Toxoplasmosis

Clinical Snapshot

Toxoplasmosis is caused by Toxoplasma gondii, an obligate intracellular protozoan parasite capable of infecting essentially any warm-blooded animal, with domestic and wild cats as its only definitive host — the only species in which the parasite completes sexual reproduction and sheds environmentally resistant oocysts in feces.^[1] Three transmission routes account for the great majority of human infection: eating undercooked or cured meat containing tissue cysts (pork, lamb, and venison/wild game carry meaningfully higher risk than beef or poultry); ingesting oocyst-contaminated soil, unwashed produce, or untreated water; and direct or indirect contact with a cat's litter box or contaminated garden soil.^[1]^[2] A pharmacist's exposure-history questions — recent undercooked meat, gardening without gloves, a new or outdoor cat, an unchanged litter box — are frequently what actually points toward the diagnosis, since routine serologic screening is deliberately not universal in Canada (see Assessment & Diagnosis).

In an immunocompetent host, primary infection is asymptomatic in the large majority of cases and, when symptomatic, is typically a mild, self-limited illness that does not require antiparasitic treatment — a genuinely important, easily over-treated point covered fully in Choose Initial Treatment. This chapter is organized around four clinically distinct pictures that share one parasite and one diagnostic toolkit: the ordinary immunocompetent primary infection (usually no treatment needed); primary infection acquired during pregnancy, where the entire clinical significance shifts to the risk of congenital transmission and which is this chapter's counseling centerpiece; reactivation disease in an immunocompromised host, most classically toxoplasmic encephalitis in advanced HIV/AIDS; and ocular toxoplasmosis (chorioretinitis), a distinct presentation that can occur congenitally or be reactivated later in life. One more cross-cutting point worth flagging up front: acute toxoplasmosis can produce a clinical picture resembling infectious mononucleosis and is a recognized cause of a false-positive heterophile (monospot) screening test — see this platform's Infectious Mononucleosis chapter for that test's other limitations; a compatible exposure history in a mono-like presentation should prompt toxoplasma-specific serology rather than accepting a positive monospot at face value.

Recognize the Condition

Four clinical pictures, one parasite

The toxoplasmosis spectrum

From an unnoticed primary infection to sight- and life-threatening reactivation disease.

Primary infection, immunocompetent host

Asymptomatic in an estimated 80-90% of cases. When symptomatic, presents after a 5-18 day incubation period as a mild, self-limited illness — low-grade fever, malaise, myalgia, and non-tender cervical lymphadenopathy (often posterior cervical, sometimes more diffuse) that can persist for weeks to a few months even after the acute illness otherwise resolves.^[3]^[2] Rarely progresses to more severe disease (pneumonitis, myocarditis, polymyositis, hepatitis) in an immunocompetent host — more often reported with specific, atypical, more virulent strains circulating in parts of South America than with the strains typical of North American exposure.^[2]^[4]

Primary infection in pregnancy

Clinically indistinguishable from the picture above for the pregnant patient herself — pregnancy does not make the maternal illness itself more severe.^[3] The entire clinical stakes are the risk of transplacental (congenital) transmission to the fetus — real, specific, and gestational-age-dependent — covered fully in Special Populations.

Reactivation disease, immunocompromised host

Occurs almost exclusively through reactivation of dormant tissue cysts established during an often entirely unnoticed primary infection years earlier, rather than through new (primary) infection, once cell-mediated immunity is sufficiently impaired — classically toxoplasmic encephalitis in advanced HIV/AIDS, and less commonly disseminated disease or myocarditis in a transplant recipient (see Special Populations).^[5]

Ocular toxoplasmosis (chorioretinitis)

A focal necrotizing retinochoroiditis that can arise congenitally (from transplacental infection, sometimes not clinically apparent until years or decades later) or from reactivation of a dormant retinal cyst, or, less classically, from newly acquired postnatal infection. Presents with blurred vision, floaters, eye pain, photophobia, and scotomas, and can threaten vision directly when a lesion involves the macula or optic nerve (see Red Flags & Refer).^[4]

Parasite biology in brief — why reactivation and delayed ocular disease both happen

T. gondii exists in three forms relevant to this chapter: tachyzoites, the rapidly dividing form responsible for acute, active infection and tissue invasion; bradyzoites, a slow-dividing form contained within tissue cysts that establish a lifelong latent reservoir, preferentially in brain, retina, and skeletal/cardiac muscle; and sporozoites, contained within the oocysts shed only by cats. After primary infection, the initial tachyzoite phase is normally controlled by an intact cell-mediated immune response, and the parasite persists indefinitely as encysted bradyzoites rather than being fully eradicated. This single fact explains two of this chapter's four clinical pictures at once: reactivation encephalitis occurs when severe immunosuppression allows dormant brain cysts to reactivate into destructive tachyzoites, and a meaningful proportion of ocular disease represents local reactivation of a dormant retinal cyst — sometimes years to decades after an entirely unnoticed primary infection — rather than a new exposure.^[4]^[5]

Congenital toxoplasmosis — the clinical spectrum in the newborn

The classic teaching triad of congenital toxoplasmosis — chorioretinitis, hydrocephalus, and intracranial calcifications — is the exception, not the rule: the great majority of congenitally infected infants are subclinically infected and appear entirely normal at birth, with no obvious sign to prompt suspicion without deliberate testing.^[4] When present, clinical findings span a wide spectrum: chorioretinitis (the single most common manifestation, and one that can appear for the first time well into childhood or young adulthood even when the newborn exam was normal), hydrocephalus, intracranial calcifications, microcephaly, seizures, sensorineural hearing loss, hepatosplenomegaly, jaundice, thrombocytopenia, and, in the most severely affected infants infected very early in gestation, a combination approaching the full classic triad.^[4] This subclinical-at-birth pattern is the central reason confirmed or highly probable congenital infection is treated for an extended course regardless of how well the newborn looks (see Choose Initial Treatment and Special Populations), and why lifelong ophthalmologic follow-up matters even after an apparently uneventful neonatal course (see Monitoring & Follow-Up).

