Toxoplasma gondii Detection by Nested Polymerase Chain Reaction in Lens Aspirate and Peripheral Blood Leukocyte in Congenital Cataract Patients: The First Report from a Tertiary Eye Hospital in India

Vision Research Foundation, L & T Microbiology Research Centre, Chennai, India.
Current Eye Research (Impact Factor: 1.64). 07/2007; 32(7-8):653-7. DOI: 10.1080/02713680701471123
Source: PubMed
To detect T. gondii DNA and specific antibodies in lens aspirates (LA) and peripheral blood leucocytes (PBL) of congenital cataract patients.
ELISA for T. gondii antibodies on sera nPCR for T. gondii DNA (B1 gene) on LA and PBL were performed for 52 patients.
T. gondii DNA was detected in 29 (55.8%) of the 52 patients (LA-14, PBL-13, LA and PBL-2, and specific IgM in 2 sera). nPCR in PBL was more sensitive than ELISA (p<0.005).
nPCR is a sensitive technique to detect T. gondii from LA and PBL in congenital cataract patients.


Available from: Mahalakshmi Balasubramanian, May 19, 2015
Current Eye Research, 32:653–657, 2007
Informa Healthcare USA, Inc.
ISSN: 0271-3683 print / 1460-2202 online
DOI: 10.1080/02713680701471123
To xoplasma gondii Detection by Nested
Polymerase Chain Reaction in Lens
Aspirate and Peripheral Blood Leukocyte
in Congenital Cataract Patients: The First
Report from a Tertiary Eye Hospital in India
B. Mahalakshmi,
K. Lily Therese,
G. Shyamala,
U. Devipriya,
and H. N. Madhavan
Vision Research Foundation,
L&TMicrobiology Research
Centre, Chennai, India
ABSTRACT Purpose:Todetect T. gondii DNA and specific antibodies in lens
aspirates (LA) and peripheral blood leucocytes (PBL) of congenital cataract
patients. Methods: ELISA for T. gondii antibodies on sera nPCR for T. gondii
DNA (B1 gene) on LA and PBL were performed for 52 patients. Results: T.
gondii DNA was detected in 29 (55.8%) of the 52 patients (LA-14, PBL-13, LA
and PBL-2, and specific IgM in 2 sera). nPCR in PBL was more sensitive than
ELISA (p < 0.005). Conclusion:nPCRisasensitive technique to detect T. gondii
from LA and PBL in congenital cataract patients.
KEYWORDS T. gondii in lens aspirate; B1 gene of T. gondii; T. gondii in congenital cataract;
nested PCR for T. gondii
Congenital/infantile cataract is the most serious type of childhood cataract
because of its potential for inhibiting or restricting early visual development.
Prevention of visual impairment due to congenital and infantile cataract is an
important component of the World Health Organization international pro-
gram for the elimination of avoidable blindness by 2020.
The prevalence of
blindness among children in different region of the world varies from 0.2–
1.5/ 1000 children. This corresponds to an estimate of 1.4 million blind chil-
dren worldwide.
Congenital cataract affects about 3/10,000 newborns in India
and is a significant cause of blindness in children, often leading to lifelong
visual disability.
The various causes of congenital cataract include prena-
tal infections due to Rubella, To xoplasma gondii (T. gondii), Cytomegalovirus
(CMV), and Treponema pallidum, prenatal drug exposure, prenatal ionizing
radiations, prenatal/peri-natal metabolic disorders, hereditary, or unknown
Received 8 March 2007
Accepted 16 May 2007
Correspondence: K. Lily Therese,
Vision Research Foundation,L&T
Microbiology Research Centre, 18
College Road, Chennai 600006, India.
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Congenital toxoplasmosis can result from transpla-
cental transmission of T. gondii infection. The preva-
lence of congenital toxoplasmosis in the USA and Eu-
rope is 1 and 1–10 per 10,000 live births, respectively.
Most cases of congenital toxoplasmosis present as a
subclinical or chronic infection. After months or even
years, these children develop the signs and symptoms of
central nervous system involvement, developmental de-
lay, and ocular disease with retinochoroidal lesions, stra-
bismus, and blindness. Clinical signs of active infection
are retinochoroiditis, hydrocephalus, microcephaly,
cerebral calcification, seizure, psychomotor retarda-
tion, organomegaly, jaundice, rash, and fever. The
most common ocular sequelae in these patients are
retinochoroidal scar, cataract, microphthalmia, phthi-
sis bulbi, strabismus, nystagmus, and optic atrophy.
