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Pediatric Toxoplasmosis Medication

  • Author: Itzhak Brook, MD, MSc; Chief Editor: Russell W Steele, MD  more...
Updated: Sep 16, 2015

Medication Summary

The currently recommended drugs for T gondii infection act primarily against the tachyzoite form but do not eradicate the encysted form (bradyzoite). Effective treatment mandates the administration of combination of 2 agents effective against the pathogen. Leucovorin (folinic acid) should be administered concomitantly to avoid bone marrow suppression. Pyrimethamine is the most effective agent and is included in most drug regimens. Unless circumstances arise that preclude using more than one drug, a second drug, such as sulfadiazine, atovaquone, or clindamycin, should be added. Other effective agents include sulfamerazine and sulfamethazine, which are not available in the United States.[10]

The efficacy of azithromycin, clarithromycin, atovaquone, dapsone, and cotrimoxazole (ie, trimethoprim-sulfamethoxazole) is unclear; therefore, they should be used only as alternatives in combination with pyrimethamine. The most effective available therapeutic combination is pyrimethamine plus sulfadiazine or trisulfapyrimidine (ie, combination of sulfamerazine, sulfamethazine, and sulfapyrazine). These agents are active against tachyzoites and are synergistic when used in combination.

A study that compared the effects of trimethoprim-sulfamethoxazole vs placebo in reducing the risk of recurrences of Toxoplasma gondii retinochoroiditis reported that trimethoprim/sulfamethoxazole therapy resulted in a 100% reduction in the recurrence of Toxoplasma gondii retinochoroiditis over 1 year of treatment.[11, 12]

Children with renal insufficiency or glucose-6-phosphate-dehydrogenase (G6PD) deficiency and those receive anticonvulsants or antiretrovirals require special attention. Because sulfadiazine is excreted in the kidneys, its dose may require adjustment for those with renal insufficiency. Sulfadiazine should not be administered to children with G6PD deficiency because it can cause hemolysis. It should be substituted with another agent such as clindamycin. Because high-dose pyrimethamine can cause hemolytic anemia in individuals with G6PD deficiency, these patients should be under close observation. Dosing adjustments may be necessary when sulfadiazine is given to those receiving phenytoin as its half-life may be prolonged.

Additional therapy with corticosteroids (prednisone, 1 mg/kg/day) should be considered with markedly elevated CSF protein (>1 g/dL) and vision-threatening chorioretinitis. Corticosteroids are administered until the elevated CSF protein or active chorioretinitis resolves. The efficacy of corticosteroid therapy has not been observed in controlled studies. No adverse effects of corticosteroids have been noted in cohort studies.


Sulfonamide antimicrobials

Class Summary

These agents exert bacteriostatic action through competitive antagonism with para-aminobenzoic acid (PABA). Microorganisms that require exogenous folic acid and do not synthesize folic acid (pteroylglutamic acid) are not susceptible to the action of sulfonamides. Resistant strains are capable of using folic acid precursors or preformed folic acid. In serum, these agents exist in 3 forms: free, conjugated (ie, acetylated and possibly others), and protein bound. The free form is considered to be therapeutically active.



This is a bacteriostatic agent that acts synergistically with pyrimethamine to treat T gondii.

Trimethoprim/sulfamethoxazole (Bactrim, Bactrim DS, Septra DS, Sulfatrim)


Blocks 2 consecutive steps in the biosynthesis of nucleic acids and proteins essential to many bacteria

Trimethoprim: Inhibits dihydrofolate reductase, thereby blocking production of tetrahydrofolic acid from dihydrofolic acid

Sulfamethoxazole: Inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid


Antiprotozoal and antimycobacterial agents

Class Summary

Protozoal infections occur throughout the world and are a major cause of morbidity and mortality in some regions. Patients who are immunocompromised are especially at risk. Primary immune deficiency is rare, whereas secondary deficiency is more common. Immunosuppressive therapy, cancer and its treatment, HIV infection, and splenectomy may increase vulnerability to infection. Infectious risk is proportional to neutropenia duration and severity. Protozoal infections are typically more severe in immunocompromised patients than in immunocompetent patients.

Dapsone, a sulfone that has been widely used in the treatment of leprosy, has been administered in combination with pyrimethamine for prophylaxis against malaria.