Risk Factors

Eating undercooked, rare, or cured/smoked meat — pork, lamb, and venison/other wild game carry meaningfully higher tissue-cyst risk than beef or poultry; tasting meat before it is fully cooked is a specific, common exposure worth asking about directly.^[1]
Unwashed or unpeeled fruits and vegetables, and untreated or unfiltered water, that may be contaminated with oocyst-bearing soil.^[1]
Gardening or handling soil/sand without gloves — outdoor soil and children's sandboxes can harbor oocysts from cat defecation.^[2]
Cat litter box exposure, particularly changing litter without gloves and without prompt hand hygiene, and particularly for a cat that hunts or is fed raw/undercooked meat (see Non-Pharmacologic Treatment for the specific, reassuring detail about how briefly cats actually shed infectious oocysts).
Unpasteurized dairy, particularly unpasteurized goat's milk.
Immunocompromise — advanced HIV/AIDS (particularly CD4 <100 cells/mm³), solid organ or hematopoietic stem cell transplantation, and other significant iatrogenic immunosuppression are risk factors for reactivation disease rather than for acquiring new infection (see Special Populations).^[5]
Solid organ transplantation with a seropositive donor into a seronegative recipient — a specific, well-recognized transmission route distinct from reactivation of the recipient's own latent infection, classically relevant for heart transplantation given tissue cysts in donor myocardium (see Special Populations).
Occupational exposure — veterinary staff, abattoir/meat-processing workers, and laboratory personnel handling the organism.
Blood transfusion and needlestick/laboratory accidents are recognized but uncommon transmission routes.

Red Flags & Refer

Toxoplasmosis is usually a low-stakes diagnosis in an immunocompetent, non-pregnant adult, but a specific, short list of presentations changes the plan to urgent evaluation and referral:

Confirmed or strongly suspected primary maternal infection during pregnancy — refer promptly to obstetrics/maternal-fetal medicine for confirmatory testing and treatment planning; do not wait for a routine prenatal visit (see Special Populations and Choose Initial Treatment).^[3]
New focal neurologic deficit, headache, confusion, seizure, or fever in a patient with advanced HIV (CD4 <100 cells/mm³) or significant iatrogenic immunosuppression — evaluate urgently for toxoplasmic encephalitis with contrast-enhanced brain imaging; this is a genuine medical emergency, not a routine outpatient workup.^[5]
New floaters, blurred vision, eye pain, photophobia, or a visual field defect — refer urgently to ophthalmology, especially in a patient with HIV, a history of ocular toxoplasmosis, or a compatible exposure history; a lesion involving or threatening the macula or optic nerve can cause rapid, permanent vision loss if treatment is delayed (see Assessment & Diagnosis).^[4]
A newborn with any sign suggestive of congenital infection — hydrocephalus, microcephaly, chorioretinitis found on newborn ophthalmologic exam, intracranial calcifications, seizures, hepatosplenomegaly, jaundice, or thrombocytopenia — needs immediate pediatric infectious diseases involvement, regardless of whether antenatal screening or treatment occurred.^[4]
Unexplained fever, myocarditis, or graft dysfunction in a heart transplant recipient, particularly with a known donor/recipient T. gondii serologic mismatch — consider transplant-associated toxoplasmosis and involve the transplant infectious diseases team.

Assessment & Diagnosis

Serology — the diagnostic mainstay, with real interpretive limitations

Diagnosis in a non-pregnant, immunocompetent adult is rarely pursued at all, since treatment is usually not needed regardless of the result (see Choose Initial Treatment). When testing is indicated, IgG and IgM serology are the initial tests: IgG indicates past or current exposure and, once positive, generally remains positive for life; IgM appears early but has a well-documented, clinically important limitation — it can remain detectable for months to years after the acute infection has resolved, so a positive IgM alone does not reliably confirm a recent infection.^[2] This is the same limitation-of-a-single-test-in-isolation pattern this platform's Infectious Mononucleosis chapter describes for the heterophile test — a positive result needs interpretation in clinical context, not automatic acceptance.

IgG avidity testing is the specific tool used to resolve this ambiguity: antibody avidity (binding strength) starts low early after infection and matures to high avidity over roughly 3-5 months. A high-avidity result reliably excludes infection acquired in the preceding 3-5 months — genuinely useful for timing a pregnancy-relevant infection relative to conception or a specific trimester. A low-avidity result is less definitive: it is consistent with recent infection but does not prove it, since avidity maturation is variable and can remain low for longer than 5 months in a minority of patients — low avidity therefore requires correlation with the clinical picture and repeat testing rather than being treated as confirmatory on its own.

Canada's screening policy — deliberately not universal

Unlike some countries that perform routine monthly serologic screening throughout pregnancy, SOGC does not recommend routine universal toxoplasma screening for pregnant patients at low risk in Canada. Screening should be offered specifically to pregnant patients considered at risk for primary infection (a compatible exposure history, or symptoms suggestive of acute infection) and to patients who are immunosuppressed or HIV-positive, given their risk of reactivation disease.^[3] This is a genuinely important, easily assumed-otherwise point for pharmacist counseling: a pregnant patient without a specific risk factor should not automatically be offered — or expect — a toxoplasma screening test at every prenatal visit.

If acute infection is suspected (a compatible exposure history, symptoms, or an initial equivocal result), repeat serologic testing in 2-3 weeks, and consider starting spiramycin immediately rather than waiting for the repeat result if clinical suspicion is genuinely high — the treatment's purpose is to reduce placental transmission risk while the diagnosis is being confirmed, not only after it is certain (see Choose Initial Treatment).^[3]

Amniocentesis and fetal diagnosis

Amniocentesis for amniotic fluid PCR testing should be offered when maternal primary infection is diagnosed, when serologic testing cannot confirm or exclude acute infection, or in the presence of abnormal ultrasound findings suggestive of congenital infection (ventriculomegaly, intracranial calcifications, hepatosplenomegaly, ascites, or growth restriction).^[3] Timing matters specifically: amniocentesis should not be performed before 18 weeks' gestation, and should be performed no less than 4 weeks after the suspected acute maternal infection — both rules exist specifically to reduce the occurrence of false-negative results from testing too early in the window before fetal infection (if present) becomes PCR-detectable.^[3]

Ultrasound surveillance

Serial obstetric ultrasound is used to monitor for findings suggestive of congenital infection throughout a pregnancy with confirmed or suspected maternal infection, and factors into the amniocentesis decision above.^[3]

Newborn diagnosis

Maternal IgG crosses the placenta, so a positive IgG in a newborn reflects maternal antibody and is not diagnostic on its own; congenital infection is confirmed instead through IgM or IgA serology in the infant (which does not cross the placenta), PCR testing of placental tissue, cord blood, or cerebrospinal fluid, and a full evaluation — ophthalmologic exam and neuroimaging — of every exposed infant regardless of whether the newborn appears clinically well.^[4]

