Toxoplasmosis is caused by the protozoan Toxoplasma gondii. It commonly infects intermediate hosts such as humans through contact with cat feces or consumption of undercooked meat containing cysts. In the eye, it most often causes retinochoroiditis which can lead to vision loss. Diagnosis is usually based on clinical findings, though serology and imaging tests provide supporting evidence. Treatment involves anti-protozoal medications such as sulfadiazine combined with pyrimethamine and corticosteroids to reduce inflammation. Recurrences are common in immunocompromised patients.

1. PARISITIC INFECTION

2. TOXOPLASMA

3. • Toxoplasmosis iscaused by Toxoplasma
gondii
• an obligate intracellular protozoan.
• It infests 10%of adults in northern
temperatecountries and 50%of
adults in Mediterranean and
tropical countries.
LIFE CYCLE
• definitive host - cat
• intermediate hosts -mice, livestock,
birds& humans.
• Oocysts are excreted in cat faecesand
then ingested by intermediate hosts
via contaminated water

5. SOURCES OF INFECTION
• Undercooked Lamb,Pork,Chicken
• Contamination of cat faeces in the environment –water contaminated
with cat feces
• Raw vegetables contaminated with cat feces.
• Organ transplantation
• Blood transfusion

6. Bradyzoite:
• isan inactive stage lying dormant within cystsin tissues such asthe eye,brain and skeletal
muscle
• consumption of undercooked meat (or eggs) froman intermediate host can lead to
infestation.
Tachyzoites:
• Releasedfrom rupture of Bradyzoitecysts
• Are the proliferating active form
• stimulate an inflammatory reaction.

7. Congenital toxoplasmosis:
• 40%of primary maternal infections result in congenital infection;
• Transplacental transmission ishighest during the third trimester.
• Therisk of severe disease developing in the fetus isinversely proportional to
gestationalage
• early pregnancy - result in spontaneous abortion, stillbirth, or severe
congenital disease
• late pregnancy - asymptomatic, normal-appearing infantwith latent
infection.

8. Theclassicpresentation (Sabin’s tetrad) includes
• retinochoroiditis,
• hydrocephalus or microcephaly,
• intracranial calcifications, and
• cognitive impairment, occurring in lessthan 10%of infected children.
• fetal death occurs in 10%of all congenital toxoplasmosis.
• Neurological and visceral involvement may be subclinical
• Retinochoroiditis occur in over 75%,leaving scarsthat are commonly alater incidental
finding
• 25%of these become blind in 1 or both eyes.

9. Retinochoroidal scars in congenital toxoplasmosis macular lesion

10. Retinochoroidal scars in congenital
toxoplasmosis :
(B) multiple peripheral scars on wide-feld
imaging;
(C) wide-feld autofluorescence
image of the same eye

11. Acquired toxoplasmosis in immunocompetent adults
• subclinical in 80–90%
• Cervical lymphadenopathy, fever, malaise and pharyngitis are common features in
symptomatic patients
• Earlyretinitis may occur in about 20%.
Toxoplasmosis in immunocompromised patients
• may be acquired or result from reactivation of pre-existing disease.
• constitutional symptoms + meningoencephalitis, pneumonitis, retinochoroiditis
can occur.

12. Ocular features
• Themost common causeof ocular toxoplasmosis is from intrauterine
infection
• Toxoplasmosis constitutes 20–60%of all posterior uveitis.
• Retinochoroiditis isthe most common manifestation of ocular
toxoplasmosis, but it is often accompanied by a granulomatous anterior
uveitis
• Reactivation at previously inactive cyst-containing scarsis the rule in the
immunocompetent
• Recurrent episodes of inflammation are common and occur when the cysts rupture and
release hundreds of tachyzoites into normal retinal cells

13. Symptoms
• Unilateral acute or subacute onset of floaters,
• blurring and photophobia.
SIGNS
• Spill-over’ anterior uveitis iscommon
• It may be granulomatous or resemble Fuchsuveitis
syndrome
• IOPmay
be elevated
• A single inflammatory focus of fluffy white retinitisor
retinochoroiditis associated with apigmented scar
• satellite lesion is typical.
• Lesionstend to involve the posteriorpole. Typical satellite lesion adjacent to
toxoplasma retinitis scar

