Borrelia burgdorferi by serological assays, immunoblot analysis, therapeutic results and exclusion of other infectious agents of ocular disease. Of the eleven patients reported here with clinical manifestations of ocular Lyme borreliosis, 6 had chorioretinitis, 1 papillitis, 2 iridocyclitis, 1 occlusion of the arteriae centralis retinae, 1 neuritis retrobulbaris and 1 neuroretinitis. Diagnostic confirmation of LB was in most patients done by serological tests and/or by immunoblot method in serum. In the last few years we have also done culture and molecular diagnostic methods polymerase chain reaction (PCR)) in serum and cerebrospinal fluid. The patients were treated with 2 g of ceftriaxon i.v. per day for 14-21 days and/or with doxucyclin orally in a daily dose of 2 x 100 mg for 2-4 weeks. The therapeutic effect was followed up by regression of clinical symptoms (better visual acuity of the infected eye) and in changing of the specific antibody titer in serological tests. The authors emphasise the more detailed diagnostic proceedings of ocular Lyme borreliosis in patients with suspected Lyme borreliosis, an algorithm which contains data about residence in endemic area for LB, positive contact with ticks and/or the history of erythema migrans or any other Lyme borreliosis-like symptoms. For diagnostic confirmation it is necessary to use enzymeimmunoassay and immunoblot methods in serum, cerebrospinal fluid and aqueous humor, and isolation by culture or PCR can be used in the same diagnostic samples. Ocular Lyme borreliosis is an underdiagnosed disorder, because it is often unrecognised by ophthalmologists and due to weak seropositivity and seronegativity in the late ocular Lyme borreliosis. This is especially important in a highly endemic area for Lyme borreliosis like northwest Croatia, a border area of the central European andemic area for Lyme borreliosis.

PMID: 15628679 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=15628679

Coll Antropol. 2005;29 Suppl 1:137-9. Links

Paralytic strabismus as a manifestation of lyme borreliosis.
Zrinscak O,
Masnec-Paskvalin S,
Corak M,
Bacani B,
Mandic Z.
University Department of Ophthalmology, Clinical Hospital, Systers of Mercy, Zagreb, Croatia. ozrinscak@yahoo.co.uk

Lyme disease is a multi-system organ disorder caused by Borrelia burgdorferi. Although ocular manifestations have been reported, these remain a rare feature of the disease. This report shows a 49-years old patient that has been bitten by a tick and as consequence of which developed symptoms of the Lyme disease. In 1998 the patient was hospitalized in our Eye Clinic due to operating treatment of the paralytic strabismus (abductal nerve paralysis), as a rare feature of the Lyme disease. Postoperative squint angle was significantly reduced, but without any temporal movement. Diplopia was still present, though slightly reduced with the use of prism eyeglasses. The improvement of the quality of life was achieved, as well as the patient's satisfaction.

PMID: 16193697 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum



.J Fr Ophtalmol. 2005 Dec;28(10):1095-100

[Onset of Leber's hereditary optic neuropathy in association with borreliosis]
[Article in French]

Macarez R,
Bazin S,
Lagauche D,
Soullie B,
Giordano P,
May F,
Guigon B.
Service d'Ophtalmologie, HIA Clermont Tonnerre, BP 41, 29240 Brest-Armees.

INTRODUCTION: The diagnosis of Lyme disease in the presence of an acute optical neuritis always raises a difficult diagnostic problem. We present a case of Lyme-associated Leber's hereditary optic neuropathy (LHON). OBSERVATION: A 17-year-old Eurasian young man presented with left-eye visual impairment for 1 month. This loss of vision acuity in the left eye is related to an optic neuropathy. Mitochondrial DNA testing showed a G to A substitution at position 11778 confirming a diagnosis of LHON. The family history disclosed a case of LHON in a maternal cousin. The mother's family is Asian. Besides, serum examination of anti-Borrelia antibodies was performed and was positive against Borrelia burgdorferi garinii. The patient history indicated that he had been possessing a dog and was living in an endemic area of Lyme disease. But he did not recall receiving a tick bite nor having any erythema chronicum migrans. Initial examination showed bilateral green-red axis colour vision defects which made us fear bilateralisation of the optic neuropathy, which occurred 2 months later (that is 3 months after the onset of symptoms on the left eye). An antibiotic treatment by ceftriaxone was administered for 4 weeks all in all; and a long term ubidecarenone therapy was established. At present, after a 1-year follow up, the eyes' conditions remains unchanged. CONCLUSION: To our knowledge, this would be the first case reporting such an association, in which we can discuss the fortuitous character or the role of the infectious factor in the developing of the mitochondrial pathology. This observation also raises the problem of the positive diagnosis of Lyme disease when tick bite and erythema are absent or underestimated.

PMID: 16395203 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=16395203

Przegl Epidemiol. 2002;56 Suppl 1:85-90. Links

[Ophthalmic manifestations in Lyme borreliosis]
[Article in Polish]

Zagorski Z,
Biziorek B,
Haszcz D.
Katedra i I Klinika Okulistyki Akademii Medycznej w Lublinie.

We reviewed ophthalmic manifestations in Lyme borreliosis, concentrating on clinical and laboratory diagnosis, differential diagnosis and treatment options. Ocular involvement may occur in every stage of the disease. Conjunctivitis and episcleritis are the most frequent manifestations of the early stage. Neuro-ophthalmic disorders and uveitis occur in the second stage whereas keratitis, chronic intraocular inflammation and orbital myositis have been reported in the third stage of borreliosis.

PMID: 12194235 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=12194235







J Neuroophthalmol. 1994 Jun;14(2):77-80. Links

Transient worsening of optic neuropathy as a sequela of the Jarisch-Herxheimer reaction in the treatment of Lyme disease.
Strominger MB,
Slamovits TL,
Herskovitz S,
Lipton RB.
Department of Ophthalmology, Montefiore Medical Center, Bronx, NY 10467.

A 58-year-old woman developed neurologic and neuroophthalmologic manifestations of Lyme disease, including a radiculomyelitis, cranial neuritis and mild right optic neuropathy. Upon treatment with intravenous ceftriaxone a Jarisch-Herxheimer reaction occurred with encephalopathy, mild fever, worsening radiculomyelitis, and deterioration of her visual acuity. Intravenous methylprednisolone was given, and the visual acuity recovered over 72 hours. This case suggests that transient worsening of optic neuropathy can develop as a sequela of the Jarisch-Herxheimer reaction in the treatment of Lyme disease.

PMID: 7951931 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=7951931

Oftalmologia. 2006;50(1):16-20. Links

[Lyme disease--a relatively new entity]
[Article in Romanian]

Tsirmpas MD,
Tsirmpas D.
Clinica de Oftalmologie, Spitalul Clinic de Urgenta, Militar Central, Bucuresti.

PURPOSE: To bring in the attention of the medical personnel a relatively new discovered disease with serious consequences, that is often mistaken with a great multitude of miscellaneous syndromes. Also we want to highlight that it is not a rare disease taken into account its endemicity in Europe and consequently in Romania. SUMMARY: Lyme disease is a bacterial infection caused by a spirochete named "Borrelia Burgdorferi" transmitted to humans by a minuscule tick. It is a multi-systemic illness with ocular involvement as well. The disease mimics other pathologic conditions and because of this goes frequently undiagnosed and consequently untreated. Its ocular involvement may vary from a mild conjunctivitis to uveitis, optic neuritis and sometimes lead to blindness. The disease is endemic in Romania. If it is correctly diagnosed it can be successfully treated with specific antibiotics administrated orally or i.v.

PMID: 16773934 [PubMed - indexed for MEDLINE]





J Neuroophthalmol. 1994 Mar;14(1):15-20. Links

Ophthalmic manifestations in Lyme borreliosis. A review.
Bergloff J,
Gasser R,
Feigl B.
Department of Ophthalmology, University of Graz, Austria.

Lyme borreliosis is an emerging tick-borne spirochetal infection characterized by a broad variety of symptoms, ranging from neurologic disorders and different skin manifestations to cardiac symptoms. Many ocular and neuro-ophthalmic symptoms have recently been attributed to Lyme disease. Especially in endemic areas ophthalmologists need to be aware of Borrelia burgdorferi as a possible causal agent. The aim of this paper is to present a short review of the literature of ophthalmic disorders resulting from Borrelia burgdorferi infections.

PMID: 8032473 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=8032473





Am J Ophthalmol. 1995 Feb;119(2):127-35. Links Comment in:

Am J Ophthalmol. 1995 Aug;120(2):263-4.

Diagnosis and clinical characteristics of ocular Lyme borreliosis.
Karma A,
Seppala I,
Mikkila H,
Kaakkola S,
Viljanen M,
Tarkkanen A.
Department of Ophthalmology, University of Helsinki, Finland.