Immunocompromised host with neurologic symptoms

For suspected toxoplasmic encephalitis, contrast-enhanced brain MRI is preferred over CT for its greater sensitivity, classically showing multiple ring-enhancing lesions, often at the basal ganglia or corticomedullary junction, together with a positive toxoplasma IgG (reactivation disease in a seronegative patient is rare enough that a negative IgG should prompt reconsideration of the diagnosis).^[5] The key differential is primary CNS lymphoma, which can look similar radiographically; a genuinely useful diagnostic approach in a patient with a compatible presentation and imaging is a 10-14 day empiric treatment trial, with clinical and radiographic improvement supporting the toxoplasmosis diagnosis and reserving brain biopsy for patients who do not improve (see Treatment Failure/Next Step).^[5]

Ocular disease

Diagnosis of ocular toxoplasmosis is primarily clinical, made by dilated fundoscopic examination showing a focal necrotizing retinochoroiditis, often adjacent to an old pigmented chorioretinal scar from a prior episode, with overlying vitreous inflammation. Serology is supportive, not diagnostic on its own — a positive IgG is common in the general population and does not, by itself, confirm that a given retinal lesion is actively caused by toxoplasmosis; a false sense of diagnostic confirmation from serology alone is a genuine pitfall here (see Common Errors to Avoid).^[4]

Treatment Targets

Avoid unnecessary antiparasitic treatment of an ordinary, self-limited primary infection in an immunocompetent, non-pregnant adult, where treatment adds risk without meaningful benefit.
Reduce placental transmission risk in confirmed maternal infection during pregnancy through correctly timed spiramycin, switched to pyrimethamine-sulfadiazine-folinic acid once fetal infection is confirmed or highly likely.
Deliver genuine, specific, actionable prevention counseling to pregnant and at-risk patients on food safety, produce handling, and cat litter box precautions — the highest-yield pharmacist contribution in this condition.
Recognize and treat reactivation disease (toxoplasmic encephalitis) promptly in an immunocompromised host, and maintain appropriate primary and secondary prophylaxis in patients at ongoing risk.
Preserve vision in ocular toxoplasmosis by identifying vision-threatening lesions early and combining antiparasitic therapy with adjunctive corticosteroids only when genuinely indicated and only after antiparasitic treatment has started.
Use folinic acid (leucovorin), never plain folic acid, alongside every pyrimethamine-containing regimen.
Ensure every congenitally exposed infant receives full diagnostic testing, extended treatment when infection is confirmed, and long-term ophthalmologic follow-up regardless of how the newborn appears clinically.

Choose Initial Treatment

Step 1 — Immunocompetent, non-pregnant host: usually no antiparasitic treatment

Not routinely treated ordinary primary toxoplasmosis in an immunocompetent adult is self-limited and does not require antiparasitic therapy in the great majority of cases; manage with reassurance and symptomatic care (see Drug Tables).^[2] Consider treatment only for severe or persistent symptoms (constitutional symptoms lasting beyond several weeks, or visceral involvement such as myocarditis, pneumonitis, or hepatitis) — this is uncommon enough that it should prompt specialist infectious diseases input rather than routine empiric antiparasitic prescribing.^[2]

Step 2 — Pregnancy, maternal infection confirmed, fetal infection not yet confirmed

1st line spiramycin (no Drug Database entry — see Drug Tables for why) to reduce the risk of placental transmission while fetal infection status is being determined. Spiramycin is a macrolide that concentrates in placental tissue but crosses the placenta poorly itself — it acts to reduce the parasite burden at the maternal-placental interface rather than treating an already-infected fetus, which is exactly why the regimen changes (Step 3) once fetal infection is confirmed or highly likely.^[3] Start as soon as acute maternal infection is confirmed or strongly suspected — do not wait for a repeat serology result if clinical suspicion is high (see Assessment & Diagnosis).^[3]

Step 3 — Fetal infection confirmed or highly likely, or maternal infection acquired at or after ~18 weeks' gestation

Switch to Combo: pyrimethamine + sulfadiazine + folinic acid (leucovorin) — this combination, not spiramycin, is what actually treats established or strongly suspected fetal infection, and is also used when maternal infection itself was acquired later in pregnancy.^[3] Do not simply continue spiramycin once amniotic fluid PCR is positive or ultrasound findings are abnormal — this is a genuine, consequential switch, not an optional escalation (see Common Errors to Avoid). See Drug Tables for indication-specific dosing; sulfadiazine near the time of delivery carries a theoretical risk of displacing bilirubin and contributing to neonatal hyperbilirubinemia, a recognized but accepted trade-off managed jointly with obstetrics/maternal-fetal medicine and pediatrics around the time of delivery rather than a reason to withhold treatment of confirmed fetal infection.

Step 4 — Confirmed congenital infection in the newborn

Combo: pyrimethamine + sulfadiazine + folinic acid (leucovorin) for an extended course (commonly 12 months) under pediatric infectious diseases direction, regardless of whether the infant appears clinically well — subclinical-at-birth is the norm for congenital infection, not the exception (see Recognize the Condition), and undertreating an asymptomatic-appearing infected newborn risks the delayed chorioretinitis and neurodevelopmental sequelae this extended course is meant to prevent.^[4]

Step 5 — Toxoplasmic encephalitis (advanced HIV/AIDS or other severe immunosuppression)

Preferred acute regimen Combo: pyrimethamine + sulfadiazine + folinic acid (leucovorin) for a minimum of 6 weeks, then transition to a lower-dose secondary prophylaxis (maintenance) regimen continued until sustained immune reconstitution (see Special Populations for the discontinuation criteria).^[5] Sulfa allergy/intolerance substitute clindamycin for sulfadiazine, keeping pyrimethamine and folinic acid — a genuinely effective alternative combination, though clindamycin does not treat as broad a range of concurrent CNS pathogens as sulfadiazine can.^[5] This is the same drug (pyrimethamine + folinic acid) and the same underlying combination logic as pregnancy/congenital treatment above, at CNS-specific doses (see Drug Tables) — a genuinely useful pattern to recognize across this chapter's four clinical pictures.

