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Purpose@#With changing fungal epidemiology and azole resistance in Aspergillus species, identifying fungal species and susceptibility patterns is crucial to the management of aspergillosis and mucormycosis. The objectives of this study were to evaluate performance of panfungal polymerase chain reaction (PCR) assays on formalin-fixed paraffin embedded (FFPE) samples in the identification of fungal species and in the detection of azole-resistance mutations in the Aspergillus fumigatus cyp51A gene at a South Korean hospital. @*Materials and Methods@#A total of 75 FFPE specimens with a histopathological diagnosis of aspergillosis or mucormycosis were identified during the 10-year study period (2006–2015). After deparaffinization and DNA extraction, panfungal PCR assays were conducted on FFPE samples for fungal species identification. The identified fungal species were compared with histopathological diagnosis. On samples identified as A. fumigatus, sequencing to identify frequent mutations in the cyp51A gene [tandem repeat 46 (TR46), L98H, and M220 alterations] that confer azole resistance was performed. @*Results@#Specific fungal DNA was identified in 31 (41.3%) FFPE samples, and of these, 16 samples of specific fungal DNA were in accord with a histopathological diagnosis of aspergillosis or mucormycosis; 15 samples had discordant histopathology and PCR results. No azole-mediating cyp51A gene mutation was noted among nine cases of aspergillosis. Moreover, no cyp51A mutations were identified among three cases with history of prior azole use. @*Conclusion@#Panfungal PCR assay with FFPE samples may provide additional information of use to fungal species identification. No azole-resistance mediating mutations in the A. fumigatus cyp51A gene were identified among FFPE samples during study period.
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Background@#The aim of this study was to describe the clinical and microbiological characteristics of infective arthritis and to analyze risk factors for Gram-negative bacterial infections that cause infective arthritis. @*Materials and Methods@#Patients admitted between 2009 - 2018 with infective arthritis in a single-tertiary hospital were evaluated retrospectively. @*Results@#A total of 181 patients were enrolled in this study. Of them, 135 were native joint infection patients and 46 were prosthetic joint infection patients. The most common site of infective arthritis was the knee (63.6%), followed by the shoulder (17.7%), and the hip (9.9%).The most frequently identified microorganisms were Staphylococcus aureus (51.1%), followed by Streptococci sp. (21.1%), Enterobacteriaceae (8.4%), and coagulase-negative-Staphylococci (CNS;8.4%). Infections due to Gram-negative bacteria and fungi made up 13.7% and 3.2% of all cases, respectively. Additionally, 20% and 4.2% of the cases involved methicillin-resistant S. aureus (MRSA) and MRCNS. We found that bacteriuria, infective arthritis in the hip, and steroid use at admission are independent risk factors for Gram-negative bacterial infections. @*Conclusion@#Infective arthritis with methicillin-resistant microorganisms reached up to about 25% in a single-tertiary hospital in Korea. In case of suspected urinary tract infection, infective arthritis of the hip joint, or steroid use at admission time among infective arthritis patients, empirical treatment covering Gram-negative microorganisms can be considered.
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Background@#The aim of this study was to describe the clinical and microbiological characteristics of infective arthritis and to analyze risk factors for Gram-negative bacterial infections that cause infective arthritis. @*Materials and Methods@#Patients admitted between 2009 - 2018 with infective arthritis in a single-tertiary hospital were evaluated retrospectively. @*Results@#A total of 181 patients were enrolled in this study. Of them, 135 were native joint infection patients and 46 were prosthetic joint infection patients. The most common site of infective arthritis was the knee (63.6%), followed by the shoulder (17.7%), and the hip (9.9%).The most frequently identified microorganisms were Staphylococcus aureus (51.1%), followed by Streptococci sp. (21.1%), Enterobacteriaceae (8.4%), and coagulase-negative-Staphylococci (CNS;8.4%). Infections due to Gram-negative bacteria and fungi made up 13.7% and 3.2% of all cases, respectively. Additionally, 20% and 4.2% of the cases involved methicillin-resistant S. aureus (MRSA) and MRCNS. We found that bacteriuria, infective arthritis in the hip, and steroid use at admission are independent risk factors for Gram-negative bacterial infections. @*Conclusion@#Infective arthritis with methicillin-resistant microorganisms reached up to about 25% in a single-tertiary hospital in Korea. In case of suspected urinary tract infection, infective arthritis of the hip joint, or steroid use at admission time among infective arthritis patients, empirical treatment covering Gram-negative microorganisms can be considered.
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Mineralocorticoids influences on acid-base homeostasis by the regulation of urine acidification. But its mechanism of acion is not well known in human. This study compared the acid-base status and the indices of urine acidification before and after mineralocorticoid administration in human, and analyzed the effect of mineralocorticoids on human acid-base homeostasis. We administered 9a-fludrocortisone in 6 chronic renal failure patients and 6 normal controls 0.5mg daily for 7 days. The results were as following: 1) After administration of 9a-fludrocortisone in patients group, serum aldosterone level changed from 120.2+/-71.0pg/mL to 44.8+/-32.2pg/mL(mean+/-SD, p< 0.05). Serum HCO- level was not changed. Urine ammonium excretion was incresed from 24.6+/-12.3 mmol/day to 43.7+/-19.0 (p<0.05), but there were no change in urine pH and urine anion gap, Serum potassium level decreased from 5.5+/-0.7mBq/L to 4.1+/-0.5mEq/L (p<0.05), and TTKG increased from 3.9 to 8.9(p<0.05). 2) After administration of 9a-fludrocortisone in control group, serum aldosterone level changed from 99.7+/-44.5pg/mL to 25.1+/-3 mL(p<0.05). Serum HCO- level was not changed. Urine ammonium excretion was incresed from 44.3+/-21.6mmoVday to 76.3+/-19.6(p<0.05), but there were no change in urine pH and urine anion gap. Serum potassium level decreased from 4.8+/-0.5mEq/L to 3.9+/-0.2mHq/L(p< 0.05), but there was no change in TTKG. 3) No patient or control showed any discomfort after 9-fludrocortisone administration, and there was no elevation in diastolic blood pressure, increase in body weight, electrolyte abnormality. In summary, after 9alpha-fludrocortisane administration, urinary ammonium excretion increased in both patients and control group, and this phenomenon occured with correction of hyperkalemia without urine pH change. This result implies urinary ammonium excretion increase by mineralocorticoid. In human increase in renal distal acidification by mineralocorticoid is due to increase in renal ammoniagenesis rather than stimulation on proton excretion.