Updated June 2015
How does lyme disease affect the eye?
Fortunately, involvement of the eye is uncommon in lyme disease. But when the eyes can be affected in many different ways by the disease.
In the early stage of the disease, many persons have conjunctivitis. In this condition, commonly called pink eye, the eyes are red and uncomfortable, and there is a discharge of pus. Unlike many forms of conjunctivitis, the type that occurs in lyme disease is not contagious.
In later stages of the disease, inflammation of the eye may develop. Parts of the eye that may be affected include the uvea, the middle layer inside the eye, the cornea, part of the outer coat of the eye; the iris, the colored circle around the pupil, and the choroid, a layer of blood vessels in the eye. Ocular symptoms can include sensitivity to light and floaters (spots in front of the eyes).
Inflammation of the optic nerve (optic neuritis) also can occur, which results in visual loss. Loss of vision can result from inflammation in the brain as well.
Persons who develop Bell’s palsy may be unable to blink or close their eyes. This dries the cornea and can result in an infection or even a hole in the cornea, which can endanger vision if not treated promptly.
Bacterial tick-borne diseases caused by Bartonella spp., Borrelia burgdorferi sensu lato, Coxiella burnetii, and Rickettsia spp. among patients with cataract surgery
Tomasz Chmielewski, Joanna Brydak-Godowska, Beata Fiecek, Urszula Rorot, Elżbieta Sędrowicz, Małgorzata Werenowska, Dorota Kopacz, Agata Hevelke, Magdalena Michniewicz, Dariusz Kęcik, Stanisława Tylewska-Wierzbanowska
Laboratory of Rickettsiae, Chlamydiae and Spirochetes, National Institute of Public Heath – National Institute of Hygiene, Warsaw, Poland
Med Sci Monit 2014; 20:927-931 / DOI: 10.12659/MSM.890149 / Published: 2014-06-05
Background: Clinical data have shown that tick-borne diseases caused by Borrelia burgdorferi sensu lato, Bartonella spp., Coxiella burnetii, and Rickettsia spp. can affect the central nervous system, including the eye. The aim of this study was to establish a relationship between the incidence of cataract and evidence of bacterial infections transmitted by ticks.
Results: Microbiological analysis revealed the presence of Bartonella sp. DNA in intraoperative specimens from the eye in 1.8% of patients. Serological studies have shown that infections caused by B. burgdorferi sensu lato and Bartonella sp. were detected in 34.8% and 4.6% of patients with cataract surgery, respectively.
Conclusions: Presence of DNA of yet uncultured and undescribed species of Bartonella in eye liquid indicates past infection with this pathogen. Specific antibodies to B. burgdorferi sensu lato and Bartonella sp. are detected more frequently in patients with cataract compared to the control group. This could indicate a possible role of these organisms in the pathological processes within the eyeball, leading to changes in the lens. Further studies are needed to identify Bartonella species, as well as to recognize the infectious mechanisms involved in cataract development.
Case report: papillitis as the sole ocular sign in Lyme disease
Published Date July 2012 Volume 2012:6 Pages 1093—1097
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.
Blurred Vision – Inflammatory Causes
Conjunctivitis is the most common ophthalmologic involvement during the first stage of Lyme disease. Choroiditis, exudative retinal detachment, keratitis, iridocyclitis, and retinal vasculitis have also been reported at this stage or early in stage 2. I have seen one patient with recurrent iritis who finally cleared when diagnosed as having Lyme disease and treated with intravenous antibiotics. The usual presentation of stage 2 is neurologic or cardiac symptoms.
The neurologic symptoms are three times more common, with facial nerve palsy the leading sign. The sixth and optic nerves are much less frequently involved. These manifestations are much rarer than conjunctivitis. Neurologic involvement includes the form of meningitis with headache and stiff neck. Spinal fluid examination reveals a lymphocytic pleocytosis with 15 to 700 white blood cells per milliliter. There is also a slight elevation of the protein and a normal glucose level. These findings may falsely suggest septic meningitis rather than Lyme meningitis. Other neurologic signs and symptoms are peripheral neuropathy and cranial-nerve palsies, particularly of the seventh cranial nerve. The latter occurs in up to 10% of patients in the course of Lyme disease and not uncommonly is bilateral.