Step 6 — HIV: primary prophylaxis (Toxoplasma IgG-positive, CD4 <100 cells/mm³)

Preferred sulfamethoxazole/trimethoprim — the same regimen already used for Pneumocystis jirovecii pneumonia prophylaxis in this population, a genuinely convenient dual-purpose choice.^[5] If not tolerated Combo: dapsone + pyrimethamine + folinic acid (leucovorin) at prophylactic doses.^[5] Discontinue primary prophylaxis once CD4 count rises and is sustained above the threshold used for secondary prophylaxis discontinuation, per current HIV opportunistic-infection guidance and in coordination with the patient's HIV care team (see Special Populations).^[5]

Step 7 — Ocular toxoplasmosis (chorioretinitis)

Small peripheral lesion, immunocompetent host, vision not threatened can reasonably be observed without systemic treatment, since many such lesions are self-limited — a genuine, easily overlooked nuance rather than a reason to treat every positive fundoscopic finding.^[4]

Vision-threatening lesion — involving or threatening the macula, optic nerve, or major retinal vessels, or with significant vitritis — classic triple therapy is Combo: pyrimethamine + sulfadiazine + folinic acid (leucovorin) plus an oral corticosteroid, started roughly 3 days after antiparasitic therapy is underway, not before or at the same time — starting the corticosteroid first risks unchecked organism proliferation.^[6] Alternative regimens clindamycin-sulfadiazine-corticosteroid, or trimethoprim/sulfamethoxazole-corticosteroid, are reasonable substitutions, and a randomized trial found intravitreal clindamycin plus dexamethasone, administered by ophthalmology, a genuinely acceptable alternative to the classic systemic regimen — more convenient, with a more favourable systemic side-effect profile, though it is a specialist procedure rather than a routine oral prescribing decision.^[6]

Central teaching point across every pyrimethamine-containing regimen in this chapter — use folinic acid (leucovorin), never plain folic acid. Pyrimethamine works by inhibiting the parasite's dihydrofolate reductase enzyme; folinic acid (leucovorin, an already-reduced folate) can be taken up by human cells to bypass that same blocked step, rescuing the patient's bone marrow from pyrimethamine-induced suppression without rescuing the parasite, which cannot use exogenous folinic acid the same way. Plain folic acid does not have this selective, human-cell-only rescue effect and risks interfering with the regimen's antiparasitic activity — this is a genuinely easy substitution error for a pharmacist to catch at order-verification or dispensing, since folic acid is a far more commonly stocked, cheaper, and more familiar supplement than folinic acid.

Non-Pharmacologic Treatment

Prevention counseling — the highest-yield pharmacist contribution in this condition

Cook meat thoroughly — to a safe internal temperature throughout (whole cuts of beef, veal, and lamb to at least 63°C/145°F with a 3-minute rest; ground meat to at least 71°C/160°F; poultry to at least 74°C/165°F) — and do not taste meat before it is fully cooked.^[1]
Freezing meat reduces but does not reliably eliminate tissue-cyst risk — it is a useful adjunct, not a substitute for thorough cooking.^[1]
Wash and, where practical, peel all fruits and vegetables before eating, cutting, or peeling, and wash hands, cutting boards, and utensils that contacted raw meat before they touch other food.^[1]
Avoid unpasteurized dairy, particularly unpasteurized goat's milk.
Cat litter box precautions — ideally, someone other than the pregnant or immunocompromised patient changes the litter box during pregnancy or significant immunosuppression. If that is not possible, wear disposable gloves, change the litter daily, and wash hands thoroughly immediately afterward. The daily-change detail is not arbitrary: oocysts shed in cat feces take roughly 1-5 days after being shed to sporulate and become infectious, so litter removed before that window has passed is not yet capable of transmitting infection.^[2]
Wear gloves when gardening or handling outdoor soil or sand (including children's sandboxes), and wash hands afterward — outdoor soil can be contaminated with oocysts from any cat that has defecated in the area, not only an owned cat.^[2]
Reassurance worth giving explicitly: a pregnant or immunocompromised patient does not need to give away or avoid petting a household cat — direct contact with the animal itself does not transmit infection; it is contact with feces (litter box, contaminated soil) that matters, and this distinction genuinely changes how counseling lands with an anxious, cat-owning patient.^[2]
Cats shed infectious oocysts for only a relatively brief period — typically 1-3 weeks — following their own first exposure to the parasite, most often early in life; most adult cats, especially those kept exclusively indoors and not fed raw meat, are not actively shedding oocysts at any given time. Keeping cats indoors and feeding only commercial cat food (not raw or undercooked meat) reduces the cat's own infection risk and, by extension, the household's exposure risk.
Avoid adopting or handling unfamiliar stray or new outdoor cats during pregnancy or significant immunosuppression, since a newly acquired cat is more likely to be in — or approaching — its own primary-infection shedding window.

