One in 150 Australians have retinal scars caused by the Toxoplasma parasite


One in 150 Australians have retinal scars caused by the Toxoplasma parasite, according to new Flinders University analysis.

With the condition putting people at risk of further attacks of toxoplasmosis that can progressively damage the retina and lead to vision loss, experts are calling for increased awareness of the risks of eating raw and undercooked meat.

Closely associated with cats, Toxoplasma is a parasite that causes the infectious disease known as toxoplasmosis. Many animals around the world are infected, generally contracting the disease in environments soiled by infected cats or by consuming other infected animals.

For humans, while domestic cat feces can be a carrier, the most common route of infection is by eating undercooked or raw meat sourced from infected livestock.

“Considering Australia’s substantial population of feral cats that are known to be infected, alongside high levels of farming and diets rich in meat, it’s imperative we understand the prevalence of the disease across the country,” says study senior author Professor Justine Smith, Strategic Professor in Eye & Vision Health at Flinders University.

“While there is no cure or vaccine, the symptoms of toxoplasmosis vary depending on the age, health and genetics of the infected individual. Many people are asymptomatic, but the most common disease that we see in the clinic is retinal inflammation and scarring known as ocular toxoplasmosis.

“Studies around the world show that 30% to 50% of the global population is infected with Toxoplasma, but despite knowing that, what we didn’t know was how common the related eye disease was.”

In the study, published in the journal Ophthalmology Retina, Professor Smith and her team analyzed retina photographs of more than 5,000 people living in the Busselton area in Western Australia, previously collected to evaluate the prevalence of glaucoma and age-related macular degeneration for a long-term healthy aging study.

Three specialized ophthalmologists, including Professor Smith, assessed the scans for toxoplasmic retinochoroiditis, with positive cases confirmed with antibody blood tests.

“Among the 5,000 people, we found eight participants with blood test-confirmed toxoplasmic retinal scars. Add to that that about three-quarters of the retinal lesions would be in a position not visible in these particular photographs, we were able to estimate the prevalence of ocular toxoplasmosis to be one per 149 persons,” says Professor Smith.

The work represents the first effort to quantify the rate of ocular toxoplasmosis in Australia, with the findings indicating the condition can be considered common.

With previous research showing the infection can lead to reduced vision in more than 50% of eyes and even blindness, the authors say it is important for people understand the risk factors of toxoplasmosis and ways to avoid it.

“While people are often familiar with pregnant women needing to avoid cat litter trays, we also need everyone to know that preparation of meat is an important risk factor,” says Professor Smith.

Research by Professor Smith in 2019 highlighted a high prevalence of Toxoplasma in Australian lamb sold in supermarkets.

“Add to that that it’s now becoming more common to prepare meat in and out of restaurants to be purposefully undercooked or raw, then the likelihood of people becoming infected with Toxoplasma increases.

“We need people to be aware this disease exists, so they can make informed decisions about how they prepare and eat their meet. The parasite can be killed easily by cooking the meat to an internal temperature of 66ºC (or medium) or by freezing it prior to cooking.”

The research follows on from a series of papers recently published by Professor Smith and team on the condition, including one that uses new technology retinal imaging to show the changes that occur in ocular toxoplasmosis at the tissue-level, and another that highlights the best clinical practice for managing the disease.

“Prevalence of Toxoplasmic Retinochoroiditis in an Australian Adult Population: a Community-Based Study,” by Lisia B. Ferreira, João M. Furtado, Jason Charng, Maria Franchina, Janet M. Matthews, Aus A.L. Molan, Michael Hunter, David A. Mackey and Justine R. Smith will be published in the journal Ophthalmology Retina.


Treatment of ocular toxoplasmosis remains controversial. Some clinicians do not treat small peripheral retinal lesions, while others treat all patients in order to reduce recurrences and complication rates. Typically, toxoplasmic retinochoroiditis in immunocompetent patients is expected to resolve within 1 to 2 months [117].