Papilledema has been reported in five patients with some decrease in vision, but only one had increased intracranial pressure and a pseudotumor-like syndrome. One case of Lyme disease with disc edema, decreased vision, and an altitudinal defect has been reported.
Atlas Of Ophthalmology – Disorders of the eye caused by borrelia (Lyme) infection
Optician Online : Lyme disease
This article is best viewed in a PDF Format.
Lyme disease is caused by infection with Borrelia spirochaetes (B burgdorferi, B afzelii and B garinii). The organisms are transmitted through the bite of ticks of the Ixodes ricinus complex in the US, Europe and Asia. After an incubation period of several days, the spirochaetes disseminate haematogenously to multiple organs.
A history of environmental exposure (such as camping in an endemic area) is significant. Flu-like symptoms often accompany the rash. Common symptoms of systemic disease include headache, fatigue, chills and arthralgias. Neck stiffness or photophobia may reflect meningitis. Common ocular symptoms include blurred or double vision, pain and photophobia.
Lyme disease is renowned for its protean clinical manifestations. Its progression is described in three stages, although all may co-exist.
● Stage 1: A pathognomonic, localised skin rash (Erythema migrans) develops. Erythema migrans consists of single large erythematous skin lesion, often with a pale or indurated centre (‘bull’s-eye’), that may expand over several days. Conjunctivitis or periorbital oedema may occur
● Stage 2 reflects organ dissemination: The skin, joints, heart, and central nervous system are most commonly involved. Possible ocular signs are listed below
● Stage 3: Appears in 60 per cent of untreated patients after months to years, typically with a large joint oligoarticular arthritis. Chronic encephalopathy and neuropathy are observed occasionally. On ocular examination, a red eye may reflect conjunctivitis or episcleritis. Reduced acuity, impaired colour vision, and relative afferent pupillary defect vision occur with optic neuritis. Keratitis produces corneal clouding and vascularisation. There may be anterior or posterior uveitis: Iritis may manifest ciliary injection and aqueous cells or flare posterior uveitis or retinitis may show vitreous flare, opacities or discolouration, elevation of the retina with retinal detachment, and disc swelling with optic neuritis.
Potentially life and vision-threatening. Optic neuritis may cause blindness, particularly in children.
[Ocular manifestations of Lyme disease]
Med Mal Infect. 2007 Jul-Aug;37(7-8):518-22. Epub 2007 Mar 21.
[Article in French]
Service d’ophtalmologie, université Paris-VI, CHU de la Pitié-Salpêtrière, 47-83, boulevard de l’Hôpital, 75651 Paris cedex 13, France. email@example.com
Despite the wide spectrum of clinical entities, eye involvement remains a rare event in patients with Lyme borreliosis. Most of ocular manifestations occur during the late phase of the disease. The infection needs to be considered along with more conventional causes of ocular inflammation, particularly in regions where Lyme disease is common. The pathogenesis of this condition remains controversial. Direct ocular infection and a delayed hypersensitivity mechanism may be involved at different disease stages. Uveitis and optic neuritis are the most common ocular complications. Serological testing lacks sensitivity and specificity. In atypical cases, ocular fluids sampling and analysis may be proposed. PCR seems to be an interesting diagnostic tool, allowing genotypic analysis. In the majority of cases, therapeutic strategy should be based on the association of antibiotics and corticosteroids. A new course of antibiotics may be prescribed to patients with chronic or relapsing inflammation due to bacterial persistence in ocular tissues.
PMID: 17376626 [PubMed – indexed for MEDLINE]
Ocular Signs of Lyme 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, 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.
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.
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, 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.
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.
Retina. 1996;16(6):505- 9.
Long-term follow-up of chronic Lyme neuroretinitis.
Karma A, Stenborg T, Summanen P, Immonen I, Mikkilä H, Seppälä 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.
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]
____________ _________ _________ _________ _________ _________ _
Int Ophthalmol Clin. 2001 Winter;41(1) :83-102.
Ray S, Gragoudas E.
Harvard Medical School, Massachusetts Eye and Ear Infirmary, 243 Charles Street, Boston, MA 02114, USA.
