presentation made during uveitis session.

2.  O.T is a recurrent retinochoroiditis caused by
the organism Toxoplasma gondii, and
represents the most common cause of
infectious posterior uveitis worldwide.

3.  Most successful obligate intracellular
parasite.
 Apicomplexan parasite infecting one third of
the human population.
 Sexual reproduction occurs in intestine of
members of the Felidae family among which
cat represents the definitive host.

5.  Tachyzoite (6-7 mm) is the active
proliferative form; present in intermediate
and definitive during acute infections .
 It is able to penetrate any nucleated cell and
circulate all over the body, leading to cell
lysis, direct tissue damage, subsequently to
potentially destructive immune response.

6.  Tachyzoite differentiate
into bradyzoites ,
forming tissue cyst
which are the latter
forms and remains in
host tissue without
eliciting any significant
inflammatory
response.

7.  Definitive hosts gets infected by either ingesting meat containing
tissue cysts/tachyzoites from intermediate hosts, or by ingesting
sporulated oocysts , present in the soil and shed in the faeces of
another hosts.
 Once in the intestine , the parasite invades enterocytes and
reproduces asexually and sexually.
 Felines shed oocysts 3-18 days after oral infection, gets matures in
the soil into sporulated oocysts, become infective after 1-21 days,
and persists for up to 18 months

8.  Manifests as a focal retinochoroiditis with necrotizing
granulomatous inflammation of retina with reactive granulomatous
involvement of choroid, vitreous,anterior uvea.
 Mononuclear infiltrates .
 Disruption/Migration of RPE.
 After resolution CR Scar is seen.
 Pathogenesis depends upon a delicate balance between host
immunity and parasite virulence.
 Adaptive immune response is mediated by CD4+ T lymphocytes
and macrophages.
 Th-1 helper reaction leads to pro-inflammatory cytokines : IL-12,
Interferon-Ý and TNF-


9.  Type I : highly virulent : Strong
proinflammatory response
 Type II : least virulent
 Type III : less virulent.

10.  Systemic Disease
 Fever, malaise and variable lymphadenopathy.
 Pneumonitis
 Hepatitis
 Myocarditis
 Encephalitis
 Congenital T : IUFD, anaemia, thrombocytopenia, cutaneous rash,
hepatitis,pneumonitis,myocarditis and even encephalitis.
 Sabin’s Tetrad : Hydrocephalus, Intracranial calcifications,
Mental retardation and chorioretinits which occurs in less than
10 % of infected newborns .
 However, 80% of these infected newborns will manifest with
chorioretinitis.

12.  Retinochoroiditis : active : whitish yellowish
exudates in inner retina with retinal edema.
 Begins from margin of satellite lesion.
 Involves full thickness of retina.
 Inflammatory cellular infiltrates may lead to
granulomatous precipitates on the posterior hyaloid
and to denser vitreous bands/haze – ‘headlight in
the fog’
 Periarterial lipidic exudates (Kyrielis arteriolitis).
 Granulomatous or non-granulomatous iridocyiclitis.
 Retinochoroidal lesion – ‘wagon –wheel’ scar

15.  Essentially clinical, based on presence of necrotising
chorioretinitis.
 Serological findings are supportive
 IgG Antibodies specific to T.gondii – previous exposure
 Absence of specific IgG & IgM exclused possibility of
Toxoplasmosis
 IgM &/or IgA Ab, IgG Ab (High level)- Congenital
Toxoplasmosis.
 PCR of ocular fluids.
 Goldman-Witmer or Witmer-Desmonts Coefficient : Serum
titer of sp. T.gondii Ab vs globulin titers.
 Positivity of Vitreous sample > Aqueous humor samples.

16.  May be self-limited
 Worsening of Intraocular inflammation as
well as development of sight threatening
complications indicates the necessity of
treatment.

17.  A lesion within temporal arcade
 A lesion abutting the optic nerve or threatening
a large retinal vessels.
 A lesion that has induced a large degree of
hemorrhage.
 A lesion that has induced enough of a vitreal
inflammatory response that the visual acquity
has dropped two line after acute infections
 Multiple recurrences that developed marked
vitreal condensation.

18. Drugs Dosage Precaution
Sulfadiazine 1 gm QID for Adults,
50-100mg/kg for children
G6PDH,Crystalluria,
Hepato-renal failure,SJS,
BM supp.
Pyrimethamine 100 mg followed by 25-
50 mg/day, 1mg/kg/day
Teratogenic, HR failure,
BM suppression- Use of
folinic acid
Clindamycin 300 mg QID, 10-25
mg/kg/day
HR
failure,Psudomembranou
s colitis
Azithromycin 250-500 mg/day,5
mg/kg/day
GI disturbances
Sulfamethoxazole /
Trimethoprim
800/160 mg BD,40-
50/8—10 mg/kg/day
HR failure, G6PDH
Deficiency, Sulfa
hypersensitivity
Spiramycin 1.5 million IU (500
mg)QID
High levels in
placenta,GI abnormailty
Atovaquone (Mepron) 750 mg qid, 30
mg/kg/day
Liver failure, not for
lactation/gestation.

19.  Cryotherapy of peripheral lesions : Excess
may lead to condensation and membrane
formation.
 Photocoagulation
 Anti – VEGF
 Vitrectomy and lensectomy
 HAART therapy.

20. • Avoiding ingestion of raw/undercooked meat
,(-20 to -4˚c) overnight destroys tissue cysts.
• Drinking only filtered or boiled water.
• Carefully washing vegetables/fruits before
consumption.
• Using gloves and washing hands after
manipulating soil/meat.
• Avoid contact with felines & their faeces.

21. Reference:
- Nussenblatt and whitecup 4th
edition
- Myron yanoff 4th edition