1.Chancroid: Report of Three Case.
Korean Journal of Dermatology 1980;18(2):127-131
Chancroid is an acute localized, autoinoculable venereaI disease caused by Haemophilus ducreyi, characterized clinicaIly by painful ulceration at the site of incubation, and frequently accompanied by regional lymphadenopathy, and short incubation period. Three cases of chancroid were seen in Won Ju city, Kangwondo, Korea. All of the patients were male, and painful ulcers developed on genital region in 2 to 3 days after sexual contacts. Direct smear showed the characteristic "school-of-fish" arrangement of Haemophilus ducreyi by Gram stain. There were no regional lymphadenopathies and VDRL test were negative. Treatments were done with sulfisoxazole (Gantrisin) in case I, with sulfamethoxydiazine(Bayrena) and streptomycin in case 2, and with sulfamethoxydiazine and tetracycline in case 3 with exccllent results.
Chancroid*
;
Gangwon-do
;
Haemophilus ducreyi
;
Humans
;
Korea
;
Lymphatic Diseases
;
Male
;
Streptomycin
;
Sulfameter
;
Sulfisoxazole
;
Tetracycline
;
Ulcer
2.A Case of Toxic Epidermal Necrolysis.
Korean Journal of Dermatology 1974;12(3):175-178
A case of Toxic epidermal necrolysis in 19 th years old man is presented. This patient has been suffering from erythematous patches and bullae over entire body including vesicles, erosions, and fissures on both lips since 2 days ago after taking some drugs (analgetics, aspirin, chloramphenicol, sulfisoxazole, erythromycine.) for treatment of tonsillitis. Furthermore, it is very difficult for us to say why the disease has occured. Toxic Epidermal Necrolysis (TEN) by talking drugs or Staphylococcal Scalded Skin Syndrpme (4S) by staphylococcus aurues because staphylococcus aureus was found on bacteriai culture from his throat swab. He was treated with corticosteroid, antibiotics and fluids for 20 days with good result. Literature was briefly reviewed.
Anti-Bacterial Agents
;
Aspirin
;
Chloramphenicol
;
Humans
;
Lip
;
Palatine Tonsil
;
Pharynx
;
Skin
;
Staphylococcus
;
Staphylococcus aureus
;
Stevens-Johnson Syndrome*
;
Sulfisoxazole
;
Tonsillitis
3.Epidemiological Study of Serratia marcescens Isolates by Molecular Analysis.
Sung Yong SEOL ; Dong Taek CHO ; Yoo Chul LEE ; Haeng Seop SHIN ; Hee Kyung CHANG ; Sung Joe BAE
Journal of the Korean Society for Microbiology 1997;32(5):503-520
Ninety-two strains of Serratia marcescens isolated from 5 hospitals were analyzed for plasmid profile, antimicrobial drug resistance pattern, biotyping, and production of pigment. Ninety-three percents of strains were resistant to chloramphenicol (Cm), tetracycline (Tc), sulfisoxazole (Su), cefazolin (Cz), ampicillin (Ap), and rifampin (Rf). A majority of strains were susceptible to amikacin (Ak), ciprofloxacin (Ci), and cefotaxim (Ct). Fifty-four resistance patterns were found in 94 strains and the most prevalent resistance pattern was CmTcSuApCzRf. Seventeen (17.4%) isolates could transfer their partial resistance to E. coli or Klebsiella pneumoniae by conjugation. Twenty-seven plasmid profiles in 54 strains (58.7%) were detected, however no predominant patterns were seen in isolates from each hospital. Eleven biotypes were detected. The common types were A3b (29.4%) and A8b (27.1%), predominant types were found in each hospital. Twenty strains from 4 of 5 hospitals showed consistence of 3 types. These results indicate that plasmid profile analysis, Grimont biotyping, and resistance pattern type of strains in combination are useful as an epidemiological tool for S. marcescens isolates and some of isolates were confirmed as nosocomial strains.
