eMedicine Specialties > Ophthalmology > Infectious Disease

Toxoplasmosis: Treatment & Medication

Author: Lihteh Wu, MD, Consulting Surgeon, Department of Ophthalmology, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Coauthor(s): Teodoro Evans, MD, Retina Fellow, St Michael's Hospital, University of Toronto, Canada; Rafael Alberto García, MD, Chief of Outpatient Services, Department of Ophthalmology, Hospital México of San José, Costa Rica
Contributor Information and Disclosures

Updated: Jul 27, 2007

Treatment

Medical Care

  • Because it is a self-limited condition, treatment of systemic acquired toxoplasmosis is usually not recommended.
  • In the case of ocular toxoplasmosis, several therapeutic regimens have been recommended. Triple drug therapy refers to pyrimethamine, sulfadiazine, and prednisone. Quadruple therapy refers to pyrimethamine, sulfadiazine, clindamycin, and prednisone. Pyrimethamine should be combined with folinic acid to avoid hematological complications. The duration of treatment varies depending on the patient's response but usually lasts for 4-6 weeks.
  • During pregnancy, spiramycin and sulfadiazine can be used in the first trimester. Throughout the second trimester, spiramycin, sulfadiazine, pyrimethamine, and folinic acid are recommended. Spiramycin, pyrimethamine, and folinic acid may be used during the third trimester.
  • Corticosteroids
    • Topical corticosteroids are used depending on the anterior chamber reaction.
    • Depot steroid therapy is absolutely contraindicated in the treatment of ocular toxoplasmosis. The high-dose medication in close proximity to ocular tissues apparently overwhelms the host's immune response, leading to rampant necrosis and the potential for a blind, phthisical globe.
    • Systemic corticosteroids are used as an adjunct to minimize collateral damage from the inflammatory response.
  • Topical cycloplegic agents are used depending on the anterior chamber reaction and the degree of pain. They are also used to prevent formation of posterior synechiae.
  • Antitoxoplasmic agents include the following:
    • Sulfadiazine
    • Clindamycin
    • Pyrimethamine
    • Atovaquone
    • Azithromycin

Surgical Care

  • Photocoagulation or cryotherapy
    • Caution must be exercised if photocoagulation or cryotherapy is being considered in the treatment of intraocular toxoplasmosis.
    • Intraretinal hemorrhages, vitreous hemorrhage, and retinal detachment have been reported as complications of such treatment. Tissue cysts can exist in a normal-appearing retina.
  • Pars plana vitrectomy may be indicated in cases of retinal detachment secondary to vitreous traction or in cases where vitreous opacities persist.

Consultations

Vitreoretinal consultation is desired if pars plana vitrectomy is being considered. Consultations with internal medicine or infectious disease specialists are always recommended.

Activity

No restrictions of activity are necessary.

Medication

The mere presence of a focus of retinitis is not always an indication for treatment. Generally, small peripheral lesions heal spontaneously and may be followed conservatively. On the other hand, lesions within the vascular arcade, lesions near the optic disc (Jensen papillitis), lesions in the papillomacular bundle, or large lesions irrespective of location are treated. Patients with severe debilitating vitreitis are also treated aggressively.

In a prospective trial, treatment with several regimens failed to shorten the duration of inflammatory activity or to prevent recurrences. However, treatment did reduce the size of the ultimate chorioretinal scar. In addition, experts differ on their preferred initial treatment. In a report, one third of respondents preferred triple therapy (ie, pyrimethamine, sulfadiazine, prednisone), and a little more than one quarter of respondents preferred quadruple therapy (ie, pyrimethamine, sulfadiazine, clindamycin, prednisone).

Antibiotics

Therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.


Pyrimethamine (Daraprim)

A diaminopyrimidine that acts as a potent inhibitor of dihydrofolate reductase and is synergistic with sulfonamides.

