Colonization Rate, Risk Factor for Acquisition and Genetic Diversity of Vancomycin-Resistant Enterococci (VRE) Isolated from Rectal Culture of Patients in Intensvie Care Units from Ten Large Hospitals in Korea / 감염

BACKGROUND: VRE have become an emerging nosocomial pathogen in Korea, but there has not been nationwide study on the colonization of VRE among high risk groups of hospitalized patients. The purpose of this study was to determine the prevalence of rectal colonization of VRE among patients hospitalized in the intensive care unit (ICU), to study the risk factors for nosocomial acquisition of VRE among those patients, to define the genetic diversity of VRE strains in major hospitals in Korea. METHODS: Between January the 20th and 30th of 2000, a point surveillance study was conducted in the ICU of the ten large hospitals, which were located nationwide. Surveillance rectal swab cultures for detecting VRE were obtained among 214 patients admitted to the ICU during the study period. To isolate VRE, rectal swab cultures were performed on Enterococcosel(R) agar that containing 6 microgram/mL of vancomycin. Minimal inhibitory concentrations (MICs) of vancomycin and teicoplanin were determined by agar dilution method. For the genotyping of VRE isolates, the detection of vanA, vanB, vanC1 and vanC2 gene by polymerase chain reaction was done. Pulsed-field gel electrophoreis (PFGE) was used for elucidating the genetic relatedness of VRE isolates. To identify the risk factors for rectal VRE colonization, patients harboring VRE were compared to patients who were not colonized with this organism. RESULTS: The rectal colonization rate of VRE was variable from 9.7% to 51.9% according to hospital. 64 VRE strains which were isolated from 63 patients included 37 E. feacium. 26 E. gallinarum and 1 E. casseliflavus isolates. Therefore the colonization rate of clinically significant vanA type VRE was 17.3% (37/ 214). 37 E. feacium. 26 E. gallinarum and 1 E. casseliflavus isolates were presented as vanA, vanC1 and vanC2 genotypes, respectively. Risk factors for rectal VRE colonization included the presence of chronic illness, previous use of broad spectrum antibioitcs es-pecillay vancomycin, and prolonged stay in ICU. Various PFGE patterns are noted among vanA type VRE isolates, so individual acquisition of VRE during stay in the majority of ICUs were suggested. But there is some evidence of focal VRE spread within the ICU and between hospitals. CONCLUSION: This study demonstrated the high rectal colonization rate (17.3%) of clinically significant vanA type VRE among patients admitted to the ICUs of ten large hospitals located nation-widely. This study suggested that practicing HICPAC guidelines, restricted vancomycin usage and periodic surveillance cultures in patients with high risk factors are important in preventing the emergence and spread of VRE infection among ICU patients.

A Case of Pulmonary Embolism Caused by Aspergillus in a Child with Acute Lymphoblastic Leukemia / 대한소아혈액종양학회지

Pulmonary embolism is not a frequent cause of morbidity and mortality in patients with or without malignancies. Pulmonary embolism should be ruled out when sudden tachypnea and pulmonary hypertension develop in leukemic children, and chest radiograph shows no or minimal abnormalities. A 14-year-old girl with acute lymphoblastic leukemia was admitted due to neutropenic fever and dyspnea. Chest computed tomography and ventilation/perfusion scan showed pulmonary embolism, and embolectomy revealed aspergillosis. Invasive aspergillosis is the major opportunistic fungal pathogen in neutropenic patient and an important cause of death. The critical elements of successful management of invasive aspergillosis complicating neutropenia and pulmonary embolism are early diagnosis, initiation of aggressive doses of amphotericin B, reversal of immune suppression and feasible surgical resection of the lesions. To the best of our knowledge, this is the first report of pulmonary embolism caused by Aspergillus in an immunocompromised setting in Korea and we present a case report with a brief review.

The Expression of BDNF mRNA in the Hippocampal Formation after Febrile Seizure / 대한소아신경학회지

PURPOSE: Neuronal damage induced by febrile seizure(FS) has been implicated in the pathogenesis of medial temporal sclerosis, the pathologic hallmark of temporal lobe epilepsy. Recent data indicate that prolonged FSs induce transient structural changes of some hippocampal pyramidal neurons and long-term functional changes of hippocampal circuitry. In this study we have investigated the expression of brain-derived neurotrophic factor(BDNF) in the hippocampal formation after FSs with in situ hybridization histochemistry using riboprobe. METHODS: FSs were induced in 21 day-old male Sprague-Dawley rats(five rats for each group), which had a mean weight of about 100g. Exposure to hyperthermia was achieved by maintaining the water in the beaker at a temperature of 45 degrees C by pacing it in a temperature-controlled water bath. The rats were decapitated at appropriate times(0 hr, 30 min, 1 hr, 2 hr, 3hr, 6 hr, 12 hr and 24 hr) after FSs. In situ hybridization histochemistry was performed. The probe used in these studies were riboprobe complementary to the sequence 641-729 of rat BDNF. RESULTS: The induction of BDNF mRNA was observed in the dentate gyrus at 30 min after FSs. The expression in the dentate gyrus was gradually increased, peaked at 3 hr after FSs, and almost returned to basal level at 24 hr after FSs. The significant induction of BDNF mRNA was also observed in the CA3 area of hippocampus from 2 hr to 3 hr after FSs. CONCLUSION: These observations suggest that BDNF is the gene whose expression can be altered by FSs and these gene might be related to pathologic alterations after FSs.