Taking into account the benign natural course and the possibility of toxicity to the antiparasitic drugs, the therapeutic approach of each individual with active infection would probably lead to unnecessarily high rates of drug-induced morbidity. Subsequently, treatment is adjusted to each patient individually. The decision of commencing treatment in cases of active retinochoroiditis is based on several parameters. Some of the most important are the following:

Patients’ immune status

Characteristics of the active lesion (i.e., location and size)

  • Visual acuity
  • Clinical course
  • Grading of vitreous haze
  • Macular edema
  • Edema of the optic disk
  • Vascular occlusion
  • Possible adverse effects of available drugs
  • Other parameters (newborns, pregnancy, allergies).

The treatment of ocular toxoplasmosis includes both antimicrobial drugs (Table ​(Table3)3) and corticosteroids (topical and oral) and is maintained for 4–6 weeks. The main target of the antimicrobial treatment at the stage of active retinitis is to control the parasites’ multiplication [118]. Currently, the number of randomized control trials in the setting of toxoplasmic retinochoroiditis is restricted [119]. Another issue regarding the therapeutic approach of chronic infections is the fact that antiparasitic drugs may be ineffective against tissue cysts [120].

Table 3

Available drug options for toxoplasmosis

MedicationAdult dosePediatric dose
PyrimethamineLoading dose: 100 mg (1st day)Treatment dose: 25 mg twice daily for 4–6 weeksInfants1 mg/kg once daily for 1 yearChildrenLoading dose: 2 mg/kg/day divided into 2 daily doses for 1–3 days (maximum: 100 mg/day)Treatment dose: 1 mg/kg/day divided into 2 doses for 4 weeks; (maximum: 25 mg/day)
Folinic acid15 mg daily5 mg every 3 days
Trimethoprime—sulfamethoxazolOne tablet twice daily for 4–6 weeks6–12 mg TMP/kg/day in divided doses every 12 h
Sulfadiazine4 g daily divided every 6 hCongenital toxoplasmosisNewborns and Children < 2 months: 100 mg/kg/day divided every 6 hChildren > 2 months: 25–50 mg/kg/dose 4 times/dayToxoplasmosis in children > 2 monthsLoading dose: 75 mg/kgTreatment dose: 120–150 mg/kg/day, divided every 4–6 h (maximum dose: 6 g/day)
Clindamycin150–450 mg/dose every 6–8 h (maximum dose: 1.8 g/day) (usually 300 mg every 6 h)8–25 mg/kg/day in 3–4 divided doses
AzithromycinLoading dose: 1 g (1st day)Treatment dose: 500 mg once daily for 3 weeksChildren ≥ 6 months: 10 mg/kg on first day (maximum: 500 mg/day) followed by 5 mg/kg/day once daily (maximum: 250 mg/day)
Spiramycin2 g per day in two divided doses15 kg = 750 mg20 kg = 1 g30 kg = 1.5 g
Atovaquone750 mg every 6 h for 4–6 weeks40 mg/kg/day divided twice daily (maximum dose: 1500 mg/day)
TetracyclineLoading dose: 500 mg every 6 h (first day)Treatment dose: 250 mg every 6 h for 4–6 weeksChildren > 8 years: 25–50 mg/kg/day in divided doses every 6 h
Minocycline100 mg every 12 h not to exceed 400 mg/24 h for 4 to 6 weeksChildren > 8 yearsInitial: 4 mg/kg followed by 2 mg/kg/dose every 12 h (Oral, I.V.)
g, gram; I.V., intravenous; kg, kilogram; mg, milligram; TMP, trimethoprime
Modified from: Bonfioli and Orefice [99] and readjusted according to the protocols of the Department of Ophthalmology (Ocular Inflammation Service) of the University Hospital of Ioannina, Greece

The first choices include one of the following combination regimens: (1) pyrimethamine, sulfadiazine, folinic acid and prednisone; (2) pyrimethamine, clindamycin, folinic acid and prednisone; (3) pyrimethamine, sulfadiazine, clindamycin, folinic acid and prednisone. Trimethoprim-sulfamethoxazole can also be a good alternative of sulfadiazine concerning first choice combination regimens. Alternative combination regimens include: (1) trimethoprim—sulfamethoxazole and prednisone; (2) clindamycin, spiramycin, and prednisone; (3) clindamycin, sulfadiazine, and prednisone; (4) pyrimethamine, azithromycin, folinic acid and prednisone; (5) pyrimethamine, atovaquone, folinic acid and prednisone; (6) sulfadiazine, atovaquone and prednisone; (7) tetracycline and prednisone; (8) minocycline and prednisone [93, 121]. The exact therapeutic drug regimens are summarized in Table ​Table22.