Adult

75 mg PO qd or 50 mg PO bid loading dose, followed by 25 mg PO bid

Pediatric

1 mg/kg/d divided bid; after 2-4 d, dose is decreased to half and continued 4 more wk

Concurrent use of antifolic acids, such as methotrexate, and pyrimethamine may increase risk of bone marrow suppression; discontinue pyrimethamine therapy if signs of folate deficiency develop; mild hepatotoxicity may occur with concomitant administration of lorazepam and pyrimethamine

Documented hypersensitivity; megaloblastic anemia resulting from a folate deficiency

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

If signs of folate deficiency develop, reduce dose or discontinue drug depending on patient response; caution in hepatic or renal impairment; monitor for toxoplasmosis by performing semiweekly blood counts, including platelet counts; may precipitate hemolytic anemia in patients with G-6-PD deficiency, generally in presence of other stressful events


Sulfadiazine (Microsulfon)

Exerts bacteriostatic action through competitive antagonism with para-aminobenzoic acid (PABA).

Adult

2-4 g PO single dose, loading dose, followed by 1 g PO qid

Pediatric

<2 months: Not established
>2 months: 75 mg/kg (or 2 g/m2) as loading dose, followed by maintenance dose of 120-150 mg/kg/d (4 g/m2/d) in 4-6 divided doses; not to exceed 6 g/d

Increases effect of oral anticoagulants and oral hypoglycemic agents; sulfadiazine effects are decreased when administered concurrently with PABA or PABA metabolites of drugs, such as proparacaine, tetracaine, sunscreens, and procaine

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Adverse effects include a skin rash and renal crystallization, which can be avoided by large intake of fluids; treatment should be stopped if crystalluria, albuminuria, or hematuria develops; caution in impaired renal or hepatic function or G-6-PD deficiency; adjust dose in renal insufficiency


Trimethoprim and sulfamethoxazole (Bactrim, Bactrim DS, Septra, Septra DS)

Exerts bacteriostatic action through competitive antagonism with para-aminobenzoic acid (PABA). Double strength (DS) tab contains 800 mg of sulfamethoxazole and 160 mg of trimethoprim. Regular strength tab contains 400 mg of sulfamethoxazole and 80 mg of trimethoprim.

Adult

1 DS tab PO bid for first 2 wk; then, 1 regular tab PO bid for next 3-4 wk

Pediatric

<2 months: Not recommended
>2 months: 8 mg/kg/d of trimethoprim plus 40 mg/kg/d of sulfamethoxazole divided bid

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly patients; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine

Documented hypersensitivity; megaloblastic anemia secondary to folate deficiency; breastfeeding

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBCs frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, give 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholics, elderly patients, those receiving anticonvulsant therapy, those with malabsorption syndrome); hemolysis may occur in individuals with G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); give fluids to prevent crystalluria and stone formation


Clindamycin (Cleocin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes causing RNA-dependent protein synthesis to arrest. Some animal evidence exists that clindamycin is effective in the eradication of the encysted form.

Adult

300 mg PO qid

Pediatric

8-16 mg/kg/d divided tid/qid

Increases duration of neuromuscular blockade, induced by tubocurarine and pancuronium; erythromycin may antagonize effects of clindamycin; antidiarrheals may delay absorption of clindamycin

Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis by allowing overgrowth of Clostridium difficile


Azithromycin (Zithromax)

Binds to the 50S ribosomal subunit and interferes with protein synthesis. Treats mild-to-moderate microbial infections.

Adult

500 mg PO day 1, followed by 250 mg/d for the next 4 d

Pediatric

Not established

May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum and/or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine

Documented hypersensitivity; hepatic impairment; do not administer with pimozide

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Site reactions can occur with IV route; bacterial or fungal overgrowth may result with prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function, prolonged QT intervals, or pneumonia; caution in hospitalized, geriatric, or debilitated patients

Ubiquinone analogs

Inhibit ATP synthesis, which, in turn, causes inhibition of metabolic enzymes, causing the suppression of parasite growth.


Atovaquone (Mepron)

A hydroxynaphthoquinone that inhibits the mitochondrial electron transport chain by competing with ubiquinone at the ubiquinone-cytochrome-c-reductase region (complex III). The inhibition of electron transport by atovaquone will result in the inhibition of nucleic acid and ATP synthesis in the parasites. Atovaquone has shown activity against bradyzoites in animal models of toxoplasmosis.

Adult

750 mg (5 mL) PO bid

Pediatric

Not established

May increase zidovudine serum levels; coadministration with rifampin and rifabutin may decrease atovaquone levels; atovaquone may decrease levels of TMP-SMZ

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in elderly patients and in hepatic and renal impairment; adverse effects include rash, pruritus, headache, and nausea

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli. In cases where anterior uveitis is present, topical corticosteroids are used to treat the inflammation.