The prevalence of congenital toxoplasmosis in India
is not known. The present study was undertaken to de-
termine the association of T. gondii in congenital cataract
patients in an ophthalmic hospital-based study. For this
purpose, nested polymerase chain reaction (nPCR) tar-
geting B1 gene of T. gondii
was applied on the lens
aspirate (LA) and the peripheral blood leukocyte (PBL)
of patients undergoing therapeutic lensectomy. The re-
sults were correlated with anti T. gondii antibodies assay
on the serum samples of the same patients.
Patients and Specimens
A total of 52 children less than one year of age clin-
ically diagnosed to have congenital cataract and un-
dergoing therapeutic lensectomy over a period of 14
months (February 2005 to April 2006) at the tertiary
care ophthalmic hospital, Sankara Nethralaya, Chen-
nai, India, were included in the study. Lensectomy was
done by extracapsular cataract extraction. The lens as-
pirate (LA) was collected in a syringe attached to a vit-
reous cutter at the beginning of the lensectomy and im-
mediately transported to the laboratory. The LA spec-
imen obtained after lensectomy was diluted in 1 ml
of Dulbecco’s modified Eagle medium with 3% fetal
calf serum and stored at –80
C until further use. The
diluted specimen was used for DNA extraction. Hep-
arinized blood and serum samples from all 52 patients
were collected at varying periods 2 days to 3 months
prior to surgery.
Separation of Peripheral Blood Leukocyte (PBL) from
EDTA Blood: Te n milliliters of blood collected in a cen-
trifuge tube containing 20 mg of EDTA was allowed
to settle in an upright position for 30–60 min at room
temperature. The leukocyte-rich plasma was then trans-
ferred to an Eppendorf vial using a sterile Pasteur pipette
and centrifuged at 3000 rpm for 10 min. The leukocyte
deposit was resuspended in 200 µlofthe plasma and
30 µlofthe PBL was used for DNA extraction.
ELISA for Detection of Specific
T. gondii IgG and IgM Antibodies
The52sera were tested for the presence of specific
anti-T. gondii IgM antibodies (T. gondii IgM abs) and
anti-T. gondii IgG antibodies (T. gondii IgG abs) using
commercially available bioelisa Toxo IgG and bioelisa
Toxo IgM kit (BIOKIT, SA, Spain) following the manu-
facturer’s instructions. The serum was tested at dilution
of 1:100 along with the controls in each run. Results
were read at 490 nm in an ELISA plate reader (Bio-Tek
Model EL-311, Highland Park, Winooski, VT, USA).
Serum showing the presence of anti-T. gondii antibodies
at 1:100 dilutions was considered positive.
Nested Polymerase Chain Reaction
(nPCR) Using Primers Coding for the
B1 Gene
Positive Control-Tachyzoites of T. gondii: Heat-killed
Cinawater bath for 30 min) RH strain of
T. gondii maintained in mice (obtained from Dr. Dubey,
PGIMER,Chandigarh, India) was used as the positive
Extraction of DNA:DNA was extracted from heat-
killed T. gondii tachyzoites by the method of Miller
et al.
One hundred microliters of the diluted LA
specimen and approximately 50 µlofthe PBL from
the EDTA blood was used for DNA extraction us-
ing the clinical genomic DNA mini prep kit (Biogene
Inc., Los Angeles, CA, USA) as per the manufacturer’s
PrimersTargeting theB1GeneofT. gondii: Primers and all
the reagents used for PCR were obtained from Sanmar
Speciality Chemicals Pvt. Ltd., (formerly Bangalore,
Genei), Bangalore, India. Nested primers targeting the
B1 gene
included outer sense primers for the first
round of amplification consisting of upstream primer
and down-
stream primer 5
TC 3
which generates a 193-bp product (nucleotides
B. Mahalakshmi et al. 654
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Page 2
694–887). The inner set of II round of primers consist-
ing of upstream primer 5
and downstream primer 5
generate a 96-bp product
(nucleotides 757–853) after amplification by nPCR. The
nPCR protocol followed was as given earlier.