Despite the growing list of agents that can present as neuroretinitis, nearly one-half remain idiopathic. However, many of the candidate etiologies are treatable conditions, and accurate diagnosis can result in visual rehabilitation. A complete workup in patients presenting with acute neuroretinitis should include a thorough history and general medical evaluation. Exposure history should be thoroughly explored, including recent travel, unpasteurized and uncooked foods, sexual experience, and animal contacts. A detailed physical examination should be performed to note hidden rashes and inoculation sites and should include routine measurements of blood pressure and heart rate. Laboratory tests should be tailored to the history and may include complete blood count; erythrocyte sedimentation rate; bacterial, fungal, and viral blood cultures; antinuclear antibody test; angiotensin- converting enzyme; anti-double- stranded DNA; and C3. Serological evaluation should look for syphilis, Lyme disease, histoplasmosis, brucellosis, chlamydia, HIV, toxoplasmosis, Epstein-Barr virus, viral hepatitis B and C, and tuberculin skin test. Neuroretinitis is a clinical entity in which there is inflammation of the retinal architecture and optic nerve. There are numerous entities that can cause a picture of neuroretinitis ranging from vascular to infectious to autoimmune. With regards to the infectious etiologies, it is interesting to note that many of these organisms are obligate intracellular pathogens. The microorganisms B. henselae, T. gondii, R. typhi, T. pallidum, Mycobacterium tuberculosis, Histoplasma capsulatum, and various viruses, such as HIV, mumps, and HSV, are known intracellular agents. Other major infectious agents, such as B. burgdorferi and Leptospirosis spp. are known to remain sequestered within the circulatory system. It is possible that in this way these agents are able to breach the delicate blood-brain barrier. The implication of such findings on the treatment and management of neuroretinitis remains to be explored. Interestingly, the vast majority of infected patients do not develop neuroretinitis or demonstrate CNS involvement. Detailed examination of this variability may provide further insight into the pathogenic properties of these infectious agents, host tissue susceptibility, and mechanisms of blood-retina barrier integrity. A detailed retinal examination can provide an unobstructed view of the CNS. Careful inspection of this delicate interface may reveal subtle findings critical for accurate and rapid diagnosis of underlying systemic pathology. The varied visual and neurological symptoms of neuroretinitis attest to the fact that this is a disease of both the retina and contiguous neuronal elements. Such involvement significantly elevates the risk to the patient and emphasizes the need for early detection and prompt treatment.
PMID: 11198149 [PubMed – indexed for MEDLINE]
Ocular Immunology & Uevitis Foundation:
Lijing Yao, MD
Ocular manifestations of Lyme disease may occur at any stage but are more common in the last two stages. The most common ocular finding in stage I is conjunctivitis.
During the second and third stages, ocular involvement includes anterior, intermediate, and posterior uveitis, endophthalmitis, keratitis (stromal opacities, punctuate superficial keratitis or peripheral ulcerative keratitis), and conjunctivitis.
Neuroophthalmic features can also occur, including involvement of third, sixth, and seventh cranial nerves (Bell’s palsy, most common), optic nerve (optic neuritis and perineuritis, papilledema, ischemic optic neuropathy, optic nerve atrophy).
Other possible ocular involvement includes retinal hemorrhages, exudative retinal detachments, cystoid macular edema, blepharitis, scleritis and episcleritis.
The most commonly reported ocular syndromes in stage II are conjunctivitis and uveitis. Bilateral interstitial keratitis has been described as a characteristic feature in the late stage of Lyme disease.
Ophthalmic problems with Lyme:
• Lyme disease is characterized by dermatological, neurological, cardiac,
rheumatic, and ophthalmic manifestations that result from tick-borne
transmission of the spirochete Borrelia burgdorferi.
• Three chronological stages:
1.Primary or initial phase—rash at the site of tick bite (erythema chronicum
migrans) and flu-like symptoms.
2. Secondary or dissemination stage—further dermatological, cardiac, and
3. Tertiary or late stage—arthritis, meningoencephalitis, cranial neuropathy,
peripheral neuropathy, carditis.
• Conjunctivitis, most common manifestation in stage 1.
• Cranial nerve palsies, optic nerve inflammation can occur in stage 2.
• Corneal, uveal, and retinal inflammation can occur in stage 3.
Loads more info in article 🙂
Lyme Disease & the eye