14. • De novo foci not associated with an old scar
• Vitritis may be severeand impair fundus visualization.
• ‘Headlight in the fog’ isthe classicdescription of awhite
• retinal inflammatory nidus viewed through vitritis

15. • Rarely, blood vessels crossing over the active retinitis may suffer occlusion
• sheathing of vessels-common
• more commonly in the proximity of the lesion, but can also occur far from it .
• These vessels do not suffer the risk of occlusion
• sheathing disappears very quickly with therapy.
• This vascular response represents an immune mediated reaction.
• Also in the vicinity of the acute focus arteries may show multiple small deposits on
their surface, which are known as Kyrieleis plaques, are very suggestive of
toxoplasmosis .
• These vessels do not show leakage on fluorescein angiography and do not suffer
occlusion.

16. OTHER MANIFESTATIONS
• Optic disc oedema is common.
• Retinochoroiditis absent in acute phase of acquired disease,with activity
consisting of anterior uveitis,vitritis and retinal vasculitis; typical retinal scarsmay
form later.
• Neuroretinitis israre, marker of acutely acquired rather than reactivated
infection.
• Punctate outer retinal toxoplasmosis isan atypical manifestation featuring
clusters of small (25–75µm diameter) grey–white lesions.

17. • On an average, the inflammation lasts for ~4 months.
• About one-third of the patients haverecurrent attacks.
There are three main morphologic variants.
1st variant:
• lesions are larger than 1DD dense, and elevated.
• largely destructive lesions and associated with significant vitritis and anterior
chamberreaction.
• Prompt therapy isusually necessaryregardless of the location of the lesion.
Second variant :
• punctate lesions of the inner retina
• The inflammation is mild, and no therapy is necessary unless the lesion is close to the
macula and threatens vision.
Third variant :
• chr by punctate lesions on outer retina & mild vitritis.
• Lesionsslowly resolve spontaneously but also tend to recur in adjacent areas.

18. Immunocompromisedhost
• Extensiveand fulminant retinal involvement ,bilateral , may be diffcult to
distinguish from viral retinitis.
• But vitritis is still there as the patient in not as immunocompromised as in
CMV infection
• Papilloedema is another potential manifestation in the presence of encephalitis and
raised intracranial pressure.
Immunocompromised: Large area of retinitis which
is progressively enlarging in a leukaemia patient on
chemotherapy

19. Complications of toxoplasmosis retinochoroiditis include
• posterior synechiae
• macular edema,
• dragging of the macula secondary to aperipheral lesion,
• retinal detachment,
• chorioretinal vascular anastomosis,
• choroidal neovascularization,
• branch retinal artery or vein occlusions,
• optic nerve atrophy
• cataract, and
• Glaucoma
• Unilateral pigmentary retinopathy simulating retinitis pigmentosa (asa late
sequela of recurrent ocular toxoplasmosis )

20. Common complications of Toxoplasma retinitis.
(A) Macular involvement, at presentation and (B) following treatment;

21. Common complications of Toxoplasma retinitis.
(C) juxtapapillary lesion involving the optic nerve head

22. Uncommon complications of Toxoplasma retinitis. (A) Periarteritis resulting in branch
retinal artery occlusion; (B) FA shows extensive non-perfusion at the posterior pole;

23. Uncommon complications of Toxoplasma retinitis.(C) serous macular
detachment; (D) FA of (C) shows hyperfluorescence d/t pooling of
dye;

24. Uncommon complications of Toxoplasma retinitis. (E) choroidal
neovascularization adjacent to an old scar; (F) FA of (E) shows
corresponding hyperfluorescence

25. Progression of Toxoplasma retinitis. (A) Moderate activity;
(B) 3 months later, following antibiotic treatment

26. Investigations:
•Diagnosis is usually based on clinical examination findings.
Serology
• TORCH TITRE -antibody
• IgG antibodies appear after the first 2 weeks of infection, detectable throughout
life.
• IgM antibodies -acute phase of the infection, detectable upto 1 year
• newborns –IgM confirms congenital infection
Ig A first to appear after birth
• the presence of IgG antibodies may indicate passive transfer of maternal antibodies
in utero.
• IgA antibodies usually disappear by 7 months.

