[Microsporidium spp. infection in an immunocompromised child diagnosed by polymerase chain reaction]. / Immün sistemi baskilanmis bir çocukta Microsporidium spp. Enfeksiyonunun polimeraz zincir reaksiyonu ile tanimlanmasi

Microsporidium spp. may lead to a variety of clinical pictures like sinusitis, keratoconjunctivitis, hepatitis, myositis, peritonitis, nephritis, encephalitis and pneumonia in case of immune deficiencies. In this report, a case of diarrhea due to Microsporidium spp. has been presented. A four years old male patient who was followed with the diagnosis of myotonic dystrophia, was admitted to the hospital with the complaints of respiratory distress and fever. Due to the history of recurrent infections, further investigations was carried out to clarify the immunological status of the patient, and the total IgA and IgM levels were found as 14 mg/dl and 30 mg/dl, respectively (normal values were; 18-160 and 45-200 mg/dl, respectively). Following bronchoscopy done to enlighten respiratory distress, the patient developed high fever and watery diarrhea. Since bacteriological cultures of the stool yielded Shigella spp., antimicrobial therapy with ciprofloxacin was initiated. Parasitological examination of the stool done by Weber's modified trichrome dye, yielded Microsporidium spp. microscopically and albendazole was added to the treatment. Presence of Microsporidium spp. was confirmed by polymerase chain reaction with the use of C1 and C2 primers (Metabion, Germany) targeted to Microsporidium spp. and besides a 270 bp band specific for Encephalitozoon intestinalis was also obtained. This case emphasized that in case of diarrhea the stool samples of the immunocompromised patients should be evaluated in terms of Microsporidium spp. in addition to the routine parasitologic examinations.

Protozoan protein tyrosine phosphatases.

The aim of this review is to provide a synthesis of the published experimental data on protein tyrosine phosphatases from parasitic protozoa, in silico analysis based on the availability of completed genomes and to place available data for individual phosphatases from different unicellular parasites into the comparative and evolutionary context. We analysed the complement of protein tyrosine phosphatases (PTP) in several species of unicellular parasites that belong to Apicomplexa (Plasmodium; Cryptosporidium, Babesia, Theileria, and Toxoplasma), kinetoplastids (Leishmania and Trypanosoma spp.), as well as Entamoeba histolytica, Giardia lamblia, Trichomonas vaginalis and a microsporidium Encephalitozoon cuniculi. The analysis shows distinct distribution of the known families of tyrosine phosphatases in different species. Protozoan tyrosine phosphatases show considerable levels of divergence compared with their mammalian homologues, both in terms of sequence similarity between the catalytic domains and the structure of their flanking domains. This potentially makes them suitable targets for development of specific inhibitors with minimal effects on physiology of mammalian hosts.

Efecto de la ciclosporina A en ratones C57BL/6 infectados con encephalitozoon intestinalis / Cyclosporine A effect in mice C57BL/6 infected with Encephalitozoon intestinalis

Introducción. Encephalitozoon intestinalis es un microsporidio parásito del intestino, que puedediseminarse en pacientes inmunocomprometidos. Existen referencias de modelos animales inmunosuprimidos para el estudio de la microsporidiosis utilizando fármacos que producen supresión total de la respuesta inmune; sin embargo, no se han estudiado los efectos deinmunosupresores con acción selectiva sobre los componentes de esta respuesta. Objetivo. Evaluar el efecto de la inmunosupresión con ciclosporina A (CsA) en ratones C57BL/ 6 infectados con E. intestinalis.Materiales y métodos. Se utilizaron 80 ratones C57BL/6 distribuidos en cuatro grupos: infectados, inmunosuprimidos e infectados, inmunosuprimidos no infectados y controles. La inmunosupresión con CsA (50 mg/kg) se realizó vía intraperitoneal durante todo el estudio. En la semanas 2, 3, 4 y 6 posteriores a la infección se obtuvo sangre para determinar los anticuerpos, y materia fecal para evaluar la cinética de excreción de esporas. Además, se extrajeron varios órganos para estudiar la histopatología y observar la posible diseminación del parásito. Resultados. La producción de anticuerpos IgG fue mayor en los ratones inmunocompetentes infectados que en los inmunosuprimidos infectados con E. intestinalis. No se encontró elparásito en órganos diferentes al intestino delgado en los dos grupos infectados. Sin embargo, la excreción de esporas, tanto en heces como en líquido duodenal, fue mayor en el grupo inmunosuprimido infectado. Conclusión. La CsA en el modelo en ratón no indujo la diseminación de E. intestinalis ni la exacerbación de la enfermedad, pero contribuyó al aumento en la cinética de excreción deesporas y la disminución de la producción de anticuerpos IgG en los ratones inmunosuprimidos infectados.