PURPOSE: To establish a diagnosis, in a group of patients we studied the characteristics of ocular Lyme borreliosis. METHODS: During a two-year period, 236 patients with prolonged external ocular inflammation, uveitis, retinitis, optic neuritis, or unexplained neuro-ophthalmic symptoms were examined for Lyme borreliosis. Antibodies to Borrelia burgdorferi were measured by indirect ELISA and western blot. Cerebrospinal fluid was also analyzed by polymerase chain reaction. RESULTS: Ocular Lyme borreliosis was diagnosed in ten patients on the basis of medical history, clinical findings, and serologic test results. Results of ELISA disclosed that five patients were seropositive, two patients showed borderline reactivity, and three patients were seronegative. Four of the five patients with borderline or negative results by ELISA had a positive result by western blot analysis. In one seropositive patient, polymerase chain reaction verified a gene of B. burgdorferi endoflagellin from the vitreous and cerebrospinal fluid specimen. In five of the six patients with known onset of the Borrelia infection, the ocular disorder appeared as a late manifestation. Abnormalities of the posterior segment of the eye, such as vitreitis, retinal vasculitis, neuroretinitis, choroiditis, and optic neuropathy were seen in six patients. Bilateral paralytic mydriasis, interstitial keratitis, episcleritis, and anterior uveitis were seen in one patient each. CONCLUSIONS: Late-phase ocular Lyme borreliosis is probably underdiagnosed because of weak seropositivity or seronegativity in ELISA assays. Ocular borrelial manifestations show characteristics resembling those seen in syphilis.

PMID: 7832219 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=7832219







Am J Med. 1995 Apr 24;98(4A):60S-62S. Links

Ocular manifestations of Lyme disease.
Lesser RL.
Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, Connecticut, USA.

Although ocular manifestations of Lyme disease have long been noted, they remain a rare feature of the disease. The spirochete invades the eye early and remains dormant, accounting for both early and late ocular manifestations. A nonspecific follicular conjunctivitis occurs in approximately 10% of patients with early Lyme disease. Keratitis occurs often within a few months of onset of disease and is characterized by nummular nonstaining opacities. Inflammatory syndromes, such as vitritis and uveitis, have been reported; in some cases, a vitreous tap is required for diagnosis. Neuro-ophthalmic manifestations include neuroretinitis, involvement of multiple cranial nerves, optic atrophy, and disc edema. Seventh nerve paresis can lead to neurotrophic keratitis. In endemic areas, Lyme disease may be responsible for approximately 25% of new-onset Bell's palsy. Criteria for establishing that eye findings can be attributed to Lyme disease include the lack of evidence of other disease, other clinical findings consistent with Lyme disease, occurrence in patients living in an endemic area, positive serology, and, in most cases, response to treatment. Management of ocular manifestations often requires intravenous therapy.

PMID: 7726193 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=7726193

Retina. 1996;16(6):505-9.

Long-term follow-up of chronic Lyme neuroretinitis.
Karma A,
Stenborg T,
Summanen P,
Immonen I,
Mikkila H,
Seppala I.
Department of Ophthalmology, University of Helsinki, Finland.

PURPOSE: The authors report sequential fluorescein angiographic and color photographic findings of the fundi and response to treatment in a patient with chronic Lyme neuroretinitis. METHODS: A Lyme enzyme-linked immunosorbent assay with purified 41-kd flagellin as antigen was used to detect immunoglobulin G and immunoglobulin M antibodies to Borrelia burgdorferi in serum, cerebrospinal fluid, and vitreous. The changes were documented by fluorescein angiography and color photography tests performed during a 5 1/2 year follow-up. RESULTS: The diagnosis of Lyme neuroretinitis was based on the history of erythema migrans and positive Lyme enzyme-linked immunosorbent assay tests from cerebrospinal fluid and vitreous and by the exclusion of other infectious and systemic diseases and uveitis entities. Fluorescein angiography results disclosed bilateral chronic neuroretinal edema with areas of cystoid, patchy, and diffuse hyperfluorescence peripapillary and in the macular areas. The hyperfluorescent lesions enlarged despite a 9-month period of antibiotic therapy. CONCLUSION: Lyme borreliosis may cause neuroretinitis with unusual angiographic findings. Chronic Lyme neuroretinitis may be unresponsive to antibiotic therapy.

PMID: 9002133 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=9002133

J Fr Ophtalmol. 1990;13(6-7):339-42. Links

[Oculomotor paralysis and Lyme disease]
[Article in French]

Bienvenot M,
Tranchant C,
Flament J,
Warter JM,
Sahel J.
Clinique Ophtalmologique, Hopital Civil, Strasbourg.

Lyme disease is an infectious multi system disorder caused by the spirochete Borrelia Burgdorferi. Neurologic syndromes occurring during the second stage of the illness are common and the neurologic feature is extremely variable. We report a case of Lyme disease with diplopia. In contrast with most reported cases of ocular motor involvement in Lyme disease, no other systemic symptoms were detected. The serodiagnosis, although mildly positive, was confirmed by western blot antibodies analysis and evaluation of CSF antibodies. Symptoms readily vanished 3 days after the introduction of antibiotherapy. The efficacity of antibiotic therapy on the quality and timing of functional recovery justifies the use of this therapy.

PMID: 2290005 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2290005

Ophthalmology. 1990 Jun;97(6):699-706. Links

Neuro-ophthalmologic manifestations of Lyme disease.
Lesser RL,
Kornmehl EW,
Pachner AR,
Kattah J,
Hedges TR 3rd,
Newman NM,
Ecker PA,
Glassman MI.
Department of Ophthalmology and Visual Science, Yale University School of Medicine, New Haven, CT 06510.

Lyme disease is a tick-borne spirochetal infection characterized by skin rash, neurologic, cardiac, and arthritic findings. The authors report six patients with Lyme disease who had neuro-ophthalmologic manifestations. One patient had meningitis with papilledema, two had optic neuritis, and one had neuroretinitis. Three patients had sixth nerve paresis, two of whom cleared quickly, whereas multiple cranial nerve palsies and subsequent optic neuropathy developed in another. Early recognition of neuro-ophthalmologic findings can help in the diagnosis and treatment of Lyme disease.

PMID: 2374674 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2374674

Surv Ophthalmol. 1990 Nov-Dec;35(3):191-204

Lyme disease: neurologic and ophthalmic manifestations.
Winterkorn JM.
Department of Ophthalmology, North Shore University Hospital-Cornell University Medical College, Manhasset, New York.

Lyme disease is tick-borne infection which produces early and late manifestations in many organ systems. Prominent symptoms and signs occur in skin, heart, joints and nervous system. Many ocular and neuro-ophthalmic abnormalities recently have been attributed to Lyme disease, but some cases have not been well established as direct sequelae. This review of the contemporary state of knowledge about Lyme disease was undertaken so that more rigorous criteria can be applied in future diagnosis.

PMID: 2274849 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2274849



Ned Tijdschr Geneeskd. 1991 Aug 17;135(33):1500-2. Links

[Aspecific eye disorders in Lyme disease]
[Article in Dutch]

Jager M,
Kuiper H.
Academisch Ziekenhuis, afd. Oogheelkunde, Leiden.

Lyme disease shows a large variety of clinical signs and symptoms. Ocular disease may occur in the disseminated stage of the disease. Ocular signs are often not specific of Lyme disease. In the presence of unexplained ocular disease it may be wise to consider Lyme disease as a possible diagnosis. Diagnosis and therapy in two Lyme disease patients with ocular disease are discussed.

PMID: 1922471 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=1922471

Klin Monatsbl Augenheilkd. 1991 Jan;198(1):44-7. Links

[Bilateral Leber's neuroretinitis stellata in Borrelia burgdorferi seroconversion]
[Article in German]

Schonherr U,
Lang GE,
Meythaler FH.
Augenklinik mit Poliklinik der Universitat Erlangen-Nurnberg.

We report on a 22-year-old white female with bilateral Leber's stellate neuroretinitis occurring 5 weeks after a viral-like illness. Serological tests revealed a seroconversion for Borrelia burgdorferi indicating an etiological connection. During therapy with 200 mg doxycycline daily for 2 weeks on systemically steroids the optic disc swelling and macular star figure resolved. Visual acuity improved from 0.4 to 1.0 in this time period. It is important that the ophthalmologist should consider Lyme-Borreliosis in isolated neuroretinitis, because the prognosis depends on the time when treatment is initiated.

PMID: 2023374 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=2023374



Klin Monatsbl Augenheilkd. 1992 Aug;201(2):83-91. Links

[Ocular findings in infection with Borrelia burgdorferi]
[Article in German]

Reim H,
Reim M.
Augenklinik, Medizinischen Fakultat, Rheinisch-Westfalischen Technischen Hochschule Aachen.

During the years 1988 to 1990 ten patients were observed in the eye clinic of RWTH Aachen with ocular findings of infection with Borrelia burgdorferi. 6 of them showed neuro-ophthalmological signs, 4 had uveitis. In both groups recent infections were documented in fresh and chronic stages of the disease, lasting longer than one year. The various clinical pictures of the disease following infection with Borrelia burgdorferi are described. As a vaccination against Borreliosis is not yet available, it is important to detect the antibodies against Borrelia burgdorferi early enough, to initiate an effective treatment.

