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Ocular Manifestations of Leptospirosis

Leptospirosis

Rathinam SR

Uveitis Service, Aravind

Eye Hospital and PG
Institute of Ophthalmol
ogy, Madurai, India
Correspondence:
Rathinam SR
E-mail:
rathinam@aravind.org

PubMed ID

ABSTRACT
ABSTRACT

Leptospiral uveitis is a common entity in tropical countries. Ocular manifestations are noted in the second
phase of illness, but these remain under-diagnosed mainly because of the prolonged symptom-free period
that separates the systemic manifestations from detection of ocular manifestations.
Varying ophthalmic presentations and the intrinsic nature of different types of uveitis to mimic one another
also challenge the accuracy of the diagnosis. Of the individual ocular signs, the combination of acute, non
granulomatous, panuveitis, hypopyon, vasculitis, optic disc edema, membranous vitreous opacities and absence
of choroiditis or retinitis have high predictive value for the clinical diagnosis of leptospiral uveitis. Geographic
location of the patient, occupation, socio-economic status, risk factors related to exposure, past history of
fever or jaundice also aid in diagnosis.
Steroids are the mainstay of treatment for leptospiral uveitis. Depending upon the severity and anatomical
location of inflammatory lesion, topical, peri-ocular and/or systemic steroids are given. The prognosis is generally
good, even when the inflammation is severe.

: 16333191

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KEY WORDS: Hypopyon, Leptospiral, Tropical uveitis, Waterborne zoonosis

eptospirosis, Borreliosis, and Syphilis are three impor

tant spirocheatal diseases, which can cause systemic
infectious disease and after a latent period they result in uvei
tis, an immunological disorder. [1,2] Leptospires are very thin,
spiral-shaped, tightly coiled, gram-negative aerobic, spirochetes
with a unique flexuous type of motility. The genus is divided
into two species: the pathogenic leptospires, L interrogans and
non-pathogenic leptospires, L biflexa. Infected rodents and
other animals pass the bacteria in their urine contaminating
the soil and water reservoirs. They enter the humans through
an intact mucosa or abraded skin, resulting in a bacteraemia,
disseminating into various organs such as the kidneys, liver,
lungs, heart and the central nervous system. A febrile illness,
headache, severe fatigue and muscle pain may be the clinical
features of the leptospiremic acute phase; however the sever
ity of fever varies from asymptomatic presentation to mild,
moderate or severe form and is not sufficiently characteristic
for an early diagnosis.[1,3-5] After 4 to 7 days of the initial bacter
aemia, the leptospires are rapidly eliminated by the immune
system from all host tissues except from immunologically privi
leged places like the brain and eyes. This results in immuno
logical diseases like uveitis, which may manifest after 2 days
4 years after the systemic infection. Usually, uveitis begins
around three to six months after the initial leptospiral ill
ness.[2,6,7]

Ocular involvement is seen both in the systemic bacteraemic

phase as well as in the immunological phase. The incidence of
ocular signs during acute systemic phase varies from 2% to
J Postgrad Med September 2005 Vol 51 Issue 3

90%. However, in some instances, the ocular manifestations

may be sub-clinical or of such low order as to be overlooked;
they are usually found by those who search for it. [2,8-11] During
this stage one may also see conjunctival congestion without
any conjunctival discharge, chemosis, and sub-conjunctival
haemorrhage. Presence of yellow sclera and circum-corneal
congestion is regarded as pathognomomic sign of severe sys
temic leptospirosis. Martins reported a high incidence of ad
ditional ocular signs in the acute phase of leptospirosis includ
ing optic disc oedema, retinal vasculitis, retinal haemorrhage
and hard exudates. None of these patients with leptospirosis
had uveitis in the systemic phase.[8]
Uveitis is a potentially blinding inflammatory disease of the
eye and it includes a large group of diverse etiologies.[11-13] Lept
ospiral uveitis was first reported by Weil in 1866 in his original
article and subsequently, several authors found its varying pres
entations.[7-32] The precise incidence of uveitis in systemic lept
ospirosis is not known and it ranges from 3% to 92%.[3] Euro
pean authors reported an incidence of 10% to 44%, while Brand
and Heath reported figures of 13% and 2% from Israel and the
United States, respectively.[3,22,23] In a uveitis clinical set up,
Vassilev, as cited by Duke Elder, reported leptospiral uveitis to
contribute to 10% of all uveitis cases.[21] But the incidence prob
ably depends largely on the awareness with which the ocular
signs are searched for.[26] Although it is one of the common
entities in tropical countries, it remains under diagnosed. The
prolonged symptom-free period between the systemic and ocu
lar manifestations makes it difficult for the ophthalmologist
189