Prednisone (Deltasone, Meticorten, Orasone)

Used to limit inflammatory damage. Use of oral corticosteroids without antibiotic coverage may produce an immunodeficiency state that results in rapid spread of tachyzoites and widespread retinitis. Antiparasitic agents should be stopped only after the steroids have been stopped. They should never be used without antiparasitic coverage in the treatment of ocular toxoplasmosis. Corticosteroids are probably not indicated in patients who are immunosuppressed. Some specialists wait 24-48 h after the initiation of antibiotic therapy before starting prednisone, while others begin antibiotics and prednisone simultaneously.

Adult

60-100 mg/d PO for 1-2 wk; then, taper over 2-3 wk

Pediatric

Not established

Drugs, such as phenobarbital, phenytoin, and rifampin, induce hepatic enzymes and, therefore, increase the clearance of corticosteroids; other drugs, such as ketoconazole, inhibit clearance of corticosteroids, adjust dose accordingly; corticosteroids have an unpredictable effect on anticoagulants, so coagulation indices should be monitored

Documented hypersensitivity; systemic fungal infections

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Secondary adrenocortical insufficiency may be induced; in periods of stress, may require increased dosage; immunizations should be withheld when the patient is taking corticosteroids; caution in diabetics, hypertensives, and patients with known hypersecretory gastric disease (internal medicine consultation imperative in these instances)


Prednisolone acetate 1% (Pred Forte)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. Frequency of application depends on degree of ocular inflammation.

Adult

1 gtt qid up to q1h

Pediatric

Administer as in adults; nasolacrimal duct occlusion is recommended to minimize systemic absorption

Documented hypersensitivity; herpetic, bacterial, or fungal keratitis

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Caution in hypertension; known to cause cataract formation with long-term use; suspect fungal invasion in any persistent corneal ulceration where a corticosteroid has been used or is in use (obtain fungal cultures when appropriate)

Folic acid derivatives

Used to counteract toxic effects of folic acid antagonists that act by inhibiting dihydrofolate reductase.


Leucovorin (Wellcovorin)

Reduced form of folic acid that does not require enzymatic reduction reaction for activation. Allows for purine and pyrimidine synthesis, both of which are needed for normal erythropoiesis.

Adult

5-15 mg IV/IM 3 times/wk together with a combination of pyrimethamine and sulfonamide

Pediatric

Not established

May enhance toxicity of 5-fluorouracil; in large doses, may counteract antiepileptic effect of phenobarbital, phenytoin, and primidone

Documented hypersensitivity; pernicious anemia or vitamin deficient megaloblastic anemias

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Do not administer intrathecally or intraventricularly

Cycloplegics

As in any eye with uveitis, posterior synechiae often form if a pupil is not mobilized. Anticholinergic agents, such as cyclopentolate, atropine, and homatropine, block the sphincter muscle of the iris and the muscle in the ciliary body that is responsible for accommodation to produce mydriasis and paralysis of accommodation.


Cyclopentolate 0.5%, 1%, 2% (AK-Pentolate, Cyclogyl)

Prevents muscle of ciliary body and sphincter muscle of iris from responding to cholinergic stimulation. Induces mydriasis in 30-60 min and cycloplegia in 25-75 min. Infants should not be given concentrations >0.5%.

Adult

1% solution: 1 gtt qid

Pediatric

Administer as in adults

Decreases effects of carbachol and cholinesterase inhibitors

Documented hypersensitivity; narrow-angle glaucoma

Pregnancy

C - Safety for use during pregnancy has not been established.

Precautions

Exercise caution in patients (eg, elderly persons) where increased intraocular pressure may be present; can cause toxic anticholinergic systemic adverse effects (common in children, especially infants) but incidence rare when used sparingly; compressing lacrimal sac by digital pressure for 1-3 min following application may minimize systemic absorption

More on Toxoplasmosis

Overview: Toxoplasmosis
Differential Diagnoses & Workup: Toxoplasmosis
Treatment & Medication: Toxoplasmosis
Follow-up: Toxoplasmosis
Multimedia: Toxoplasmosis
References

References

  1. Atmaca LS, Simsek T, Batioglu F. Clinical features and prognosis in ocular toxoplasmosis. Jpn J Ophthalmol. Jul-Aug 2004;48(4):386-91. [Medline].

