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Toxoplasmosis Medication

  • Author: Murat Hökelek, MD, PhD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Oct 20, 2015
 

Medication Summary

Currently recommended drugs in the treatment of toxoplasmosis act primarily against the tachyzoite form of T gondii; thus, they do not eradicate the encysted form (bradyzoite). Pyrimethamine is the most effective agent and is included in most drug regimens. Leucovorin (ie, folinic acid) should be administered concomitantly to prevent bone marrow suppression. Unless circumstances preclude using more than 1 drug, a second drug (eg, sulfadiazine, clindamycin) should be added.[53, 54, 55]

The efficacy of azithromycin, clarithromycin, atovaquone, dapsone, and cotrimoxazole 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 trisulfapyrimidines (eg, a combination of sulfamerazine, sulfamethazine, and sulfapyrazine). These agents are active against tachyzoites and are synergistic when used in combination.

Careful attention to dosing regimen is necessary because it differs depending on patient variables (eg, immune status, pregnancy). Pyrimethamine may be used with sulfonamides, quinine, and other antimalarials and with other antibiotics.

Nonpregnant patients

Immunocompetent, nonpregnant patients typically do not require treatment. Treatment of nonpregnant patients is described below.

The 6-week regimen is as follows:

  • Pyrimethamine (100mg loading dose orally followed by 25-50 mg/day) plus sulfadiazine (2-4 g/day divided 4 times daily) OR
  • Pyrimethamine (100-mg loading dose orally followed by 25-50 mg/day) plus clindamycin (300 mg orally 4 times daily)
  • Folinic acid (leucovorin) (10-25 mg/day) should be given to all patients to prevent hematologic toxicity of pyrimethamine
  • Trimethoprim (10 mg/kg/day) sulfamethoxazole (50 mg/kg/day) for 4 weeks

Sulfadiazine or clindamycin can be substituted for azithromycin 500 mg daily or atovaquone 750 mg twice daily in immunocompetent patients or in patients with a history of allergy to the former drugs

Consider steroids in patients with radiologic midline shift, clinical deterioration after 48 hours, or elevated intracranial pressure.

Pregnant patients

The diagnosis of acute infection is often difficult to make during pregnancy, and the administration of empiric antimicrobial therapy is discouraged.

Substantial controversy exists regarding the efficacy of treatment during pregnancy in terms of reducing the risk of fetal exposure and the subsequent development of clinical disease such as retinochoroiditis or CNS abnormalities.

Controversy also exists regarding the optimal regimen for treating maternally acquired infection. Spiramycin and pyrimethamine-sulfonamide are used, but given the infrequency of fetal infection and the asymptomatic nature of most fetal infections, treatment effects are difficult to measure. Spiramycin appears to be somewhat more easily tolerated than pyrimethamine-sulfonamide.

A dosing regimen for pregnant patients is as follows:

  • Spiramycin 1 g orally every 8 hours
  • If the amniotic fluid test result for T gondii is positive: 3 weeks of pyrimethamine (50 mg/day orally) and sulfadiazine (3 g/day orally in 2-3 divided doses) alternating with a 3-week course of spiramycin 1 g 3 times daily for maternal treatment OR
  • Pyrimethamine (25 mg/day orally) and sulfadiazine (4 g/day orally) divided 2 or 4 times daily until delivery (this agent may be associated with marrow suppression and pancytopenia) AND
  • Leucovorin 10-25 mg/day orally to prevent bone marrow suppression

Patients with AIDS

Patients with AIDS are treated with pyrimethamine 200 mg orally initially, followed by 50-75 mg/day orally plus folinic acid 10 mg/day orally plus sulfadiazine 4-8 g/day orally for as long as 6 weeks, followed by lifelong suppressive therapy or until immune reconstitution.

Suppressive therapy for patients with AIDS (CD4 count < 100 cells/μL) is pyrimethamine 50mg/day orally plus sulfadiazine 1-1.5 g/day orally plus folinic acid 10 mg/day orally for life or until immune reconstitution.

