Antimicrobial treatment of Acinetobacter infections may be limited because of the emergence of extended-spectrum -lactamase (ESBL)-and carbapenemase-producing multiresistant strains (7,13). Non-TEM-, non-SHV-derived ESBLs (such as PER and VEB) have been documented in Acinetobacter isolates from Europe and Asia (7) but not yet from the Americas.Recently, an increasing trend has been documented in carbapenem and extended-spectrum cephalosporin resistance in Acinetobacter isolates in Buenos Aires. Indeed, data from the Whonet-Argentina Network showed that, in 2004, more than 80% of Acinetobacter isolates were resistant to extendedspectrum cephalosporins. In addition, imipenem resistance increased from 5% to 54%, in the period from 2000 to 2004 (M. Galas, unpublished results). National ESBL surveillance is performed by Whonet-Argentina Network participants using a modification of the CLSI antibiogram (8), consisting of a synergy test with ceftazidime or cefepime and amoxicillin-clavulanic acid (distance between disks, 20 mm, center to center).FAV-1 and M5179 were the first putative ESBL-producing Acinetobacter baumannii strains isolated at two hospitals in Buenos Aires in 2000 and 2003, respectively. FAV-1 was a colonizer from the urine of a patient hospitalized for lung transplantation. M5179 was from the peritoneal fluid of a patient with hemolytic-uremic syndrome. Strains were confirmed to be A. baumannii by using the API 20NE system (bioMérieux, Marcy l'Etoile, France) combined with their ability to grow at 44°C.MICs (micrograms per milliliter) for FAV-1 and M5179 determined by agar dilution (10) were, respectively, as follows: ticarcillin, 1,024 and 1, 024; piperacillin, 512 and 256; piperacillin-tazobactam, 512 and 0.5; ampicillin-sulbactam, 8 and 8; cefotaxime, 64 and 64; cefotaxime-clavulanate, 64 and 8; ceftazidime, 64 and 512; ceftazidime-clavulanate, 16 and 2; cefepime, 64 and 64; cefepime-clavulanate, 16 and 4; aztreonam, 512 and 512; imipenem, 8 and 0.5; meropenem, 8 and 0.5; amikacin, 128 and 32; gentamicin, 2 and 32; trimethoprimsulfamethoxazole, 128 and 8; ciprofloxacin, 32 and 0.12; rifampin, 2 and Ͼ32; minocycline, 0.5 and Ͻ0.25. EDTA (0.4 mM) did not affect carbapenem MICs.Attempts to transfer the ceftazidime (FAV-1 and M5179) or imipenem (FAV-1) resistance marker by conjugation or electroporation to Escherichia coli ER1793 (6) were unsuccessful.Isoelectric focusing analysis (6) revealed ESBL bands at pIs of 5.4 (FAV-1) and 7.4 (M5179) and narrow-spectrum -lactamase bands at pIs of 6.9, 9.4 (FAV-1), and 5.4 (M5179). A band at a pI of 9.4 was inhibited by oxacillin (1 mM) (probable
We report the first case of human infection due to Pseudomonas fulva. P. fulva caused acute meningitis following the placement of a drainage system in a 2-year-old female. Additionally, the isolate displayed a VIM-2 carbapenemase in a class 1 integron context. CASE REPORTA 2-year-old female was brought to our center after 30 days of treatment in another center due to a history of fever, malaise, and partial food rejection. A sample of urine was taken for a bacteriological culture, and empirical treatment with amoxicillin was begun. The urinalysis showed pathological sediment with more than 25 leukocytes per field, pyuria, and bacteriuria. The urinary culture yielded Ͼ10 5 CFU of Proteus penneri per ml. Based on the susceptibility test result, amoxicillin was discontinued and a 1-week course of trimethoprimsulfamethoxazole (TMP-SMX) therapy was prescribed. Since she did not recover, she was hospitalized in the same center for evaluation. After 48 h, she presented a poor general state with signs of meningismus. Therapy with ceftriaxone (150 mg/kg/ day) was started. A computerized axial tomography (CAT) test, performed after lumbar puncture, revealed ventricular dilatation. The cerebrospinal fluid (CSF) cytochemical analysis was normal, and the CSF culture was negative.Due to a torpid evolution and because the patient presented facial paralysis, she was referred to Ricardo Gutierrez Children's Hospital, where a new brain CAT was performed showing progressive hydrocephalus. In order to drain the CSF, an external catheter was placed in the lateral ventricle. A presumptive diagnosis of meningitis with a bad evolution or tuberculous meningitis was made. Empirical treatment with vancomycin (60 mg/kg/day) (intravenous [i.v.]), cefotaxime (220 mg/kg/day) (i.v.), and