Overview.
Toxoplasmic encephalopathy is a parasitic disease of the brain caused by the protozoan Toxoplasma gondii and is the leading cause of death from toxoplasmosis. Because the blood-brain barrier prevents antibodies from entering the central nervous system, approximately 50% of patients with Toxoplasma gondii are associated with cerebral toxoplasmosis. Toxoplasmosis is classified as congenital or acquired according to the route of infection.
Etiology
Acquired toxoplasmic encephalopathy is mainly infected by eating undercooked meat, eggs and unpasteurized milk containing toxoplasmosis; it can also be infected through skin and mucous membrane injury or through blood transfusion or organ transplantation; contact with soil and water contaminated by oocysts is also an important means of transmission. Arthropods (flies, cockroaches) carrying oocysts can also be transmitted.
Classification
1. Acquired toxoplasmosis encephalopathy
The incubation period ranges from 3 days to 2 years. It can be a primary encephalopathy or part of systemic toxoplasmosis, and is most common in immunocompromised people. Clinical manifestations may include meningitis, diffuse encephalopathy, seizures, intracranial space-occupying lesions or mental abnormalities.
2. Congenital toxoplasmic encephalopathy
When pregnant women are infected, it may cause miscarriage, preterm labor or stillbirth. Surviving infants may have developmental abnormalities such as hydrocephalus, microcephaly, and mental defects.
Symptoms
Some patients with Toxoplasma gondii may have fever, myalgia, malaise, enlarged lymph nodes, liver and spleen. Choroiditis, iritis, retinitis, etc. may also occur; headache, nausea, vomiting, fundus optic papillae edema may occur in those with increased cranial pressure; hemiparesis and aphasia may occur in those with parenchymal brain damage.
Diagnosis
1. The clinical manifestations of toxoplasmosis are very complicated, and it is easy to miss and misdiagnose. The diagnosis of Toxoplasmosis encephalopathy is mainly confirmed by epidemiologic history, pathogenetic testing and imaging.
2. The imaging CT features of toxoplasmosis encephalopathy are cortical multilocular granulomas, striated or punctate calcifications in the basal ganglia, or bilateral symmetrical calcified shadows of the brain mainly around the ventricles and signs of hydrocephalus. MRI features irregular long T1 and long T2 abnormal signal areas in the periventricular white matter and cortical areas may be accompanied by hydrocephalus. Differential diagnosis should be differentiated from viral encephalitis, bacterial encephalitis and parasitic infections, intracerebral tumors, primary epilepsy, cerebrovascular lesions and psychiatric diseases.
Examination
1. Lumbar puncture cerebrospinal fluid examination: increased white blood cell count mainly of lymphocytes, accompanied by increased eosinophils and protein.
2. Serum and cerebrospinal fluid are positive for anti-toxoplasma antibodies.
3. Single or multiple hypodense lesions are seen on cranial CT.
4. Toxoplasma trophozoites are detected in cerebrospinal fluid, lymph nodes, and brain biopsy.
Treatment
1. Sulfadiazine
Oral or intramuscular injection. Combination of sulfisoxazole and sulfa potentiator (TMP) can enhance the efficacy.
2. Ethylaminopyrimidine
Administer in divided doses for 1 month.
3. Other treatments
Add prednisone or dexamethasone if choroidal optic neuritis is complicated. For immunocompromised patients, add levamisole or transfer factor. Seizures, increased cranial pressure and paralysis should be treated accordingly.
Prevention
1. Strengthen the monitoring and isolation of domestic animals, poultry and suspected animals.
2. Strengthen the quarantine of meat, dietary hygiene and management of raising cats, do not eat raw or half-raw meat, unsterilized dairy products, and make regular routine examination of toxoplasmosis for pregnant women in order to prevent the occurrence of congenital toxoplasmosis.
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