Toxoplasmosis chorioretinitis

Dear Doctor Paul
Greetings!!
I am Gopal from India. I am a Ph. D. Scholar at IIT Roorkee India.
I am suffering from Toxoplasmosis Retinochoroditis. I have scars in my left eye from infections when I was a child (around 5 years old) and low vision since then (6/60 with or without lenses).
Around 10 years back, my right eye also acquired the infection. I had introvitiols, introvenals, oral medication (clindamycin). Since then, the infection has re-occurred many times. I am losing vision by the day and the infection is spreading slowing all over the retina.
I saw your video on Youtube and I am observing the symptoms you mentioned (ear infections and memory losses). I request you to suggest me as I am not satisfied with the diagnosis provided to me.
I request for some stable solution.
Also, If you know some good doctor in the field in India whom I can visit. Please suggest.
I will be grateful to you. Hoping for a positive response
======================
My Response:

Toxoplasma gondii is one of the most common pathogens to cause chorioretinitis (a posterior uveitis) in immunocompetent hosts. Immunocompetent adults with ocular toxoplasmosis can present with visual loss, especially if chorioretinitis affects the macular region. Floaters are often the presenting sign if chorioretinitis is extramacular. In addition, certain asymptomatic patients may have scarring noted on routine examination without evidence of active chorioretinitis.

Ocular disease can be due to acute infection or reactivation disease.

Acute ocular disease – Acute ocular disease can be seen in adults and is also associated with congenital infection. It is estimated that in the United States, about 2 percent of Toxoplasma-infected people develop chorioretinitis, which may not be recognized in the acute phase but found later as a retinal scar. Children with congenital toxoplasmosis can develop retinochoroiditis associated with visual impairment.

Reactivation disease – Those with reactivation disease are infected either in utero or postnatally. Patients with reactivation disease often have bilateral involvement, in comparison to adults with acute infection who typically present with unilateral ocular disease. Patients older than 40 years of age are at higher risk of recurrence than younger patients, and a relapsing and remitting course can develop after a prolonged disease-free interval. In immunocompetent hosts, reactivations are almost always chorioretinitis and not lymphadenopathy or febrile illness.

It is well established that T. gondii can be divided into different genotypes and that different genotypes differ in pathogenicity. This explains why acquired T. gondii infection in South and Central America has high rates of posterior uveitis compared with other geographic areas.

Diagnosing ocular disease — Ocular toxoplasmosis should be considered in a patient who presents with visual loss or floaters. The diagnosis of ocular disease is typically suggested by findings on ophthalmologic examination and supported by serologic testing and/or aqueous humor analysis.

Exam findings – Findings on ophthalmologic examination usually include extensive iritis and vitritis, accompanied by whitish retinal lesions representing chorioretinitis. However, chorioretinitis and choroidal neovascularization may be masked by the vitreous inflammation and require angiography for detection.

Serologic testing – Serologic testing to detect the presence of IgM and IgG antibodies should be performed to support the diagnosis of ocular toxoplasmosis.

Aqueous humor analysis – Aqueous humor analysis (eg, polymerase chain reaction [PCR] or antibody testing), if available, can also be used to help diagnose intraocular disease if the diagnosis is unclear (eg, atypical exam findings and/or negative serology). The use of aqueous humor analysis was evaluated as a diagnostic method in 137 immunocompetent patients with posterior uveitis resulting from a suspected infectious etiology. Intraocular antibody production and PCR were used to test for a variety of pathogens including T. gondii, herpes simplex virus, varicella zoster virus, and cytomegalovirus. Of the 37 patients with positive results, 75 percent had evidence of toxoplasma infection; most were diagnosed using measurements of intraocular antibody production.

Treatment — The decision to treat chorioretinitis depends upon several factors, including: the degree of inflammation; the patient’s visual acuity; and the size, location, and persistence of the lesion. The treatment of ocular disease should be done in conjunction with an ophthalmologist experienced in the diagnosis and treatment of chorioretinitis or uveitis.

