Analysis of Reporting Time for Identification of Methicillin-Resistant Staphylococcus aureus Carriers Using ChromID MRSA

We assessed the reporting times for identification of nasal methicillin-resistant Staphylococcus aureus (MRSA) carriers in 2011 in a university-affiliated hospital using surveillance cultures incubated for 1 and 2 days with ChromID MRSA (bioMerieux, France). Of 2,732 nasal swabs tested, MRSA was detected in 829 (85.6%) and 140 (14.4%) swabs after 1 and 2 days of incubation, respectively, and the median reporting times for positive specimens were 33.7 hr (range, 18.2-156.9 hr) and 108.1 hr (range, 69.8-181.0 hr), respectively. Detection rate after 1-day incubation was 85%. Additional 1-day incubation improved detection rate; however, it prolonged the reporting times of positive specimens approximately up to 4 days because of the need for confirmatory tests such as species identification and susceptibility tests. Following a 2-day culture with ChromID MRSA, rapid confirmatory tests are warranted to reduce delay in identifying MRSA carriers.

A Case of der(19)t(1;19) in Refractory Anemia with Ring Sideroblasts Associated with Marked Thrombocytosis

Translocation between chromosomes 1 and 19 is well documented in ALL. Here, we report a case of refractory anemia with ring sideroblasts associated with marked thrombocytosis with der(19)t(1;19). A 67-yr-old man was admitted to our hospital with anemia and thrombocytosis. The aspirated bone marrow showed erythroid and megakaryocytic hyperplasia and dyspoiesis. Iron staining showed that the ring sideroblasts increased in number. Bone-marrow cell karyotyping showed 46,XY,der(19)t(1;19)(q23;p13)[9]/46,XY,del(5)(q21)[2]/46,XY[9]. PCR analysis showed the absence of the TCF3-PBX1 rearrangement. The patient was treated with hydroxyurea and intermittent blood transfusion. It is known that t(1;19)(q23;p13) leads to a TCF3-PBX1 fusion gene, whose product is a powerful transcriptional activator that plays a key role in the development of ALL. However, t(1;19) has rarely been reported in myeloid neoplasms and the TCF3-PBX1 fusion gene has not been detected. This implies that other genes might be involved in the TCF3-PBX1 rearrangement, or an alternative TCF3-PBX1 fusion transcript with a different breakpoint has not been detected to date. Further research and case studies, including the use of molecular analysis techniques, are required to evaluate the clinical and prognostic significance of t(1;19) in the development of myeloid neoplasms.