PMID: 1434386 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=1434386

Br J Ophthalmol. 1992 Mar;76(3):181-2. Links

Intermediate uveitis and Lyme borreliosis.
Breeveld J,
Rothova A,
Kuiper H.
Department of Ophthalmology, Academic Medical Centre, Amsterdam, The Netherlands.

A case of chronic intermediate uveitis and associated classic snowbanking (pars planitis) with severe cystoid macular oedema probably due to Lyme borreliosis is reported. Despite a disease duration of 10 years the patient's ocular symptoms and visual acuity responded promptly to intravenous ceftriaxone treatment. This case demonstrates that periodic reevaluation of patients with intermediate uveitis is necessary to obtain a specific diagnosis which may include Lyme borreliosis.

PMID: 1540569 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=1540569

J Neuroophthalmol. 1997 Jun;17(2):108-21. Links

Neuro-ophthalmic manifestations of Lyme disease.
Balcer LJ,
Winterkorn JM,
Galetta SL.
Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia, USA.

Lyme disease is a multisystem disorder caused by infection with the Borrelia burgdorferi spirochete. The diagnosis of Lyme disease usually is based on several clinical criteria, with supportive data from laboratory testing. The presence of the bullseye skin lesion, erythema migrans, is the single pathognomonic criterion. In the 20 years since the initial description of Lyme disease in the United States, B. burgdorferi has been implicated as an etiologic agent in numerous ophthalmic and neuro-ophthalmic syndromes, involving most structures from the cornea to the cranial nerves. Neuro-ophthalmic and ocular manifestations of Lyme disease include meningitis with papilledema, cranial neuropathies, follicular conjunctivitis, nummular keratitis, and intraocular inflammation. Although an association with Lyme disease has been purported for numerous other syndromes, a definite causal relationship has not been proved in many cases. During a period of rapidly increasing awareness of Lyme disease, a high index of suspicion and poorly defined criteria for its presence have resulted in over-diagnosis of Lyme disease. In the authors' experience, the incorrect diagnosis of Lyme disease initially has been made in patients with allergic conjunctivitis, keratoconus, morning glory syndrome, craniopharyngioma, meningioma, CNS lymphoma, paraneoplastic syndrome, multiple sclerosis, sarcoid, syphilis, and functional illness. Nevertheless, this treatable infection must be an important consideration in the differential diagnosis of certain ocular or neurologic diseases.

PMID: 9176782 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=9176782



Int Ophthalmol Clin. 1997 Spring;37(2):13-28. Links

The ocular manifestations of Lyme disease.
Zaidman GW.
New York Medical College, Valhalla, USA.

LD (with its ocular manifestations) is a worldwide disorder that is increasing in frequency. It is a treatable multisystemic disease that presents in three stages of severity. It can present with unusual forms of conjunctivitis, keratitis, cranial nerve palsies, optic nerve disease, uveitis, vitreitis, and other forms of posterior segment inflammatory disease. A patient with any of these ocular manifestations should be questioned for exposure to an area endemic for LD, tick bites, skin rash, or arthritis. Such patients should undergo serological testing. If the clinical presentation is suggestive of LD, a course of oral antibiotics should be used (unless the patient gives a history of adequate therapy). Topical corticosteroids can be used for anterior segment inflammation. An antibiotic therapeutic trial can be used for posterior segment or neuroophthalmic disease. Systemic corticosteroids without concomitant antibiotics should not be used in the treatment of ocular LD. If ocular LD is discovered and treated early, response to therapy usually is satisfactory.

PMID: 9269595 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=9269595

Eur J Ophthalmol. 1997 Jul-Sep;7(3):251-5. Links

The significance of serum anti-Borrelia antibodies in the diagnostic work-up of uveitis.
Mikkila H,
Seppala I,
Leirisalo-Repo M,
Karma A.
Department of Ophthalmology, University of Helsinki, Finland.

PURPOSE: To assess the utility of testing uveitis patients for anti-Borrelia antibodies in an area endemic for Lyme borreliosis. METHODS: We examined 161 uveitis patients for serum antibodies to Borrelia burgdorferi by Lyme ELISA. Antibodies were determined in patients with uveitis of unknown etiology and non-selectively from patients with an established diagnosis. RESULTS: Concentrations of antibodies to B. burgdorferi were elevated in 26 uveitis patients (16.1%), with elevated IgG in 11 of them (6.8%). In four of these patients Lyme borreliosis was a highly suggestive cause of uveitis because of a history of tick bites, systemic symptoms, response to antibiotic therapy, and/or a positive polymerase chain reaction result. Other causes of uveitis were ruled out. All these patients had vitritis. CONCLUSIONS: Non-selective testing of uveitis patients for Lyme antibodies is not reasonable even in endemic areas. We recommend using the Borrelia antibody test only in cases of uveitis of unknown cause, especially in patients with vitritis or other symptoms of Lyme borreliosis.

PMID: 9352279 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=9352279

Acta Ophthalmol Scand. 1997 Dec;75(6):716-9. Links

The etiology of uveitis: the role of infections with special reference to Lyme borreliosis.
Mikkila H,
Seppala I,
Leirisalo-Repo M,
Immonen I,
Karma A.
Department of Ophthalmology, University of Helsinki, Finland.

PURPOSE: To assess the distribution of different uveitis entities and to evaluate their associations with infections, especially Lyme borreliosis. METHODS: During a one-year period 160 consecutive uveitis patients were evaluated in a university clinic. Selected tests were performed depending on the medical history of the patient and the clinical picture of the ocular inflammation. RESULTS: Uveitis was classified into selected entities for 74.4% of the patients. A direct infection was suggested to be linked with uveitis in 23 patients (14.4%). Lyme borreliosis, toxoplasmosis, and herpetic infections were the most frequently seen, in seven patients (4.3%) each. All patients with Lyme uveitis had manifestations of the posterior segment of the eye, such as vitritis, retinal vasculitis, neuroretinitis, chorioretinitis, or optic neuropathy. CONCLUSION: Infections are an important cause of uveitis in a university clinic. Lyme borreliosis is a newly recognised uveitis entity which should be kept in mind in the differential diagnosis of intermediate or posterior uveitis in areas endemic for Lyme borreliosis.

PMID: 9527338 [PubMed - indexed for MEDLINE]

Klin Oczna. 1997;99(2):129-32. Links

[Clinical manifestation and diagnosis of ocular borreliosis]
[Article in Polish]

Biziorek B,
Zagorski Z,
Jedrzejewski D,
Haszcz D.
Katedry i l Kliniki Okulistyki AM w Lublinie.

PURPOSE: To present severe involvements of Borrelia burgdorferi in the etiology of uveitis, optic neuritis and other ocular inflammatory conditions. METHODS: IgM and IgG antibodies for Borrelia burgdorferi were detected by ELISA. Since May 1995 we have examined 78 patients for borreliosis. RESULTS: Borreliosis was diagnosed in 11 patients (4 males, 7 females; aged 7 to 48 ). 7 persons remembered being bitten by a tick, 3 months to 3 years before the onset of ocular symptoms. All patients had systemic symptoms and signs. Ocular manifestations were as follows: nonspecific chronic conjunctivitis in 4 patients, keratitis in 2, diminished corneal sensation in 1, iritis in 1, intermediate uveitis and perivasculitis in 1, posterior uveitis in 3, retinal haemorrhage in 1, optic neuritis in 1, optic disc oedema in 2, sixth nerve paresis in 1 patient. CONCLUSIONS: We emphasize the importance of performing serological tests for borreliosis in patients with uveitis, inflammatory diseases of unknown etiology, optic neuritis and other neuro-ophthalmic conditions.

PMID: 9379664 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=9379664

Nervenarzt. 1997 Oct;68(10):792-800

[Ocular myositis]
[Article in German]

Berkhoff M,
Sturzenegger M,
Schroth G,
Hess CW.
Neurologische Klinik, Inselspital, Universitat Bern.

We report a young woman presenting with "painful diplopia" caused by inflammation of external eye muscles affecting both eyes sequentially. Orbital MRI disclosed swelling, signal hyperintensity and enhancement of isolated eye muscles. Corticosteroid treatment led to a complete remission within a few days. The compiled data of a literature review enclosing 52 sufficiently documented patients diagnosed as orbital myositis is reported with respect to clinical features, laboratory findings, associated disease, value of imaging procedures (CT,MRI). Therapeutic aspects and differential diagnosis are reviewed.

PMID: 9441251 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=9441251

J Emerg Med. 1998 May-Jun;16(3):437-8

Lyme disease complicated by the Jarisch-Herxheimer reaction.
Maloy AL,
Black RD,
Segurola RJ Jr.
The Department of Emergency Medicine, Hospital of Saint Raphael, New Haven, Connecticut 06511, USA.

