Ocular toxoplasmosis is caused by the protozoan Toxoplasma gondii. It commonly presents as focal necrotizing retinochoroiditis and can cause vision loss. While most infections are asymptomatic, it can be life-threatening for newborns and immunocompromised patients. People become infected through contact with cat feces or consuming undercooked meat containing cysts. Recurrent lesions are common due to the parasite's ability to form dormant tissue cysts. Treatment aims to reduce inflammation and inhibit parasite replication, but cannot eliminate the infection entirely.

1. Ocular Toxoplasmosis
Dr. Md. Mominul
Islam
Fellow (Vitreo-Retina)
Ispahani Islamia Eye
Institute And
Hospital Dhaka
Bangladesh

2. Introduction
Common zoonosis
Caused by Toxoplasma Gondii
Life threatening disease (newborn and
immnosuprresed patients)
Asymptomatic in immuno competent patient
Congenital or Acquired
Both eye may affected

3. Epidemiology
Represent with posterior uveitis
50-85% in Brazil
25% in USA
Prevalence: (not well determind)
0.6-2% in USA
10-17.7% in Brazil

4. Transmission
Beef
Undercooked lamb , pork, chicken
Environment contaminated by feces of infected cats
family
Organ transplantation
Blood transfusion
Water

5. Biology And Life Cycle
Obligate , intracellular protozoan
Both sexual and asexual reproduction
Definitive host – Members of cat family
Intermediate host- Hundreds of species including
mammals, birds
Host tissue - Muscle
- Retina
- Nervous tissue
- Body fluid

6. Contd
Three forms
Oocyte
Trachyzoite
Bradyzoit
(tissue cyst)

7. Genetics
Type- I
• Very
virulent
• Postnatal
acquired
ocular
infection
Type-II
• Less
virulent
• Congenital
infection
and
toxoplasmic
encephalitis
Type-III
• Less
virulent

8. Pathogenesis
In immunocompetent patients is characterized
histologically by
Foci of granulomatous chorioretinal inflammation
Coagulative necrosis of the retina with sharply
demarcated borders
Inflammatory changes can be widespread in the eye
and involve choroid, iris, and trabecular meshwork

9. Contd
In Immunosuppressed
Have both tachyzoites and tissue cysts in areas of
retinal necrosis and within retinal pigment epithelial
cells.
Parasites can occasionally be found in the iris, choroid,
vitreous, and optic nerve

11. Ocular presentation
Symptoms
Floaters
Blurring or loss of vision
Sign (The hallmarks)
necrotizing
retinochoroiditis
Satellite lesion adjacent
to old hyperpigmented
scars
Vitreous inflammation
Anterior uveitis
Retinal vasculitis is also
present (occationally)

13. Contd
New or Acute lesion
• Intensely white
• Focal lesion overlying
vitreous inflammatory
haze (head light in the
fog)
• Acute anterior uveitis
Healed lesion
• Border become more
defined
• Hyperpigmented after
several months
• Large scar will have
atrophic center
(devoid of all choroidal
retinal elements)

15. Investigation
Serological test
PCR

16. Differential Diagnosis
Infectious:
Rubella
Cytomegalovirus
Syphilis
Herpes simplex
Tuberculosis
Toxocariasis

17. Contd
Non-infectious:
Retinal and choroidal coloboma
Retinoblastoma,
Retinopathy of prematurity
Gyrate atrophy
Retinal vascular membrane
Serpiginous choroidopathy

18. Outcome And Complication
Central vision will be lost
Permanent loss of vision
Sudden loss of vision.

19. Treatment and Prevention
Available drugs do not eliminate tissue cysts and
cannot prevent chronic infection
No treatment has proven to be superior or even more
effective than no treatment
Antitoxoplasmic agents and systemic steroids have
never been studied in large clinical trials

20. Pyrimethamine:
75–100 mg loading dose given over 24 hours, followed by 25–
50 mg daily for 4–6 weeks depending on clinical response
Sulfadizine:
“Classic” therapy:
2.0–4.0 g loading dose initially, followed by 1.0 g given 4
times daily for 4–6 weeks, depending or clinical response
The combination of pyrimethamine, sulfadiazine, and
corticosteroids
Prednisone:
40–60 mg daily for 2 to many weeks depending on clinical
response; taper off before discontinuing
pyrimethamine/sulfadiazine
Folinic acid:
5.0 mg tablet, 2–3 times weekly during pyrimethamine
therapy

21. Contd
Other Drugs:
Trimethoprim and sulfamethoxazole.
Systemic or intraocular clindamycin
The duration of treatment depends on the individual
clinical picture
Steroid treatment is often administered systemically and
always associated with antitoxoplasmic drugs
 Local drops are used when anterior uveitis is present

22. Take Whom Massage
Wrong concepts in ocular toxoplasmosis
 All cases congenital
 Must present as a “retinochoroiditis”
 Vertical transmission (pregnancy) only once in life
 Cats and meat are the only source
 No treatment to avoid recurrences
 All patients need antitoxoplasmic drugs for 4–6
weeks
 Recurrences are related only to local factors

23. Thank you