The ‘classic therapy’ consists of pyrimethamine, sulfadiazine and a systemic corticosteroid (most commonly prednisone) [122]. It was found that none of three therapies (i.e., Classic therapy; Clindamycin with sulfadiazine and oral steroid; Trimethoprim with sulfamethoxazole and oral steroid) reduced the duration of posterior pole retinitis compared to control subjects with peripheral lesions that received no treatment [118]. Additionally, treatment did not affect the rates of recurrence. However, it was shown that the classic regimen was more effective in the reduction of the size of the lesion(s) in comparison with treatments or no treatment. The same study reported that the classic treatment may be more suitable for foveal or adjacent to the fovea lesions. [118].

The use of pyrimethamine and sulfadiazine for treating ocular toxoplasmosis was introduced in the 1950s [28]. The possibility of medication-related adverse events (including gastrointestinal and dermatological side effects, leukopenia and thrombocytopenia) should always be taken into account. Therefore, blood testing should be carried out every week throughout treatment and folinic acid must be also prescribed [48]. Sulfadiazine is a sulfonamide antimicrobial that can cause hypersensitivity reactions, such as skin rashes.

Trimethoprim-sulfamethoxazole is defined by good tolerability, wide availability and low cost. However, sulfonamide-related reactions may occur [122]. Trimethoprim-sulfamethoxazole with prednisone was found to be relatively well-tolerated, but as effective as the classic therapy in the reduction in lesions’ size [118]. In contrast, a relevant study reported comparable outcomes among trimethoprim-sulfamethoxazole with prednisolone and classic therapy in two randomized groups [123]. Additionally, the role of trimethoprim-sulfamethoxazole in preventing the recurrences of toxoplasmic retinochoroiditis calls for further investigation [124].

Clindamycin can be added to the triple regimen, converting it to ‘quadruple therapy’ [122], which has been found to improve vision and/or intraocular inflammatory markers [125]. On the contrary, Rothova et al. [118] reported a smaller reduction in lesion size in those treated with clindamycin, sulfadiazine and corticosteroid compared to the classic therapy. Pseudomembranous colitis can be caused by clindamycin, and diarrhea consists an indication for cessation of the drug. The intravitreal use of clindamycin and dexamethasone has been also assessed by recent studies. [126–129]. A substantially larger reduction in size of lesions was found in T. gondii IgM-positive patients who were treated with classic treatment in comparison with those who received intravitreal treatment [129]. Topical treatment seems to be suitable for individuals with recurrent infection, due to the concerns regarding systemic drug toxicities. On the other hand, this approach would not be recommended in patients with immunodeficiency (e.g., HIV-patients) due to the risk of fulminant disease [130]. Intravitreal treatment (1 mg clindamycin with or without 400 μg dexamethasone) [128] may also be necessary in cases with fovea involvement or active lesion(s) within zone 1 as an adjunctive to systemic therapy [129, 131].

Two other antiparasitic drugs, atovaquone and azithromycin [93, 122], were found to have promising results in experimental studies, but do not show favorable outcomes in preventing recurrences of retinochoroiditis in humans.

The comparison of the efficacy of classic therapy and pyrimethamine plus azithromycin showed no difference between the two groups but the adverse events in those treated with azithromycin were less frequent and less severe [132].

Although their benefit has been completely delineated, systemic steroids can be added to the therapeutic regimen against toxoplasmic retinochoroiditis. However, the doses prescribed and timing of administration may widely differ among uveitis specialists. Corticosteroids are usually initiated 3 days after the start of antibiotic therapy and must be suspended at least 10 days before the antimicrobial drugs [133]. If given without antimicrobials (e.g., in cases of initial misdiagnosis or atypical presentation), systemic steroids can lead to legal blindness in most patients [133]. Systemic corticosteroids are usually avoided in immunocompromised patients [122]. This category of patients is treated with a maintenance antimicrobial therapy while being immunocompromised (e.g., trimethoprim-sulfamethoxazole). Periocular corticosteroid injections are generally unpopular [122], as their administration has been correlated to detrimental results, especially in patients that have not received an antiparasitic therapy [134]. Intravitreal administration of relatively short-acting dexamethasone has been successfully combined with clindamycin. Intravitreal injection of triamcinolone acetonide, which is longer acting, has not been widely practiced [135], and therefore, there is no standard consensus on this approach [136].