A 31-year-old woman diagnosed with Lyme disease was treated with amoxicillin. One hour after the first antibiotic dose, the patient became acutely ill. She developed hypertension, fever, and rigors. Shortly afterward, she became hypotensive and required fluid resuscitation. This systemic illness, the Jarisch-Herxheimer reaction, was first noted in association with antibiotic therapy for neurosyphilis. Thus, the institution of antibiotic therapy may be complicated by the Jarisch-Herxheimer reaction.

PMID: 9610974 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=9610974

Graefes Arch Clin Exp Ophthalmol. 1999 Mar;237(3):225-30

The laboratory diagnosis of ocular Lyme borreliosis.
Mikkila H,
Karma A,
Viljanen M,
Seppala I.
Department of Ophthalmology, Helsinki University Central Hospital, Finland.

BACKGROUND: A study was carried out to evaluate indirect enzyme-linked immunosorbent assay (ELISA), immunoblot analysis, and polymerase chain reaction (PCR) in the diagnostic work-up of ocular Lyme borreliosis. METHODS: Twenty patients with ocular Lyme borreliosis were examined. IgG and IgM antibodies to Borrelia burgdorferi were measured by ELISA in serum, and in cerebrospinal fluid (CSF) when indicated, and immunoblot analysis of B. burgdorferi IgG antibodies in serum was performed. A nested PCR was used to detect a segment of a gene coding for B. burgdorferi endoflagellin. The samples used in PCR testing were serum and CSF and in isolated cases conjunctiva and vitreous. RESULTS: Seventeen patients had elevated Borrelia antibodies in serum or CSF by ELISA. Seven patients, including two with negative ELISA, had a positive immunoblot. Seven of the 13 patients in whom PCR was examined during clinically active disease had a positive PCR result. Immunoblot analysis gave a negative result from the sera of five PCR-positive patients. CONCLUSIONS: For efficient diagnosis of ocular Lyme borreliosis, immunoblot analysis and PCR should be used in addition to ELISA. A positive PCR seems to be associated with a negative immunoblot.

PMID: 10090586 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=10090586

Br J Ophthalmol. 1999 Oct;83(10):1149-52

Ocular manifestations in children and adolescents with Lyme arthritis.
Huppertz HI,
Munchmeier D,
Lieb W.
Children's Hospital, University of Wurzburg, Wurzburg, Germany.

BACKGROUND: Lyme arthritis is the most frequent late manifestation of Lyme borreliosis and has been associated with ocular inflammation. METHODS: A group of 153 children and adolescents with arthritis, 84 of whom had Lyme arthritis and 69 other causes of arthritis, were followed prospectively for 22-73 (median 44) months in the course of a national study. RESULTS: Three of 84 patients with Lyme arthritis had ocular inflammation (4%), including keratitis, anterior uveitis, and uveitis intermedia. All three had symptoms of decreased visual acuity. Whereas anterior uveitis disappeared without sequelae, a corneal scar and a permanent loss of visual acuity in the patients with keratitis and intermediate uveitis remained. Systematic examination of all patients revealed no further ocular involvement. Of 69 patients with other causes of arthritis who were followed in parallel as a control group, four of 15 patients with early onset pauciarticular juvenile rheumatoid arthritis had chronic anterior uveitis and two of 12 patients with juvenile spondyloarthropathy had acute anterior uveitis. CONCLUSIONS: Ocular involvement with keratitis, anterior uveitis, and intermediate uveitis may occur in children and adolescents with Lyme arthritis. Visual loss appears to be symptomatic, making regular ocular screening of such patients unnecessary.

PMID: 10502576 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... s=10502576

Int Ophthalmol Clin. 1993 Winter;33(1):9-22. Links

The ocular manifestations of Lyme disease.
Zaidman GW.
Department of Ophthalmology, Westchester County Medical Center Valhalla, NY 10595.

Lyme disease (with its ocular manifestations) is a worldwide disorder that is rapidly increasing in frequency. It is a treatable, multisystemic disease that presents in three stages of severity. It can present with unusual forms of conjunctivitis, keratitis, cranial nerve palsies, optic nerve disease, uveitis, vitritis, and other forms of posterior segment inflammatory disease. A patient with any of these ocular manifestations should be questioned for exposure to an area endemic for Lyme disease, tick bites, skin rash, or arthritis. Such patients should undergo serological testing. If the clinical presentation is suggestive of Lyme disease, a course of oral antibiotics should be used (unless the patient gives a history of adequate therapy). Topical corticosteroids can be used for anterior segment inflammation. An antibiotic therapeutic trial can be used for posterior segment or neuroophthalmic disease. Systemic corticosteroids without concomitant antibiotics should not be used in the treatment of ocular Lyme disease. If ocular Lyme disease is discovered and treated early, response to therapy is usually satisfactory.

PMID: 8349429 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=8349429



J Clin Neuroophthalmol. 1993 Sep;13(3):155-61; discussion 162. Links

First isolation of Borrelia burgdorferi from an iris biopsy.
Preac-Mursic V,
Pfister HW,
Spiegel H,
Burk R,
Wilske B,
Reinhardt S,
Bohmer R.
Max v. Pettenkofer Institut fur Hygiene u. Medizinische Mikrobiologie, LM-Universitat Munchen, Germany.

The persistence of Borrelia burgdorferi in six patients is described. Borrelia burgdorferi has been cultivated from iris biopsy, skin biopsy, and cerebrospinal fluid also after antibiotic therapy for Lyme borreliosis. Lyme Serology: IgG antibodies to B. burgdorferi were positive, IgM negative in four patients; in two patients both IgM and IgG were negative. Antibiotic therapy may abrogate the antibody response to the infection as shown by our results. Patients may have subclinical or clinical disease without diagnostic antibody titers. Persistence of B. burgdorferi cannot be excluded when the serum is negative for antibodies against it.

PMID: 8106639 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=8106639



J Neurol. 1993 May;240(5):278-83. Links

Borrelia burgdorferi myositis: report of eight patients.
Reimers CD,
de Koning J,
Neubert U,
Preac-Mursic V,
Koster JG,
Muller-Felber W,
Pongratz DE,
Duray PH.
Friedrich-Baur-Institute, Clinic for Internal Medicine Innenstadt, Munich, Germany.

Myositis is a rare manifestation of Lyme disease of unknown pathogenesis. This study describes the course of disease in eight patients with Lyme disease, aged 37-70 years, all of whom were suffering from histologically proven myositis. The clinical, electrophysiological, and myopathological findings are reported. One patient showed signs and symptoms of myositis of all limbs. In six patients myositis was localized in the vicinity of skin lesions, arthritis or neuropathy caused by Borrelia burgdorferi. In another patient suffering from pronounced muscle weakness of the legs and cardiac arrest, inflammation of the myocardium, the conducting system and skeletal muscles was revealed at autopsy. Muscle biopsy revealed lymphoplasmocellular infiltrates combined with few fibre degenerations in three patients. The lymphoplasmocellular infiltrates were found predominantly in the vicinity of small vessels. Several spirochetes were stained in six of seven muscle biopsy samples by means of the immunogold-silver technique. Culturing of B. Burgdorferi from the muscle biopsy samples was, however, unsuccessful. Antibiotic treatment succeeded in curing the myositis in four of six patients. In one patients signs and symptoms improved. One patient died from cardiac arrest caused by myocarditis and Guillain-Barre syndrome. The outcome is unknown in one patient. Clinical and myopathological findings indicate that Lyme myositis can be caused either by local spreading of B. burgdorferi or an unknown antigen or toxin from adjacent tissues or haematogenously.

PMID: 8326331 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/quer ... ds=8326331



Am J Ophthalmol. 1993 Nov 15;116(5):571-5. Links

Long-term effects of ceftriaxone treatment on intraocular Lyme borreliosis.
Suttorp-Schulten MS,
Kuiper H,
Kijlstra A,
van Dam AP,
Rothova A.
Netherlands Ophthalmic Research Institut
soijuv
 
Viestit: 3010
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja Sailairina » Su Kesä 03, 2012 11:17

http://savotta.helsinki.fi/halvi/tiedot ... enDocument


LL HELENA MIKKILÄ VÄITTELEE 4.12.1998 AIHEESTA
SILMÄN BORRELIOOSI - DIAGNOOSI JA KLIININEN KUVA


LYHENNELMÄ VÄITÖSKIRJATYÖSTÄ:

Lymen borrelioosi on Borrelia burgdorferi -bakteerin aiheuttama ja
punkkien levittämä infektiotauti, joka voi aiheuttaa oireita lähes
minkä tahansa elimen taholta. Väitöskirjassa käsiteltiin Lymen
borrelioosiin liittyvien silmämuutosten taudinkuvaa sekä
diagnostiikkkaa. Lisäksi tutkittiin Lymen borrelioosin osuutta
silmänsisäisten tulehdusten, uveiittien, aiheuttajana ja selvitettiin
kannattaako uveiittipotilailta rutiininomanisesti määrittää
borreliavasta-aineet.