Patients with AIDS, CNS toxoplasmosis, and evidence of midline shift or increased intracranial pressure may also benefit from steroid therapy.

Diagnosing toxoplasmosis in the absence of definitive tissue or culture evidence may be perilous because serology may be misleading and a false-positive IgM result is somewhat common. Consequently, empiric therapy should be avoided.

Retinitis

The mere presence of a focus of retinitis is not always an indication for treatment. Small, peripheral lesions generally heal spontaneously and may be followed conservatively. On the other hand, lesions in 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. (See the image below.)

Acute macular retinitis associated with primary ac Acute macular retinitis associated with primary acquired toxoplasmosis, requiring immediate systemic therapy

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 retinochoroidal 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).

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Sulfonamide

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.

Sulfonamide antimicrobials exist as 3 forms in serum: free, conjugated (ie, acetylated and possibly others), and protein bound. The free form is considered therapeutically active.

Sulfadiazine

 

Through competitive antagonism of PABA, sulfadiazine interferes with microbial growth. It is useful in the treatment of toxoplasmosis.

Trimethoprim and sulfamethoxazole (Bactrim DS, Septra DS)

 

Trimethoprim/sulfamethoxazole exerts bacteriostatic action through competitive antagonism with PABA. The double-strength tablet contains 800 mg of sulfamethoxazole and 160 mg of trimethoprim. The regular strength tablet contains 400 mg of sulfamethoxazole and 80 mg of trimethoprim.

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Antibiotics, Other

Class Summary

Antimicrobials with activity against mycobacteria may be used

Dapsone

 

Dapsone is bactericidal and bacteriostatic against mycobacteria. Its mechanism of action is similar to that of sulfonamides, ie, it is a competitive antagonist of PABA, preventing the formation of folic acid and inhibiting bacterial growth.

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Lincosamide Antimicrobials

Class Summary

These agents are used to treat serious skin and soft-tissue staphylococcal infections. They are also effective against aerobic and anaerobic streptococci (except enterococci). They inhibit bacterial growth, possibly by blocking the dissociation of peptidyl transfer ribonucleic acid (t-RNA) from ribosomes, causing RNA-dependent protein synthesis to arrest.

Clindamycin (Cleocin)

 

Clindamycin is an alternative to sulfonamides. It may be beneficial when used with pyrimethamine in the acute treatment of CNS toxoplasmosis in patients with AIDS.

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Antiprotozoal Agents

Class Summary

Protozoal infections occur throughout the world and are a major cause of morbidity and mortality in some regions. Immunocompromised patients are especially at risk. Primary immunodeficiency 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.

Pyrimethamine (Daraprim)

 

This is a folic acid antagonist that selectively inhibits plasmodial dihydrofolate reductase. Pyrimethamine is highly selective against plasmodia and T gondii. A synergistic effect occurs when it is used conjointly with a sulfonamide to treat toxoplasmosis. Folinic acid should be given to all patients to prevent hematologic toxicity of pyrimethamine

Atovaquone (Mepron)

 

Atovaquone is a hydroxynaphthoquinone that inhibits the mitochondrial electron transport chain by competing with ubiquinone at the ubiquinone-cytochrome-c-reductase region (complex III). Inhibition of electron transport by atovaquone results in inhibition of nucleic acid and adenosine triphosphate (ATP) synthesis in parasites.

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Macrolides

Class Summary

Spiramycin is a macrolide antibiotic with an antibacterial spectrum similar to erythromycin and clindamycin. It is bacteriostatic at serum concentrations but may be bactericidal at achievable tissue concentrations. The mechanism of action is unclear, but it acts on the 50S subunit of bacterial ribosomes and interferes with translocation. Absorption from the GI tract is irregular (20-50% of the oral dose is absorbed). Following oral administration, peak plasma levels are achieved within 2-4 hours. Spiramycin has a longer half-life than erythromycin and sustains higher tissue levels.