Two negative (reagent) controls (one for the first
round and amplified in the second round and another
reagent control for the second round) and positive con-
trol (using 2 µlofT. gondii DNA from RH strain) were
included in each PCR run. The PCR results were con-
sidered valid only when the negative controls were neg-
ative and the positive control (T. gondii DNA) were pos-
itive at the end of I and II rounds of nPCR. Visual-
ization of the PCR product was done by subjecting 10
µlofamplified reaction mixture to electrophoresis in
2% agarose gel incorporating 5µg /ml of ethidium bro-
mide in 1X Tris-Borate buffer (pH –8.2 to 8.6) and docu-
mented on gel documentation system (Vilber Lourmat,
Marne La Vallee, Cedex, France).
Precautions of nPCR: To prevent contamination,
DNA extraction, PCR preparation, PCR amplification,
and analysis of the amplified product were done in
physically separated rooms. PCR preparation was per-
formed on a laminar flow workbench with single-use
aliquots of reagents and dedicated pipettes. Sterile filter
guarded tips were used for the addition of specimens
and also for the extracted DNA.
Statistical Analysis of Results
The results of ELISA and nPCR were statistically
analysed by Fisher Exact test and Chi-square test.
ELISA for Specific Anti-T. gondii IgM and IgG
Abs: Anti-T. gondii IgM alone was detected in 2/52
(3.8%) patients and anti-T. gondii IgG alone in 5/52
(9.6%) patients. Both anti-T. gondii IgG and IgM abs
were not simultaneously detected in any of the 52
nPCR for the Detection of B1 Gene of T. gondii Genome:
nPCR was positive in 15 (28.8%) LA and in 16 (30.8%)
PBLofthe 52 patients. Among these nPCR positive
specimens, T. gondii DNA was detected in both the LA
and PBL of 2 patients, in LA alone in 13 patients, and in
PBL alone in 14 patients. Figure 1 shows the results of II
round of nPCR using primers targeting the B1 gene of
FIGURE 1 Agarose gel electrophoretogram of the II round of
nPCR using nested primers targeting the B1 gene of T. gondii
genome on both LA (n = 7) and PBL (n = 7) from collected 7
patients with congenital cataract. N2: Negative control II round.
N1: Negative control I round. Lanes 1–16: LA and PBL from con-
genital cataract patients. Lanes 10, 11, 15, and 16: Positive for T.
gondii DNA. Lanes 1–9, 12–14: Negative for T. gondii DNA. PC:
DNA from tachyzoites of standard RH strain of T. gondii. MW:
Molecular weight marker ϕX DNA Hinf I digest.
T. gondii on the LA and PBL of the study group. nPCR
for T. gondii DNA was negative in both LA and PBL in
23 patients in this study group.
Correlation of Results of ELISA and nPCR on LA and
PBL:Ofthe 13 nPCR-positive LA specimens, anti-T.
gondii IgM abs was detected in one and IgG abs in 4
patients. Among the 14 PBL nPCR-positive specimens,
IgM abs was detected in one patient. Out of the two
patients with nPCR being positive for both LA and
PBL, IgM was detected in one patient (Table 1). The
results of detection of anti-T. gondii IgM abs and the
nPCR for T. gondii genome on the LA and PBL were
statistically significant respectively (Fischers Exact test;
p < 0.005). The results of nPCR for B1 gene of T. gondii
genome on LA and PBL were not statistically significant
(Chi-square test, P = 0.83). In this study population,
T. gondii genome was detected in 55.8% (29/52) of the
congenital cataract patients.
TABLE 1 Comparison of the Results of nPCR Using Primers
Targeting the B1 Gene in the Lens Aspirate and the Leukocyte
Fraction and ELISA for the Detection Specific anti T. gondii Anti-
bodies in the Serum of 52 Patients with Congenital Cataract
Results of specific anti-
T. gondii antibodies in serum
IgM pos IgM neg IgM neg
Results of nPCR for IgG neg IgG pos IgG neg
T. gondii genome (n = 02) (n = 05) (n = 45)
LA pos PBL pos (n = 13) 01 04 08
LA pos PBL neg (n = 14) 01 13
LA neg PBL neg (n = 02) 01 01
LA neg PBL neg (n = 23) 23
LA: lens aspirate; PBL: peripheral blood leukocyte.
Anti-T. gondii IgG and IgM were not simultaneously detected in any
of 52 serum samples. The results of detection of anti-T. gondii IgM abs
and the nPCR for T. gondii genome on the LA and PBL were statistically
significant, respectively (Fischer Exact test p < 0.005). The results of nPCR
for B1 gene of T. gondii genome on LA and PBL were not statistically
significant (Chi-square test, P = 0.83).