27. Ocular fluid
Goldmann–Witmer coefficient(GWC)
• Calculating the ratio of specifc IgG in aqueous humour to that in serum
• A ratio of greater than 3 is considered diagnostic of local antibody production.
PCR of intraocular fluid is variably sensitive but highly specific and can be
diagnostic in clinically uncertain cases

28. • Sabin Feldman dye test-
 The classic gold standard serology test, uses live T.gondii tachyzoites to detect IgG
antibodies .
 High sensitivity and specificity
 Not frequently performed, owing to the risk for laboratory-acquired infections
 Available in very few reference laboratories in North America.
• Western blot analysis –to identify cytoplasmic antigens of T.gondii

29. Imaging.
• Macular OCT will demonstrate any macular oedema if vitritis is not preventative.
• B-scan ultrasonic imaging can be used to exclude retinal detachment in the presence
of severe vitritis.
• FAF may facilitate monitoring of inflammatory activity
Toxoplasma –active –full thickness involvement
Healed- full thickness atrophy

30. • Usually self –resolving in Immunocompetent patients –resolves in 4- 8 weeks
INDICATIONS FOR TREATMENT
• Lesions threatening fovea or optic nerve
• Lesions within temporal arcades
• Lesions with moderate to severe vitritis
• Lesions greater than 1 DD
• Persistent disease for > 1 month
• Presence of multiple active lesions
• 2 line drop in visual acuity
• Immunocompromised

31. TREATMENT
• TRIPLE THERAPY
• Sulfadiazine –pyrimethamine – Corticosteroids

32. • Trimethoprim –Sulfamethoxazole (160/800mg) combination is now preferred
 Can cause bone marrow suppression
 CBC,Serum Creatinine and Liver enzymes should be tested at baseline and at 7
days
 Contraindicated in pediatric patients <2 years
 Risk of SJS and TEN
 Hypersensitivity to sulphonamides – fever, maculopapular
rash
• If hypersensitivity, can switch to Clindamycin 300 mg QID alone OR
Azithromycin(500 mg/day) alone or in combination with pyrimethamine
(50md/day) –Has less side effects also –is accepted for sight threatening toxo
• QUADRUPLE THERAPY –Triple therapy + Clindamycin 300 mg qid

33. • Spiramycin 400 mg 3 times /day
• Atovaquone 750mg qid for 3 months –also very effective in CNS toxoplasmosis
• Treatment of congenital toxoplasmosis in neonateswith antimicrobials (pyrimethamine
and sulfonamides plus folinic acid)for one year may reduce the frequency of subsequent
development of retinochoroidal scars.

34. • Prednisolone (1 mg/kg)
 given initially and tapered according to clinicalresponse
 should alwaysbe used in conjunction with aspecific anti Toxoplasmaagent
 Most frequently pyrimethamine combined with sulfadiazine (‘classic’ or
‘triple’ therapy, sometimes supplemented with clindamycin)
 Systemic steroids should be avoided in immunocompromised
patients
• In AIDS pyrimethamine is avoided or used at alower dosage because of possible pre-existing bone
marrow suppression and the antagonistic effect of zidovudine when the drugs are combined.
• In AIDS Initial dose BACTRIM DS BD for 6 weeks ,then BACTRIM DS OD lifelong
• For recurrent infection –prophylaxis BACTRIM DS alternate / BACTRIM DS twice a week for 21 months

