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Toxoplasmosis is the most common cause of infectious retinochoroiditis (inflammation of the retina and the choroid) worldwide. It is caused by the protozoan parasite, Toxoplasma gondii. Where treatment is indicated, toxoplasmosis is managed with the triad of systemic pyrimethamine, sulfadiazine and corticosteroids.


Toxoplasmosis is an infection caused by the unicellular, obligate intracellular protozoan parasite, Toxoplasma gondii.

The two most important serotypes to be aware of are:

  • Type 1: causes more severe disease, found in Latin America

  • Type 2: a less aggressive serotype, found in Europe/North America

T. gondii has three infectious stages:

  1. Tachyzoites - the proliferating active infectious form

  2. Bradyzoites - the latent form, lying dormant within cysts in tissues such as the eye and brain

  3. Sporozoites - the soil form, excreted in oocysts in cat faeces

The definitive host for T. gondii is the cat, however, humans, a variety of other mammals, reptiles and birds may serve as intermediate hosts. T. gondii resides in the intestinal tract of animals, particularly cats, and is shed in cat faeces which contaminate the soil and water. Other animals (e.g. cattle, sheep) may become infected when grazing, and can pass the infection to humans eating undercooked meats.

T. gondii can be transmitted to humans via different routes:

  • Congenital (transmitted from mother to foetus via the placenta)

  • Acquired, from consuming undercooked meat or contaminated foods

The risk of acquiring the infection can be minimised by good hygiene measures (e.g. hand washing before preparing/eating food, not eating undercooked meat and unwashed vegetables).


An estimated 1 billion people are infected with T. gondii globally, although the majority never have symptoms. Infection rates are higher in tropical regions, and lower in dry, cold regions.


Toxoplasmosis can produce a retinochoroiditis (inflammation of the retina and choroid). The retinitis is necrotising, with vasculitis and destruction of the retina.

Clinical features

Systemic features

The majority of those infected will never experience symptoms and will not be aware that they’re infected. However, some people may experience flu-like symptoms after a 1-2 week incubation period, including mild fever, lymphadenopathy, malaise, muscle/joint pain, headache, sore throat and skin rash.

Toxoplasmosis, more seriously, can cause hepato- or splenomegaly, and rarely can involve the lungs, CNS or heart.

Ocular features

Ocular symptoms vary, but may include floaters, blurred vision or photophobia during active disease. Patients with secondary iritis may experience eye pain and redness too.

Ocular signs can be classified as classic and atypical findings.

Classic findings:

  • A single inflammatory focus of fluffy white retinitis with overlying vitreous inflammation. Lesions tend to involve the posterior pole.

  • A nearby pigmented retinochoroidal scar (”satellite lesion”)

  • Vitritis (vitreous inflammation) may be severe and impair visualisation of the fundus. The “headlight in the fog” sign describes a white retinal inflammatory focus viewed through vitritis

  • Posterior uveitis. ‘Spill-over’ anterior uveitis is common (which may be granulomatous or resemble Fuch’s uveitis syndrome, FUS). Inflammatory ocular hypertension (in 10-15% of cases) may follow

  • Retinal vasculitis (more commonly venous than arterial)

  • Granulomatous and stellate keratic precipitates

  • Optic disc oedema is common

Atypical findings which may accompany retinochoroiditis:

  • Scleritis

  • Retinal detachment

  • Branch retinal vein occlusion

  • Papillitis

  • Neuroretinitis

  • Multifocal diffuse necrotising retinitis

Atypical findings independent of retinochoroiditis:

  • Unilateral neuroretinitis (characterised by optic disc oedema and a ‘macular star’)

  • Unilateral pigmentary retinopathy mimicking retinitis pigmentosa

Extensive and fulminant retinal involvement (which may be bilateral) is generally only seen in immunocompromised patients.

From left to right: 1) Fundus picture showing the “headlight in the fog appearance” in a patent with acquired toxoplasmosis. 2) Fundus picture showing a typical punched-out macular scar of a healed congenital toxoplasmosis lesion. Images courtesy of Sudharshan et al.

Congenital toxoplasmosis

Most cases of congenital toxoplasmosis are asymptomatic. Foetal involvement is related to the duration of gestation at the time of maternal infection, tending to be more severe the earlier the stage of pregnancy. Severe cases present similarly to other intrauterine infections (e.g. rubella or cytomegalovirus), with:

  • Low birth weight

  • Hydrocephalus

  • Prematurity

  • Seizures

  • Hepato- or splenomegaly

  • Jaundice

  • Death (10% of all congenital toxoplasmosis)

Evidence of retinal infection is found in 〜80% of known infected babies, and is usually bilateral. In babies born with congenital toxoplasmosis, the infection can cause a retinitis which resolves spontaneously. However, the inflammation may result in scar formation, which contains T. gondii in an inactive, encysted form. The T. gondii in these scars are generally inactive, however they may later re-activate causing the signs and symptoms described above (e.g. pain, redness and blurred vision).


Toxoplasmosis is predominantly a clinical diagnosis, but the clinician can be reassured using serology. Toxoplasma IgG antibodies are detectable in the serum within 1-2 weeks of the initial infection, and provide evidence of exposure to T. gondii in the past. If the IgG titres for toxoplasmosis are negative in an immunocompetent patient, then toxoplasmosis is ruled out. It is however possible that an immunocompromised patient can have an active toxoplasmosis infection with negative IgG titres.

In difficult or atypical cases, PCR to detect T. gondii DNA in the aqueous humour and vitreous fluid is highly sensitive and specific.


Toxoplasmosis usually self-resolves without treatment within a few months within immunocompetent hosts.

Some ocular lesions may warrant treatment:

  • Macular threatening or optic nerve lesions

  • Larger lesions

  • Lesions that have caused marked visual impairment

  • If the host is pregnant or immunocompromised

If treatment is indicated, toxoplasmosis is managed medically; surgery is only warranted to treat complications of toxoplasmosis e.g. retinal detachments. The classic triple therapy used in the treatment of toxoplasmosis is systemic pyrimethamine, sulfadiazine and corticosteroids. Sometimes, oral clindamycin is also given.

N.B. pyrimethamine is a folate antagonist, hence folinic acid (leucovorin) is simultaneously administered to prevent bone marrow suppression.


The prognosis in terms of visual acuity depends upon the location of the active infection, the degree of inflammation and whether complications have resulted from ocular inflammation. 〜25% of eyes have permanently reduced vision.

Patients with toxoplasmosis should be followed up in the long-term as recurrences can occur. Recurrences tend to occur at the margins of old scars, but may also occur elsewhere in the fundus.


  1. Salmon, John F., and Jack J. Kanski. Kanski’s Clinical Ophthalmology: A Systematic Approach. Ninth Edition, Elsevier, 2020.

  2. Toxoplasmosis - American Association for Pediatric Ophthalmology and Strabismus. Accessed 22 Dec. 2022.

  3. ‘What Is Toxoplasmosis?’ American Academy of Ophthalmology, 16 May 2022,

  4. Sudharshan, S., et al. ‘Current Approach in the Diagnosis and Management of Posterior Uveitis’. Indian Journal of Ophthalmology, vol. 58, no. 1, 2010, pp. 29–43. PubMed Central,

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