Ophthalmic manifestations in Lyme borreliosis 
OPHTHALMIC MANIFESTATIONS 
IN LYME BORRELIOSIS 
J. Bergloff, R. Gasser 
ABSTRACT 
Lyme Borreliosis is a multisystem disorder caused by tbe spirocbete Borrelia burgdorferi. Altbougb many 
ocular manifestations bave been attributed to Lyme Borreliosis, tbey remain a rare clinical feature of tbe 
disease. The spirochetes invade the eye early and remain dormant, accounting for both early and late ocular 
manifestations wbich range from conjunctivitis and keratitis to intraocular inflammatory syndromes and neuro-
ophthalmic manifestations. Especially in endemic areas, ophthalmologists need to be aware of Borrelia 
burgdorferi as a possible causal agent. Tbe aim of tbis article is to present a short review of opbthalmic 
disorders resulting from Borrelia burgdorferi infections. 
KEY WORDS 
Borrelia burgdorferi, Lyme Borreliosis, eye, ophthalmic manifestations 
INTRODUCTION 
There bas been a growing awareness of Lyme 
Borreliosis (LB) during recent years. Borrelia burgdorferi 
(Bb) infection can be associated witb a variety of 
signs and symptoms including neurologic, dermatologic, 
cardiac and ophtbalmic disorders. The infectious 
agent causing LB is tbe spirocbete Bb wbich is 
transmitted by ixodid ticks (1,2). Recently, Bb has 
also been found in mosquitoes and deer flies (3). 
The clinical course of LB is divided into tbree 
stages ( 4,5). Stage I directly follows the bite by an 
infected tick. Patients develop a typical skin lesion, 
erytbema migrans (EM) (6) and, in some cases, 
non-specific intluenza-like symptoms and fever. After 
several weeks, spirochetes spread throughout tbe 
body and patients may develop neurological, skin 
acta dennatovenerologica A.P.A. Vol 5, 96, No 3-4 
and cardiac manifestations (Stage 11) ( 4,7-9). Stage 
III is mainly cbaracterized by polyartbritis, progressive 
encephalomyelitis similar to multiple sclerosis ( 4,5,8) 
and skin disorders with acrodermatitis cbronica 
atropbicans (10). However, not every patient follows 
tbis course (6,11,12). In fact, no clear line can be 
drawn between tbe tbree stages, neither witb respect 
to tirne of occurrence nor to symptoms. 
Bb bas been isolated from blood, cerebrospinal 
fluid and various tissues (7,13). Althougb Borrelia 
bas also been identified histologically in tbe iris, tbe 
retina and in the vitreous humour (14-19), little 
attention has been focused on the ophthalmic 
manifestations of LB. Since LB can be associated 
with a number of ophthalmic manifestations, · Bb 
sbould be considered as a possible causal agent. 
However, strict criteria should be applied to avoid 
147 
Ophthalmic manifestations in Lyme borreliosis 
overdiagnosis. The aim of this article is to review 
the reported ophthalmic disorders associated with 
Bb infection. 
OPHTHALMIC MANIFESTATIONS OF 
BORRELIABURGDORFERIINFECTION 
1. OPHTHALMIC MANIFESTATIONS 
IN STAGE I (SEE TABLE 1) 
1.1. Conjunctivitis, periorbital edema (5,13,18,20,21) 
Follicular conjunctivitis with photophobia and peri-
orbital edema have been observed in 10% of patients 
m the early stages of LB. 
2. OPHTHALMIC MANIFESTATIONS 
IN STAGE II (SEE TABLE 1) 
2.1. UVEITIS 
2.1.1. Iridocyclitis (5,17-20, 22-37): Several case reports 
of LB and granulomatous iritis with posterior synechia 
have been published. Kauffmann and Wormser showed 
that panuveitis with disseminated chorioretinitis may 
follow iridocyclitis (19). 
2.1.2. Pars planitis (25,27,28,31,35,38-40): Chronic 
intermediate uveitis with classic snowbanking and 
severe cystoid macular edema was reported by Bree-
veld et al. (38). In spite of the fact that the patient 
had suffered for 10 years, the ocular symptoms 
responded promptly to intravenous antibiotic therapy. 
Another case of pars planitis associated with facial 
palsy was presented by Winward et al. (35). 
2.1.3. Vitritis (15,22,27,28,35,38,41-43): Several case 
reports of vitritis have been described. In 1991 
Rothova et al. reported a case of spiderweb vitritis 
in the Lancet ( 43). Although it is only one single 
case report, it demonstrates the variety of ophthalmic 
manifestations of LB. Kuiper et al. observed vitritis 
in association with Lyme meningitis and cranial 
polyneuritis 6 weeks after a tick bite causing EM 
( 42). Winward et al. described severa} patients with 
positive laboratory findings of borreliosis who had 
recurrent bilateral vitritis and granulomatous iridocyclitis 
relatively resistant to therapy (35). 