35. Pregnancy.
• Treatment of recurrent ocular toxoplasmosis during pregnancy should be chosen
carefully and only started if clearlynecessary
• Management should be multidisciplinary.
• Severalof the drugs discussed above have the potential to harm the fetus.
• Intravitreal therapy for reactivated disease,or systemic treatment with azithromycin,
clindamycin and possibly prednisolone may be appropriate.
• Specifc treatment to prevent transmission to the fetus isnot generally given except
in newly acquired infection.
• Spiramycin (treatment dose, 400 mg 3 times daily) reduces the rate of tachyzoite
transmission to the fetus and may be used safely without undue risk of
teratogenicity

36. DIFFUSE UNILATERALSUBACUTE
NEURORETINITIS(DUSN)

37. HISTORY
• Donald Gass
• Described as ‘Unilateral wipe out syndrome’
• Young adults
• Visual loss accompanied by optic atrophy, retinal vascular
attenuation and pigmentary retinopathy in one eye
• clusters of grey-white lesions that migrated to different
areas of the fundus over time.
• Noted a small curvilinear glistening white structure
approximately 400 microns in length with tapered ends in
the vicinity of the active lesions.
• The white worm like structure moved with the crops of
grey-white lesions.

38. WORM
• Ancylostoma caninum (dog hookworm)
• Baylisascaris procyonis (raccoon round worm)-can
cause neural larva migrans –
(neurodegenerative)devastating.
LARVA MIGRANS
• Patient gives a significant history of cutaneous larva
migrans (few months to upto a year back from the
presenting ocular feature.)
• The nematode burrows through the skin and may
cause an eruption on the dorsum of the foot
The small DUSN worm coiled into a ring
(arrow) in the vicinity of the active lesions

39. PATHOGENESIS
• White lesions appears to be a reaction of the local tissue to the presence of the
worm.
• The byproducts or waste products of the worm presumably incite a toxic reaction in
the retinal receptors causing the inflammatory response in the form of vitreous cells
and retinal vasculitis and loss of the vision.
• Consecutive optic atrophy ensues secondary to destruction of retinal elements

40. CLINICAL FEATURE
• Young
• Male
• c/o diminution of vision,floater
• Characteristic retinal lesion ,mild disc edema, mild vitritis
• Vision loss is out of proportion to the fundus appearance
• The white lesions are clustered within a small zone and fade over a few weeks leaving
pigment mottling.
• As the disease progresses, there may be an increase in the number of vitreous cells and
the retinal vessels begin to narrow with some amount of sheathing.
• As disease progresses- white lesion disappear without any sequele or sometimes
pigmentation.
• Disc pallor may progress.
• Sometimes, anterior uveitis, hemorhages ,vascular sheathing.

41. • Careful observation in the vicinity of the
white lesion shows a small white nematode
which is gently tapered at both ends.
• The disease is believed to be caused by two
worms, the smaller worm measuring 400 to
500 microns in length and the larger worm
measuring approximately 1500 to 2000
microns in length.
• The smaller worm propels itself by slow
coiling and uncoiling movements and moves
rather slowly in the subretinal space
• the larger worm moves at a faster pace.
C/o floaters and decline in vision 6/12.
Afferent pupillary defect, relative central scotoma
and small white lesions in the posterior pole.
History of travel to Mexico 6 months prior with
cutaneous
larva migrans at that time

42. • A careful history will reveal travel of the affected individual to an endemic area.
• Endemic in United states, unusual cases reported from France, UK,Germany
• Repeated examination in the vicinity of the greywhite lesions may be required to
identify the worm.
• When the worm hasn’t been found with multiple examinations, a 50 micron laser
burn placed in the vicinity of the suspected site of the worm often stimulates
movement of the worm. This confirms the location of the worm which can then
be treated.

43. • Vitritis
• Papillitis
• One must search for the worm when these gray white
outer retinal lesions are present
• Rates of nematode identification range from 33%-52% !!!!

