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Introduction
Demographics
Occurence
Clinical features
Diagnosis
Treatment
Outcome
Toxoplasmosis is a systemic zoonotic infection caused by the protozoan parasite Toxoplasma gondii.
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.
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 microscopic oocysts 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:
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 is one of the TORCH complex infections 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.
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.
Dermatological manifestations are rare.
Skin lesions of congenital toxoplasmosis:
Skin lesions of acute acquired toxoplasmosis:
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:
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. gondii DNA in amniotic fluid during pregnancy.
Patients with impaired immunity without evidence of prior T. gondii infection and pregnant women can take the following precautions:
Pretransplant serology screening of transplant donors and recipients is recommended. Chemoprophylaxis with cotrimoxazole for transplant recipients improves survival.
Treatment is required for:
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.
Reactivation of toxoplasmosis can be fatal in immunocompromised patients.