Silmän borrelioosin oireita ja löydöksiä tutkittiin 20 potilaalla,
joilla diagnosoitiin Lymen borrelioosi. Heistä kymmenellä todettiin
silmänsisäinen tulehdus, viidellä keskushermostoon liittyvä silmäoire,
neljällä silmän ulkoinen tulehdus ja yhdellä silmänsisäinen
verenkiertohäiriö. Monilla potilailla esiintyi epätavallisia oireita:
viisi potilasta kärsi poikkeuksellisen kovista silmä- tai
kasvokivuista ja kolmella oli jatkuvaa voimakasta valonarkuutta.
Eräiden potilaiden silmämuutokset, kuten mustuaisen toimintahäiriöt
ja sarveiskalvon tai verkkokalvon tulehdukset muistuttivat
syfiliksessä eli kupassa tavattavia.

Silmän borrelioosin laboratoriodiagnostiikka perustui vasta-aineiden
määritykseen ELISA-menetelmällä sekä kahteen uuteen menetelmään, ns.
vasta-aineiden immunoblottaustestiin ja borrelian DNA:n osoittamiseen
polymeraasiketjureaktiolla (PCR). Valtaosalla potilaista vasta-aineita
todetiin ELISA-menetelmällä. Osalla potilaista laboratoriodiagnoosi
varmistui kuitenkin vasta immunoblottaus- tai PCR-testillä. Kahdella
potilaalla borreliabakteerin DNA:n osoitus onnistui silmänäytteestä,
joko sidekalvolta tai silmän lasiaisesta. Silmän borrelioosin
diagnostiikassa tulisikin ottaa uudet immunoblottaus- ja PCR-testit
käyttöön ELISA-menetelmän lisäksi.

Lymen borrelioosin osuutta silmänsisäisen tulehduksen aiheuttajana
tutkittiin 160 potilaalla. Heistä 23:lla tulehduksen aiheuttajaksi
osoittautui infektio ja jopa seitsemällä Lymen borrelioosia pidettiin
syynä silmätautiin. Lymen borrelioosi tulisikin ottaa huomioon
silmänsisäisen tulehduksen taustaa selvitettäessä. Rutiininomainen
borreliavasta-aineiden määrittäminen silmänsisäistä tulehdusta
sairastavilta ei kuitenkaan ole tarpeen, sillä koholla olevat
vasta-aineet eivät yksin riitä Lymen borrelioosin diagnoosiin. Omassa
aineistossa vain pienellä osalla potilaista, joilla todettiin
kohonneita borreliavasta-aineita, silmänsisäisen tulehduksen syynä
pidettiin borrelioosia. Näillä kaikilla potilailla oli silmän takaosan
tulehdus. Muilla vasta-aine-positiivisilla silmätulehdukseen löytyi
jokin muu todennäköisempi aiheuttaja ja kohonneet borreliavasta-aineet
olivat luultavimmin jäänne aiemmin sairastetusta infektiosta tai
jonkin muun bakteerin tai yleistaudin aiheuttama ns. väärä
positiivinen tulos. Vasta-aineet tulisikin määrittää lähinnä, jos
potilaalla on muita borrelioosin oireita tai löydöksiä, tai jos
potilaalla on silmän takaosan tulehdus, jonka aiheuttaja ei ole
tiedossa.

Julkaisussa on 140 sivua ja se on painettu Hakapaino Oy:ssä,
ISBN-numero on 951-910529-0.

______________

http://onlinelibrary.wiley.com/doi/10.1 ... 0637.x/pdf
The etiology of uveitis:

The role of infections with special reference to Lyme borreliosis

_____

http://www.ophsource.org/periodicals/op ... 61-6420(99)00128-1/abstract

The expanding clinical spectrum of ocular lyme borreliosis

Results
Four patients presented with a neuro-ophthalmologic disorder, five had external ocular inflammation, 10 patients had uveitis, and one had branch retinal vein occlusion. One patient developed episcleritis and one patient developed abducens palsy within 2 months of the infection incident. In the remaining 14 patients in whom the time of infection was traced, the ocular manifestations appeared in the late stage of Lyme borreliosis. Two patients with a neuro-ophthalmologic disorder and one with external ocular inflammation experienced severe photophobia, whereas the main reported symptom of the patients with uveitis was decreased visual acuity. Four patients with external ocular disease and one with a neuro-ophthalmologic disorder experienced severe periodic ocular or facial pain. Retinal vasculitis developed in seven patients with uveitis.

Conclusions
Lyme borreliosis can cause a variety of ocular manifestations, which develop mainly in the late stage of the disease. Photophobia and severe periodic ocular pain can be characteristic symptoms of Lyme borreliosis. In the differential diagnosis of retinal vasculitis, Lyme borreliosis should be taken into account, especially in endemic areas.

______


http://www.duodecimlehti.fi/web/guest/e ... usinnumero

Jarish-Herxheimerin reaktio on komplikaatio, joka liittyy spirokeettojen aiheuttamien tautien hoitoon. Sen tyypillisiä oireita ovat aiempien oireiden paheneminen, kuume, vilunväristykset sekä nivel- ja lihaskivut. Seuraavassa kuvataan potilas, jonka silmäoireet pahenivat kyseisen reaktion seurauksena. Potilas sairasti Lymen borrelioosiin liittyvää episkleriittiä. Suonensisäisen keftriaksonihoidon alussa hänelle kehittyi iriitti ja sarveiskalvon reunahaavauma...

___________

http://www.aikakauskirjaduodecim.fi/web ... usinnumero

"Silmäoireista lievää sidekalvotulehdusta esiintyy Lymen taudin varhaisvaiheessa. Levinneen taudin oireisiin saattavat kuulua iriitti, korioretiniitti, retinavaskuliitti, keratiitti, hyaliitti ja optikusneuriitti. Silmien valonarkuus on melko yleinen oire, joka saattaa liittyä meningiittiin (Hytönen ym. 2008)."

__________

http://www.duodecimlehti.fi/web/guest/e ... usinnumero

"Uveiitti ei ole vain mikä tahansa silmän sisällä esiintyvä tulehdus, jota hoidetaan kortikosteroideilla. Jos uveiitin aiheuttajaksi todetaan infektio, oikein valittu mikrobihoito on tarpeen usein yhdessä paikallisen tai systeemisen kortikosteroidihoidon kanssa. Toisaalta eräät uveiittioireyhtymät eivät reagoi kortikosteroideihin eivätkä muuhunkaan hoitoon. Tällainen tauti on esimerkiksi ns. Fuchsin heterokrominen sykliitti. Joskus kortikosteroidihoito on jopa vasta-aiheinen. Tällaisesta on viitteitä Lymen borrelioosiin liittyvässä uveiitissa (Karma ym. 1993)."

__________
Sailairina
 
Viestit: 513
Liittynyt: Ma Tammi 19, 2009 16:04
Paikkakunta: Kaarina

ViestiKirjoittaja soijuv » Ke Elo 29, 2012 14:43

Silmän näköhermon nystyn tulehdus (papilliitti) ainoa oire Borrelioosista.
Hoito: IV keftriaksoni + suun kautta doksisykliiniä + steroideja. Toinen sai ainoastaan iv keftriaksonin. (2012)

http://www.dovepress.com/case-report-pa ... ticle-OPTH

Case report: papillitis as the sole ocular sign in Lyme disease

Authors: McVeigh K, Vakros G

Published Date July 2012 Volume 2012:6 Pages 1093 - 1097
DOI: http://dx.doi.org/10.2147/OPTH.S32601

Katherine McVeigh, Georgios Vakros
Department of Ophthalmology, Raigmore Hospital, Inverness, United Kingdom

Background: Lyme disease is a spirochetal disease responsible for a multitude of ocular and systemic manifestations, and patients may present to ophthalmologists and general clinicians with a wide variety of generalized and ocular signs which can result in chronic and disabling sequelae. Here we report two cases of patients suffering with Lyme disease who developed a rare associated papillitis.
Methods: A 48-year-old Scottish man presented with diminished visual acuity, painful ocular eye movements, photophobia, and mild ataxia. Fundus examination revealed bilateral disc swelling with associated hemorrhages in the right eye. Following exclusion of raised intracranial pressure as the cause of the findings, enzyme-linked immunosorbent assay and Western blot serology confirmed a positive result for Borrelia burgdorferi which, along with ophthalmic signs and exposure to an endemic area, confirmed the diagnosis of Lyme disease. A 79-year-old gentleman presented with intermittent short-duration ?gray film? in his left eye. Fundus examination revealed left optic disc swelling. He was positive for Lyme?s serology and his condition was treated with 2 weeks of intravenous ceftriaxone.

Results: The first patient?s inflammation resolved and visual acuity returned to normal following a course of high-dose steroids and intravenous ceftriaxone, followed by oral doxycycline. The second patient?s condition improved with high-dose intravenous ceftriaxone.

Conclusion: These patients highlight the fact that Lyme disease should be considered as a differential diagnosis for patients presenting with papillitis. With the incidence of this disease rising and more cases being reported, practitioners in Lyme-endemic areas need to be aware of the various manifestations so that appropriate referrals for treatment can be made.