Steroid eye drops are widely prescribed for controlling anterior uveitis [122]. Their frequency depends on the severity of inflammatory activity in the anterior segment. Apart from topical steroids, mydriatics and hypotensive agents are also added when required. Mydriatics are important for the prevention of posterior synechiae (or breaking them if they have already developed) and for pain relief.

Immunocompromised patients are treated with the antimicrobial regimens described above, for 6 or more weeks. After complete resolution of the lesions, the patient starts on secondary prophylaxis, with sulfadiazine, pyrimethamine and folinic acid or clindamycin, pyrimethamine and folinic acid. In asymptomatic individuals with a CD4 count above 200 cells/μL for six months or more, prophylaxis for toxoplasmosis can be stopped, but patients must be followed up for detecting signs of recurrence [93]. In HIV patients with toxoplasmic retinochoroiditis, neuroimaging is crucial to rule out central nervous system (CNS) toxoplasmosis lesions. Treatment includes ongoing suppressive therapy with pyrimethamine and sulfadiazine [137].

In pregnancy, the highest risk regarding the adverse effects of antiparasitic drugs is during the first trimester [138]. Consequently, a multidisciplinary assessment between the ophthalmologist, the obstetrician and an infectious disease physician is vital in cases where an intervention is required.

A serological investigation is necessary in women with toxoplasmic chorioretinitis during pregnancy, to define when the infection was acquired. Reactivation of a latent infection (acquired before gestation) leading to toxoplasmic chorioretinitis does not present a higher risk for transmission of T. gondii to their offspring compared to pregnant women with an acquired infection before gestation but no signs of active ocular toxoplasmosis [139].

When a toxoplasmic retinochoroiditis is attributed to a recently acquired infection, treatment must be administered not only for treating the ophthalmic disease but also for reducing the risk of transmission to the fetus [140]. During pregnancy, the therapeutic regimens are: (1) First trimester: spiramycin, and sulfadiazine; (2) Second trimester (> 14 weeks): spiramycin, sulfadiazine, pyrimethamine, and folinic acid; (3) Third trimester: spiramycin, pyrimethamine and folinic acid. Medications are given in lower doses for three weeks and can be repeated, if required, after 21 days [121].

Moreover, treating the mother lessens the possibility of congenital transmission. Classic therapy is contraindicated as pyrimethamine is considered to be teratogenic and sulfadiazine can cause bilirubin encephalopathy [141]. Clindamycin and azithromycin or clindamycin and atovaquone (± systemic corticosteroid) are discussed as alternatives [141]. The recurrences of toxoplasmic retinochoroiditis pose minimal risk to the embryo. Thus, preventing vertical transmission alone is not an indication for treatment [142].

When a toxoplasmic infection occurs during or immediately before pregnancy, the risk of transmission to the fetus and congenital toxoplasmosis is significantly higher. This condition requires coordinated management together with a perinatologist, for a more detailed approach, the reader is referred to the study of Montoya and Remington [140].

The severity of toxoplasmic retinochoroiditis is multifactorial and varies widely in different geographical areas. Due to the increased risk of detrimental intraocular complications, the lack of large controlled studies does not justify changes to the standard therapy for this clinical entity.

Two surveys of the American Uveitis Society (AUS), in 1991 [143] and 2001 [122], highlighted a substantial shift in favor of treating both mild and severe disease [122]. Atypical presentations and immunocompromisation are considered as an indication for commencing treatment [44]. Well-designed large interventional studies are required to shed more light on the therapeutic approach of ocular toxoplasmosis.

reference link :

More information: Lisia B. Ferreira et al, Prevalence of Toxoplasmic Retinochoroiditis in an Australian Adult Population: a Community-Based Study, Ophthalmology Retina (2022). DOI: 10.1016/j.oret.2022.04.022


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