ABSTRACT
Objective To explore the clinical characteristics of systemic disseminated infection caused by Mycobacterium fortuitum (M.fortuitum), and improve the diagnostic rate and understanding of the disease.Methods One case of systemic disseminated M.fortuituminfection was reported, and analyzed in combination with relevant literatures.Results Patient was with multiple systemic involvement (including lung, lymph node, skin, joint), lymph node tissue culture was positive for M.fortuitum, patient was given clarithromycin+levofloxacin+linezolid for treatment, disease was remitted.Conclusion Systemic disseminated M.fortuituminfection is rare, and patient with GATA2 deletion and IFN-γautoantibody may be a potential mechanism, diagnosis is mainly based on pathological morphology and microbiological detection, but positive rate is low, diagnosis is difficult.
ABSTRACT
Mendelian susceptibility to mycobacterial diseases (MSMD)is a rare congenital disorder characterized by susceptibility to poorly virulent mycobacteria,such as Bacille Calmette-Guerin vaccine or non-tuberculous environmental mycobacteria.The interferon-γ'(IFN-γ)/interleukin-12 (IL-12) pathway is central to controlling mycobacterial infections,in which several genes had been identified.IFN-γ secretion is impaired in patients with IL-12p40 and IL-12 receptor β1 deficiency,where the response to IFN-γ is impaired in patients with IFN-γ receptor 1,IFN-γ receptor 2,and signal transducer and activator of transcription 1 deficiencies.Furthermore,germline mutations in the cytochrome b (-245) beta subunit,interferon regulatory factor 8,ubiquitin-like modifier,RORC and TYK2 have been identified as the genes which are responsible for MSMD.These patients do not generally have associated infections,apart from salmonellosis.Now,the pathogenesis,molecular,clinical,laboratory features,treatment and prognosis were described,in order to support the clues for pediatrician's clinical practice.
ABSTRACT
Se presenta información reunida retrospectivamente sobre casos de micobacteriosis originados por Mycobacterium simiae (n = 4) y "M. sherrisii" (n = 6). Los casos ocurrieron entre pacientes con sida (n = 6), historia de silicosis (n = 2) o tuberculosis previa (n = 1). Un caso se perdió luego de diagnosticado y nueve fueron tratados con esquemas terapéuticos basados en claritromicina, etambutol y quinolonas. La respuesta fue muy pobre: cinco pacientes fallecieron (cuatro eran HIV positivos), tres permanecieron crónicos y sólo uno curó. Estas micobacterias originaron 2.1% de los casos de micobacteriosis registrados en un período de ocho años. La distinción de estas micobacterias raras de otras más frecuentes por métodos moleculares rápidos, parece ser clínicamente útil para advertir sobre la dificultad que puede presentar el tratamiento. Sin embargo, la diferenciación genotípica entre M. simiae y "M. sherrisii" parecería no ser clínicamente relevante, dado que no quedaron expuestas características que distingan a los pacientes afectados por los dos microorganismos tan estrechamente relacionados.
A revision of mycobacterial disease due to M simiae (n = 4) and "M. sherrisii" (n = 6) identified during an eight-year period is presented. Cases occurred among patients with AIDS (n = 6), previous history of silicosis (n = 2) or tuberculosis (n = 2). One case was lost to follow-up and the remaining nine responded poorly to chemotherapy based on clarithromycin, ethambutol and fluoroquinolones. Five patients died of whom four were HIV-positive, three remained chronic and one was cured. These microorganisms originated 2.1% of mycobacterioses cases detected in an eight-year period. Timely identification of this group of uncommon mycobacteria by molecular methods seems to be clinically relevant in order to warn of difficulties inherent to the treatment. However, the distinction between both closely related microorganisms might not be crucial for case management as no distinctive characteristics were evident among patients affected by M. simiae or "M. sherrisii".