Dapsone with trimethoprim is used as an alternative to trimethoprim-sulfamethoxazole for the treatment of mild to moderate Pneumocystis carinii pneumonia; dapsone alone can be used for prophylaxis. Dapsone and pyrimethamine have also been used in patients with HIV and low CD4+ T-cell counts to prevent T gondii encephalitis.



Mechanism of action similar to that of sulfonamides—competitive antagonists of PABA prevent formation of folic acid, inhibiting growth.

Pyrimethamine (Daraprim)


Pyrimethamine is a folic acid antagonist that selectively inhibits dihydrofolate reductase. It is highly selective against plasmodia and T gondii. Pyrimethamine has a synergistic effect when used conjointly with a sulfonamide to treat T gondii.

Atovaquone (Mepron)


Inhibits electron transport chain in mitochondria, which in turn inhibits synthesis of nucleic acid and ATP.


Lincosamide antimicrobials

Class Summary

These agents inhibit bacterial growth, possibly by blocking the dissociation of peptidyl transfer ribonucleic acid (tRNA) from ribosomes, causing RNA-dependent protein synthesis to arrest.

Clindamycin (Cleocin)


Clindamycin is used as an alternative to sulfonamides. It may be beneficial when used with pyrimethamine in short-term treatment of CNS toxoplasmosis in patients with AIDS.


Macrolide antimicrobials

Class Summary

Azithromycin, which belongs to the azalide subclass of macrolide antibiotics, is administered orally. Azithromycin is derived from erythromycin; however, it differs chemically from erythromycin in that a methyl-substituted nitrogen atom is incorporated into the lactone ring.

Azithromycin (Zithromax, Zmax)


Azithromycin acts by binding to the 50S ribosomal subunit of susceptible microorganisms, in that way interfering with microbial protein synthesis. Nucleic acid synthesis is not affected. Azithromycin concentrates in phagocytes and fibroblasts, as demonstrated by in vitro incubation techniques. In vivo studies suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues. The drug is used to treat mild to moderate microbial infections.

Clarithromycin (Biaxin, Biaxin XL)


Semisynthetic macrolide antibiotic that reversibly binds to P site of 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl t-RNA from ribosomes, thereby inhibiting bacterial growth.



This product is not available in the US. Spiramycin is the drug of choice for maternal or fetal toxoplasmosis. It is used as an alternative therapy in other patient populations when pyrimethamine and sulfadiazine cannot be used.



Class Summary

Supplemental folinic acid is coadministered to prevent hematologic adverse effects caused by bone marrow suppression.



Leucovorin, also called folinic acid, is a derivative of folic acid used with folic acid antagonists, such as sulfonamides and pyrimethamine.



Class Summary

Glucocorticoids have anti-inflammatory properties and cause profound and varied metabolic effects, modifying the body’s immune response to diverse stimuli.

Prednisone (Prednisone Intensol, Rayos)


This agent elicits mild mineralocorticoid activity and moderate anti-inflammatory effects; controls or prevents inflammation by controlling rate of protein synthesis, suppressing migration of polymorphonuclear leukocytes (PMNs) and fibroblasts, reversing capillary permeability, and stabilizing lysosomes at cellular level; in physiologic doses, corticosteroids are administered to replace deficient endogenous hormones; in larger (pharmacologic) doses, they decrease inflammation

Contributor Information and Disclosures

Itzhak Brook, MD, MSc Professor, Department of Pediatrics, Georgetown University School of Medicine

Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Immunocompromised Host Society, International Society for Infectious Diseases, Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric Infectious Diseases Society, Society for Experimental Biology and Medicine, Society for Pediatric Research, Southern Medical Association, Society for Ear, Nose and Throat Advances in Children, American Federation for Clinical Research, Surgical Infection Society, Armed Forces Infectious Diseases Society

Disclosure: Nothing to disclose.


Murat Hökelek, MD, PhD Professor, Department of Clinical Microbiology, Istanbul University Cerrahpasa Medical Faculty, Turkey

Murat Hökelek, MD, PhD is a member of the following medical societies: American Society for Microbiology, Turkish Society for Parasitology

Disclosure: Nothing to disclose.

Hakan Leblebicioglu, MD Chairman, Professor, Department of Infectious Diseases and Clinical Microbiology, Ondokuz Mayis University School of Medicine, Turkey

Hakan Leblebicioglu, MD is a member of the following medical societies: American Society for Microbiology, European Society of Clinical Microbiology and Infectious Diseases

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.


Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

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Toxoplasma gondii trophozoites in tissue culture.
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