2.1.4. Chorioretinitis (5,15,22,31,44,45): Two cases of 
bilateral diffuse chorioiditis, cystoid macular edema 
and exsudative retinal detachment have been described. 
These patients also suffered from lymhocytic meningitis 
secondary to LB. The dramatic improvement of 
ocular complaints in these patients after doxycycline 
therapy suggests LB as a possible cause. 
148 
2.1.5. Pigmentepitheliitis (16,33,46,47): Bialasiewicz 
et al. observed a patient with hyper- and depig-
mentations in the macular region in association with 
Bb seroconversion ( 46). It was similar to pigment-
epitheliitis. Recently, Wiegand described cases of 
presumed acute multifocal posterior placoid 
pigmentepitheliopathy in association with LB (33,47). 
Further investigations need to prove the relevance 
of this coincidence. 
2.1.6. Retinal vasculitis (5,22,28,31,37,48): Several 
cases of retinal vasculitis in LB associated with 
vitritis and pars planitis have been presented. One 
patient with positive Bb serology developed retinal 
neovascularization and cystoid macular edema. He 
received oral tetracycline therapy and showed marked 
improvement. In two other cases of severe retinal 
vasculitis associated with Bb infection, surgical therapy 
was applied after antibiotic treatment was unsuccessful 
(28). Retina} vasculitis can be expected to occur in 
LB as similar findings are frequently seen in the 
later stages of syphilis, another spirochetal infection 
(28). 
2.2. Endophthalmitis (17,19) 
Kauffmann et al. described a patient who showed 
severe unilateral panendophthalmitis following an 
insect bite causing EM (19). A lensectomy and 
vitrectomy were performed; Lyme spirochetes were 
found in the vitreous specimens. 
2.3. Neuro-ophthalmic manifestations 
2.3.1. Optic neuropathy 
2.3.1.1. Optic neuritis (5,8,16,18,22,24,29,31,35,49-51): 
To date, there are only a few reports of optic 
neuritis associated with LB. Winward et al. observed 
a case of bilateral optic neuritis and mild vitritis 
(35). In these patients, central scotoma and afferent 
pupillary defect were present as well as other 
neurologic manifestations. 
2.3.1.2. Anterior ischemic optic neuropathy (32,34, 
52,53): A case of ischemic optic neuropathy secondary 
to LB with an inferior altitudinal field defect was 
reported by Schechter et al. (53). Pizzarello et al. 
described another case of ischemic neuropathy 
following a tick bite causing EM (52). Temporal 
artery specimens showed the typical appearance of 
giant cell arteritis, but a silver stain suggested 
spirochetes within the multinucleated giant cells. 
Ceftriaxone therapy led to a marked improvement 
of visual acuity. 
2.3.1.3. Optic atrophy (11,18,20,25,34,48,54,55): Optic 
acta dennatovenerologica A.P.A. Vol 5, 96, No 3-4 
Ophthalmic manifestations in Lyme borreliosis 
Table I. Ophthalmic manifestations of Lyme Borreliosis by stage. 
conjunctivitis 
periorbital edema 
photophobia 
uveitis 
iridocyclitis 
pars planitis 
vitri tis 
chorioretinitis 
pigmen tepi theli tis 
AMPPPE* 
retinal vasculitis 
endophthalmitis 
neuro-ophthalmic manifestations 
optic neuropathy 
optic neuritis 
ischemic neuropathy 
optic atrophy 
papilledema 
pseudotumor cerebri 
Leber's neuroretinitis 
cranial nerve palsy 
oculomotor palsy (III, IV, VI) 
facial nerve palsy 
pupillary disorders 
Argyll Robertson pupil 
Horner's Syndrome 
paralytic mydriasis 
keratitis 
interstitial keratitis 
peripheral ulcerative keratitis 
episcleritis 
myositis 
neuro-ophthalmic manifestations 
optic neuritis 
ocular nerve palsies 
visual field defects 
nystagmus 
primary affect 
erythema migrans 
lymphadenosis cutis benigna 
generalization 
fever, malaise, cephalea 
organic manifestations 
dermatologic 
multiple erythemata 
neurologic 
meningitis 
radiculoneuritis 
cranial neuritis 
cardiac 
myocarditis 
pericarditis 
artrioventricular block 
rheumatologic 
mono-, oligoarthritis 
organic manifestations 
dermatologic 
acrodermatitis chronica atrophicans 
neurologic 
progressive encephalomyelitis 
rheumatologic 
oligo-, polyarthritis 
chronic erosive arthritis 
* AMPPPE = acute multifocal posterior placoid pigmentepitheliopathy 
acta dermatovenerologica A .P.A. Vol 5, 96, No 3-4 
IgG negative 
IgM negative 
IgG increasing 
IgM high 
IgG high 
IgM low 
149 
Ophthalmic manifestations in Lyme borreliosis 
neuritis, ischemic neuropathy and chronic papilledema 
in pseudotumor cerebri may each be responsible for 
optic disc atrophy in patients with chronic LB. 