44. Late stages
• Dense scotomas
• RAPD
• Progressive optic atrophy
• Degenerative RPE
• Marked narrowing of the
arteries.
Diffuse and focal pigmentation Of the
RPE

45. • increased internal limiting membrane
reflex (Oréfice’ssign),
• subretinal tunnels (Garcia’ssign)
• the most common features seen in
early and late DUSN are
• subretinal tracks (91.7%),
• focal RPE changes (89.3%),
• small white subretinal spots (80.2%)

49. FFA -EARLY STAGES
• Early hypoflourescence
• Late hyperflourescence with
staining
• Leakage of dye from ONH
• LATE STAGES
• Hyperflourescence
from RPE window
defects
• Delay in retinal perfusion

50. • ICGA in Late stages shows
hypocyanescence corresponding to the
hypopigmented lesions in fundus and a
hypercyanescence at the macula

51. FFA
• Lesions –initial hypo-hyper
• Hot disc
• Pigment mottling-window defect
Showing initial hypofluorescence (A) and late staining of the lesions(B)

52. • OCT
• Shows diffuse retinal thinning and
RNFL atrophy
• Focal retinal edema in areas affected by
the worm

53. DUSN OTHER PARASITIC INFECTIONS
OUTER RETINA IS AFFECTED INNER RETINA IS AFFECTED
NO RPE CHANGES AND SCARRING SCARRING
DUSN MEWDS
NO SUCH HISTORY HISTORY OF FLU LIKE
ILLNESS
CHILDREN AND
YOUNG ADULTS
YOUNG ADULT WOMEN
HYPOFLOURESCENT HYPERFLOURESCENT
DOTS IN EARLY PHASES
OF FFA
DUSN APMPPE AND OTHER
WHITE DOT
SYNDROMES
NO SCARRING SCARRING
UNILATERAL BILATERAL

54. Other
differentials
POHS – Bilateral , Clear vitreous
without inflammatory cells, No
vessel narrowing

55. TREATMENT
• Laser photocoagulationto the worm - Confluent laser burns approximately 100 to 200
microns in size can be placed over the worm, which causes minimal inflammatory
response- New lesions cease to occur and the old lesions fade.
Confluent 200 microns argon laser burns applied
directly to the worm seen
The small DUSN worm coiled into a ring (arrow) in
the vicinity of the active lesions

56. Scatter laser applied to the quadrant with
active lesions to disrupt the blood retinal
barrier
Mid-peripheral fundus showing both active and
inactive lesions. Repeated examinations failed to
find the worm
If worm couldn’t be localized- if active inflammation (means retinal blood barrier
disrupted) –give oral anti-helmith Albendazole 400 mg BD for 3 days - see patient again
after 5 days - worm staggers in the subretinal space and die - causing white
inflammatory reaction.
If no significant inflammation- apply laser burns over the seemingly apparent lesion –
causes disruption of blood retinal barrier-give antihelmith-exam again after 5 days and
few weeks later to check arrest of visual loss and resolution of active lesion
3 days post-laser and albendazole, 3
new active lesions are seen. The
lesions are believed to be sited where
the worm staggered before death

57. OCULAR CYSTECERCOSIS

58. INTRODUCTION
• Cause-larvae of the adult tapeworm Taenia solium (Pig)and Taenia saginata(cow)
• LIFE CYCLE- Human definitive host –eggs excreted in stools—contaminate food
and water –pig/cow is intermediate host---pig consume this contaminated food--
-hematogenous dessimination occurs and cyst are formed in multiple tissue –
cytecercosis in human occur by consumption of this undercooked pork/beef
• Cysticerci may be found in almost any tissue. most frequently-are skin, skeletal
muscle, heart, eye, CNS

60. Modes of infestation:
• 1) contaminated food and water with the Taenia solium eggs (hetero-infection);
• 2) reinfection by ingestion ova of the existing parasite (external auto-infection)- feco –
oral route;
• 3) retrograde peristalsis causing the transport of mature proglottids bearing eggs
from bowel to stomach (internal auto-infection).