Rathinam: Ocular Leptospirosis

to link uveitis to leptospirosis. Lack of laboratory facilities fur

ther challenges the accuracy of the diagnosis. Sturman et al in
their exhaustive review of related world literature have cited[6]
numerous reports of leptospiral uveitis, and have identified a
broad spectrum of clinical manifestations that includes iritis,
iridocyclitis, papillitis, membranous vitreous opacities, vascu
litis and panuveitis. Edward, Feign, Woods, Duke Elder, and
others [2,3,10,11] also have contributed informative and extensive
descriptions of leptospiral uveitis. Two recent studies from
South India have identified non-granulomatous uveitis, hy
popyon, cataract, vitreous inflammatory reaction, retinal vas
culitis and papillitis as more common ocular manifestations
of leptospirosis [Table 1].[7,31]
Leptospiral uveitis commonly affects the young and middle
aged patients, men more often than women, mainly because
of the increased chance of exposure to leptospiral-contami
nated water or soil.[1-5,30] It may occur as single, self-limited or
recurrent episodes.[3,15,30] Bilateral and unilateral presentations
are found to be equally prevalent.[7,31] The primary anatomical
location of inflammation is either the anterior segment or pan
uveitis involving anterior, middle and posterior segment of the
eye. Doret classified leptospiral uveitis into a mild anterior
uveitis and a severe panuveitis with noticeable vitreous opaci
ties.[18] Anterior uveitis is usually insidious and mild[26] in con
trast to pan-uveal inflammation, which may be acute, severe
and relapsing.[6,9] The onset and severity of leptospiral uveitis
is variable, with its severity not necessarily correlating with that
of systemic disease.[3]
Slit lamp bio-microscopic examination of the anterior segment
of the eye revealed the presence of inflammatory cell collec
tion or non-granulomatous keratic precipitates (KPs) at the
back of the cornea. Like Fuchs hetrochromic iridocyclitis, these
KPs are fine, white and often diffusely distributed on the cor
neal endothelium, however presence of acute circum corneal
congestion, inflammatory cells and flare in anterior chamber
can indicate leptospiral uveitis and differentiate this from Fuch
heterochromic uveitis. Inflammatory reaction of the anterior
chamber ranges from moderate to severe scale.[7] In case of
severe inflammation, the cells gravitate down to form hy
popyon. Hypopyon has been noted to occur in 12 % of pa
tients with leptospiral uveitis [Figure 1].[7, 31] In tropical coun-

Table 1: Ocular signs in Leptospiral Uveitis

Early

Late

190

Conjunctival congestion without discharge

Conjunctival chemosis
Subconjunctival haemorrhage
Corneal stromal opacities
Non-granulomatous keratic precipitates
Inflammatory cells in the anterior chamber
Hypopyon
Cataract
Vitreous inflammatory reaction
Vitreous membrane
Hyperemic disc
Optic neuritis
Retinal vasculitis
Retinal haemorrhage
Neuroretinitis

