Toxoplasmosis is a systemiczoonoticinfection caused by the protozoanparasiteToxoplasma gondii.
Who gets toxoplasmosis?
T gondii infects up to one-third of the world's population. Prevalence of the infection varies with the age of the population studied and by geographic location. The likelihood of having antibodies to T gondii present in the blood (indicating past infection) increases with increasing age. In New Zealand, around 20% of people aged 16–24 and 34% of people aged 25–44 years have had past infection with T. gondii.
How does infection with toxoplasmosis occur?
T. gondii is an intestinal parasite of cats, but can infect virtually all warm-blooded vertebrates. Cats become infected by eating infected rodents, birds, or other small animals. The cat then sheds millions of microscopicoocysts in its faeces for 1–3 weeks. Mature cats are unlikely to shed T. gondii if they have been previously infected. Humans can become infected via the following routes of transmission:
Foodborne transmission is the most common — ingestion of the parasiticcysts in undercooked, contaminated meat (especially pork, lamb, and venison) or poor kitchen hygiene when handling raw contaminated meat.
Zoonotic (animal-human) transmission — accidental ingestion of oocysts in cat faeces for example, after cleaning a cat's litter box, after gardening, or eating unwashed fruit or vegetables from a garden.
Congenital (mother-child) transmission — a pregnant woman who acquires a new infection with T gondii can pass the infection to her unborn child. The incidence of congenital toxoplasmosis is approximately 1 per 1000 live births in the United States. Generally if a woman has previously been infected with T gondii and is exposed again during pregnancy, the unborn child will be protected because the mother will already have immunity. If a pregnant woman has impaired immunity, reactivation of T gondii infection can lead to congenital infection.
Rarely T gondii can be transmitted via organ donation or blood transfusion.
What are the clinical features of toxoplasmosis?
In healthy individuals, infection with T. gondii goes unnoticed. Some people (around 10%) experience 'flu-like symptoms with enlarged lymph nodes and, in rare instances, chorioretinitis (inflammation in the eye). Very rarely, myocarditis, pneumonitis, or encephalitis may occur. After an acute infection the parasite remains in the body in an inactive (encysted) state and can become reactivated if immunity is impaired.
In patients with impaired immunity (for example, drug-induced immunosuppression, HIV/AIDS) toxoplasmosis can be life-threatening. The illness is usually caused by reactivation of chronic infection. Encephalitis and pneumonitis is common in these patients.
Congenital toxoplasmosis
Congenital toxoplasmosis is one of the TORCH complexinfections and has a range of clinical presentations, from mild to severe disease. Symptoms may be present in the newborn period or may not be apparent for many years. Infection is more severe if the transmission is in early pregnancy. Congenital T. gondii infection can result in miscarriage, stillbirth, or neonatal death. Most affected newborns are symptom-free at birth; however 10% have chorioretinitis with blindness and in 20% there is more generalised disease (such as fever, anaemia, jaundice, and enlargement of the liver and spleen) or neurological symptoms (deafness, seizures, and intellectual disability). Chorioretinitis and other neurological symptoms may develop later in life.
Eye disease in toxoplasmosis
Toxoplasmosis eye disease (chorioretinitis) can result from congenital or acquired (eg, foodborne or zoonotic) T. gondii infection. Eye infection leads to acute inflammation of the retina, which resolves leaving scarring. The eye disease can reactivate months or years later, each time causing more damage to the retina. Symptoms include eye pain, blurred vision, photophobia, and blindness.
Lesions may be telangiectaticmacules, papules, or vesicles
Cases of acute dermatomyositis-like syndrome have been described.
How is toxoplasmosis diagnosed?
The diagnosis of toxoplasmosis is usually made by serology, ie, the detection of Toxoplasma-specific antibodies in the blood. Several tests are available to detect these antibodies within several weeks of infection:
Dye test
Indirect fluorescent antibody test
Enzyme immunoassays (ELISA).
Serologic tests may be unreliable in patients with impaired immunity.
Diagnosis can also be made by direct observation of T. gondii in stained tissue sections, cerebrospinal fluid (CSF), blood, or other biopsy material including skin. [see Toxoplasmosis pathology]
Polymerase chain reaction (PCR) can be used to detect T. gondiiDNA in amniotic fluid during pregnancy.
What is the treatment for toxoplasmosis?
Prevention
Patients with impaired immunity without evidence of prior T. gondii infection and pregnant women can take the following precautions:
Avoid eating undercooked meat and eggs, and unpasteurised milk
Wash hands after touching raw meat and practice good kitchen hygiene
Wash fruits and vegetables before eating
Wash hands after gardening or handling soil
Avoid contact with cat faeces.
Pretransplant serology screening of transplant donors and recipients is recommended. Chemoprophylaxis with cotrimoxazole for transplant recipients improves survival.
Specific measures
Treatment is required for:
Acute infection
Active lesions caused by T. gondii (for example, in the skin or eye)
Congenital infection
Toxoplasmosis in patients with impaired immunity.
The most effective treatment is sulfadiazine in combination with pyrimethamine. For patients allergic to sulfonamides, clindamycin is used. Trimethoprim plus sulfamethoxazole is used for immunocompromised patients with central nervous system disease. Ivermectin has been reported to be effective in an immunocompetent host.
Currently recommended medications treat the active form of T gondii (tachyzoite stage), but do not eradicate the inactive, encysted form of the parasite.
What is the outcome of toxoplasmosis?
Reactivation of toxoplasmosis can be fatal in immunocompromised patients.
References
Adhikari M, Dhakal S, Bhattarai S, Rai U. Toxoplasmosis presenting as nonhealing cutaneous ulcer. Case Rep Pathol. 2020;2020:8874800. doi:10.1155/2020/8874800 Journal
Lupi O, Bartlett BL, Haugen RN, et al. Tropical dermatology: tropical diseases caused by protozoa [published correction appears in J Am Acad Dermatol. 2009 Dec;61(6):1059]. J Am Acad Dermatol. 2009;60(6):897–928. doi:10.1016/j.jaad.2009.03.004 PubMed
Rand AJ, Buck AB, Love PB, Prose NS, Selim MA. Cutaneous acquired toxoplasmosis in a child: a case report and review of the literature. Am J Dermatopathol. 2015;37(4):305–10. doi:10.1097/DAD.0000000000000072 PubMed
Robert-Gangneux F, Meroni V, Dupont D, et al. Toxoplasmosis in transplant recipients, Europe, 2010-2014. Emerg Infect Dis. 2018;24(8):1497–1504. doi:10.3201/eid2408.180045 Journal