RESUMEN
Cysticercosis, a disease of economic and public health importance, is caused by Cysticercus cellulosae, the metacestode stage of Taenia solium. Experimental induction of cysticercosis was achieved in young pigs by feeding an optimum dose of 20,000 T. solium (Indian strain) eggs after immunosuppression, to assess the effect of albendazole and development of the immune response to cysticercus antigens before and after treatment. Histopathological studies revealed the presence of cysticerei in liver, lungs and muscles. Treatment with albendazole at 15 mg kg-1 body weight daily for 30 days starting from day 0 or 15 days post-infection resulted in 100% cure rates. Increases in antibody titre to crude soluble extract and a Sephadek G-200 purified antigenic fraction of Cysticercus cellulosae were found on days 25, 40 and 55 post-infection in untreated pigs and those in which treatment started on day 15 post-infection, whereas no increase in antibody response was observed in pigs in which treatment started on day 0.
Asunto(s)
Albendazol/uso terapéutico , Antihelmínticos/uso terapéutico , Cisticercosis/tratamiento farmacológico , Cysticercus/efectos de los fármacos , Animales , Anticuerpos Antihelmínticos/sangre , Antígenos Helmínticos , Cisticercosis/inmunología , Cisticercosis/parasitología , Cysticercus/inmunología , Modelos Animales de Enfermedad , Evaluación Preclínica de Medicamentos , Cinética , Hígado/parasitología , Hígado/patología , Parasitosis Hepáticas/tratamiento farmacológico , Parasitosis Hepáticas/inmunología , Parasitosis Hepáticas/parasitología , PorcinosRESUMEN
After peritoneal macrophages had been exposed to different concentrations of nifedipine (10-120 ng mL-1) there was a significant increase (P less than 0.001) in the percentage of Leishmania donovani infected macrophages compared with controls. Parasite load was also significantly increased (P less than 0.001) in nifedipine-treated, L. donovani infected, BALB/c mice, compared with untreated, infected mice, post-inoculation. Peak chemiluminescence responses were significantly depressed (P less than 0.001) in nifedipine-treated infected mice compared with untreated mice post-inoculation. It is suggested that availability of intracellular calcium is a factor in the defense mechanism of inflammatory cells in L. donovani infections.