  2. Auer C, Bernasconi O, Herbort CP. Toxoplasmic retinochoroiditis: new insights provided by indocyanine green angiography. Am J Ophthalmol. Jan 1997;123(1):131-3. [Medline].

  3. Bonfioli AA, Orefice F. Toxoplasmosis. Semin Ophthalmol. Jul-Sep 2005;20(3):129-41. [Medline].

  4. Bosch-Driessen EH, Rothova A. Recurrent ocular disease in postnatally acquired toxoplasmosis. Am J Ophthalmol. Oct 1999;128(4):421-5. [Medline].

  5. de Boer JH, Verhagen C, Bruinenberg M, Rothova A, de Jong PT, Baarsma GS, et al. Serologic and polymerase chain reaction analysis of intraocular fluids in the diagnosis of infectious uveitis. Am J Ophthalmol. Jun 1996;121(6):650-8. [Medline].

  6. Desmonts G. Definitive serological diagnosis of ocular toxoplasmosis. Arch Ophthalmol. Dec 1966;76(6):839-51. [Medline].

  7. Desmonts G, Daffos F, Forestier F, Capella-Pavlovsky M, Thulliez P, Chartier M. Prenatal diagnosis of congenital toxoplasmosis. Lancet. Mar 2 1985;1(8427):500-4. [Medline].

  8. Dodds EM. Toxoplasmosis. Curr Opin Ophthalmol. Dec 2006;17(6):557-61. [Medline].

  9. Engstrom RE Jr, Holland GN, Nussenblatt RB, Jabs DA. Current practices in the management of ocular toxoplasmosis. Am J Ophthalmol. May 15 1991;111(5):601-10. [Medline].

  10. Fine SL, Owens SL, Haller JA, Knox DL, Patz A. Choroidal neovascularization as a late complication of ocular toxoplasmosis. Am J Ophthalmol. Mar 1981;91(3):318-22. [Medline].

  11. Friedmann CT, Knox DL. Variations in recurrent active toxoplasmic retinochoroiditis. Arch Ophthalmol. Apr 1969;81(4):481-93. [Medline].

  12. Ghartey KN, Brockhurst RJ. Photocoagulation of active toxoplasmic retinochoroiditis. Am J Ophthalmol. Jun 1980;89(6):858-64. [Medline].

  13. Giles CL. The treatment of Toxoplasma uveitis with pyrimethamine and folinic acid. Am J Ophthalmol. Oct 1964;58:611-6. [Medline].

  14. Glasner PD, Silveira C, Kruszon-Moran D, Martins MC, Burnier Júnior M, Silveira S, et al. An unusually high prevalence of ocular toxoplasmosis in southern Brazil. Am J Ophthalmol. Aug 15 1992;114(2):136-44. [Medline].

  15. Goto K, Kurita M, Masuhara N, Iijima Y, Saeki K, Ohno S. The prevalence of Toxoplasma antibody in patients with various ocular diseases in central Japan. Graefes Arch Clin Exp Ophthalmol. Aug 1996;234(8):493-5. [Medline].

  16. Guex-Crosier Y, Auer C, Bernasconi O, Herbort CP. Toxoplasmic retinochoroiditis: resolution without treatment of the perilesional satellite dark dots seen by indocyanine green angiography. Graefes Arch Clin Exp Ophthalmol. Jun 1998;236(6):476-8. [Medline].

  17. Henderly DE, Genstler AJ, Smith RE, Rao NA. Changing patterns of uveitis. Am J Ophthalmol. Feb 15 1987;103(2):131-6. [Medline].

  18. Hercos BV, Muinos SJ, Casaroli-Marano RP. [Utility of ultrasonography in toxoplasmic uveitis]. Arch Soc Esp Oftalmol. Feb 2004;79(2):59-65. [Medline].

  19. Holland GN. Ocular toxoplasmosis: a global reassessment. Part I: epidemiology and course of disease. Am J Ophthalmol. Dec 2003;136(6):973-88. [Medline].