Indications — Patients with evidence of inactive ocular toxoplasmosis do not require treatment. However, we suggest antimicrobial treatment (with or without adjunctive steroids) for patients with iritis, vitritis, or chorioretinitis if the lesions have one of the following characteristics :

They are located within the vascular arcades

They are adjacent to the optic disk

They are larger than 2 optic disc diameters

They have an atypical presentation

We also treat individuals infected in South or Central America with a more pathogenic strain of T. gondii.

Although most cases of active ocular toxoplasmosis resolve spontaneously over the course of four to eight weeks, limited data suggest that systemic antimicrobial therapy (with or without glucocorticoids) is associated with a reduction in active retinochoroiditis and/or improved vision. As an example, 149 patients with ocular toxoplasmosis were evaluated in a prospective multicenter study. Patients with central lesions were treated with one of three different antimicrobial regimens in combination with glucocorticoids, whereas those with peripheral lesions did not receive systemic therapy. Approximately half of the 35 patients treated with a pyrimethamine-containing regimen had a reduction in the size of the retinal inflammatory lesion compared with 20 percent (8 of 41) who did not receive systemic therapy.

Antimicrobial therapy for ocular disease — Ocular toxoplasmosis is treated with similar agents as those used for systemic disease. The duration depends upon the clinical response.

Preferred regimens — Our preferred regimen for nonpregnant adults with chorioretinitis is pyrimethamine (100 mg) plus sulfadiazine (2 grams) given as a single loading dose on the first day of treatment. This is followed by pyrimethamine (25 mg daily) plus sulfadiazine (500 mg four times daily) plus leucovorin (10 mg daily) for a minimum of six weeks.

If a pyrimethamine-containing regimen cannot be used, we administer trimethoprim-sulfamethoxazole (TMP-SMX; 160 mg TMP/800 mg SMX) twice daily for six weeks. After the first six weeks, we then administer therapy with one double-strength tablet taken every other day for one year. This suppressive regimen has been found to reduce the risk of recurrent disease.

Alternative regimens — If a patient is intolerant to first-line regimens, we administer atovaquone (750 mg four times a day) in combination with pyrimethamine (100 mg loading dose followed by 25 mg daily) plus leucovorin (10 mg per day) for a minimum of six weeks. Atovaquone can be given alone if pyrimethamine is not tolerated or not available; however, it must be given for at least three months.

Azithromycin 500 mg daily for a minimum of six weeks is another option. This regimen has been shown to be effective, but resolution of findings is slower than with the pyrimethamine-sulfadiazine combination.

Intravitreal clindamycin (0.1 mg/0.1 mL) with one to three injections administered over a period of six weeks can also be used. The number of injections is based upon disease activity on examination. This regimen can be difficult for a nonretina specialist to perform.

Adjunctive glucocorticoids — We administer glucocorticoids to patients with significant vitreous inflammation and retinal vasculitis to help preserve vision. There are no definitive data to guide the best way to administer glucocorticoids.

We typically initiate prednisone (40 mg once a day) three days after antimicrobial therapy has been started. We delay glucocorticoid therapy by three days to reduce the organism burden and minimize the likelihood that glucocorticoids will exacerbate the infection. This approach has been used in clinical trials evaluating different treatment regimens for ocular disease.

We continue the 40 mg daily dose until the inflammation clears up in the eye, and the posterior pole and vitreous normalize, which can take a few weeks. After that, we taper the glucocorticoids (eg, prednisone 30 mg for one week, 20 mg for one week, 10 mg for two weeks, 5 mg for two weeks).

If an intravitreal injection of clindamycin is used, intravitreal-injected dexamethasone (1 mg/0.1 mL) may be used rather than oral prednisone as an adjunctive glucocorticoid.

Frequency of follow-up — Patients on therapy require frequent ophthalmologic examinations to monitor the response to therapy. The frequency of follow-up depends upon the proximity of the lesion to the central vision. As an example, patients with central lesions should be seen at least once weekly.

Duration of treatment — Patients with ocular disease should be treated for a minimum of six weeks. Ocular findings that support treatment discontinuation include resolution of inflammation and retinitis. Lesion activity and cessation of vasculitis on fluorescein angiography are also useful to help if determine if treatment can be stopped.

The ultimate duration also depends upon the specific regimen. Certain agents (eg, TMP-SMX, atovaquone monotherapy) require a longer course of treatment than others.

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