Keywords: Lyme disease, ocular papillitis, Borrelia burgdorferi
soijuv
 
Viestit: 3010
Liittynyt: Ke Tammi 21, 2009 14:16

ViestiKirjoittaja soijuv » Su Syys 09, 2012 20:05

Borrelia-bakteeri voi aiheuttaa erilaisia silmäongelmia, kuten konjuktiviitin.

BMJ 2012; 345: e4721.

Ocular inflammation as a manifestation of Lyme borreliosis.


Jael M Howlett, specialist trainee year 1, ophthalmology1,

Adam P Booth, consultant ophthamologist1

Royal Eye Infirmary, Plymouth PL4 6P, UK.

jaelhowlett@hotmail.com

Lyme disease has several important ophthalmic manifestations that are important to highlight.
1 Self limiting follicular conjunctivitis is probably the most common early ocular manifestation and occurs within the ?...
soijuv
 
Viestit: 3010
Liittynyt: Ke Tammi 21, 2009 14:16

Re: BORRELIOOSI/SILMÄSAIRAUDET

ViestiKirjoittaja soijuv » Ma Loka 21, 2013 12:21

http://www.ebm-guidelines.com/xmedia/duo/duo70192.pdf

Jarisch–Herxheimerin reaktio
Lymen borrelioosiin liittyvän
episkleriitin hoidossa

TAPAUSSELOSTUS
Lymen borrelioosi on spirokeetta Borrelia
burgdorferin aiheuttama ja puutiaisten väli-
tyksellä leviävä monimuotoinen sairaus. Ta-
vallisimpia borrelioosin oireita ovat erythema mi-
grans -ihottuma, niveloireet sekä keskus- ja ää-
reishermoston oireet. Silmässä borrelioosin on
kuvattu aiheuttavan mm. konjunktiviittia, kera-
tiittia, episkleriittiä, iriittiä sekä lasiaisen, korioi-
dean tai neuroretinan tulehduksia, verkkokalvon
vaskuliittia, näköhermon tulehdusta sekä silmää
liikuttavien lihasten halvauksia (Karma ja Mikkilä
1996).
Lymen borrelioosin varhaisvaihetta erythema
migrans -ihottumineen hoidetaan yleensä suun
kautta otettavalla amoksisilliini- tai doksisykliini-
kuurilla. Vaikeiden myöhäisoireiden kuten pitkit-
tyvien ja näköä uhkaavien silmäoireiden hoidossa
käytetään suonensisäistä keftriaksonia. Tätä seu-
raa vielä suun kautta otettava antibioottikuuri,
joka on yleensä amoksisilliinin ja probenesidin
yhdistelmä.

Oma potilas
Potilas on vuonna 1942 syntynyt nainen, joka lähetettiin
HYKS:n silmäklinikkaan toistuvan, kivuliaan, molemminpuo-
lisen episkleriitin takia joulukuussa 1993. Toukokuussa 1986
potilas oli sairastanut ranteen niveltulehduksen. Silmäoireet
alkoivat kesäkuussa 1986. Seuraavien kahdeksan vuoden ai-
kana episkleriitti esiintyi toistakymmentä kertaa. Viimeisten
vuosien aikana potilaalla oli esiintynyt myös toistuvia lihas-,
nivel- ja kasvokipuja sekä voimakasta väsymystä. Potilas ei
ollut huomannut punkinpuremia eikä erythema migrans
-ihottumaa. Kesänsä hän oli viettänyt pääkaupunkiseudulla.
Oikean silmän näöntarkkuus oli normaali (1.0). Ohimon-
puoleisessa sidekalvossa ja episkleerassa esiintyi lievää surkas-
tumaa. Vasemman silmän näöntarkkuus oli heikentynyt
(0.6). Sidekalvo oli voimakkaasti punoittava, ja ylätempo-
raalialueella oli todettavissa kyhmymuodostusta. Ohimon-
puoleiset episkleeran suonet olivat laajentuneet. Etukam-
miot ja lasiaistilat olivat rauhalliset eikä silmänpohjissa to-
dettu poikkeavaa. Vasemman silmän episkleriittialue vaihtoi
sittemmin paikkaa nasaalipuolelle (kuva 1).
Potilasta tutkittiin anamneesin pohjalta sidekudostauteja
ja sarkoidoosia ajatellen. Tumavasta-aineiden, reumatekijän,
HLA-B27-tekijän, seerumin ACE:n ja lysotsyymin arvot oli-
vat kuitenkin normaalit. Sen sijaan borrelian IgG-vasta-
ainearvo todettiin ELISA-menetelmällä suurentuneeksi
(1 900, viitealue <500). IgM-arvo oli viitealueella (<1 800).
Borrelian IgG-vasta-aineiden »immunoblot»-testin tulos oli
myös vahvasti positiivinen. Treponema pallidum -hemagg-
lutionaatiotesti antoi negatiivisen tuloksen.
Potilasta hoidettiin aluksi paikallisella ja suun kautta otet-
tavalla prednisonilääkityksellä, joka auttoi vain ohimeneväs-
ti. Koska borrelioosiepäily oli vahva ja potilaalla esiintyi tois-
tuvia, kivuliaita episkleriitin pahenemisvaiheita, aloitettiin
kahden viikon suonensisäinen keftriaksonihoito huhtikuussa
1994. Neljä päivää hoidon aloittamisen jälkeen potilaalla
todettiin iriitti sekä koko sarveiskalvon ympäri ulottuva reu-
nahaavauma (kuva 2). Silmän syvemmät osat olivat terveet.
Iriitti ja sarveiskalvon haavaumatauti paranivat paikallisella
hydrokortisonilääkityksellä. Keftriaksonin jälkeen antibioot-
tihoitoa jatkettiin suun kautta otettavalla kolmen kuukau-
den pituisella amoksisilliini-probenesidilääkityksellä. Kun hoi-
to oli jatkunut kaksi kuukautta, potilaalle tehtiin seerumin
borrelian polymeraasiketjureaktiotesti (PCR). Sen tulos
osoittautui positiiviseksi. Lokakuussa 1994 potilas sai velä
toisen kolmen kuukauden pituisen amoksisilliinikuurin, kos-
ka vasen silmä punoitteli uudelleen. Pitkäkestoisten anti-
bioottihoitojen myötä episkleriitti vähitellen rauhoittui ja
nivel- ja lihasoireet sekä voimakas väsymys vähenivät.
Hel-
mikuussa 1995 toistettu seerumin borrelian PCR antoi
negatiivisen tuloksen ja ELISA-menetelmällä tehdyn vasta-
ainetestin tulos oli normaalistunut.

1993). JHR:n etiologia ei ole selvinnyt varmasti.
Erään teorian mukaan sen aiheuttaa endotoksii-
nien vapautuminen sprirokeettojen hajoamisen
yhteydessä. Toisen teorian mukaan JHR:n syynä
on valkosolujen pyrogeenin vapautuminen kuol-
leiden spirokeettojen fagosytoosin yhteydessä.
Kolmannen selityksen mukaan hoito aikaansaa
immunokompleksien muodostumisen ja tunte-
mattoman antigeenin vapautumisen (Bryceson
1976, Strominger 1994).
JHR:n oireita ovat aiempien oireiden pahen-
tuminen sekä yleisoireina kuume, vilunväristyk-
set, hypotensio sekä lihas- ja nivelkivut. Silmä-
oireiden pahenemista JHR:n seurauksena on ai-
emmin kuvattu sekä syfiliksessä että Lymen bor-
relioosissa. Jo vuosisadan alkupuolella Moore ra-
portoi syfiliittisen iriitin pahenemisesta arseeni-
hoidon aikana (Moore ja Gieske 1931). Wein-
stein ym. (1981) kuvasivat syfiliittistä optikus-
neuriittia sairastavan potilaan, jolla lihaksensisäi-
nen bentsyylipenisilliinihoito sai aikaan yleisoirei-
den ohella myös näöntarkkuuden heikentymisen.
Äskettäin Strominger ym. (1994) raportoivat
borrelioosiin liittyvän optikusneuriitin pahene-
misen suonensisäisen keftriaksonihoidon yhtey-
dessä.
Tässä kuvatulle potilaalle kehittyi iriitin lisäksi
sarveiskalvon reunahaavauma. Sarveiskalvon ja
kovakalvon välinen raja-alue eli limbus on im-
munologisesti aktiivinen alue. On esitetty, että
sarveiskalvon reunahaavauman syntymekanismi-
na on antigeeni-vasta-ainekompleksien kertymi-
nen limbuksen stroomaan, mikä aiheuttaa komp-
H. Mikkilä
K u v a 1. Vasemman silmän sidekalvon ja episkleeran
suonet ovat huomattavasti laajentuneet episkleriitin
merkkinä.
K u v a 2. Neljä päivää suonensisäisen keftriaksonihoidon
aloittamisesta potilaan vasempaan silmään kehittyi iriitti ja
koko sarveiskalvon ympäri ulottuva reunahaavauma (nuoli).
Pohdinta
Potilaan diagnoosi ja sen myötä oikea hoito
viivästyivät kahdeksalla vuodella, koska silmän
borrelioosia ei osattu epäillä. Diagnoosia vaikeut-
ti se, että potilas ei muistanut saaneensa punkin
puremia eikä erythema migrans -ihottumaa. Hän
oli kuitenkin sairastanut niveltulehduksen, joka
on tunnetuimpia borrelioosiin liittyviä oireita.
Suonensisäisen antibioottihoidon seurauksena
kehittyi sarveiskalvon reunahaavauma sekä iriitti.
Kyseinen reaktio tulkittiin Jarisch–Herxheimerin
reaktioksi (JHR). Se on jo pitkään tunnettu spi-
rokeettojen aiheuttamien tautien hoitoon liitty-
vänä komplikaationa (Jarisch 1895, Herxheimer
ja Krause 1902). Lymen borrelioosissa JHR
esiintyy 2–14 %:lla potilaista antibioottihoidon
yhteydessä (Steere ym. 1983, Christen ym.