  20. Holland GN. Ocular toxoplasmosis: a global reassessment. Part II: disease manifestations and management. Am J Ophthalmol. Jan 2004;137(1):1-17. [Medline].

  21. Holland GN. Reconsidering the pathogenesis of ocular toxoplasmosis. Am J Ophthalmol. Oct 1999;128(4):502-5. [Medline].

  22. Holland GN, Muccioli C, Silveira C, Weisz JM, Belfort R Jr, O'Connor GR. Intraocular inflammatory reactions without focal necrotizing retinochoroiditis in patients with acquired systemic toxoplasmosis. Am J Ophthalmol. Oct 1999;128(4):413-20. [Medline].

  23. Jabs DA, Green WR, Fox R, Polk BF, Bartlett JG. Ocular manifestations of acquired immune deficiency syndrome. Ophthalmology. Jul 1989;96(7):1092-9. [Medline].

  24. Johnson MW, Greven GM, Jaffe GJ, Sudhalkar H, Vine AK. Atypical, severe toxoplasmic retinochoroiditis in elderly patients. Ophthalmology. Jan 1997;104(1):48-57. [Medline].

  25. Kimball AC, Kean BH, Fuchs F. Congenital toxoplasmosis: a prospective study of 4,048 obstetric patients. Am J Obstet Gynecol. Sep 15 1971;111(2):211-8. [Medline].

  26. Koo L, Young LH. Management of ocular toxoplasmosis. Int Ophthalmol Clin. 2006;46(2):183-93. [Medline].

  27. Lakhanpal V, Schocket SS, Nirankari VS. Clindamycin in the treatment of toxoplasmic retinochoroiditis. Am J Ophthalmol. May 1983;95(5):605-13. [Medline].

  28. Mahalakshmi B, Therese KL, Madhavan HN, Biswas J. Diagnostic value of specific local antibody production and nucleic acid amplification technique-nested polymerase chain reaction (nPCR) in clinically suspected ocular toxoplasmosis. Ocul Immunol Inflamm. Apr 2006;14(2):105-12. [Medline].

  29. Manku H, McCluskey P. Diagnostic vitreous biopsy in patients with uveitis: a useful investigation?. Clin Experiment Ophthalmol. Dec 2005;33(6):604-10. [Medline].

  30. McCannel CA, Holland GN, Helm CJ, Cornell PJ, Winston JV, Rimmer TG. Causes of uveitis in the general practice of ophthalmology. UCLA Community-Based Uveitis Study Group. Am J Ophthalmol. Jan 1996;121(1):35-46. [Medline].

  31. Mets MB, Holfels E, Boyer KM, Swisher CN, Roizen N, Stein L, et al. Eye manifestations of congenital toxoplasmosis. Am J Ophthalmol. Sep 1996;122(3):309-24. [Medline].

  32. Nicholson DH, Wolchok EB. Ocular toxoplasmosis in an adult receiving long-term corticosteroid therapy. Arch Ophthalmol. Feb 1976;94(2):248-54. [Medline].

  33. Ongkosuwito JV, Bosch-Driessen EH, Kijlstra A, Rothova A. Serologic evaluation of patients with primary and recurrent ocular toxoplasmosis for evidence of recent infection. Am J Ophthalmol. Oct 1999;128(4):407-12. [Medline].

  34. Pearson PA, Piracha AR, Sen HA, Jaffe GJ. Atovaquone for the treatment of toxoplasma retinochoroiditis in immunocompetent patients. Ophthalmology. Jan 1999;106(1):148-53. [Medline].

  35. Perkins ES. Ocular toxoplasmosis. Br J Ophthalmol. Jan 1973;DA - 19730719(1):1-17. [Medline].

  36. Ronday MJ, Ongkosuwito JV, Rothova A, Kijlstra A. Intraocular anti-Toxoplasma gondii IgA antibody production in patients with ocular toxoplasmosis. Am J Ophthalmol. Mar 1999;127(3):294-300. [Medline].

  37. Rothova A, Bosch-Driessen LE, van Loon NH, Treffers WF. Azithromycin for ocular toxoplasmosis. Br J Ophthalmol. Nov 1998;82(11):1306-8. [Medline].