tuberculostatic drugs (isoniazid, 5 mg/ kg/day; rifampin, 10 mg/kg/day; streptomycin, 15 mg/kg/day; pyrazinamide, 20 mg/kg/day) was started. Since the lumbar puncture was traumatic, CSF chemistry and cell count were not carried out; however, the CSF culture obtained by lumbar puncture (for bacteria, fungi, and mycobacteria) was negative.After 9 days of having the catheter drainage in place, the patient showed no neurological sign improvement. The catheter was changed, and a CSF sample for bacterial culture was taken with negative results. The CSF cell count was 8 leukocytes/mm 3 , and protein and glucose contents were 17 mg/dl and 70 mg/dl, respectively. Vancomycin was suspended, and the patient continued with ceftriaxone, and despite a negative result for the detection of Mycobacterium tuberculosis by PCR, the patient continued on tuberculosis drugs until the culture was finished.As indicated by neurosurgery, a nuclear magnetic resonance test was carried out, showing a lesion that occupied the midbrain and pons consistent with a probable ependymoma.On the eighth day after the new drainage system was placed, the patient was in very poor condition; therefore, internal ventriculoperitoneal shunting and performing a brain biopsy of the mass were considered. A new...
RESUMENLa forma infantil de la enfermedad de Pompe conduce al óbito antes del año de vida por miocardiopatía o insuficiencia ventilatoria. Presentamos la experiencia de siete años de terapia de reemplazo enzimático en un niño diagnosticado a los 7 días de vida; se trata del seguimiento más prolongado en el país. El tratamiento fue bien tolerado, sin reacciones adversas asociadas. Los parámetros ecocardiográficos y electrocardiográ-ficos se normalizaron progresivamente en el primer año y se mantuvieron estables. El niño logró rolar y sentarse sin sostén, pautas que se perdieron a partir del tercer año. Ingresó en respirador a los 16 meses. Se mantiene vivo con 7 años de edad, con debilidad muscular generalizada grave. El niño superó notablemente la edad promedio de sobrevida y de ingreso a respirador. Fue clara la mejoría cardíaca, pero el beneficio sobre el músculo esquelético fue limitado. Palabras clave: enfermedad de Pompe, terapia de reemplazo enzimático, alfa-glucosidasa ácida, Argentina, Myozyme ® . SUMMARYThe infantile form of Pompe disease drives children to death before the first year of life due to cardiomyopathy and respiratory insufficiency. We present the seven-year follow-up experience with enzyme replacement therapy on a child with Pompe disease, being the longest follow-up in the country. The treatment was well tolerated without adverse reactions. The echocardiographic and electrocardiographic parameters clearly improved during the first year and remain stable. Motor milestones (like rolling over or sitting down without support) were initially achieved, but, after the third year were getting lost. The average age of ventilator dependence was also delayed (16 months). The 7-year old patient remains alive with severe generalized muscle weakness. The child notably overcame the average age of survival and onset of ventilator dependence. Although the cardiovascular improvement was clear, enzyme replacement therapy efficacy on skeletal muscle was limited in this patient. La forma infantil de la enfermedad de Pompe se caracteriza por hipotonía, debilidad muscular y miocardiopatía, aunque también se aprecia dificultad para alimentarse, retraso motor, hepatomegalia y dificultad respiratoria. Generalmente, estos niños mueren antes del año de vida 3,4 por fallo cardiorrespiratorio. 5El mayor avance en el tratamiento de la enfermedad de Pompe fue el desarrollo de la terapia de reemplazo enzimático, que consiste en realizar infusiones periódicas de alfa-glucosidasa ácida humana recombinante.El objetivo del presente artículo es presentar la experiencia de siete años de seguimiento de un niño con enfermedad de Pompe infantil, en tratamiento con terapia de reemplazo enzimático. CASO CLÍNICOPrimer hijo de padres no cosanguíneos, nacido de término. A los 5 días presentó cianosis peribucal, palidez, hipotonía y bradicardia, por lo que ingresó a cuidados intensivos neonatales. El electrocardiograma presentó intervalo PR acortado y complejos QRS gigantes. El ecocardiograma mostró miocardiopatía hipertrófica no obstru...
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