845
TAPAUSSELOSTUS
L
ymen borrelioosi on spirokeetta Borrelia
burgdorferin aiheuttama ja puutiaisten väli-
tyksellä leviävä monimuotoinen sairaus. Ta-
vallisimpia borrelioosin oireita ovat erythema mi-
grans -ihottuma, niveloireet sekä keskus- ja ää-
reishermoston oireet. Silmässä borrelioosin on
kuvattu aiheuttavan mm. konjunktiviittia, kera-
tiittia, episkleriittiä, iriittiä sekä lasiaisen, korioi-
dean tai neuroretinan tulehduksia, verkkokalvon
vaskuliittia, näköhermon tulehdusta sekä silmää
liikuttavien lihasten halvauksia (Karma ja Mikkilä
1996).
Lymen borrelioosin varhaisvaihetta erythema
migrans -ihottumineen hoidetaan yleensä suun
kautta otettavalla amoksisilliini- tai doksisykliini-
kuurilla. Vaikeiden myöhäisoireiden kuten pitkit-
tyvien ja näköä uhkaavien silmäoireiden hoidossa
käytetään suonensisäistä keftriaksonia. Tätä seu-
raa vielä suun kautta otettava antibioottikuuri,
joka on yleensä amoksisilliinin ja probenesidin
yhdistelmä.
Oma potilas
Potilas on vuonna 1942 syntynyt nainen, joka lähetettiin
HYKS:n silmäklinikkaan toistuvan, kivuliaan, molemminpuo-
lisen episkleriitin takia joulukuussa 1993. Toukokuussa 1986
potilas oli sairastanut ranteen niveltulehduksen. Silmäoireet
alkoivat kesäkuussa 1986. Seuraavien kahdeksan vuoden ai-
kana episkleriitti esiintyi toistakymmentä kertaa. Viimeisten
vuosien aikana potilaalla oli esiintynyt myös toistuvia lihas-,
nivel- ja kasvokipuja sekä voimakasta väsymystä. Potilas ei
ollut huomannut punkinpuremia eikä erythema migrans
-ihottumaa. Kesänsä hän oli viettänyt pääkaupunkiseudulla.
Oikean silmän näöntarkkuus oli normaali (1.0). Ohimon-
puoleisessa sidekalvossa ja episkleerassa esiintyi lievää surkas-
tumaa. Vasemman silmän näöntarkkuus oli heikentynyt
(0.6). Sidekalvo oli voimakkaasti punoittava, ja ylätempo-
raalialueella oli todettavissa kyhmymuodostusta. Ohimon-
puoleiset episkleeran suonet olivat laajentuneet. Etukam-
miot ja lasiaistilat olivat rauhalliset eikä silmänpohjissa to-
dettu poikkeavaa. Vasemman silmän episkleriittialue vaihtoi
sittemmin paikkaa nasaalipuolelle (kuva 1).
Potilasta tutkittiin anamneesin pohjalta sidekudostauteja
ja sarkoidoosia ajatellen. Tumavasta-aineiden, reumatekijän,
HLA-B27-tekijän, seerumin ACE:n ja lysotsyymin arvot oli-
vat kuitenkin normaalit. Sen sijaan borrelian IgG-vasta-
ainearvo todettiin ELISA-menetelmällä suurentuneeksi
(1 900, viitealue <500). IgM-arvo oli viitealueella (<1 800).
Borrelian IgG-vasta-aineiden »immunoblot»-testin tulos oli
myös vahvasti positiivinen. Treponema pallidum -hemagg-
lutionaatiotesti antoi negatiivisen tuloksen.
Potilasta hoidettiin aluksi paikallisella ja suun kautta otet-
tavalla prednisonilääkityksellä, joka auttoi vain ohimeneväs-
ti. Koska borrelioosiepäily oli vahva ja potilaalla esiintyi tois-
tuvia, kivuliaita episkleriitin pahenemisvaiheita, aloitettiin
kahden viikon suonensisäinen keftriaksonihoito huhtikuussa
1994. Neljä päivää hoidon aloittamisen jälkeen potilaalla

Jarish–Herxheimerin reaktio on komplikaatio, joka liittyy spirokeettojen aiheuttamien
tautien hoitoon. Sen tyypillisiä oireita ovat aiempien oireiden paheneminen, kuume,
vilunväristykset sekä nivel- ja lihaskivut. Seuraavassa kuvataan potilas, jonka silmäoireet
pahenivat kyseisen reaktion seurauksena. Potilas sairasti Lymen borrelioosiin liittyvää
episkleriittiä. Suonensisäisen keftriaksonihoidon alussa hänelle kehittyi iriitti ja sarveis-
kalvon reunahaavauma.

todettiin iriitti sekä koko sarveiskalvon ympäri ulottuva reu-
nahaavauma (kuva 2). Silmän syvemmät osat olivat terveet.
Iriitti ja sarveiskalvon haavaumatauti paranivat paikallisella
hydrokortisonilääkityksellä. Keftriaksonin jälkeen antibioot-
tihoitoa jatkettiin suun kautta otettavalla kolmen kuukau-
den pituisella amoksisilliini-probenesidilääkityksellä. Kun hoi-
to oli jatkunut kaksi kuukautta, potilaalle tehtiin seerumin
borrelian polymeraasiketjureaktiotesti (PCR). Sen tulos
osoittautui positiiviseksi. Lokakuussa 1994 potilas sai velä
toisen kolmen kuukauden pituisen amoksisilliinikuurin, kos-
ka vasen silmä punoitteli uudelleen. Pitkäkestoisten anti-
bioottihoitojen myötä episkleriitti vähitellen rauhoittui ja
nivel- ja lihasoireet sekä voimakas väsymys vähenivät. Hel-
mikuussa 1995 toistettu seerumin borrelian PCR antoi
negatiivisen tuloksen ja ELISA-menetelmällä tehdyn vasta-
ainetestin tulos oli normaalistunut.
1993). JHR:n etiologia ei ole selvinnyt varmasti.
Erään teorian mukaan sen aiheuttaa endotoksii-
nien vapautuminen sprirokeettojen hajoamisen
yhteydessä. Toisen teorian mukaan JHR:n syynä
on valkosolujen pyrogeenin vapautuminen kuol-
leiden spirokeettojen fagosytoosin yhteydessä.
Kolmannen selityksen mukaan hoito aikaansaa
immunokompleksien muodostumisen ja tunte-
mattoman antigeenin vapautumisen (Bryceson
1976, Strominger 1994).
JHR:n oireita ovat aiempien oireiden pahen-
tuminen sekä yleisoireina kuume, vilunväristyk-
set, hypotensio sekä lihas- ja nivelkivut. Silmä-
oireiden pahenemista JHR:n seurauksena on ai-
emmin kuvattu sekä syfiliksessä että Lymen bor-
relioosissa. Jo vuosisadan alkupuolella Moore ra-
portoi syfiliittisen iriitin pahenemisesta arseeni-
hoidon aikana (Moore ja Gieske 1931). Wein-
stein ym. (1981) kuvasivat syfiliittistä optikus-
neuriittia sairastavan potilaan, jolla lihaksensisäi-
nen bentsyylipenisilliinihoito sai aikaan yleisoirei-
den ohella myös näöntarkkuuden heikentymisen.
Äskettäin Strominger ym. (1994) raportoivat
borrelioosiin liittyvän optikusneuriitin pahene-
misen suonensisäisen keftriaksonihoidon yhtey-
dessä.
Tässä kuvatulle potilaalle kehittyi iriitin lisäksi
sarveiskalvon reunahaavauma. Sarveiskalvon ja
kovakalvon välinen raja-alue eli limbus on im-
munologisesti aktiivinen alue. On esitetty, että
sarveiskalvon reunahaavauman syntymekanismi-
na on antigeeni-vasta-ainekompleksien kertymi-
nen limbuksen stroomaan, mikä aiheuttaa komp-

K u v a 1. Vasemman silmän sidekalvon ja episkleeran
suonet ovat huomattavasti laajentuneet episkleriitin
merkkinä.
K u v a 2. Neljä päivää suonensisäisen keftriaksonihoidon
aloittamisesta potilaan vasempaan silmään kehittyi iriitti ja
koko sarveiskalvon ympäri ulottuva reunahaavauma (nuoli).

