Toxoplasmosis is caused by the protozoan Toxoplasma gondii. It can cause congenital infection in fetuses if a woman is infected during pregnancy. Clinical features in infants may include chorioretinitis, hydrocephalus, or intracerebral calcifications. Ocular features include posterior uveitis, retinitis, or chorioretinitis. Diagnosis is usually based on clinical examination and serology. Treatment involves pyrimethamine, sulfadiazine, and prednisolone (triple therapy), along with folate supplementation to prevent side effects. Maintenance therapy may be used long-term in immunocompromised patients to prevent reactivation.

1. TOXOPLASMOSIS
DR. ANITA KUMARI
ANTERIOR SEGMENT FELLOW
SCEH, LAHAN

2. INTRODUCTION
• Toxoplasmosis is caused by Toxoplasma gondii
• Derived from Greek word “Toxon” means bow
• An obligate intracellular protozoan
• Cat - definitive host
• Intermediate hosts including mice, livestock, birds
and humans

3. PATHOGENESIS
TOXOPLASMOSIS LIFE CYCLE

4. CLINICAL FEATURES
• Systemic features-
1. Congenital toxoplasmosis
- Mother –symptom free/mild constitutional
manifestations
- Severity of fetal involvement related to the duration
of gestation at the time of maternal infection
- Fetal abnormalities range from chorioretinitis,
hydrocephalus, convulsions and intracerebral
calcifications to only mild effects, such as slightly
diminished vision

5. • Strabismus, nystagmus and microphthalmia can also
be seen, usually in infants infected early in
development
• Infants infected late in gestation may have a fever,
rash, hepatomegaly, splenomegaly, pneumonia,
chorioretinitis or a generalized infection.
• Many infected infants are asymptomatic at birth;
however, some will develop learning and visual
disabilities

7. CONGENITAL TOXOPLASMOSIS

8. 2. Postnatal childhood acquisition
- 50% of of cases of childhood toxoplasmosis
3. Acquired toxoplasmosis in immunocompetent patients
- Subclinical in 80-90%
- Cervical lymphadenopathy, fever, malaise, pharyngitis are
common
- Early retinitis- upto 20%
4. Toxoplasmosis in immunocompromised patients
- Acquired or reactivation of pre-existing disease
- Meningoencephalitis, pneumonitis, retinochoroiditis

9. Ocular features-
Symptoms- U/L , floaters, blurring, photophobia
Signs –
- Posterior uveitis 20-60%
- Spill over anterior uveitis
- A single inflammatory focus of fluffy white retinitis or
chorioretinitis associated with pigmented
scar(satellite lesion)
- Vitritis, optic disc oedema, neuroretinitis

10. TOXOPLASMOSIS FUNDUS PHOTO

13. MANAGEMENT
Investigation
• Diagnosis is usually based on clinical examination
findings.
1. Serology - Toxoplasma IgG antibodies are detectable in
the serum within 1–2 weeks of initial infection
 Positivity to IgM antibodies usually means that infection
has been acquired within the last year, and so helps to
distinguish between acute (newly acquired) and chronic
infection
 Occasionally IgM is positive due to persistence or
reactivation following earlier infection

14. 2. PCR testing of intraocular fluid sensitive (16– 67%) but highly
specific
 can be diagnostic in clinically uncertain cases
 Aqueous and vitreous probably give similar yields

15. 3. Ocular fluid antibody assessment - Calculating the ratio
(Goldmann–Witmer coefficient) of specific IgG in aqueous
humour to that in serum seems to be a reasonably sensitive (48–
90%) investigation
4. 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

16. Treatment
• Prednisolone (1 mg/kg) is given initially and tapered according to
clinical response
• Pyrimethamine - loading dose of 75–100 mg for 1–2 days
followed by 25–50 mg daily for 4 weeks in combination with oral
folinic (not folic) acid 5 mg thrice a week to retard
thrombocytopenia, leukopenia and folate deficiency.
• Sulfadiazine 1 g 4t/daily for 3–4 weeks is usually given in
combination with pyrimethamine.
• Intravitreal therapy with clindamycin (1 mg) and dexamethasone
(400 µg) may be as effective as triple therapy in reactivated
infection; two to three injections (two-weekly intervals) may be
required

17. • Azithromycin 250–500 mg daily- reducing the rate of recurrence of
retinochoroiditis
• Clarithromycin may be a good alternative to azithromycin
• Co-trimoxazole (trimethoprim 160 mg/sulfamethoxazole 800 mg)
twice daily in combination with prednisolone
• Clindamycin 300 mg four times daily may be added to triple
therapy or used instead of pyrimethamine
• Atovaquone theoretically attacks encysted bradyzoites, but does
not seem to prevent recurrence in vivo; dosing is 750 mg two to
four times daily
• Topical steroid and mydriatic may be given for anterior uveitis
• Antimicrobial maintenance therapy is used in
immunocompromised patients

18. COMPLICATION
• Serous rhegmatogenous /exudative RD
• Optic neuritis
• Choroidal neovascularization
• Periarteritis
• Serous macular detachment

19. TOXOPLASMOSIS VITREOUS HAZE WITH RD

21. Home work
• What are the parasites which affect eyes?
• What is triple therapy in toxoplasmosis?
• Define oocyst, bradyzoites, tachyzoites?
• Life cycle of toxoplasma gondii ?
• How to prevent toxoplasmosis infection ?

22. Thank you