Bertuch et al. described a case of progressive optic 
disc pallor following a presumed diagnosis of LB 
without previously observed optic nerve disorders 
(55). 
2.3.1.4. Papilledema (5,11,18-20,27,35,37,39,48,49,51,56-
58): Optic disc edema may result from various 
causes. Only a minority of patients with Lyme 
meningitis develop disc edema. The latter leads to 
blurred vision and is usually not associated with 
elevated intracranial pressure (39). Optic perineuritis 
(11,18,19,57) is probably the reason for disc swelling 
in the cases described by Kauffmann et al. and 
Reik et al. (11,19). LB associated pseudotumor 
cerebri with increased cerebrospinal fluid pressure 
has been reported in several cases (35,49,56-58). 
2.3.1.5. Leber's stellate neuroretinitis (5,20,48,49,59,60): 
This disorder is caused by vasculitis of the optic 
nerve head, causing distinct disc edema, venous 
congestion and star-shaped lipoid exudation. It has 
been reported in viral diseases and neurolues. Recently, 
a few cases of Leber's stellate neurretinitis in LB 
have also been observed (59). 
2.3.2. CRANIAL NEUROPATHY 
2.3.2.1. Facial nerve palsy (8,11,27,28,35,49,51,54,56,61-
65): Facial nerve palsy, occasionally associated with 
exposure keratitis, is the most common cranial 
neuropathy occurring in approximately 50% of patients 
with Lyme meningitis. Sometimes it is the only 
manifestation of the disease, although multiple re-
currences have also been observed (35). 
2.3.2.2. Oculomotor palsy (8,9,11,24,30,31,35,42,49, 
51,62,63,66,67): Cranial neuropathy with oculomotor, 
trochlear and abducens nerve palsies have been 
reported. Diplopia is the typical ocular complaint in 
this case. These palsies may occur individually or in 
combination with other neurologic abnormalities. LB 
has been reported in children suffering from late 
onset strabismus and diplopia (31,66). 
2.3.3. Pupillary disorders (11,22,68) 
In the literature, there are only anecdotal reports 
about the association of pupillary dysfunction and 
LB. Argyll-Robertson pupil was described in Reik's 
report in 1986 (11). This disorder is also common 
in neurolues. A case with reversible Horner's Syndrome 
was observed by Glauser et al. (68). Karma et al. 
reported a case of bilateral paralytic mydriasis (22). 
150 
3. OPHTHALMIC MANIFESTATIONS 
IN STAGE III (SEE TABLE 1) 
3.1. CONJUNCTIVITIS AND EPISCLERITIS 
(51,69-71) 
Zaidman observed a case of chronic LB with 
tarsoconjunctival scarring, symblepharon and episcleritis 
(71). These manifestations are common in autoimmu-
nological eye diseases. Thus, an immune-pathogenesis 
can also be considered in this case of late LB. 
3.2. KERATITIS 
3.2.1. Interstitial keratitis (5,19,31,49,55,69,70,72-77): 
Interstitial keratitis in chronic spirochetal infections 
(Treponema pallidum) is well known. In LB, several 
cases with scattered hazy infiltrates of the deep and 
superficial stroma have been observed. Only one 
patient, however, exhibited corneal neovascularization 
unlike the typical syphilitic keratitis parenchymatosa 
with early stromal vascularization (19,74). It is 
interesting to note that these cases of Lyme-associated 
interstitial keratitis responded to local steroids but 
not to antibiotic therapy, thus suggesting an immun-
pathologic origin (74). 
3.2.2. Peripheral ulcerative keratitis: A patient with 
peripheral ulceration secondary to LB was presented 
(78). It should be mentioned that this manifestation 
is commonly seen in autoimmune diseases. 
3.3. ORBITAL MYOSITIS (79) 
A single case of orbital myositis was described in 
the literature: a five year-old girl with typical mani-
festations of late LB. This child developed unilateral 
orbital pain, proptosis and diplopia. Computerized 
tomography disclosed myositis of the medial and 
inferior rectus muscle and haziness of the retrobulbar 
fat. Complete resolution was seen after corticoid 
therapy. 
3.4. NEURO-OPHTHALMIC MANIFESTATIONS 
The typical CNS manifestation in chronic LB is a 
progressive encephalomyelitis with fatigue, dementia, 
multiple . cranial nerve palsies as well as cerebellary 
and extrapyramidal defects and recurrent strokes (80). 