Pharmacologic Treatment Options

Drug / intervention	Role	Dose / use	Important adverse effects	Teaching points
Acetaminophen Alternative	Symptomatic relief only, immunocompetent primary infection	650-1000 mg PO Q4-6H PRN, max 3-4 g/day	Hepatotoxicity with excessive use	Supportive care is the entire treatment for the great majority of immunocompetent primary infections — see Choose Initial Treatment.
Spiramycin Preferred	Pregnancy — maternal infection confirmed, fetal infection not yet confirmed	1 g (3 million IU) PO three times daily until delivery or until fetal infection is excluded/confirmed	GI upset, rare hypersensitivity	Reduces placental transmission risk but does not reliably treat established fetal infection; not routinely stocked — obtained via Health Canada's Special Access Programme, so arrange access as early as possible.
Pyrimethamine Preferred	Core agent for confirmed/suspected fetal infection, congenital infection, toxoplasmic encephalitis, and ocular disease — always with folinic acid	Indication-specific — see Drug Tables	Bone marrow suppression (megaloblastic anemia, leukopenia, thrombocytopenia), rash	Always co-administered with folinic acid (leucovorin), never plain folic acid — see the central teaching point in Choose Initial Treatment.
Sulfadiazine Preferred	Paired with pyrimethamine for confirmed fetal/congenital infection, toxoplasmic encephalitis, and ocular disease	Indication-specific — see Drug Tables	Crystalluria (ensure adequate hydration), rash including rare SJS/TEN, hemolysis in G6PD deficiency, sulfa hypersensitivity	No oral sulfadiazine product exists in this database (only a topical silver sulfadiazine burn-cream formulation, a different product entirely) — left unlinked rather than mis-linked.
Leucovorin calcium (folinic acid) Preferred	Co-administered with every pyrimethamine-containing regimen in this chapter, without exception	Indication-specific — see Drug Tables	Generally well tolerated	Rescues host bone marrow from pyrimethamine toxicity without rescuing the parasite — plain folic acid does not have this selective effect and should not be substituted.
Clindamycin Alternative	Sulfa-allergic/intolerant substitute for sulfadiazine in toxoplasmic encephalitis or ocular disease (with pyrimethamine + folinic acid), or intravitreal (ophthalmology-administered) for ocular disease	Indication-specific — see Drug Tables	GI upset, rare C. difficile-associated diarrhea	A genuinely effective alternative, though it does not cover as broad a range of concurrent CNS pathogens as sulfadiazine when used for encephalitis.
Sulfamethoxazole/trimethoprim Preferred	HIV primary prophylaxis (IgG-positive, CD4 <100 cells/mm³) — preferred agent; also an alternative ocular-disease regimen with a corticosteroid	Prophylaxis: 1 DS tablet PO daily (or per current OI guideline schedule)	Sulfa hypersensitivity, marrow suppression, hyperkalemia	The same regimen already used for Pneumocystis jirovecii pneumonia prophylaxis in this population — a convenient dual-purpose first choice.
Dapsone Alternative	HIV primary prophylaxis when sulfamethoxazole/trimethoprim is not tolerated (with pyrimethamine + folinic acid)	Prophylactic dosing — see Drug Tables	Hemolysis (screen for G6PD deficiency first), methemoglobinemia	Screen for G6PD deficiency before starting given the hemolysis risk, particularly relevant given overlapping G6PD considerations with sulfonamide-based regimens.
Atovaquone Alternative	Further alternative when both sulfamethoxazole/trimethoprim and dapsone-based regimens are not tolerated, or as a treatment alternative in sulfa/pyrimethamine intolerance	Per current OI guideline; must be taken with a fatty meal for adequate absorption	GI upset, rash	Absorption is meaningfully reduced without dietary fat — a genuine, easily missed counseling point that can silently undermine efficacy.
Prednisone Special situation	Adjunctive therapy for vision-threatening ocular chorioretinitis (macular/optic nerve involvement or significant vitritis)	Typically 40 mg PO once daily, started ~3 days after antiparasitic therapy begins, then tapered — see Drug Tables	Hyperglycemia, insomnia, mood change; GI upset	Never start before antiparasitic therapy is underway — an unchecked organism can proliferate if the corticosteroid is started first or alone.
Dexamethasone Special situation	Intravitreal (ophthalmology-administered, with intravitreal clindamycin) alternative to the classic systemic ocular-disease regimen	Administered by ophthalmology per the injection protocol — not a routine oral prescribing decision	Injection-related and typical corticosteroid effects	An evidence-based specialist alternative from a randomized trial — a genuinely useful option to know exists, not one a community/outpatient pharmacist would initiate.

Special Populations

Pregnancy — the counseling centerpiece of this chapter

Transmission risk rises with gestational age at maternal infection, while the severity of fetal disease when transmission does occur falls — a genuinely important, non-intuitive pattern that shapes everything else in this section. A peer-reviewed meta-analysis found vertical transmission rates of roughly 5% (first trimester), 13% (second trimester), and 32% (third trimester) of confirmed maternal infections, with an overall transmission rate around 20%.^[7] At the same time, when transmission does occur, disease is more severe with earlier gestational age at infection — first-trimester transmission, though the least likely to occur, carries the highest risk of severe congenital disease, while third-trimester transmission, though the most likely to occur, is more often subclinical or mild at birth.^[7]^[4] Confirmed maternal infection is also associated with meaningfully increased risk of miscarriage, fetal anomaly, and stillbirth compared with an uninfected pregnancy, independent of congenital transmission specifically.^[7]

Screening in Canada is risk-based, not universal — offered to patients with a specific exposure history or compatible symptoms, and to immunosuppressed or HIV-positive patients (see Assessment & Diagnosis).^[3] Prevention counseling (food safety, produce handling, cat litter box precautions — see Non-Pharmacologic Treatment) is therefore the single most broadly applicable intervention, since it reaches every pregnant patient rather than only those already flagged for screening.

Treatment follows a gestational-age- and fetal-infection-status-driven switch: spiramycin when maternal infection is confirmed before roughly 18 weeks and fetal infection is not yet confirmed, switching to pyrimethamine-sulfadiazine-folinic acid once fetal infection is confirmed or highly likely, or when maternal infection itself is acquired later in pregnancy (see Choose Initial Treatment). Delivery planning should involve maternal-fetal medicine and pediatrics jointly, particularly given the sulfadiazine-near-term bilirubin consideration noted in Choose Initial Treatment.

Reactivation disease in HIV/AIDS

Toxoplasma-seropositive patients with CD4 counts below 100 cells/mm³ are at meaningful risk of reactivation toxoplasmic encephalitis and should receive primary prophylaxis (see Choose Initial Treatment).^[5] Following successful acute treatment of confirmed encephalitis, secondary prophylaxis (maintenance therapy) at reduced doses is continued until sustained immune reconstitution — current guidance supports discontinuation once the patient has completed initial therapy, remains asymptomatic, and has maintained a CD4 count above 200 cells/mm³ for more than 6 months in response to antiretroviral therapy; restart if the CD4 count subsequently falls back below that threshold.^[5]

Solid organ and hematopoietic stem cell transplantation

A seropositive donor organ transplanted into a seronegative recipient is a specific, well-recognized transmission route distinct from reactivation of the recipient's own latent infection — classically relevant for heart transplantation, given tissue cysts that can be present in donor myocardium. Transplant centres typically use post-transplant prophylaxis (commonly sulfamethoxazole/trimethoprim) in this serologic-mismatch scenario per institutional protocol; hematopoietic stem cell transplant recipients with pre-transplant seropositivity are separately at risk of reactivation from their own latent infection during the period of post-transplant immunosuppression.

Congenital infection and long-term pediatric follow-up

Every infant with confirmed or strongly suspected congenital infection needs the extended treatment course described in Choose Initial Treatment and long-term ophthalmologic follow-up, since chorioretinitis from congenital infection can present for the first time years after an entirely normal newborn eye exam — this is not a one-time evaluation that can be considered complete after the neonatal period (see Monitoring & Follow-Up).^[4]

Renal and hepatic impairment

Ensure adequate hydration with sulfadiazine given its crystalluria risk, which is compounded by renal impairment or volume depletion; consult product-specific and institutional dosing guidance for pyrimethamine, sulfadiazine, clindamycin, and sulfamethoxazole/trimethoprim in significant renal or hepatic impairment rather than using standard doses unmodified.