tries, leptospiral uveitis is one of the common causes of hy

popyon uveitis in contrast to Mediterranean countries where
the presence of hypopyon usually indicates Behcets syndrome,
an autoimmune uveitis. HLA B27-related uveitis is another
cause for the hypopyon, which is also common in young males
and these two can be differentiated from leptospirosis with
the help of history and systemic examination. Other ocular
immunological manifestations include interstitial keratitis,
which was seen in 18% of patients.[30] Similar corneal lesions
were also seen in equine recurrent leptospiral uveitis of
horses.[33]
Cataract is a well-recognised complication of uveitis and the
steroid treatment of uveitis.[11-13,34, 35] Once the inflammation
is controlled, a majority of uveitic cataracts remain stable or
progress only slightly. In a previous study 14% of patients with
sero-positive leptospiral uveitis developed cataract, of them
76% of the patients had visually significant cataract on their
first visit even before the steroid treatment.[31] The spontane
ous absorption of opacified lens material is rare except in pa
tients with traumatic cataract, congenital rubella and in age
related leaking Morganian cataract.[36-39] Holloway and Gowen
reported a case of spontaneous absorption of cataract. The
patient also had vitreous veils and vitreous opacities. However
etiological diagnosis of uveitis was not known.[39] Progression
of cataract in leptospirosis was rapid in these young patients
and the lens material was found absorbed in 2.5% [31] of pa
tients with leptospirosis. There is a single case report from the
United States of a missing lens nucleus in a 31-year-old pa
tient who suffered from leptospiral uveitis.[6] Horses are well
recognised to develop severe uveitis associated with rapid cata
ract formation in the setting of equine recurrent leptospiral
uveitis. Laboratory studies have demonstrated the presence of
anti-Leptospira serum antibodies in these horses that react with
lens antigens, suggesting the presence of an antigenic rela
tionship between the leptospires and lens antigens [40]; the
mechanism of cataract formation in human is not known. The
leptospiral uveitis usually responds promptly to treatment and
cataract removal and intra-ocular lens implantation result in
complete recovery of vision.[31]
The posterior uveal involvement appears to be more charac
teristic inflammatory cell collection in vitreous is an impor
tant clinical sign.[6 ,7] In fact, Sturman uses different terminol
ogy to denote the viritis, including vitreous floaters, exudates,
precipitates and vitreous membranes. All these observations
were also noted in the recently published large series of lept
ospiral uveitis from south India: 76% of cases were found to
present with significant vitreous reaction.[7, 31] Vitreous inflam
matory cells may be of grade one to four; they may aggregate
to form vitreous exudates floating in vitreous. In some of these
patients, these vitreous exudates were arranged in a linear pat
tern resembling a string of pearls, as seen in sarcoid uveitis. In
the severe form of the disease, so-called vitreous precipitates
or inflammatory cell collections at posterior vitreous face were
seen. Parsplana snow balls can also be seen.[6] Initial transient
clouding of the vitreous with inflammatory cells may be asso
ciated with the formation of peculiar membranes.[10] These
vitreous veil - like membranous opacities are either attached
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Rathinam: Ocular Leptospirosis

to the disc or they freely float in the vitreous.[6,7] [Figure 2].

Feign and Doret described membranous vitreous opacities to
be the hallmark of the disease.[3,18] These membranes may per
sist for several months, even after the patient regains visual
acuity of 6/6.[10,41] In spite of severe grade III or IV vitreous
infiltration, on presentation, when the inflammation gets un
der control, marked clearing of inflammatory cells is possible;
the total permanent opacification vitreous is rare in leptospi
ral uveitis.[3, 9] Such severe vitreous inflammatory reaction may
also be seen in other uveitis including toxoplasmosis, sarcoido
sis, acute retinal necrosis and endogenous endophthalmitis.
Toxoplasmosis, sarcoidosis and acute retinal necrosis are dif
ferentiated from leptospiral uveitis with the presence of reti
nal and choroidal inflammatory lesions, which are absent in
the latter. It is often quite difficult to differentiate leptospiral
uveitis from endogenous endophthalmitis, especially when the
vitreous cells measure up to 4+, as both are acute in nature
and fundii in both entities are not visible on presentations.
Several investigators noted the presence of hyperaemic disc in
leptospirosis[2,7,10,11,27,30] and it was seen in 3% - 64% of cases of
ocular leptospirosis in previous studies [Figure 3]. Levin re
ported a case of hyperemic optic disc with blurred margins,
parapapillary venous sheathing, and vitreous haze. Fluorescein
angiography revealed disc leakage and visual-evoked potential
testing disclosed a delayed response demonstrating the

oedema. Neuroretinitis is another clinical entity where

inflammations of optic nerve and peripapillary retinal layers
result in a macular star. There are several causes for neuroretini
tis and the infectious causes include leptospirosis.[42] Optic neu
ritis and retrobulbar neuritis were seen in few patients and
they demonstrated colour vision defect or field abnormali
ties.[30] Other neurological manifestations of the disease that
can cause visual symptoms include encephalitis, optic neuri
tis and cranial nerve paresis involving third, fourth, sixth, and
seventh cranial nerves.[6,19,27,30] Chronic headache usually fol
lows aseptic leptospiral meningitis. Hyperemic disc or papilli
tis is seen also in few other uveitic entitis like VKH syndrome,
sympathetic ophthalmia, multiple sclerosis, parsplanitis and
sarcoidosis. Absence of bilateral exudative retinal detachment
or choroidal thickening of VKH and sympathetic ophthalmia,
absence of CNS involvement and MRI finding of multiple scle
rosis, absence of characteristic chronic snow banking of
parsplanitis, absence of bilateral granulomatous uveitis of sar
coidosis help the clinician to rule out these entities when a
patient with leptospiral uveitis presents with disc oedema.
Vasculitis of renal vessels and cerebral pan arteritis, have been
reported in systemic leptospirosis.[43,44] Likewise, retinal vascu
litis was seen in 4.8% to 51% of patients with leptospiral uvei
tis [Figure 4]. It mainly affects the veins and 1% of them also
had arteritis.[7,8,31] Other common causes of uveitis with reti-

