Contents
Cysticercosis, also called cysticercosis, is a disease caused by infection with the larval form of the armed tapeworm (Taenia solium).
Wągrzyca – how do we get infected?
Cysticercosis is infected by eating armed tapeworm eggs previously excreted by the same or another person. It also happens to be self-invasive – in a person who is the ultimate host of armed tapeworms, the contents of the intestine, including eggs, may become refluxed into the stomach. Wągrzyca occurs all over the world, the highest incidence is recorded in Latin America, Southeast Asia, Africa and the Middle and Middle East.
Armed tapeworm (Taenia solium) is a larva that infects Wągryca. It is 3-5 m long, its only definitive host is humans. Tapeworm larvae – blackheads – are typically found in pigs, and humans are only an occasional intermediate host. They are several or several millimeters in diameter, and are located in the muscles, subcutaneous tissue, central nervous system, and also in the eye.
Cysticosis – the mechanism of its formation
In the stomach, oncospheres hatch from eggs, penetrate the intestinal mucosa, and then enter various organs with blood. There they settle down and transform into blackheads – the larval form of the tapeworm. Carrots have the ability to modulate the host’s immune response by secreting prostaglandins and other substances that inhibit the activation of the complement system and the secretion of cytokines.
Over time, these properties weaken, leading to onset host inflammatory response on the parasite. Inflammatory infiltrates appear especially in the central nervous system and lead to the death of the parasite. Eosinophilic granulomas form around the dead parasites, often surrounded by a swollen zone. Over time, the lesions become fibrotic or calcified and the inflammatory reaction dies out.
Cysticosis – symptoms
The larvae are found in various tissues, but only their localization in the central nervous system or in the eye leads to the occurrence of a clinically evident disease. Carrots in muscle or subcutaneous tissue are detected quite often, usually accidentally, on imaging examinations, usually as diffuse calcifications or palpable as subcutaneous nodules. Most often they do not cause any ailments or symptoms.
Neurocysticercosis, i.e. cysticercosis of the central nervous system, manifests itself with numerous clinical symptoms, depending on the location of the lesions, the number and vitality of cysticeps. Wagry can be located in:
- nerve tissue in the brain or in the meninges
- fluid spaces,
- vascular plexuses.
Typically, the most common consequence of neurocysticercosis is increased intracranial pressure, accompanied by the formation of internal hydrocephalus. The condition develops slowly, causing non-specific symptoms such as:
- headaches,
- nausea,
- dizziness.
Long-lasting intracranial hypertension leads to atrophy of the cerebral cortex, and thus – to dementia. There are also sudden, fast-growing ones symptoms of hydrocephalus, sometimes life-threatening. A common symptom of cerebral cysticercosis are also seizures. Cysticercosis is the most common cause of adult-onset seizures in countries where cysticercosis is endemic.
In rare cases, when locating tire changes, it is found chronic meningitis. It is also observed focal symptoms. Although nearly all possible combinations of these symptoms in the course of neurocysticercosis have been described, they come to the fore pyramidal symptoms. The worms located in the spider’s mantle on the base of the brain can paralyze the cranial nerves. Localization of lesions in the spinal cord is uncommon, but may be associated with severe symptoms associated with compression of the spinal cord.
In the eye, blackheads are usually located in the vitreous body, in the retina, or under the retina. The inflammatory reaction around degenerating parasites leads to:
- trouble seeing,
- visual field limitations,
- inflammation of the retina and choroid,
- retinal detachment.
How do we recognize cysticercosis?
The diagnosis of cysticercosis of the central nervous system is mainly based on imaging studies:
- computed tomography,
- nuclear magnetic resonance.
The most characteristic are multiple hypodense – small cystic lesions with an inflammatory zone surrounding them, not enhancing after contrast administration. There are also intracerebral calcifications.
Serological tests are of limited importance, ELISA tests and immunoblot are used. Finding specific antibodies in the cerebrospinal fluid is of greater diagnostic value.
- In most active cases of disease, a general examination of the fluid shows moderate mononuclear pleocytosis with elevated levels of protein and, most often, normal glucose levels.
- The lugs in the muscles are detected by X-ray examinations in the form of multiple calcifications.
- Parasites in the eye are detected by ophthalmoscopy.
- Cysticercosis of the subcutaneous tissue offers the possibility of histopathological and parasitological confirmation of the infection.
As some cases of cysticercosis are associated with autoinvasion, execution is advisable stool parasitological examination to detect possible armed tapeworm eggs and members. Such tests should be performed in all household members and people in the immediate vicinity of the patient.
Differentiation in the diagnosis of cysticercosis
The variety of clinical symptoms of cysticercosis may pose diagnostic difficulties. Neurocysticercosis should be differentiated from both primary and metastatic neoplasms of the central nervous system.
In addition, a picture of brain calcification similar to that found in neurocysticercosis can be found in:
- tuberculosis,
- disseminated histoplasmosis,
- toxoplasmosis,
- CMV infection,
- other neuroinfections.
In turn, cysticercosis of the subcutaneous tissue may be confused with multiple lipomas, while muscle cysticercosis requires differentiation from trichinosis.
Treatment of cysticercosis
Only neurocysticercosis and cysticercosis of the eye require treatment!
In cysticercosis of the central nervous system, in cases where the location of the lesions allows it, neurosurgical treatment is used, consisting in removing the parasite. In cases of hydrocephalus or increased intracranial pressure, the use of ventricular peritoneal or ventricular atrial valves is necessary.
Specific conservative treatment consists in administering praziquantel at a dose of 50 mg / kg bw daily in 3 divided doses for 10-14 days or albendazole at the dose of 15 mg / kg bw daily in 2 doses for 8-15 days. This treatment carries the risk of worsening of the patient’s general condition due to cerebral edema, which often occurs in 2-5 years. on the day of treatment as a result of an inflammatory reaction to decaying parasites. For this reason, treatment should be carried out in a hospital setting. Often, corticosteroids are given concomitantly to reduce the severity of the inflammatory response.
Antiepileptic drugs are also symptomatic. Surgical removal of the lesion is the treatment of choice in cysticercosis. Sometimes anti-inflammatory therapy is introduced, usually specific treatment is not used.
What’s the prognosis?
In cases with hydrocephalus, the prognosis for cysticercosis is serious. Concomitant chronic meningitis often leads to clogging of the valve system, which usually requires reoperation and significantly increases the risk of death. However, in some patients, despite anticonvulsant treatment, these symptoms persist.
Usually asymptomatic cases have a good prognosis, spontaneous disappearance of changes occurs. Keep in mind that visual damage in ocular cysticercosis is often irreversible, although complete loss of vision is rare.
Literature
1. Del Brutto OH: Neurocysticercosis, Semin Neurol 2005; 25(3): 243-251.
2. Garcia HH, Gonzalez AE, Evans CAW, Gilman RH: Taenia solium cysticercosis, Lancet 2003; 362: 547-556.
Source: J. Cianciara, J. Juszczyk, Infectious and parasitic diseases; Czelej Publishing House