Breastfeeding

Management decisions in a breastfeeding parent should involve obstetrics/infectious diseases given the specialized nature of these regimens; this is not a routine community-pharmacy breastfeeding-compatibility question to answer in isolation.

Monitoring & Follow-Up

Pregnancy: serial ultrasound surveillance through the remainder of pregnancy in confirmed or suspected maternal infection, coordinated with maternal-fetal medicine; reassess the treatment regimen (spiramycin vs. pyrimethamine-sulfadiazine-folinic acid) whenever new amniocentesis or ultrasound information becomes available (see Choose Initial Treatment).^[3]
Every pyrimethamine-containing regimen: monitor CBC (looking specifically for megaloblastic anemia, leukopenia, and thrombocytopenia) at baseline and periodically through treatment, and increase folinic acid dosing (per specialist direction) if cytopenias develop rather than stopping folinic acid.
Every sulfadiazine-containing regimen: encourage generous fluid intake and monitor for signs of crystalluria; watch for early signs of a sulfonamide hypersensitivity reaction (rash, fever, mucosal involvement).
Toxoplasmic encephalitis: reassess clinically and radiographically at 10-14 days of acute treatment — improvement supports the diagnosis and continuation to complete a minimum 6-week acute course before transitioning to secondary prophylaxis (see Treatment Failure/Next Step for the alternative).^[5]
Ocular disease: ophthalmology follow-up through and after treatment to confirm lesion inactivation/scarring and to monitor visual acuity and intraocular pressure (relevant with corticosteroid use).
Congenitally infected infants: long-term, scheduled ophthalmologic follow-up well beyond the neonatal period and the treatment course itself, given the recognized risk of chorioretinitis presenting for the first time later in childhood or young adulthood; coordinate audiology and neurodevelopmental follow-up per pediatric infectious diseases direction.^[4]
HIV: track CD4 count trend to guide both primary-prophylaxis initiation/discontinuation and secondary-prophylaxis discontinuation decisions (see Special Populations).^[5]

Treatment Failure / Next Step

No clinical or radiographic improvement in suspected toxoplasmic encephalitis after 10-14 days of empiric treatment: reconsider the diagnosis rather than simply extending the same regimen — proceed to brain biopsy to evaluate for primary CNS lymphoma or another process, since the empiric-treatment-trial approach specifically depends on a genuine 10-14 day response check (see Assessment & Diagnosis).^[5]
Continued or progressive ocular inflammation/lesion growth on a standard oral regimen: escalate to ophthalmology for consideration of intravitreal clindamycin/dexamethasone or an alternate systemic regimen rather than simply prolonging an apparently ineffective course.^[6]
Persistent cytopenias despite folinic acid supplementation on a pyrimethamine-containing regimen: increase the folinic acid dose per specialist direction; hold pyrimethamine temporarily for severe cytopenia, with hematology input, rather than continuing unmodified.
New or worsening sulfonamide intolerance/allergy during pregnancy, congenital, or CNS treatment: switch to a clindamycin-based alternative regimen (with pyrimethamine and folinic acid retained) rather than continuing a poorly tolerated sulfa-based course (see Choose Initial Treatment).
Amniotic fluid PCR result pending or equivocal in a patient already started on spiramycin: continue spiramycin and reassess with repeat testing/ultrasound rather than switching to pyrimethamine-sulfadiazine-folinic acid prematurely on an unconfirmed result, or withholding treatment entirely while awaiting confirmation.
A newborn initially appears well but a parent/family later reports new visual symptoms in childhood or young adulthood, with a known or possible history of congenital exposure: refer for ophthalmologic evaluation for reactivation chorioretinitis rather than assuming a normal newborn exam ruled this out permanently (see Monitoring & Follow-Up).

Common Errors to Avoid

Prescribing plain folic acid instead of folinic acid (leucovorin) alongside a pyrimethamine-containing regimen — folic acid lacks the selective human-cell-only rescue effect and risks interfering with the regimen's antiparasitic activity (see the central teaching point in Choose Initial Treatment).
Continuing spiramycin after fetal infection has been confirmed by amniotic fluid PCR or strongly suggested by abnormal ultrasound findings, instead of switching to pyrimethamine-sulfadiazine-folinic acid — spiramycin reduces placental transmission risk but does not reliably treat an already-infected fetus.
Ordering (or expecting) universal toxoplasma serologic screening on every pregnant patient in Canada — SOGC specifically recommends a risk-based approach, not universal screening, for patients at low risk.^[3]
Advising a pregnant or immunocompromised patient to give away or avoid a household cat — unnecessary; direct animal contact does not transmit infection, and litter box hygiene/food safety precautions are what actually matter (see Non-Pharmacologic Treatment).
Treating a single positive IgM result as proof of recent, acute infection without avidity testing or a repeat titer — IgM can remain detectable for months to years after the acute infection has resolved.
Missing toxoplasmic encephalitis in a patient with advanced HIV and new neurologic symptoms by not considering the diagnosis or not obtaining contrast-enhanced brain imaging promptly.
Starting an oral corticosteroid for vision-threatening ocular chorioretinitis before, or at the same time as, antiparasitic therapy — this risks unchecked organism proliferation; the corticosteroid follows the antiparasitic regimen by roughly 3 days.^[6]
Assuming an infant who appears normal at birth does not have congenital toxoplasmosis — the great majority of congenitally infected infants are subclinical at birth, which is exactly why confirmed/suspected congenital infection is treated for an extended course regardless of the newborn's appearance.^[4]
Treating a positive toxoplasma IgG as proof that a specific retinal lesion currently being evaluated is actively caused by toxoplasmosis — IgG seropositivity is common in the general population and is supportive, not diagnostic, on its own.
Discontinuing long-term ophthalmologic follow-up in a congenitally infected child after an apparently successful treatment course and a normal eye exam — reactivation chorioretinitis can present for the first time years later.