These disorders are thought to be caused by occlusive 
cerebral vasculitis (5). MRI scanning shows multiple 
paraventricular and subcortical demyelinating· lesions 
(5,11,16,18,48,49) similar to those seen in multiple 
sclerosis. Ocular symptoms in progressive encephalitis 
acta dermatovenerologica A.P A. Vol 5, 96, No 3-4 
Ophthalmic manifestations in Lyme borreliosis 
are visual field defects, diplopia and/or nystagmus 
depending on the site of the cerebral lesions. 
CONCLUSION 
and subsequent immunologic reactions resulting in 
vascular occlusions in chronic stages of the disease 
(7,31,74). Bb has been cultured from blood, cerebro-
spinal fluid and directly from brain parenchyma (7,13,49), 
but it has also been identified histologically in the 
iris the retina and in the vitreous humour (14-19). 
Ophthalmic manifestations of LB are common Th~ immunlogical reactions which are believed to 
and can mimic features of other systemic disorders. play a predominant role in chronic LB (31,74), however, 
A variety of ocular disorders can be found in each have not been elucidated in detail as of yet. 
stage of LB. The growing awareness of Bb infections In early LB oral antibiotic therapy shortens the 
has certainly contributed to improved diagnosis, but duration of systemic symptoms and prevents the 
there are still diagnostic difficulties. Especially in development of delayed disease in most patients. 
cases with uveitis, optic neuritis or oculomotor nerve The specific recommendations for antibiotic therapy 
palsies, it is necessary to consider Bb as a possible have changed over the past few years, but treatment 
causal agent (35). It is advisable to investigate the failures have occurred with every regimen. Oral 
possible history of tick bites, EM and diseases such tetracycline or penicillin are the current recommended 
as arthritis. However, 30% - 40% of cases may show drugs for Stage I of LB. In later stages parenteral 
no history of tick bites. Serological tests for Bb antibiotics, such as penicillin or cephalosporins, are 
antibodies can be helpful to support the clinical required (12,18,30,34). The use of cortiocosteroids 
diagnosis of LB, but one must be aware of the fact in chronic LB is controversial. Steroids apparently 
that, in endemic areas, positive IgG titres may be an have been helpful in treating keratitis, myositis and 
occasional coincidence. On the other hand, a negative certain neurologic symptoms in Stage III of LB 
result does not necessarily exclude the diagnosis in (12,55,74,76,79). However, caution should always be 
any clinical situation. Depending on the test used, taken when using steroids in LB, since they may 
LB may be seronegative in up to 50% (34,81 ). In cause severe exacerbation of ali the clinical symptoms. 
cases with neuro-ophthalmic involvement, an exami- Once Bb infection is diagnosed, steroids should only 
nation of the CSF is recommended (66). In some be used together with high doses of intravenous 
cases of severe intraocular inflammation, a vitreous antibiotics, even in the late stages of LB. 
tap is required for diagnosis (20), however, it is The increasing number of reports of Lyme associated 
difficult to prave Bb infection histologically. Rigorous ocular disorders should alert ophthalmologists to 
criteria should be applied in order to avoid an consider Bb as a possible causal agent. Serologic 
overdiagnosis of the ocular manifestations of LB investigations for Lyme antibodies are recommended 
(30). The US. Centers for Disease Control proposed in cases with ocular inflammatory diseases, optic 
the definition of LB, as shown in Table 2 (30). neuropathies and cranial nerve palsies. In complex 
The postulated pathophysiologic mechanism of the cases interdisciplinary cooperation with neurologists 
disease is the direct bacterial invasion of the tissue and infectious disease specialists is crucial. 
Table II. Diagnostic criteria for Lyme Borreliosis according to the US. Centers for Disease Control (30) . 
endemic 
nonendemic 
* musculoskeletal, neurologic, cardiac 
acta dennatovenerologica A.P.A. Vol 5, 96, No 3-4 
l. Erythema migrans with exposure not 
more than 30 days prior to onset 
2. Involvement of one organ system * 
and positive antibody test 
l. Erythema migrans with positive 
antibody test 
2. Erythema mirgans with involvement of 
two organ systems* 
151 
Ophthalmic mani[ estations in Lyme borreliosis 
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AUTHORS' ADDRESSES 
154 
Jutta Bergkiff, MD, Department of Ophthalmology, Karl-Franzens-University Graz 
Auenbruggerplatz 4, A-8036 Graz, Austria 
Robert Gasser, MD, PhD, Department of Internal Medicine, Karl-Franzens-University Graz 
Auenbruggerplatz 15, A-8036 Graz, Austria 
acta dennatovenerologica A.P.A. Vol 5, 96, No 3-4