  38. Rothova A, Meenken C, Buitenhuis HJ, Brinkman CJ, Baarsma GS, Boen-Tan TN, et al. Therapy for ocular toxoplasmosis. Am J Ophthalmol. Apr 15 1993;115(4):517-23. [Medline].

  39. Rutzen AR, Smith RE, Rao NA. Recent advances in the understanding of ocular toxoplasmosis. In: Current Opinion in Ophthalmology. 1994;5:3-9.

  40. Sabates R, Pruett RC, Brockhurst RJ. Fulminant ocular toxoplasmosis. Am J Ophthalmol. Oct 1981;92(4):497-503. [Medline].

  41. Silveira C, Belfort R Jr, Burnier M Jr, Nussenblatt R. Acquired toxoplasmic infection as the cause of toxoplasmic retinochoroiditis in families. Am J Ophthalmol. Sep 15 1988;106(3):362-4. [Medline].

  42. Smith RE, Ganley JP. Ophthalmic survey of a community. 1. Abnormalities of the ocular fundus. Am J Ophthalmol. Dec 1972;74(6):1126-30. [Medline].

  43. Tabbara KF, Dy-Liacco J, Nozik RA, O'Connor GR, Blackman HJ. Clindamycin in chronic toxoplasmosis. Effect of periocular injections on recoverability of organisms from healed lesions in the rabbit eye. Arch Ophthalmol. Mar 1979;97(3):542-4. [Medline].

  44. Tabbara KF, O'Connor GR. Treatment of ocular toxoplasmosis with clindamycin and sulfadiazine. Ophthalmology. Feb 1980;87(2):129-34. [Medline].

  45. Van der Veen J, Polak MF. Prevalence of toxoplasma antibodies according to age with comments on the risk of prenatal infection. J Hyg Camb. 1980;85:165-174. [Medline].

  46. Wallace GD. Serologic and epidemiologic observations on toxoplasmosis on three Pacific atolls. Am J Epidemiol. Aug 1969;90(2):103-11. [Medline].

  47. Wallon M, Kodjikian L, Binquet C, Garweg J, Fleury J, Quantin C, et al. Long-term ocular prognosis in 327 children with congenital toxoplasmosis. Pediatrics. Jun 2004;113(6):1567-72. [Medline].

  48. Weiss MJ, Velazquez N, Hofeldt AJ. Serologic tests in the diagnosis of presumed toxoplasmic retinochoroiditis. Am J Ophthalmol. Apr 15 1990;109(4):407-11. [Medline].

  49. Zimmerman LE. Ocular pathology of toxoplasmosis. Surv Ophthalmol. 1961;6:832-876.

Further Reading

Keywords

Toxoplasma, Toxoplasma gondii, T gondii, congenital toxoplasmosis, acquired toxoplasmosis, toxoplasmosis in immunocompromised host, ocular toxoplasmosis, retinochoroiditis, chorioretinitis, chorioretinal scar, intraocular inflammation, intraocular toxoplasmosis

Contributor Information and Disclosures

Author

Lihteh Wu, MD, Consulting Surgeon, Department of Ophthalmology, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Lihteh Wu, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

Coauthor(s)

Teodoro Evans, MD, Retina Fellow, St Michael's Hospital, University of Toronto, Canada
Disclosure: Nothing to disclose.

Rafael Alberto García, MD, Chief of Outpatient Services, Department of Ophthalmology, Hospital México of San José, Costa Rica
Disclosure: Nothing to disclose.

Medical Editor

John D Sheppard Jr, MD, MMSc, Professor of Ophthalmology, Microbiology and Molecular Biology, Clinical Director, Thomas R Lee Center for Ocular Pharmacology, Program Director, Ophthalmology Residency Training, Eastern Virginia Medical School; President, Virginia Eye Consultants
John D Sheppard Jr, MD, MMSc is a member of the following medical societies: American Academy of Ophthalmology, American Society for Microbiology, American Society of Cataract and Refractive Surgery, American Uveitis Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

R Christopher Walton, MD, Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, Assistant Dean for Graduate Medical Education, University of Tennessee College of Medicine; Consulting Staff, Regional Medical Center, Memphis Veterans Affairs Medical Center, St Jude Children's Research Hospital
R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Healthcare Executives, American Uveitis Society, Association for Research in Vision and Ophthalmology, and Retina Society
Disclosure: Nothing to disclose.

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.