Clinical Decision Algorithm

Algorithm A — Primary infection identified during pregnancy

Suspected or confirmed primary maternal Toxoplasma infection (symptomatic, or positive/equivocal screening serology in an at-risk pregnancy)

Confirm with repeat serology in 2-3 weeks and/or IgG avidity testing; do not wait for confirmation to start spiramycin if clinical suspicion is high^[3]

Maternal infection before ~18 weeks, fetal infection not yet confirmed

Start spiramycin to reduce placental transmission risk^[3]

Offer amniocentesis for amniotic fluid PCR — no earlier than 18 weeks' gestation, and no less than 4 weeks after suspected maternal infection^[3]

Maternal infection at/after ~18 weeks, OR fetal infection confirmed/highly suspected

Switch to (or start) pyrimethamine + sulfadiazine + folinic acid — this combination, not spiramycin, treats established or likely fetal infection^[3]

Amniotic PCR negative, ultrasound normal

Continue spiramycin; ongoing serial ultrasound surveillance through the remainder of pregnancy

Amniotic PCR positive, or abnormal ultrasound findings

Fetal infection confirmed — pyrimethamine + sulfadiazine + folinic acid; maternal-fetal medicine and pediatric ID involvement for delivery planning

Every exposed newborn, regardless of maternal treatment

Congenital-infection testing (infant IgM/IgA, PCR), ophthalmologic exam, and neuroimaging — even if the infant appears entirely well^[4]

Algorithm B — New focal neurologic symptoms in an immunocompromised host

New headache, focal deficit, seizure, confusion, or fever in a patient with advanced HIV (CD4 <100 cells/mm³) or significant iatrogenic immunosuppression

Obtain contrast-enhanced brain MRI (preferred over CT) and toxoplasma IgG serology^[5]

Multiple ring-enhancing lesions, IgG-positive

Start empiric pyrimethamine + sulfadiazine (or clindamycin if sulfa-intolerant) + folinic acid; reassess clinically and radiographically at 10-14 days^[5]

Solitary lesion, IgG-negative, or atypical imaging

Lower probability of toxoplasmic encephalitis — involve neurology/infectious diseases early and consider primary CNS lymphoma and other diagnoses in parallel

Clinical and radiographic improvement at 10-14 days

Diagnosis supported — complete a minimum 6-week acute course, then transition to secondary prophylaxis until sustained immune reconstitution^[5]

No improvement at 10-14 days

Reconsider the diagnosis — proceed to brain biopsy to evaluate for primary CNS lymphoma or another process rather than continuing empiric treatment indefinitely^[5]

Drug Tables

How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Immunocompetent Host — Supportive Care Only

Antiparasitic treatment is not usually needed for a self-limited primary infection in an immunocompetent, non-pregnant adult.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Acetaminophen	Adults: 650-1000 mg PO Q4-6H PRN, maximum 3-4 g/day	Hepatotoxicity with excessive use	Increased hepatotoxicity risk with alcohol or other hepatotoxic drugs	First-choice symptomatic option for fever/malaise if genuinely needed.

Pregnancy — Maternal Infection Confirmed, Fetal Infection Not Yet Confirmed

Started as soon as acute maternal infection is confirmed or strongly suspected, without waiting for a repeat serology result if suspicion is high.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Spiramycin	Adults: 1 g (3 million IU) PO three times daily, continued until delivery or until fetal infection is excluded or confirmed	GI upset (nausea, diarrhea), rare hypersensitivity reaction	No clinically significant interactions relevant to this short-to-medium-course use	Not routinely stocked in the standard Canadian retail/hospital supply chain for this indication — obtained via Health Canada's Special Access Programme or an equivalent investigational-pharmacy pathway; arrange access as early as possible once the decision to treat is made.

Confirmed/Suspected Fetal Infection in Pregnancy, and Confirmed Congenital Infection in the Newborn

Replaces spiramycin once fetal infection is confirmed or highly likely, or when maternal infection itself was acquired at or after ~18 weeks' gestation; continued for an extended course (commonly 12 months) in a newborn with confirmed congenital infection, under pediatric infectious diseases direction.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Pyrimethamine	Pregnancy: Per maternal-fetal medicine protocol, typically a loading dose then a lower daily maintenance dose Confirmed congenital infection: Weight-based dosing per pediatric infectious diseases protocol, typically continued for 12 months	Bone marrow suppression (megaloblastic anemia, leukopenia, thrombocytopenia), rash	Additive marrow suppression with other antifolate or myelosuppressive drugs	Always co-administered with folinic acid, never plain folic acid — see the central teaching point in Choose Initial Treatment.
Sulfadiazine	Pregnancy: Per maternal-fetal medicine protocol Confirmed congenital infection: Weight-based dosing per pediatric infectious diseases protocol	Crystalluria (ensure generous fluid intake), rash including rare Stevens-Johnson syndrome/toxic epidermal necrolysis, hemolysis in G6PD deficiency, sulfa hypersensitivity	Additive crystalluria risk with dehydration; caution with other sulfonamide-sensitive patients	No oral sulfadiazine product exists in this database — only a topical silver sulfadiazine burn-cream formulation, an entirely different product, is present and was deliberately not linked here. Near-term exposure carries a theoretical bilirubin-displacement/kernicterus risk, managed jointly with obstetrics and pediatrics rather than a reason to withhold treatment of confirmed fetal infection.
Leucovorin calcium (folinic acid)	Adults/pediatrics: Per maternal-fetal medicine or pediatric infectious diseases protocol, continued for the duration of pyrimethamine therapy	Generally well tolerated	None clinically significant at these doses	Mandatory alongside pyrimethamine in this regimen — rescues host bone marrow without rescuing the parasite; increase the dose (per specialist direction) if cytopenias develop rather than stopping it.

Toxoplasmic Encephalitis — Advanced HIV/AIDS or Other Severe Immunosuppression

A minimum 6-week acute course, then transition to a lower-dose secondary prophylaxis (maintenance) regimen continued until sustained immune reconstitution.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Pyrimethamine	Acute treatment: Loading dose on day 1, then a lower daily dose for a minimum of 6 weeks Secondary prophylaxis: Reduced maintenance dose, continued until sustained immune reconstitution	Bone marrow suppression, rash	Additive marrow suppression with other antifolate or myelosuppressive drugs	Reduce to a maintenance dose for secondary prophylaxis once acute treatment is complete.
Sulfadiazine	Acute treatment: Weight-based divided dosing per current OI treatment guideline, for a minimum of 6 weeks Secondary prophylaxis: Reduced maintenance dosing	Crystalluria, rash, hemolysis in G6PD deficiency, sulfa hypersensitivity	Additive crystalluria risk with dehydration	Substitute clindamycin if not tolerated — see the alternative regimen below.
Leucovorin calcium (folinic acid)	Acute treatment and secondary prophylaxis: Per current OI treatment guideline	Generally well tolerated	None clinically significant at these doses	Continued throughout both acute treatment and secondary prophylaxis for as long as pyrimethamine is used.

