TOXOPLASMOSIS

Protozoal Uveitis

AAO READING 2021

DEFINITION

• Toxoplasmosis is the most common cause of infectious

posterior uveitis in adults and children. It is caused by the
parasite Toxoplasma gondii, a single-cell obligate intracellular
apicomplexan parasite with a worldwide distribution.
• Felines are the definitive hosts of T gondii, and humans and a
variety of other animals serve as intermediate hosts.
 LIFE CYCLE

T gondii has a complex life cycle and exists in

3 major forms:
• Oocyst, or soil form (10–12 μm), which
contains sporozoites
• Tachyzoite, or infectious form (4–8 μm)
• Tissue cyst, or latent form (10–200 μm),
which contains as many as 3000
bradyzoites
Human infection by T gondii may be either acquired or congenital. The principal
modes of transmission include :
• ingestion of undercooked, infected meat containing tissue cysts
• ingestion of contaminated water, fruit, or vegetables with oocysts
• inadvertent contact with cat feces, cat litter, or soil containing oocysts transplacental
transmission with primary infection during pregnancy
• blood transfusion or organ transplantation
Histology
 EPIDEMIOLOGI

• As of this writing, the CDC estimates that 11% of the United States population age 6 and
older has been infected with T gondii. Of that group, 2% may develop ocular
toxoplasmosis.

• The American Academy of Pediatrics estimates that the incidence of primary infection
during pregnancy in the United States is approximately 0.2–1.1 per 1000 pregnant
women, translating to 800–4400 women per year with acute T gondi infection during the
4 million yearly pregnancies in the U.S.
Pregnant women without serologic evidence of T gondii infection should be advised to take the
following precautions:
• Avoid ingestion of raw/undercooked meat (freezing at −20°C/−4°F overnight also destroys tissue
cysts).
• Drink only well-filtered or boiled water.
• Carefully wash vegetables and fruits before consumption.
• Use gloves and wash hands and kitchen utensils well after handling meat or soil.
• Avoid contact with felines and their feces (including in soil or litter boxes).
Classic Presentation of Congenital Toxoplasmosis

• Retinochoroiditis
• Hydrocephalus or microcephaly
• Intracranial calcification and cognitive impairment (Sabin’s tetrad)
occurs in less than 10% of infected children
Retinochoroidal lesions (80%) case

• the most common abnormality in patients with congenital toxoplasmosis.

• Lesions are bilateral in approximately 85% of affected individuals and carry a predilection
for the posterior pole and macula
• Posterior segment involvement may be subclinical and chronic.
• As many as 85% of infected children develop retinochoroiditis after a mean of 3.7 years, and
25% of these become blind in 1 or both eyes. Most experts recommend antiparasitic therapy
for newborns with congenital toxoplasmosis during the first year of life to reduce disease
burden, regardless of the presence of ocular and/or systemic signs.
Kyrieleis arteriolitis
• Retinochoroiditis developing in
immunocompromised and older patients may
present with atypical findings, including
large, multiple, and/or bilateral lesions, with
or without associated retinochoroidal scars.
This more severe clinical picture can also
occur in patients receiving steroids without
concomitant antiparasitic therapy (Fig 11-
31).
Ocular toxoplasmosis may simulate herpetic
ARN. Other atypical presentations include
neuroretinitis, punctate outer retinal
toxoplasmosis (PORT), unilateral pigmentary
retinopathy simulating retinitis pigmentosa, and
other forms of intraocular inflammation in the
absence of retinochoroiditis. Characteristics of
PORT include small, multifocal lesions at the
level of the outer retina, with exudation to
subretinal space and scant overlying vitreal
inflammation (Fig 11-32).
Diagnosis

In most cases, toxoplasmic retinochoroiditis is clinically diagnosed on the basis

of :
• the characteristic fundus lesion.
• Positive serologic testing for anti–T gondii IgG or IgM confirms exposure to the
parasite.