Figure 1: Hypopyon and cataract in leptospiral uveitis

Figure 3: Hyperemic disc with retinal vasculitis

Figure 2: Vitreous membranes attached to the disc

Figure 4: Retinal vasculitis

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nal vasculitis are Behcets syndrome, sarcoidosis and Eales

disease. Behcets vasculitis is occlusive in nature; the optic disc
becomes pale during its chronic course. However, the retinal
vasculitis of leptospirosis is of perivasculitis type, vascular oc
clusions and optic atrophy are not seen in this entity. Eales
disease is characterised by the absence of uveal inflammation,
neo-vascularisation and recurrent vitreous haemorrhage while
in leptospiral uveitis, uveal inflammation is the predominant
feature and it neither causes neovascularisation nor recurrent
haemorrhage. In general, vasculitis of leptospiral uveitis re
sponds well to steroid treatment.[7] The studies on pathogenesis
of vascular damage in experimental leptospirosis in the guinea
pigs revealed evidence of swollen endothelium, dilated endo
plasmic reticulum and enlarged mitochondria; open junctions
seemed to be the initial lesions followed by endothelial necro
sis.[45] The exact mechanism of vascular involvement in hu
mans is not known.
Differential diagnosis
Although leptospiral uveitis is one of the common entities, it
remains underdiagnosed mainly because of protean manifes
tations of both systemic as well as ocular presentations. Fur
ther the notorious ability of uveitic entities to mimic each other
creates a diagnostic challenge. Other non-granulomatous uvei
tis entities that can mimic leptospiral uveitis are uveitis asso
ciated with ankylosing spondilitis and Behcets syndrome. Both
of them may present with a non-granulomatous hypopyon
uveitis, in young male patients, with or without arthralgia.
However, the systemic history can help in differentiating these
disorders; moreover the Behcets syndrome has a chronic and
insidious course while leptospiral uveitis is acute on its pres
entation. As far as the posterior segment is concerned, the disc
oedema, vitreous reaction and vasculitis of leptospiral uveitis
closely mimic the uveitis of sarcoidosis. Here again the sar
coidosis is a chronic granulomatous uveitis and can be differ
entiated from acute non-granulomatous uveitis of leptospiro
sis. Endogenous endophthalmitis can rarely be mistaken for
leptospiral uveitis and vice versa, specifically when the patient
suffered from a febrile illness and was treated with intrave
nous fluids; both these histories are known risk factors for lept
ospirosis and endogenous endophthalmitis, respectively. The
laboratory work including Microscopic Agglutination Test
(MAT) for leptospirosis, blood and vitreous culture for other
bacterial and fungal causes of endogenous endophthalmitis
will help in the definitive diagnosis.
Laboratory techniques
Confirmation of clinical diagnosis of leptospirosis relies on
laboratory testing specifically when the clinical signs are not
pathognomonic. In the case of systemic leptospirosis, isola
tion of the organisms confirms the diagnosis. However, ocular
manifestations occur in the immune phase after a symptom
free latent interval challenging the isolation techniques. The
attempt to isolate the organisms from ocular fluids has rarely
succeeded in human beings,[17] although several investigators
isolated the leptospires from aqueous fluid and vitreous of
horses.[46,47] MAT is currently considered a gold standard test.