Sulfa-Allergic or Intolerant Alternative — CNS or Ocular Disease

Substituted for sulfadiazine when a genuine sulfonamide allergy or intolerance is present; pyrimethamine and folinic acid are retained.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Clindamycin	CNS disease (with pyrimethamine + folinic acid): Per current OI treatment guideline Ocular disease, intravitreal: Administered by ophthalmology per the injection protocol, not a routine oral prescribing decision	GI upset, rare C. difficile-associated diarrhea	None clinically significant at these doses beyond the general C. difficile risk of any antibiotic	Effective alternative to sulfadiazine, though it does not cover as broad a range of concurrent CNS pathogens; also used intravitreally (with dexamethasone) for ocular disease by ophthalmology.
Atovaquone	Treatment/prophylaxis: Per current OI treatment guideline, always taken with food	GI upset, rash	Must be taken with a fatty meal — absorption is meaningfully reduced without dietary fat	A further alternative when both sulfadiazine- and clindamycin-based regimens are not tolerated.

HIV — Primary Prophylaxis (Toxoplasma IgG-Positive, CD4 <100 cells/mm³)

Discontinue once CD4 count rises and is sustained above the threshold used for secondary-prophylaxis discontinuation, in coordination with the patient's HIV care team.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Sulfamethoxazole/trimethoprim	Adults: 1 double-strength tablet PO once daily, or per current OI prophylaxis guideline	Sulfa hypersensitivity, marrow suppression, hyperkalemia	Increased effect of warfarin; increased methotrexate toxicity; increased hyperkalemia risk with ACE inhibitors/ARBs/potassium-sparing diuretics	Preferred primary-prophylaxis agent — the same regimen already used for Pneumocystis jirovecii pneumonia prophylaxis in this population.
Dapsone	Adults: Prophylactic dosing per current OI prophylaxis guideline, with pyrimethamine + folinic acid	Hemolysis (screen for G6PD deficiency first), methemoglobinemia	Increased dapsone levels with trimethoprim; additive hemolysis risk with other oxidant drugs	Alternative when sulfamethoxazole/trimethoprim is not tolerated, combined with pyrimethamine and folinic acid at prophylactic doses.

Ocular Chorioretinitis — Vision-Threatening Lesion

Classic triple therapy for a lesion involving or threatening the macula, optic nerve, or major retinal vessels, or with significant vitritis; a small peripheral lesion in an immunocompetent host with no vision threat may reasonably be observed instead.

Drug	Dosage	Adverse effects	Drug interactions	Comments
Pyrimethamine	Adults: 200 mg PO once on day 1, then 50 mg PO once daily for approximately 4 weeks	Bone marrow suppression, rash	Additive marrow suppression with other antifolate or myelosuppressive drugs	Standard ocular-disease course is roughly 4 weeks; always with folinic acid.
Sulfadiazine	Adults: 2 g PO loading dose, then 1 g PO every 6 hours for approximately 4 weeks	Crystalluria, rash, hemolysis in G6PD deficiency, sulfa hypersensitivity	Additive crystalluria risk with dehydration	No oral sulfadiazine product exists in this database — see the note under the pregnancy/congenital regimen above.
Leucovorin calcium (folinic acid)	Adults: Approximately 3-25 mg PO several times weekly, per ophthalmology protocol, for the duration of antiparasitic therapy	Generally well tolerated	None clinically significant at these doses	Continued for the duration of pyrimethamine therapy; monitor CBC and increase the dose if cytopenias develop.
Prednisone	Adults: Typically 40 mg PO once daily, started ~3 days after antiparasitic therapy begins, then tapered per ophthalmology direction	Hyperglycemia, insomnia, mood change, GI upset	Increased hyperglycemia risk with other glucose-elevating drugs; increased GI bleed risk with NSAIDs	Start only after antiparasitic therapy is underway (roughly 3 days later) — never before or at the same time, to avoid unchecked organism proliferation.
Dexamethasone	Adults: Administered by ophthalmology per the intravitreal injection protocol	Injection-related effects, typical corticosteroid effects	None clinically significant for a single intravitreal administration	Intravitreal, ophthalmology-administered, with intravitreal clindamycin — an evidence-based alternative to the classic systemic regimen from a randomized trial, not a routine oral prescribing decision.

References

About Toxoplasmosis — Centers for Disease Control and Prevention. CDC, Toxoplasmosis
Clinical Care of Toxoplasmosis — Centers for Disease Control and Prevention. CDC, Toxoplasmosis
No. 285-Toxoplasmosis in Pregnancy: Prevention, Screening, and Treatment — Journal of Obstetrics and Gynaecology Canada, Society of Obstetricians and Gynaecologists of Canada (Paquet C, Yudin MH). J Obstet Gynaecol Can 2013;35(1):78-81 (Reaffirmed 2018)
Congenital Toxoplasmosis: The State of the Art — Frontiers in Pediatrics (Bollani L, Auriti C, Achille C, Garofoli F, De Rose DU, Meroni V, Salvatori G, Tzialla C). Front Pediatr 2022;10:894573
Toxoplasma gondii Encephalitis — Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV, National Institutes of Health / Centers for Disease Control and Prevention / HIV Medicine Association of the Infectious Diseases Society of America (Panel on Opportunistic Infections in Adults and Adolescents with HIV). NIH/CDC/HIVMA Adult and Adolescent OI Guidelines, current version
Randomized Trial of Intravitreal Clindamycin and Dexamethasone versus Pyrimethamine, Sulfadiazine, and Prednisolone in Treatment of Ocular Toxoplasmosis — Ophthalmology (Soheilian M, Ramezani A, Azimzadeh A, et al.). Ophthalmology 2011;118(1):134-141
A Meta-Analysis on Risks of Adverse Pregnancy Outcomes in Toxoplasma gondii Infection — PLoS ONE (Li XL, Wei HX, Zhang H, Peng HJ, Lindsay DS). PLoS One 2014;9(5):e97775

Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.