61. • Parasite reaches the posterior segment via
the short ciliary arteries.
• The macular region being thinnest and
vascularized,
• the larvae lodges itself in the subretinal space from where it
perforates and enters into the vitreous cavity.
MACULAR
HOLE
RETINAL
DETACHME
NT

62. SYMPTOMS
• Depend on the location
• Loss of vision, mass lesions, motility disorders and other
orbital or neuro-ophthalmic symptoms.
• Visualization of cysts via fundoscopy - diagnostic of the
disease.
• The cyst is seen as a spherical, and translucent cavity
associated with dense white scolex
• A living cysticercus usually induces mild inflammation in
the eye.
• However, when it dies, it is accompanied by marked
acute granulomatous inflammation.
• This severe inflammation is associated with disruption
and scarring of retina, retinal pigment epithelium and
choroid
A large cysticercosis with the dense
white area of protoscolex

63. 3 stages
• 1)The vesicular cyst is
the living cyst with a well- defined
scolex . It causes minimal or no
inflammation in the tissue.
• 2)Colloidal vesicular stgae - As larva begins to
die the cyst wall becomes leaky, releasing
toxins and causing inflammation. The cyst
becomes less translucent with a surrounding
inflammatory membrane.
• 3)Calcified nodular stage - Larvae die and
totally resorbed or calcified.

64. Posterior segment manifestations
• Vitreous cysts are more common than retinal or subretinal cysts
• Inferotemporal subretinal cyst is most frequently encountered
• Exudative RD
• Focal Chorio-retinitis
• Rarely, vitreous hemmorhage(if cyst migrates from retina into vitreous cavity)
• Translucent white cyst with dense white spot formed by the invaginated scolex with typical
undulating movements

65. Live submacular
cysticercosis
One week later, cyst migrated to
intravitreal cavity
Patient underwent pars plana
vitrectomy with complete
removal of the cyst.
Postoperative fundus
photograph shows subfoveal
scarring in the area of rupture
into the vitreous cavity

66. INVESTIGATIONS
• Opaque media- BSCAN
• Orbital and neurological manifestation need CT scan
• AC Tap-raised eosinophils
• ELISA –detect antigen, sensitivity directly linked to number of
parasitic lesions and the stage of lesions
(Only 50% of ocular cysticercosis cases test positive on ELISA,
whereas 80% of neurocysticercosis cases test positive.)
• Single lesions and calcification are more likely to be associated
with a false-negative assay result.
• Sensitivity is more if associated with multiple cysts or CSF is
analysed
• False-positive results may be caused by other parasitic
infections.
BSCAN -dead and calcified cyst throwing back
shadow (red arrow) and a
subretinal live cysticercosis with hyper-
reflective scolex (yellow arrow) with total
retinal detachment

67. Lesion superior to the nasal appeared to be a subretinal
cyst with adjacent subretinal fluid surrounding it with
chorioretinal scaring and atrophy surrounding the cyst
Outline of the cyst is captured on OCT -double-layered
cyst wall is evident .
The scolex, which represents the knoblike anterior end of
the tapeworm difficult to visualize. (Possibly, the
honeycomb invagination within the cyst is the intestine of
the larvae)

69. • It is important to do MRI or CT scan in case of ocular cysticercosis to rule out neurocysticercosis
• Neurocysticercosis can co-exist in upto 24% of the cases of ocular cysticercosis

70. TREATMENT
• Localized ocular or adnexal cysticercosis generally is treated by surgical removal because
death of the organism is associated with marked inflammation and severe damage to the
eye.
• Posterior segment involvement- PPV + cyst removal via sclerotomy site or aspirated with
vitrectomy cutter
• If ruptured cyst-complete vitrectomy should be done to remove all the vitreous debris.
• Subretinal cyst- can be removed through retinotomy site with the help of soft tip cannula.
• Subretinal cyst-poor prognosis as it can be associated with retinal detachment and fibrosis
• Orbital lesions can be treated with medical therapy under the cover of steroids to avoid
any inflammatory damage around the dying cyst

71. OCULAR TOXOCARIASIS

72. TOXOCARIASIS
• CAUSE- Nematode Toxocara
canis and Toxocara cati
(intestinal round worm)
• Definitive Host –Dog
• Dead-end host –Humans
• SOURCES OF INFECTION –
Soil contaminated with dog feces
Contact with infected pups