Pohdinta
Potilaan diagnoosi ja sen myötä oikea hoito
viivästyivät kahdeksalla vuodella, koska silmän
borrelioosia ei osattu epäillä. Diagnoosia vaikeut-
ti se, että potilas ei muistanut saaneensa punkin
puremia eikä erythema migrans -ihottumaa. Hän
oli kuitenkin sairastanut niveltulehduksen, joka
on tunnetuimpia borrelioosiin liittyviä oireita.
Suonensisäisen antibioottihoidon seurauksena
kehittyi sarveiskalvon reunahaavauma sekä iriitti.
Kyseinen reaktio tulkittiin Jarisch–Herxheimerin
reaktioksi (JHR). Se on jo pitkään tunnettu spi-
rokeettojen aiheuttamien tautien hoitoon liitty-
vänä komplikaationa (Jarisch 1895, Herxheimer
ja Krause 1902). Lymen borrelioosissa JHR
esiintyy 2–14 %:lla potilaista antibioottihoidon
yhteydessä (Steere ym. 1983, Christen ym.

846
todettiin iriitti sekä koko sarveiskalvon ympäri ulottuva reu-
nahaavauma (kuva 2). Silmän syvemmät osat olivat terveet.
Iriitti ja sarveiskalvon haavaumatauti paranivat paikallisella
hydrokortisonilääkityksellä. Keftriaksonin jälkeen antibioot-
tihoitoa jatkettiin suun kautta otettavalla kolmen kuukau-
den pituisella amoksisilliini-probenesidilääkityksellä. Kun hoi-
to oli jatkunut kaksi kuukautta, potilaalle tehtiin seerumin
borrelian polymeraasiketjureaktiotesti (PCR). Sen tulos
osoittautui positiiviseksi. Lokakuussa 1994 potilas sai velä
toisen kolmen kuukauden pituisen amoksisilliinikuurin, kos-
ka vasen silmä punoitteli uudelleen. Pitkäkestoisten anti-
bioottihoitojen myötä episkleriitti vähitellen rauhoittui ja
nivel- ja lihasoireet sekä voimakas väsymys vähenivät. Hel-
mikuussa 1995 toistettu seerumin borrelian PCR antoi
negatiivisen tuloksen ja ELISA-menetelmällä tehdyn vasta-
ainetestin tulos oli normaalistunut.
1993). JHR:n etiologia ei ole selvinnyt varmasti.
Erään teorian mukaan sen aiheuttaa endotoksii-
nien vapautuminen sprirokeettojen hajoamisen
yhteydessä. Toisen teorian mukaan JHR:n syynä
on valkosolujen pyrogeenin vapautuminen kuol-
leiden spirokeettojen fagosytoosin yhteydessä.
Kolmannen selityksen mukaan hoito aikaansaa
immunokompleksien muodostumisen ja tunte-
mattoman antigeenin vapautumisen (Bryceson
1976, Strominger 1994).
JHR:n oireita ovat aiempien oireiden pahen-
tuminen sekä yleisoireina kuume, vilunväristyk-
set, hypotensio sekä lihas- ja nivelkivut. Silmä-
oireiden pahenemista JHR:n seurauksena on ai-
emmin kuvattu sekä syfiliksessä että Lymen bor-
relioosissa. Jo vuosisadan alkupuolella Moore ra-
portoi syfiliittisen iriitin pahenemisesta arseeni-
hoidon aikana (Moore ja Gieske 1931). Wein-
stein ym. (1981) kuvasivat syfiliittistä optikus-
neuriittia sairastavan potilaan, jolla lihaksensisäi-
nen bentsyylipenisilliinihoito sai aikaan yleisoirei-
den ohella myös näöntarkkuuden heikentymisen.
Äskettäin Strominger ym. (1994) raportoivat
borrelioosiin liittyvän optikusneuriitin pahene-
misen suonensisäisen keftriaksonihoidon yhtey-
dessä.
Tässä kuvatulle potilaalle kehittyi iriitin lisäksi
sarveiskalvon reunahaavauma. Sarveiskalvon ja
kovakalvon välinen raja-alue eli limbus on im-
munologisesti aktiivinen alue. On esitetty, että
sarveiskalvon reunahaavauman syntymekanismi-
na on antigeeni-vasta-ainekompleksien kertymi-
nen limbuksen stroomaan, mikä aiheuttaa kompleksivälitteisen immunologisen tulehdusreaktion
(deLuise ja O’Leary 1991).
JHR:n ilmaantuminen viittaa epäsuorasti sii-
hen, että potilaan silmässä oli eläviä spirokeettoja
vielä kahdeksan vuoden kuluttua sairastumisen
alusta. Tätä tukee myös positiivinen borrelian
PCR. Positiivista PCR-tulostahan pidetään yleen-
sä aktiivisen infektion merkkinä (Garcia-Monco
ja Benach 1995). Borrelioosi-infektion alussa spi-
rokeetat voivat levitä ympäri elimistöä ja jäädä
pitkäksi aikaa piilemään immunologisesti suojas-
sa oleviin elimiin, kuten silmiin tai keskusher-
mostoon (Dattwyler 1988, Steere 1989).
Jarisch–Herxheimerin reaktio Lymen borrelioosiin liittyvän episkleriitin hoidon komplikaationa
JHR:n vaikeusaste ja sen mukana hoitokäytän-
tö vaihtelevat. Vaikeiden systeemisten reaktioi-
den hoitona on yleensä käytetty suun kautta otet-
tavia tai suonensisäisiä kortikosteroideja (Strom-
inger ym. 1994). Kuvatulla potilaalla JHR:ään ei
liittynyt systeemioireita ja iriitti ja sarveiskalvon
reunahaavauma paranivat paikallisella kortikoste-
roidihoidolla.
Lymen borrelioosi on pidettävä mielessä myös
silloin, kun potilas sairastaa pitkittynyttä episkle-
riittiä. Borrelioosia hoidettaessa on muistettava,
että oireiden ohimenevää pahenemista saattaa
esiintyä JHR:n seurauksena.

Kirjallisuutta
Bryceson A D: Clinical pathology of the Jarisch-Herxheimer
reaction. J Infect Dis 133: 698–704, 1976
Christen H J, Hanefeld F, Eiffert H, Thomssen R: Epidemiology
and clinical manifestations of Lyme borreliosis in childhood.
A prospective multicentre study with special regard to
neuroborreliosis. Acta Pædiatr 82 [Suppl 386]: 1993
Dattwyler R J, Volkman D J, Luft B J, ym.: Seronegative Lyme
disease: dissociation of specific T- and B-lymphocyte responses
to Borrelia burgdorferi. N Engl J Med 319: 1441–1446,
1988
Garcia-Monco J C, Benach J L: Lyme neuroborreliosis. Ann Neurol
37: 691–702, 1995
Herxheimer K, Krause I: Uber einen bei syphilitischen vorkom-
mende Quicksilberreaktion. Dtsch Med Wochenschr 28: 895–
897, 1902
Jarisch A: Therapeutische Versuche bei Syphilis. Wien Med Woc-
henschr 145: 721, 1895
Karma A, Mikkilä H: Diagnosis and treatment of ocular Lyme
borreliosis. Curr Opin Ophthalmol 7: 7–12, 1996
DeLuise V P, O’Leary M J: Peripheral ulcerative keratitis related to
Lyme disease. Am J Ophthalmol 111: 244–245, 1991
Moore J E, Gieske M: Syphilitic iritis. Ann J Ophthalmol 14: 110–
126, 1931
Steere A C: Lyme disease. N Engl J Med 321: 586–596, 1989
Steere A C, Hutchinson G J, Rahn D W, ym.: Treatment of the
early manifestations of Lyme disease. Ann Intern Med 99:
22–26, 1983
Strominger M B, Slamovits T L, Herskovitz S, Lopton R B:
Transient worsening of optic neuropathy as a sequela of the
Jarisch-Herxheimer reaction in the treatment of Lyme disease.
J Neuro-Ophthalmol 14: 77–80, 1994
Weinstein J M, Lexow S S, Ho P, Spickards A: Acute syphilitic
optic neuritis. Arch Ophthalmol 99: 1392–1395, 1981

HELENA MIKKILÄ, LL, apulaislääkäri
HYKS:n silmätautien klinikka, 00290 Helsinki
soijuv
 
Viestit: 3010
Liittynyt: Ke Tammi 21, 2009 14:16


Paluu TUTKIMUSTIETOA BORRELIOOSISTA

Paikallaolijat

Käyttäjiä lukemassa tätä aluetta: Ei rekisteröityneitä käyttäjiä ja 4 vierailijaa