RESUMO
El objetivo de este estudio fue identificar especies o genotipos del protozoario parásito Cryptosporidium presentes en heces colectadas de terneros Holstein del municipio de Manizales, Departamento de Caldas, Colombia. El ADN fue extraído a 80 muestras de materia fecal, de las cuales 11 fueron diagnosticadas positivas para Cryptosporidium spp., mediante reacción en cadena de la polimerasa (PCR). El análisis PCR-RFLP del locus 18S ADNr, identificó la presencia de Cryptosporidium parvum en todas las muestras positivas analizadas. Este hallazgo sugiere que el ganado puede ser una fuente potencial de infección por Cryptosporidium en humanos y se constituye en el primer reporte publicado de C. parvum en bovinos de Manizales, Caldas.
The objective of this study was to identify species or genotypes of Cryptosporidium parasite present in feces collected from Holstein calves in Manizales city, Caldas Department, Colombia. DNA was extracted from 80 fecal samples, which 11 were diagnosed positive for Cryptosporidium spp., by the Polymerase Chain Reaction method. PCR-RFLP analysis of 18S rDNA locus identified the presence of Cryptosporidium parvum in all samples tested positive. This finding suggests that cattle may be a potential source of human infection by Cryptosporidium, and it becomes the first published report of C. parvum in cattle in Manizales, Caldas.
RESUMO
OBJECTIVE: To determine the local prevalence and optimal therapy for children with Barrett's esophagus (BE), the authors studied children with esophageal strictures or gastroesophageal reflux (GER), or both, to diagnose BE and to follow after therapy. SUMMARY BACKGROUND DATA: Barrett's esophagus is seldom reported in children and therapeutic recommendations are unclear. Barrett's esophagus usually develops during the mucosal reparative process after acid-reflux injury to the esophageal mucosa. Risk factors for BE include conditions that are associated with GER such as mental retardation, esophageal stricture, esophageal atresia, and reversed gastric tube esophagoplasty. Barrett's syndrome increases the risk of esophageal adenocarcinoma by 30 to 40 times. METHODS: All children with the risk factors had repeated esophagoscopy and multiple mucosal biopsies before and after therapy. RESULTS: Eleven children have been documented with BE. The initial diagnoses were: GER, 5; esophageal atresia, 4; nasogastric intubation, 1; lye ingestion, 1. A gastric tube esophagoplasty had been performed in three patients with BE in the esophagus proximal to the anastomosis. Three children with mid-esophageal strictures and long segments of BE had total resection with colic interposition. An additional two patients with tight stricture were treated with colic-patch esophagoplasty without resection. The final three patients were treated with fundoplication alone. CONCLUSIONS: Barrett's esophagus can be caused by acid from gastric tubes but responds to H2 blockers and diet. Resection eliminates BE; esophagoplasty only controls the stricture and must be accompanied by fundoplication. Barrett's esophagus persists in patients with fundoplication alone if reflux control is incomplete. The authors conclude that acid reflux must be controlled to treat BE successfully or the involved segment must be resected. Esophagogastrostomy apparently predisposes to BE.