192

However, methodological complexities, including the require

ment for a continuous supply of live organisms, high specificity
for individual sero-groups leading to false negativity, and sub
jective errors in the reading limit its use in several ophthalmic
hospitals. The results of MAT have to be considered carefully
as it may offer a false negative result if the infecting serovar is
not present in the panel. A false positive result may occur due
to the presence of residual antibody in endemic areas.[48] In
this test 12 to 18 serovars that are known to be common in a
geographic area are included in the panel. The motile bacteria
in liquid medium are treated with the titrated amounts of pa
tients serum and it is examined under dark field microscopy.
When the serum contains antibodies, agglutination is seen
under dark field microscopy. Analysis of paired serum is rec
ommended, either seroconversion or a four-fold or greater rise
in antibody titre is considered diagnostic for systemic lept
ospirosis, whereas in the chronic stage or in ocular leptospiro
sis, a titre above 1:100 dilutions is taken as significant.[4,7] Other
commercially used tests which use the cross reacting antigens
are ELISA, macroscopic agglutination, indirect haemaggluti
nation, lepto dipstick, microcapsule agglutination tests, and
lateral flow assay.[1,4,5,9] Several studies are being done to find
out better antigen and to improve serological methods. Re
cently lipoprotein L 32 and an LPS antigen have been identi
fied as important serological markers.[49,50] Molecular tech
niques such as PCR based method are also under evaluation
for rapid identification.[51,52]
Pathogenesis of leptospiral uveitis
Leptospiral uveitis is a widespread disease that affects humans
as well as domestic and wild animals. Pathological study in
human ocular tissues in this disease is not yet available;[1,3,6]
however extensive studies are available in veterinary science.
Horses infected with Leptospira present with several ocular
manifestations, including recurrent iridocyclitis also known as
periodic ophthalmia or moon blindness or equine recurrent
uveitis (ERU). Ocular signs in horses include blepharospasm,
lacrimation, corneal edema, corneal opacities, hypopyon uvei
tis, vascularisation, retinal detachment, cataract formation and
lens dislocation. The common endpoint of ERU is blindness.
Several investigators isolated leptospires from vitreous sam
ples of horses that suffered from equine recurrent uveitis.[46]
The rabbit eye model for leptospiral uveitis revealed early vit
reous invasion by neutrophils, macrophages, plasma cells and
lymphocytes in 10 days and the antibody formation appeared
after the 14th day. The appearance of antibodies in the aque
ous humor coincided with the appearance of intra-ocular
plasma cells. Severe and acute fibrinous uveitis was noted on
re-infection.[53] Gsell demonstrated a significant amount of an
tibodies for Leptospira pomona in aqueous suggesting a possi
bility of local antibody production.[15] Based on the presence
of local antibody production, ERU is believed as an organ-spe
cific autoimmune disease. Kalsow reported immuno his
topathological studies on acquired and experimentally induced
leptospiral uveitis in horses. The study recognises the disease
as a distinct subset of equine uveitis of post-infectious
immuno-pathogenesis; it also emphasises a possible relevance
to human uveitis.[54] A study by Parma et al, used the immuno
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Rathinam: Ocular Leptospirosis

blotting technique, to bind serum antibodies from horses,

immunised with leptospiral serovars with antigenic fractions
from both the cornea and lens of the horses. The study hy
pothesized an antigenic mimicry between leptospiral proteins
and horse ocular antigens.[40] This antigenic mimicry was sug
gested as a possible cause for recurrent uveitis in horses. Of
note the DNA sequence related to the antigen mimicry was
detected in pathogenic serovars, and not in non-pathogenic
serovars.[55] Molecular studies on human eyes are not yet avail
able.

6.
7.

8.
9.
10.
11.
12.

Complications

13.

When uveitis is transient, complete healing is the rule, but in

cases with severe inflammation, cataract and occasionally ster
oid induced glaucoma complicate the prognosis. Cataract ex
traction with intraocular lens implantation and anti glaucoma
treatment carries good prognosis.[7,31]

14.

Treatment

18.

Treatment with anti-microbial agents (for example, Penicil

lin, Amoxycillin, Doxycycline or Ceftriaxone) is indicated in
systemic leptospirosis early in the course of the disease, and
intravenous Penicillin or Ampicillin is used in severe systemic
illness.[5,56] Steroids are the mainstay of treatment for uveitis.
Depending upon the severity, laterality and anatomical loca
tion of inflammation, topical, periocular and systemic steroids
are given.[7] It is not known whether the systemic antibiotic
treatment during the systemic phase has any protective role
on long-term complications like uveitis and there is no double
blind study on the need for additional antibiotic treatment in
leptospiral uveitis.

15.
16.
17.

19.
20.
21.
22.
23.
24.
25.
26.
27.

28.

Conclusion

29.

Leptospirosis has a worldwide distribution. Diagnosis of sys

temic leptospirosis is often missed at peripheral centres; sub
sequently the uveitis is misinterpreted as idiopathic uveitis by
the ophthalmologists. There exists a definite possibility of
underestimating the incidence of uveitis associated with lept
ospirosis. If the diagnosis is misinterpreted, young patients with
hypopyon uveitis with a history of joint pain (during systemic
leptospirosis) may mislead the ophthalmologist to diagnose
other uveitic entities that are associated with arthralgia such
as Behcets syndrome or HLA B27 related uveitis. There is a
definite need for development of clinical prediction rules to
detect the initial ocular presentation of leptospiral uveitis and
more specific and accessible molecular methods to confirm
the clinical diagnosis.

30.
31.

32.
33.

34.
35.

36.

37.
38.
39.

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J Postgrad Med September 2005 Vol 51 Issue 3