73. Systemically causes VISCERAL LARVA MIGRANS
• Low grade fever
• Pruritic nodules
• lymphadenopathy
• Hepatosplenomegaly
• Pneumonitis
• Convulsions
• Eosinophilia
• Leucocytosis

74. Symptoms
• Usually unilateral involvement
• 2-9 years of age with an average age of 7.5 years at the time of diagnosis
• Can present in adults also
• Decrease in visual acuity
• Leukocoria
• Strabismus

75. Toxocarias
is
Cover
t
Viscer
al
Ocula
r
Toxocara
chronic
endophthalmiti
s
Posterior
pole
granuloma
Periphera
l
granulom
a

76. 4 clinical presentations
• Posterior pole granuloma
• Peripheral Granuloma
• Nematode endopthalmitis
• Atypical presentation

77. Posterior pole Granuloma
• Occurs when the stage 2 larva gets
encysted in the choroid
• Raised lesion –whitish
• Vitritis
• Accounts for 44% of
toxocariasis
A.67 years/F Optic disc toxocara
granuloma, RPE atrophy and
hyperplasia
B. B-SCAN shows hyperechogenicity
of the granuloma

78. Peripheral Granuloma
• Focal white elevated nodule
• Associated with traction bands and
retinal folds extending from the lesion to
the disc
Peripheral toxocara granuloma,
retinal pigment epithelial atrophy
and hyperplasia

79. Nematode endophthalmitis
• Panuveitis with a chronic
endopthalmitis with hypopyon
• Not very painful and red
• Occurs in very young patients
• Retinal granulomas are visible once the uveitis
clears
• Can mimic retinoblastoma
• USG B Scan –Can demonstrate traction bands
and highly reflective peripheral mass

81. Atypical presentation
• Neuroretinitis
• Optic neuritis
• Optic nerve granuloma
• Mobile living larvae in the eye
• Severe Anterior uveitis
• Inflammatory mass in the iris
• Scleritis

82. D/D
• Coats disease –presents unilaterally but no uveitis is seen.
• PHPV-Unilateral and eye may be microophthalmic .Presents earlier
• ROP –history of prematurity and presents early.
RETINO BLASTOMA OCULAR TOXOCARIASIS
Mean age at presentation is
23 months
Mean age ais 7 years
No intra-ocular inflammation Intra-ocular inflammation
Family history No family history
MRI T1 HYPER
T2 HYPO
MRI T1 HYPER
T2 HYPER
CT scans may reveal calcification in retinoblastoma, but are not useful in discreminating toxocara granuloma
and noncalcified retinoblastoma.

83. • Intraocular migration is a feature of toxocara that may help clinche the diagnosis
COMPLICATIONS
• Epi-Retinal membrane
• Macular hole
• Tractional RD
• Combined RD
• Detachment of the ciliary body and anterior choroid with hypotony,
• phthisis bulbi
• Cataract
• glaucoma

84. INVESTIGATIONS
• Serum ELISA is the gold standard for the diagnosis
• A serum titre of 1:8 is taken as evidence of toxocara
• ELISA has a sensitivity and specificity of 91%
• ELISA detects the exo-antigen of the organism
• Cytologic examination of the aqueous and vitreous shows Eosinophils as opposed to
lymphocytes and malignant cells(RB)

85. Posterior pole toxocara granuloma involving macula, epiretinal membranes
in a 29-year-old female patient (Fundus photo and Bscan)

87. TREATMENT
In active vitritis
• Systemic steroids -1mg/kg/day + Albendazole 800mg BD for adults and 400mg
BD for children for 2 weeks.
• Thiabendazole -2g/day for 5 days (Maximum 3 g)
• DEC –(3-4mg/kg/day for 21 days ) with a starting minimum dose of 25mg/day for
adults
The risk of hypersensitivity reaction after the death of larvae post treatment is
less with toxocara unlike other helminths

88. SURGERY –
Indications
• RD, cataract
• ERM
• VMT
• Vitreo –papillary traction
• Vitreous opacities