[Human plerocercoidosis and sparganosis: II. A historical review on pathology, clinics, epidemiology and control].

This article is the second part of the previous review and summarizes the research advances on pathology, clinical manifestation, diagnosis, treatment, epidemiology, and control of human plerocercoidosis and sparganosis.

[Human plerocercoidosis and sparganosis: I. A historical review on aetiology].

Plerocercoid should not be confused with Sparganum. The scolex of plerocercoid has a bothrium or bothrial slit but there is no true scolex in sparganum. Plerocercoid is a developmental stage of an animal tapeworm, genus Spirometra. Sparganum is another generic name of a pseudophyllidean cestode. Plerocercoid causes benign plerocercoidosis and sparganum causes "malignant sparganosis". Plerocercoidosis is a parasitic zoonosis which can be food-borne, water-borne, contact-borne or mother-borne. During the past 20 years, there has been significant progress in studies of human plerocercoidosis and sparganosis, especially the former. Spirometra erinacei-europiea plerocercoidosis and sparganosis prolifera distributed mainly in East Asia. Spirometra mansonoides plerocercoidosis has been reported from the USA. Up to the present, approximately 1400 cases of plerocercoidosis were reported from China, Japan, Korea, USA and Thailand, and at least 16 well-documented cases of human proliferating sparganosis were reported worldwide (in Japan, China, Thailand, USA, Paraguay, Venezuela, and the Philippines). The life cycle of Sparganum is unknown. For plerocercoid, human being acts as a dead-end hosts, copepod and frogs serve as intermediate hosts, and snakes and carnivorous animals are its paratenic hosts. This review summarizes the research progress on aetiology and pathogenesis of human plerocercoidosis and sparganosis. The second part (in press) will be concentrated on their pathology, clinical manifestations, diagnosis, treatment, epidemiology, control and prevention.

[Clinical study on the treatment of severe neurocysticercosis].

OBJECTIVE: To determine the therapeutic efficacy of albendazole combined with surgical intervention on intracranial hypertension in the treatment of severe neurocysticercosis. METHODS: Seventy-four consecutive patients with severe neurocysticercosis were confirmed by neuroimaging techniques (CT and/or MRI) and ELISA for the detection of antibody to cysticerci of Taenia solium. The number of cysticerci in the brain ranged from 100 to 1160. All patients were treated with albendazole by dose-decreasing regimen. Initial tolerable dosage was defined by dose-decreasing progressively, depending on the total number of cysticerci; then the dose of albendazole was increased progressively, and ultimate dosage was 20 mg per kilogram of body weight daily. Albendazole was taken for 3-4 courses (10 days as a course). Drugs to reduce intracranial pressure were used in all patients during the treatment, including mannitol, corticosteroids and/or sodium escin. 67 patients with intracranial hypertension were treated with surgical treatment, including drainage of cerebral ventricle and/or decompression of temporal muscle. All patients received antiseizure medications to prevent the onset of seizures during the treatment. RESULTS: The combination of albendazole and surgical intervention was curative in 69 of 74 patients with neurocysticercosis after a follow-up of an average 37.2 (19-52) months. CT and/or MRI examination demonstrated that the cysts had disappeared or become calcified. Only 1 case failed because there were 1160 cysts in the brain of the patient. CONCLUSION: The combination of albendazole and surgical maneuvers to reduce intracranial pressure is a safe and effective method for treating severe neurocysticercosis.