Toxoplasmosis

Dr. Anumeha

Caused by Toxoplasma gondii Exists in three forms : Trophozoite : invasive form,responsible for the acute infection Bradyzoite (tissue cyst) : in intracellular vacuoles protected from the immune system. rupture is responsible for the latent or recurrent infection Sporozoite (oocyst): produced in cats and is found in soil contaminated with cat feces

Ocular lesions may be :

Acute Sub acute Congenital Acquired----proliferative type ----due to hypersensitivity

Congenital: From intrauterine infection. maternal infection occurs during the third trimester or can occur later Retino-choroidal lesion develop with in 6th month of life may be due to rupture of cyst and liberation of trophozoites Ocular lesions are detected late when there is: detection of defective vision, ocular deviation, or by presence of systemic and cranial complications.

Clinical picture: Lesion is first seen as a healed focus of retino-chorioditis which is frequently b/lat Near post pole, at macula also known as developmental macular coloboma ACTIVE stage: Irregular reddish brown or greyish yellow areas of lesion with pigmentation in surounding retina HEALED lesion: Heavy pigmented lesion, sharply demarked glial scar involving retina and choroid.single or multiple lesions may be there.

In worst cases:
Generalized uveitis Post synechiae KPs Isis neovascularization Lens opacities Ocular phthisis Mcrophthalmos

Systemic involvement:
neonatal jaundice Hepato-splenomegaly Interstitial pneumonitis Anaemia Leucopenia CNS involvement: hydrocephalus and convulsions Cerebral calcific deposits in healing granulomacurvilinear streaks or multiple irregular lesions

Acquired toxoplasmosis: Pt presents with floaters decreased vision pain redness, and photophobia

S/s:

iritis Vitritis papillitis retinal necrosis macular edema choroidal neovascular membranes vascular occlusions retinal detachment Complications that can result in permanent loss of vision include macular inflammation resulting in a scar, choroidal neovascular membranes, vascular occlusions, optic nerve involvement, and retinal detachment.

Fundus examination: Focal retinitis Solitary inflammatory focus called as satellite lesion just adjacent to the old pigmented scar is most common finding Associated is vacuities and detached post hyaloid face can be seen which get covered by inflammatory precipitates there is overlying vitreous haze and underlying fundus cant be seen. but white lesion can still be seen.. This is called as head light in the fog appearance

Typical satellite lesion in toxoplasmosis

Head light in the fog appearance due to overlying vitreous haze

Necrotizing lesion with adjacent vasculitis

Other fundus findings: Papillitis: secondary to juxtrapapillary retinitis

Macular scarring

lack of vitreous reaction and the presence of retinal hemorrhages due to concurrent retinal vasculitis

 Atypical lesions: In immunocompromised patients. Lesions are Bilateral Multifocal Discrete foci Pre-existing scars are absent

Course of the disease

In normal persons healing occurs with in 6-8 weeks but vitreous opacities take longer time to resolve Inflammatory focus replaced by sharply demarcated atrophic scar with hyperpigmented border Mean recurrence rate wit in 3 yrs si almost 50%

Complications: Visual loss due to: Macular involvement Optic nerve head involvement Occlusion of major blood vessel

Diagnosis: By typical fundus lesion and presence of toxoplasma antibodies

Management: Systemic steroids 1 mg/kg initially then tapered off Along with any of the following drugs: Clindamycin: 300 mg qid for 3-4 weeks Sulphadiazine: 1g qid for 3-4 weeks Pyrimethamine: loading dose of 50mg followed by 25-50mg daily for 1 month with oral folinic acid 5 mg tds for 1 week(to preent thrombocytopenia and folate deficiency)

 Co-trimoxazole around 1 gm bd for 4-6 months as monotherapy or in combination with clinda. Azithromycin: 500mg daily (less toxic)