Conditions

What is ocular toxoplasmosis?

Ocular toxoplasmosis is the most common form of infectious uveitis affecting the back of the eye.

The disease primarily involves the retina, manifesting as a white focal retinal lesion, often associated with severe vitreous inflammation (vitritis).

What causes toxoplasmosis?

Ocular toxoplasmosis is caused by a parasite, the Toxoplasma gondii. There are three principle routes of human infections:

Epidemiology of toxoplasmosis

In various places throughout the world, more than 60% of some populations have been infected with toxoplasma.

A high prevalence of infection in France is related to the high consumption of raw or undercooked meat, while a high prevalence in South and Central America is due to hot and humid climate favouring parasite survival.

How toxoplasmosis manifests?

In healthy humans that acquire toxoplasmosis during their lifetime the infection usually causes no or minimal symptoms, and the disease is usually mild because the immune system contains its spread.

It can manifest mild flu-like symptoms with tender lymph nodes and muscle aches.

However, toxoplasma remains in the person’s body in an inactive state and can later reactivate to cause inflammation.

Ocular manifestations can thus develop long after a person has been infected with toxoplasma, due to the reactivation of the inactive parasite in the retina.

Acquired ocular toxoplasmosis is usually unilateral and classically manifests with an acute inflammatory lesion of the retina, which resolves leaving a scar involving both the retina and choroid.

The presence of a whitish retinal lesion associated with severe vitreous inflammation gives the typical appearance of ‘headlight in the fog’. The disease can then reactivate in the eye months or years later, with a new area of inflammation adjacent to the old inactive scar. This clinical picture of active “satellite lesion”  at the border of a pre-existing scar has been recognised as pathognomonic for ocular toxoplasmosis.

Congenital toxoplasmosis is most commonly acquired during end of second trimester and the third trimester. The woman may not have symptoms, but there can be severe consequences for the unborn child, such as diseases of the nervous system and eyes.

In children with congenital infection, ocular toxoplasmosis usually presents with a non-active pigmented scar, more often located in the central part of the retina, the macula. Reactivation may occur many years later.

What are the symptoms of ocular toxoplasmosis?

Symptoms include floaters (dark floating spots in the vision) and decreased vision.

Permanent visual loss occurs when lesions affect the macula, the central area of the retina responsible for central vision.

Based on the scar location, children with congenital disease can present with significantly reduced visual acuity, strabismus (when the eyes do not properly align with each other when looking at an object) and nystagmus (when the eyes make repetitive, uncontrolled movements).

Diagnosis

The diagnosis is usually clinical and is made on the basis of the appearance of the lesion on eye examination.

A positive blood test result for toxoplasma (detection of antibodies) is useful to support the diagnosis.

A negative result (absence of antibodies) rules out the diagnosis of ocular toxoplasmosis.

Treatment

Although most cases of ocular toxoplasmosis resolve on their own, cases with severe ocular inflammation or with potentially sight-threatening lesions (macular lesions or lesions close to the optic nerve) need to be treated with antibiotics.

The intention of therapy is to prevent the damage to the retina and consequently the visual loss.

Different treatment regimens are used, including pyrimethamine and sulfadiazine in combination with folinic acid, pyrimethamine and azithromycin, trimethoprim-sulfamethoxazole, and clindamycin either alone or in combination.

Therapy is usually administered for at least 4–6 weeks, but that varies from patient to patient. Blood tests including blood cell and platelet count, liver and renal function tests are always recommended as part of treatment monitoring.

Systemic corticosteroids are usually added to antibiotic treatment to avoid the damage related to inflammation.

Local therapy consisting of injections of antibiotic into the eye is performed if intolerance to oral medications, contraindication to oral medications because of pregnancy, lack of response despite oral treatment, or in conjunction with oral therapy to limit tissue damage.

Complications and Prognosis

Vitreous opacification can persist despite intensive antibiotic and steroid treatment, leading to persistent floaters and blurriness.

It is important to know that in this case the floaters are due to the degeneration of the vitreous as the result of previous inflammation and not to active ocular inflammation.

Permanent visual loss occurs when the lesions affect the macula.

Other common complications include abnormal vessels growing under the retina (choroidal neovascularization) and epiretinal membrane. All these complications can affect the quality of vision.

Multimodal imaging of acute inflammatory lesion in ocular toxoplasmosis. Optos colour and optical coherence tomography (OCT) images showing the presence of characteristic yellowish retinal lesion.

Multimodal imaging of acute inflammatory lesion in ocular toxoplasmosis. Colour and optical coherence tomography (OCT) images showing the presence of a yellowish retinal lesion adjacent to an old pigmented inactive scar. This clinical picture of active “satellite lesion”  at the border of a pre-existing scar has been recognised as pathognomonic for ocular toxoplasmosis.

Multimodal imaging of acute inflammatory lesion in ocular toxoplasmosis. Colour and optical coherence tomography (OCT) images showing the presence of a yellowish retinal lesion associated with severe vitreous inflammation giving the typical appearance of ‘headlight in the fog’.

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