Azithromycin (Zithromax, Zmax)

 

Azithromycin acts by binding to the 50S ribosomal subunit of susceptible microorganisms, thereby 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 of the drug in phagocytes contributes to drug distribution to inflamed tissues. Azithromycin treats mild to moderate microbial infections.

Spiramycin

 

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

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Corticosteroids

Class Summary

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

Prednisone

 

Prednisone is used to limit inflammatory damage. The use of oral corticosteroids without antibiotic coverage may produce an immunodeficiency state that results in the rapid spread of tachyzoites and widespread retinitis. Antiparasitic agents should be stopped only after the steroids have been stopped. The steroids 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 hours after the initiation of antibiotic therapy before starting prednisone, while others begin antibiotics and prednisone simultaneously.

Prednisolone acetate 1% (Pred Forte, Omnipred)

 

This agent decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing increased capillary permeability. The frequency of application depends on degree of ocular inflammation.

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Antidotes

Class Summary

These agents are used to replenish folic acid when the patient is being treated with folic acid antagonists.

Leucovorin

 

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

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Cycloplegics/Mydriatics

Class Summary

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, Cylate)

 

This agent prevents the muscle of the ciliary body and the sphincter muscle of the iris from responding to cholinergic stimulation. It induces mydriasis in 30-60 minutes and cycloplegia in 25-75 minutes. Infants should not be given concentrations of more than 0.5%.

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Contributor Information and Disclosures
Author

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.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Joseph U Becker, MD Fellow, Global Health and International Emergency Medicine, Stanford University School of Medicine

Joseph U Becker, MD is a member of the following medical societies: American College of Emergency Physicians, Emergency Medicine Residents Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Theodore J Gaeta, DO, MPH, FACEP Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine

Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: Alliance for Clinical Education, American College of Emergency Physicians, Clerkship Directors in Emergency Medicine, Council of Emergency Medicine Residency Directors, New York Academy of Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Rick Kulkarni, MD Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

Mark L Plaster, MD, JD Executive Editor, Emergency Physicians Monthly

Mark L Plaster, MD, JD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: M L Plaster Publishing Co LLC Ownership interest Management position

Amar Safdar, MD, FACP, FIDSA Associate Professor of Medicine, Consulting Staff, Department of Infectious Diseases, Infection Control and Employee Health, MD Anderson Cancer Center, University of Texas

Amar Safdar, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, International Immunocompromised Host Society, New York Academy of Sciences, and South Carolina Medical Association

Disclosure: Nothing to disclose.

Joseph Sciammarella, MD, FACP, FACEP Major, Medical Corps, US Army Reserve; Attending Physician, Emergency Medicine, Weatherby Locums; President and Director of Education, Health Training/Consulting, Inc

Joseph Sciammarella, MD, FACP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Physicians, and American Medical Association

Disclosure: Nothing to disclose.

Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Deepika Singh, MD Staff Physician, Department of Emergency Medicine, Lawrence and Memorial Hospital, New London, CT

Deepika Singh, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Nurses Association, Emergency Medicine Residents Association, and Sigma Theta Tau International

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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Toxoplasmosis. Toxoplasma gondii tachyzoites (Giemsa stain).
Toxoplasmosis. Toxoplasma gondii tachyzoites in cell line.
Toxoplasma gondii in infected monolayers of HeLa cells (Giemsa stain).
Ophthalmic toxoplasmosis. Used with permission of Anton Drew, ophthalmic photographer, Adelaide, South Australia.
Macular scar secondary to congenital toxoplasmosis. Visual acuity of the patient is 20/400
Papillitis secondary to toxoplasmosis, necessitating immediate systemic therapy.
Acute macular retinitis associated with primary acquired toxoplasmosis, requiring immediate systemic therapy
Peripapillary scars secondary to toxoplasmosis
Perimacular scars secondary to toxoplasmosis
Inactive retinochoroidal scar secondary to toxoplasmosis
 
 
 
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