655 Toxoplasma gondii in Congenital Cataract
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The reports in literature indicate that the most com-
mon infectious agents causing congenital infections
are CMV, HSV, Erythrovirus (Parvovirus B19), Rubella
virus, Hepatitis B virus, HIV, VZV, Treponema pal-
lidum, and T. gondii.Those associated with congenital
cataract are Rubella virus, CMV, HSV, T. gondii, and
Treponema pallidum.
Congenital toxoplasmosis results
from transplacental transmission of T. gondii when the
mother has the primary infection just before or during
gestation. The incidence and the severity of congenital
infection vary with the timing of infection and have a
transmission rate of 10–15% during the first trimester,
30% during the second trimester, and 60% during the
third trimester.
The diagnosis of congenital toxoplasmosis can be
made by either indirect or direct methods. The detec-
tion of IgM or IgA antibodies to T. gondii in an in-
fant is highly sensitive for the diagnosis of congeni-
tal toxoplasmosis.
Amplification of T. gondii DNA by
PCRisalmost 100% sensitive and specific and can be
detected in most body fluids of congenitally infected
PCRamplification of amniotic fluid or fetal
blood samples obtained via cordocentesis can identify
congenitally infected fetuses while still in utero, but is as-
sociated with certain inherent procedure related risks.
In this study group of 52 congenital cataract patients,
specific anti-T. gondii IgM antibodies were detected in
only 3.8% of the patients, whereas nPCR for B1 gene
of T. gondii genome in LA and/or PBL were positive in
55.8%. nPCR alone was positive in 51.9%. nPCR for
B1 gene of T. gondii genome is 51.9% more sensitive
than ELISA for the detection of anti-T. gondii IgM abs
(statistically significant Chi-square test p < 0.001).
Among the 29 clinically diagnosed congenital
cataract patients positive by PCR for T. gondii genome
(in the LA and/or in the PBL) and/or the presence of
specific anti-toxoplasma IgM antibodies, 5 patients had
associated central nervous system involvement and 5
other patients had congenital heart disease. The other
19 patients had no systemic involvement at the time of
evaluation for congenital cataract.
Congenital toxoplasmosis of the newborn must be
differentiated from the other infectious diseases of the
TORCH group—Rubella, CMV, HSV—as well as the
other congenital infectious diseases that may simu-
late toxoplasmosis, such as syphilis, tuberculosis, and
TheLAand PBL from the 29 patients with
laboratory-proven toxoplasma infection were also ana-
lyzed for the presence of Herpes simplex virus (HSV)
DNA, Rubella virus (RV) RNA, and cytomegalovirus
(CMV) DNA. HSV-2 DNA was detected in 6 patients
(unpublished data), RV RNA in 5 patients,
and CMV
DNAinnone (unpublished data).
The detection of T. gondii genome in 13 LA and not
in the corresponding PBL and vice versa in 14 patients
needs to be studied further.
In a study by Angra et al.,
the causes of non-
traumatic cataract in 366 children in the southern part
of India were hereditary (25%), congenital Rubella syn-
drome (CRS) (15%), and undetermined (51%). The 4
major causes of visual impairment and blindness in
1411 children attending the school for the blind in India
were vitamin A deficiency, congenital ocular anomalies,
inherited retinal dystrophies, and cataract.
In another
study by Kaid Johar et al.
on pediatric nontraumatic
cataract in the western part of India, 7.2% were hered-
itary, 4.6% were due to CRS, 15% secondary cataract,
and 73% were undetermined. The association of con-
genital toxoplasmosis with congenital cataract has not
been analysed in these previous studies from India. To
the best of our knowledge, this is the first report show-
ing the association of T. gondii with congenital cataract
based on PCR on the LA from India.
It is generally recognized that extensive management
in utero and after birth certainly helps decrease the sever-
ity of the infection and the risk of ocular lesions. The
overall prognosis of congenital toxoplasmosis is satis-
factory when infection is identified early and treated ac-
cordingly. In a study of 327 children, retinal lesions were
detected between birth and one year of age in 85% of
children with proven congenital toxoplasmosis born to
mothers who were not treated during pregnancy, com-
pared to 50% of the children with lesions born to moth-
ers who were treated for toxoplasmosis. The delayed on-
set of lesions is an important consideration.
