Toxoplasmosis Medication

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dication Summary

ntly recommended drugs in the treatment of toxoplasmosis act primarily against the tachyzoite form of Ti; thus, they do not eradicate the encysted form (bradyzoite). Pyrimethamine is the most effective agent anduded in most drug regimens. Leucovorin (ie, folinic acid) should be administered concomitantly to preventmarrow suppression. Unless circumstances preclude using more than 1 drug, a second drug (eg,

iazine, clindamycin) should be added.[53, 54, 55]

fficacy of azithromycin, clarithromycin, atovaquone, dapsone, and cotrimoxazole is unclear; therefore, theyd be used only as alternatives in combination with pyrimethamine. The most effective available therapeutic

ination is pyrimethamine plus sulfadiazine or trisulfapyrimidines (eg, a combination of sulfamerazine,methazine, and sulfapyrazine). These agents are active against tachyzoites and are synergistic when used innation.

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

pregnant patients

nocompetent, nonpregnant patients typically do not require treatment. Treatment of nonpregnant patients isbed below.

-week regimen is as follows:

Pyrimethamine (100mg loading dose orally followed by 25-50 mg/day) plus sulfadiazine (2-4 g/day divided4 times daily) OR

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

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

der steroids in patients with radiologic midline shift, clinical deterioration after 48 hours, or elevatedranial pressure.

nant patients

iagnosis of acute infection is often difficult to make during pregnancy, and the administration of empiricicrobial therapy is discouraged.

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

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

ing regimen for pregnant patients is as follows:

Spiramycin 1 g orally every 8 hoursIf the amniotic fluid test result for T gondiiis positive: 3 weeks of pyrimethamine (50 mg/day orally) andsulfadiazine (3 g/day orally in 2-3 divided doses) alternating with a 3-week course of spiramycin 1 g 3 timesdaily for maternal treatment ORPyrimethamine (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) ANDLeucovorin 10-25 mg/day orally to prevent bone marrow suppression

ents with AIDS

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

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

nts with AIDS, CNS toxoplasmosis, and evidence of midline shift or increased intracranial pressure may alsot from steroid therapy.

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

d be avoided.

nitis

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

mage below.)


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

rospective trial, treatment with several regimens failed to shorten the duration of inflammatory activity or tont recurrences. However, treatment did reduce the size of the ultimate retinochoroidal scar.

dition, experts differ on their preferred initial treatment. In a report, one third of respondents preferred triple

py (ie, pyrimethamine, sulfadiazine, prednisone), and a little more than one quarter of respondents preferreduple therapy (ie, pyrimethamine, sulfadiazine, clindamycin, prednisone).

ntributor Information and Disclosuresorat Hkelek, MD, PhD Professor, Department of Clinical Microbiology, Istanbul University Cerrahpasaical Faculty, Turkey

at Hkelek, MD, PhD is a member of the following medical societies:American Society for Microbiologyandish Society for Parasitology

losure: Nothing to disclose.

ef Editorhael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart Gf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science

ter

hael Stuart Bronze, MD is a member of the following medical societies:Alpha Omega Alpha,Americanege of Physicians,American Medical Association,Association of Professors of Medicine, Infectiousases Society of America, Oklahoma State Medical Association, and Southern Society for Clinicalstigation


tional Contributorseph U Becker, MDFellow, Global Health and International Emergency Medicine, Stanford Universityool of Medicine

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


n L Brusch, MD, FACPAssistant Professor of Medicine, Harvard Medical School; Consulting Staff,artment of Medicine and Infectious Disease Service, Cambridge Health Alliance

n L Brusch, MD, FACP is a member of the following medical societies: American College of Physiciansandctious Diseases Society of America


odore J Gaeta, DO, MPH, FACEPClinical Associate Professor, Department of Emergency Medicine, Weillnell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program,artment of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor,artment of Emergency Medicine, St George's University School of Medicine

odore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: Alliance for Clinicalcation,American College of Emergency Physicians, Clerkship Directors in Emergency Medicine, Council of

ergency Medicine Residency Directors, New York Academy of Medicine, and Society for Academicergency Medicine


k Kulkarni, MDAttending Physician, Department of Emergency Medicine, Cambridge Health Alliance,sion of Emergency Medicine, Harvard Medical School

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

losure: WebMD Salary Employment

k L Plaster, MD, JDExecutive Editor, Emergency Physicians Monthly

k L Plaster, MD, JD is a member of the following medical societies: American Academy of EmergencyicineandAmerican College of Emergency Physicians

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

ar Safdar, MD, FACP, FIDSAAssociate Professor of Medicine, Consulting Staff, Department of Infectiousases, Infection Control and Employee Health, MD Anderson Cancer Center, University of Texas

ar Safdar, MD, FACP, FIDSA is a member of the following medical societies: American College ofsicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society oferica, International Immunocompromised Host Society, New York Academy of Sciences, and South Carolinaical Association
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eph Sciammarella, MD, FACP, FACEPMajor, Medical Corps, US Army Reserve; Attending Physician,ergency Medicine, Weatherby Locums; President and Director of Education, Health Training/Consulting, Inc

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


hard H Sinert, DOAssociate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine,earch Director, State University of New York College of Medicine; Consulting Staff, Department ofergency Medicine, Kings County Hospital Center

ard H Sinert, DO is a member of the following medical societies:American College of Physiciansandety for Academic Emergency Medicine


pika Singh, MDStaff Physician, Department of Emergency Medicine, Lawrence and Memorial Hospital,London, CT

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


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

losure: Medscape Reference Salary Employment

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Toxoplasmosis Medication