RESUMO
Severe periportal fibrosis is not an inevitable consequence of infection with Schistosoma mansoni. Genetic predisposition may be a deciding factor in the development of disease. To assess the contribution of genetic factors in the severity of hepatic fibrosis, the degree of familial aggregation was determined in a Kenyan population. Schistosomal fibrosis was identified with hepatic ultrasound and newly proposed World Health Organization criteria, which include both qualitative and quantitative observations. These 2 aspects of the criteria correlated well with one another. The peak prevalence of ultrasound proven fibrosis trailed 5-10 years behind peak prevalence of infection and declined sharply after age 50 years. This pattern was consistent with either resolution of severe fibrosis over 10-20 years or early death of those severely affected. Genetic predisposition appears to be a weak factor in the development of severe disease in this population, since no household or familial aggregation could be identified.
Assuntos
Cirrose Hepática/diagnóstico por imagem , Cirrose Hepática/epidemiologia , Esquistossomose mansoni/diagnóstico por imagem , Esquistossomose mansoni/epidemiologia , Adolescente , Adulto , Fatores Etários , Idoso , Animais , Biomphalaria/parasitologia , Criança , Pré-Escolar , Vetores de Doenças , Saúde da Família , Feminino , Predisposição Genética para Doença , Humanos , Lactente , Recém-Nascido , Quênia , Fígado/irrigação sanguínea , Fígado/diagnóstico por imagem , Cirrose Hepática/genética , Cirrose Hepática/patologia , Masculino , Pessoa de Meia-Idade , Veia Porta/diagnóstico por imagem , Prevalência , Esquistossomose mansoni/genética , Esquistossomose mansoni/patologia , UltrassonografiaRESUMO
Repeated selective population chemotherapy of school age children reduces infection and morbidity associated with Schistosoma haematobium infection. To examine the long-term effect of this treatment on susceptibility to re-infection and late disease, a cohort of Kenyans (n = 194) were re-examined for infection and urinary tract morbidity 7-13 years after they underwent annual ultrasonography and treatment for an average of 5 years beginning in 1984 as children. Controls were previously untreated age-matched individuals residing in the same or adjacent villages. The overall prevalence and intensity of infection were equivalent between the 2 groups. In contrast, the prevalence of bladder wall pathology was 11-fold lower in previously treated (1.5%) versus untreated subjects (17%). Severe hydronephrosis was completely reversed. These data demonstrate that treatment significantly reduced urinary tract morbidity despite re-infection, and suggest that the important risk factors for urinary tract morbidity in adulthood are cumulative intensity and duration of infection during early adolescence.
Assuntos
Hidronefrose/diagnóstico por imagem , Hidronefrose/parasitologia , Schistosoma haematobium/crescimento & desenvolvimento , Esquistossomose Urinária/tratamento farmacológico , Esquistossomicidas/uso terapêutico , Doenças da Bexiga Urinária/parasitologia , Bexiga Urinária/diagnóstico por imagem , Adolescente , Adulto , Fatores Etários , Animais , Estudos de Coortes , Seguimentos , Humanos , Quênia/epidemiologia , Análise por Pareamento , Contagem de Ovos de Parasitas , Fatores de Risco , Esquistossomose Urinária/complicações , Esquistossomose Urinária/diagnóstico por imagem , Esquistossomose Urinária/parasitologia , Ultrassonografia , Doenças da Bexiga Urinária/diagnóstico por imagem , Doenças da Bexiga Urinária/patologia , Doenças da Bexiga Urinária/prevenção & controle , Urina/parasitologiaRESUMO
The pre- and post-treatment level of eosinophiluria, as measured indirectly by the amount of free or cell bound eosinophil cationic protein (ECP) and eosinophil protein X (EPX) in urine from Schistosoma haematobium-infected Kenyan school children, were measured and compared with intensity of infection (eggs/10 ml of urine), albuminuria and pathological changes as detected by ultrasonography. ECP and EPX were determined by means of specific ELISA methods and levels were determined in both urine supernatants and extracted urine deposits (cells and cell debris). The level of ECP was significantly raised in urine supernatants from infected children compared to controls, whereas high amounts of EPX were found in urine supernatants from infected children as well as from controls. However, the amounts of cell bound ECP and EPX were significantly raised in infected children. In pre-treatment observations significant correlations were demonstrated between egg counts, albuminuria and eosinophiluria as measured by the amount of cell bound ECP and EPX, or ECP in urine supernatants. No such correlations were demonstrated with the amount of EPX in the urine supernatants. Comparable amounts of ECP and EPX could be extracted from the urine deposits from infected children, but due to the high amounts of EPX in urine deposit extracts from controls, extracted ECP gave the best discrimination between infected and non-infected children. While albuminuria disappeared in most children at the 6 week post-treatment follow-up, eosinophiluria persisted in a significant proportion of the treated children indicating continued eosinophil activity in the bladder wall. Detection and quantification of early acute inflammatory reactions using ECP/eosinophils in combination with detection of later stages of bladder pathology using ultrasound may allow for a dynamic evaluation of the pathological process, the morbidity development and post treatment pathological changes in S. haematobium infections.