If congen-
ital toxoplasmosis is undiagnosed and untreated, almost
all infected children will develop visual or neurological
impairments by adulthood. Treatment of children with
congenital toxoplasmosis for a longer period (up to one
year) resulted in less severity of the infection compared
to increased visual impairment in children who were not
treated or received treatment for a short duration.
The proven association of T. gondii infection in con-
genital cataract patients in this study group necessitates
the need for the screening of pregnant women for pri-
mary toxoplasma infection and early and appropriate
B. Mahalakshmi et al. 656
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treatment of the infected women and the growing fe-
tus to reduce the prevalence of infectious congenital
cataract in our population. These results also necessi-
tate the need to screen newborns for congenital toxo-
plasmosis to determine its prevalence in India.
The authors gratefully acknowledge the financial sup-
port of ICMR through the grant (Project no:5/3/3/3/
2003 ECD- I). We acknowledge Dr. Dubey, PGIMER,
Chandigarh, India, for the supply of inactivated stan-
dard RH strain of T. gondii.
[1] Remington JS, Thulliez P, Montoya G. Recent developments
for diagnosis of toxoplasmosis. J Clin Microbiol. 2004;42:941–
[2] Rahi JS, Dezateux C. British cataract interest group. Congenital and
infantile cataract in the United Kingdom: underlying or associated
factors. Invest Ophthalmol Vis Sci. 2000;41:2108–2114.
[3] Shamannna BR, Murali Krishnan R. Childhood cataract: magni-
tude, management, economics and impact. Community Eye Health.
[4] Jabs DA, Nguyen QD. Ocular toxoplasmosis. In: Ryan SJ, Schachat
AP, eds. Retina, Volume 2, Medical Retina. St. Louis, MO: Mosby-a
Harcourt Health Sciences Company; 2001;1531–1544.
[5] De Mata, Andrea P. Toxoplasmosis.PA: WB Saunders, Philadelphia,
PA:AHarcourt Health Sciences Company, 2002;385–410.
[6] Tabbara KF. Ocular toxoplasmosis: toxoplasmic retinochoroiditis. In:
Tabbara KF, ed. International Ophthalmic Clinics, posterior uveitis,
Part I, Volume 35, Boston: Little Brown, 1995.
[7] Klaren VNA, Kijlstra A. Toxoplasmosis: an overview with empha-
sis on ocular toxoplasmosis. Ocular Inflammation and Immunol.
[8] Jones CD, Okhravi N, Adamson P, Tasker S, Lightman S. Comparison
of PCR detection methods for B1, P30 and 18S rDNA genes of T.
gondii in aqueous humor. Invest Ophthalmol Vis Sci. 2000;41:634–
[9] Stagno S, Britt WJ, Pass RF. Laboratory diagnosis of cytomegalovirus
infections. In: Schmidt NJ, Emmons RW. Diagnostic procedures for
viral, rickettsial and chlamydial infections. Washington, DC: Ameri-
can Public Health Association, sixth edition, 1989;321–378.
[10] Miller D, Davis J, Rosa R, Diaz M, Perez E. Utility of tissue cul-
ture for detection of Toxoplasma gondii in vitreous humor of pa-
tients diagnosed with toxoplasmic retinochoroiditis. J Clin Microbiol.
[11] Mahalakshmi B, Therese KL, Madhavan HN, Biswas J. Diagnostic
value of specific local antibody production and nucleic acid am-
plification technique: nested polymerase chain reaction (nPCR) in
clinically suspected ocular toxoplasmosis. Ocular Inflammation and
Immunol. 2006;14;105–112.
[12] McCabe RE, Remington JS. Toxoplasma gondii. In: Mandel GD,
Douglas G, and Benett JE, eds., Principles and practice of infec-
tious diseases. New York, NY, Churchill Livingstone, Third Edition.
[13] Kravetz JD, Federman BG. Toxoplasmosis in pregnancy. Am J Med.
[14] Gangneux FR, Gavinet MF, Ancelle T, Raymond J, Shaefer CT, Camet
JD. Value of prenatal diagnosis and early postnatal diagnosis of con-
genital toxoplasmosis: retrospective study of 110 patients.J Clin Mi-
crobiol. 1999;37:2893–2898.