• The presence of IgM in newborns confirms congenital infection and indicates

acquired disease in adults. In cases of diagnostic uncertainty, PCR testing of
aqueous humor and vitreous fluid may be performed.
Treatment

• in the immunocompetent patient, the disease can have a self-limiting course.

The borders of the lesions become sharper and less edematous over a 6–8-
week period without treatment, and RPE hyperplasia occurs gradually over a
period of months.

• In the immunocompromised patient, the disease is often more severe and

progressive. Treatment can shorten the duration of parasitic replication,
leading to more rapid cicatrization and ultimately a smaller retinochoroidal
scar. Treatment may also reduce the frequency of inflammatory recurrences
and minimize structural complications associated with intraocular
inflammation.
Relative treatment indications include
• lesions threatening the optic nerve or fovea
• decreased visual acuity
• lesions associated with moderate to severe vitreous inflammation
• lesions greater than 1 disc diameter in size
• persistence of disease for more than 1 month
• presence of multiple active lesions
 • Treatment is indicated in immunocompromised patients (those with HIV/AIDS, with
neoplastic disease, or undergoing IMT), patients with congenital toxoplasmosis, and
pregnant women with recently acquired disease.
• The classic regimen for the treatment of ocular toxoplasmosis consists of 4–8 weeks of
pyrimethamine (loading dose, 50–100 mg; treatment dose, 25–50 mg/day) and
sulfadiazine (treatment dose, 1 g, 4 times/day). Pyrimethamine has recently become
prohibitively expensive. Folinic acid (5–10 mg/day) is added to prevent
myelosuppression (leukopenia and/or thrombocytopenia), which may result from
pyrimethamine therapy
• Potential adverse effects of sulfa compounds include skin rash, gastrointestinal intolerance, crystalluria,
kidney stones, and Stevens-Johnson syndrome.

A complete blood count may be checked approximately every 2 weeks during therapy.
• Clindamycin (300 mg, 4 times/day) may be added to the above
regimen or substituted for sulfadiazine in the case of sulfa allergy.
• Clindamycin, either alone or in combination with other drugs, has
been effective in managing acute lesions, but pseudomembranous
colitis is a potential complication.
• Clindamycin (1 mg/0.1 mL) may also be intravitreally injected in
an off-label fashion, either in combination with systemic therapy or
as monotherapy in patients who do not tolerate systemic therapy.
• Many ophthalmologists utilize trimethoprim-sulfamethoxazole (160
mg/800 mg, 2 times/day) because of its accessibility, simplicity of
administration, and cost.
• Azithromycin (500 mg daily) or atovaquone (750 mg, 2–4 times/day) may
take the place of sulfadiazine or clindamycin
• Systemic corticosteroids (approximately 0.25–0.75
mg/kg, typically not to exceed 60 mg/day) may be
considered after 48 hours of antimicrobial therapy
in immunocompetent patients. The use of systemic
corticosteroids without appropriate antimicrobial
coverage or the use of long- acting periocular and
intraocular corticosteroid formulations such as
triamcinolone acetonide is contraindicated because
of the potential for severe panophthalmitis and
loss of the eye (see Fig 11-31).
• Topical corticosteroids, however, are used liberally in the presence of
prominent anterior segment inflammation. Systemic corticosteroid
treatment may be used for 3–5 weeks, at which time inflammation begins to
subside and the retinal lesion shows signs of early cicatrization.
Antimicrobial coverage should be continued for the entire period of
systemic corticosteroid use.

• Newborns with congenital toxoplasmosis are commonly treated with

pyrimethamine and sulfonamides (plus folinic acid) for 1 year, in
consultation with a specialist in pediatric infectious diseases.
In cases of newly acquired toxoplasmosis during pregnancy,
treatment is given to prevent infection of the fetus and limit fetal
• Spiramycin (treatment dose, 400 mg 3 times/day)
• alternative medications may be needed; options include
azithromycin, clindamycin, and atovaquone (treatment dose,
750 mg every 6 hours). Sulfonamides may be used safely in the
first 2 trimesters of pregnancy.
 Thank you 

HMR, 24/11/2021