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1.
Minerva Med ; 100(2): 167-70, 2009 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-19390503

RESUMEN

The infection of endovascular stents remains one of the most problematic complications of aortic surgery. This article describes the case of a 61-year-old male with ascendant and descendent aorta endovascular stents, hospitalized for pyrexia, weight loss and back pain. Blood culture was positive for Staphylococcus hominis resistant to oxacillin and ciprofloxacin. Spiral computed tomography, magnetic resonance imaging and leukocyte-labelled scintigraphy showed that the patient developed a perigraft infection which spondylodiscitis in correspondence of D7, D8 and D9 vertebras. The biopsy CT-scan guided of vertebral inflammed tissue revealed a coagulase-negative Staphylo-coccus and the presence of numerous neutrophilis granulocytes. The reintervention for substituting an infected graft was excluded due to the high risk of death or paraplegia. A therapy with vancomycin, rifampicin and ceftazidime was started. On the basis of clinical and radiological findings, it was decided to switch empirical antimicrobial therapy to levofloxacin, minocycline and teicoplanin and a reduction of inflammation indices was observed. The patient was discharged maintaining this chronic suppressive antimicrobial therapy with a 28-day cycle of linezolid with complete regression of pain, and normalization of inflammation blood indices. After, therapy switched to teicoplanin three times a week while maintaining good clinical and radiological features. In the present, due to the high risk in performing a surgical procedure, a conservative chronic suppressive antimicrobial therapy with teicoplanin allowed to control the infection on an outpatient basis, thereby reducing the costs.


Asunto(s)
Aortitis/microbiología , Discitis/microbiología , Infecciones Relacionadas con Prótesis/microbiología , Infecciones Estafilocócicas , Staphylococcus hominis/aislamiento & purificación , Stents/efectos adversos , Antibacterianos/uso terapéutico , Aortitis/tratamiento farmacológico , Contraindicaciones , Discitis/tratamiento farmacológico , Quimioterapia Combinada , Humanos , Masculino , Persona de Mediana Edad , Implantación de Prótesis , Infecciones Relacionadas con Prótesis/tratamiento farmacológico , Reoperación , Infecciones Estafilocócicas/tratamiento farmacológico
2.
Mucosal Immunol ; 1(4): 279-88, 2008 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-19079189

RESUMEN

Loss of CD4(+) T cells in the gut is necessary but not sufficient to cause AIDS in animal models, raising the possibility that a differential loss of CD4(+) T-cell subtypes may be important. We found that CD4(+) T cells that produce interleukin (IL)-17, a recently identified lineage of effector CD4(+) T-helper cells, are infected by SIV(mac251)in vitro and in vivo, and are found at lower frequency at mucosal and systemic sites within a few weeks from infection. In highly viremic animals, Th1 cells predominates over Th17 T cells and the frequency of Th17 cells at mucosal sites is negatively correlated with plasma virus level. Because Th17 cells play a central role in innate and adaptive immune response to extracellular bacteria, our finding may explain the chronic enteropathy in human immunodeficiency virus (HIV) infection. Thus, therapeutic approaches that reconstitute an adequate balance between Th1 and Th17 may be beneficial in the treatment of HIV infection.


Asunto(s)
Linfocitos T CD4-Positivos/inmunología , Interleucina-17/inmunología , Membrana Mucosa/inmunología , Síndrome de Inmunodeficiencia Adquirida del Simio/inmunología , Virus de la Inmunodeficiencia de los Simios/fisiología , Células TH1/inmunología , Animales , Antígenos Virales/inmunología , Humanos , Linfocitos/inmunología , Macaca mulatta , Membrana Mucosa/virología , Síndrome de Inmunodeficiencia Adquirida del Simio/virología , Virus de la Inmunodeficiencia de los Simios/inmunología , Replicación Viral/fisiología
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