[15] Shyamala G, Malathi J, Moses VS, Therese KL, Madhavan HN. Nested
reverse transcriptase polymerase chain reaction for the detection of
rubella virus in clinical specimens. Indian J Med Res. 2007;125:73–
[16] Angra SK. Aetiology and management of congenital cataract. Indian
J Pediatr. 1987;54:673–677.
[17] Rahi JS, Sripathi S, Gilbert CE, Foster A. Childhood blindness in India:
causes in 1318 blind school children in nine states. Eye. 1995;9:545–
[18] Kaid Johar SR, Savalia NK, Vasavada AR, Gupta PD. Epidemiology
based etiological study of pediatric cataracts in western India. Indian
J Med Sci. 2004;58:115–121.
[19] Wallon M, Kodjikian L, Binquet C, Garweg J, Fleury J, Quantin C,
Peyron F. Long term ocular prognosis in 327 children with congenital
toxoplasmosis. Pediatrics. 2004;113:1576–1572.
[20] Segundo GRS, Silva DAO, Mineo JS, Ferreira MS. Congenital tox-
oplasmosis in Uberlˆandia, MG, Brazil. JTrop Pediatr. 2004;50:50–
657 Toxoplasma gondii in Congenital Cataract
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    [Show abstract] [Hide abstract] ABSTRACT: We undertook this study to determine the infectious aetiology of congenital cataract based on the presence of IgM antibodies to TORCHES [(Toxoplasma gondii (T. gondii), Rubella virus (RV), Cytomegalovirus (CMV), Herpes simplex virus (HSV) and Syphilis (caused by Treponema pallidum)] in the serum samples of congenital cataract patients. Serum samples collected from 593 infants and children (10 days to 12 months old) with clinically diagnosed congenital cataract at Sankara Nethralaya, a referral eye hospital in Chennai, were tested for the presence of specific IgG and IgM antibodies to T. gondii, RV, CMV, HSV by ELISA and specific treponemal antibodies by T. pallidum haemagglutination test (TPHA). IgM antibodies were detected against T. gondii in 1.7 per cent, RV in 8.4 per cent, CMV in 17.8 per cent and HSV in 5.1 per cent, and that of specific IgG in 8.9, 25.0, 66.1 and 2.6 per cent respectively. Presence of IgM antibodies to T. Gondii in the study group was significantly lower when compared to IgM antibodies to RV, CMV and HSV. All serum samples were negative for the presence of anti treponemal antibodies by TPHA. Overall, IgM antibodies to one or more of the four infectious agents were detected in 20.2 per cent of the study population, and among these co-infections to more than one infectious agents were detected in 12.5 per cent. The results of the present retrospective analysis showed association of RV, CMV, HSV and T. gondii with congenital cataract based on the presence of specific IgM antibodies.
    Full-text · Article · Apr 2010 · The Indian Journal of Medical Research
  • No preview · Article · Aug 2011 · Ocular immunology and inflammation
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    [Show abstract] [Hide abstract] ABSTRACT: PURPOSE: To report the clinical features of cataracts in eyes with ocular toxocariasis. SETTING: Department of Ophthalmology, Seoul National University Bundang Hosptal, Seongnam, South Korea. DESIGN: Retrospective observational case series. METHODS: The clinical diagnosis of ocular toxocariasis was based on the following characteristic features: retinal granuloma with or without ocular inflammation and positive results in serum antibody enzyme-linked immunosorbent assay. Patients younger than 60 years who presented with a unilateral cataract and were diagnosed with ocular toxocariasis between January 2009 and January 2012 were included. Demographic and ocular examination data for all patients showing atypical cataract features were collected. All cataracts were documented with anterior segment photography. RESULTS: Seven of 83 patients (8.4%) presented with an atypical cataract in the eye with ocular toxocariasis only. The mean patient age was 49.7 years ± 8.3 (SD) (range 38 to 59 years). All patients had small, round, white lens opacities resembling retinal granulomas. The granuloma-like opacities were located primarily in the lens midperiphery and in the subcapsular level. The lens opacity migrated in 1 patient. CONCLUSIONS: Ocular toxocariasis can cause a cataract with distinctive clinical features. These cataracts show a granuloma-like opacity primarily in the posterior subcapsular level; the opacity can migrate. FINANCIAL DISCLOSURE: No author has a financial or proprietary interest in any material or method mentioned.
    Full-text · Article · Mar 2013 · Journal of Cataract and Refractive Surgery
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