Amikacin
;
Ampicillin
;
Cefazolin
;
Cefotaxime
;
Chloramphenicol
;
Ciprofloxacin
;
Drug Resistance, Microbial
;
Epidemiologic Studies*
;
Klebsiella pneumoniae
;
Plasmids
;
Rifampin
;
Serratia marcescens*
;
Serratia*
;
Sulfisoxazole
;
Tetracycline
4.Bilirubin Metabolism and Bilirubin Encephalopathy.
Chul LEE ; Soon Min LEE ; Ran NAMGUNG
Neonatal Medicine 2013;20(3):268-275
During the last 30 years, there has been much advances in the understanding of pathogenisis of neonatal hyperbilirubinemia, but the risk of bilirubin encephalopathy are still remained for the high risk neonates. The mechanisms of bilirubin encephalopathy are not thouroughly understood. Various theories may explain bilirubin transport acoss the blood-brain barrier. Free bilirubin, not bound to albumin, can enter the brain. The permeability of the blood brain barrier to bilirubin or albuimin and bilirubin binding may play an important role in the bilirubin encephalopathy. Bilirubin binding ability of Korean infants, similar to American infants, is shown to be less than that of adults. Factors influencing bilirubin-albumin binding, such as acidosis, hypoxia, sepsis, hypothermia, hypoglycemia and immaturity should be considered for neonates at high risk of bilirubin encephalopathy. Free bilirubin is found to be significantly increased in preterm infants with low albumin level. Sulfisoxazole inhibits the bilirubin-albumin binding that resulted in increased free bilirubin concentrations even at low total bilirubin levels. Phenobarbital has no effects on bilirubin binding capacity of albumin. Phototherapy for 48 hours has no influence on bilirubin-albumin binding capacitiy and affinity. Auditory evoked repsonse (ABR) changes in the form of I, III, and IV wave reduction are associated with brainstem and cerebellum bilirubin deposition. Since early detection of bilirubin neurotoxicity is promising for improving outcome for high risk neonates, ABR and other electrophysiological measure will be useful.
Acidosis
;
Adult
;
Anoxia
;
Bilirubin
;
Blood-Brain Barrier
;
Brain
;
Brain Stem
;
Cerebellum
;
Humans
;
Hyperbilirubinemia, Neonatal
;
Hypoglycemia
;
Hypothermia
;
Infant
;
Infant, Newborn
;
Infant, Premature
;
Kernicterus
;
Permeability
;
Phenobarbital
;
Phototherapy
;
Sepsis
;
Sulfisoxazole
5.Transferable Trimethoprim Resistance in Urine Isolates of Escherichia coli.
Sung Yong SEOL ; Dong Taek CHO ; Yoo Chul LEE ; Jung Min KIM ; Haeng Seop SHIN ; Hee Kyung CHANG ; Hyang Soo HYUN
Journal of the Korean Society for Microbiology 1997;32(5):553-568
One hundred and twenty-two strains of E. coli isolated from urinary tract infection were examined for antibiogram, transferability of trimethoprim (Tp) resistance, incompatibility with F group plasmid and southem hybridization with DHFR I, II, and III probe of Tp-resistant R plasmids. 1. Among 172 Gram negative bacilli isolated from urinary tract infection, 122 (70.9%) were E. coli and 75 strains of them were resistant to trimethoprim (Tp). Most of Tp-resistant isolates were also resistant to penicillins (ampicillin, carbenicillin, and ticarcillin), aminoglycosides (kanamycin and gentamicin), and sulfisoxazole but almost all strains were susceptible to cephalosporins. 2. Most of Tp-resistant strains and E. coli transconjugant derived from them showed multiple drug resistance and various antimicrobial resistance patterns. 3. Thirty-three Tp-resistant strains (45.2%) transferred 35 Tp-resistant plasmids to E. coli recipients but among them 6 transconjugants did not show retransfer of resistance and plasmid DNA were not detected in 2 transconjugants after resistance transfer. 4. Tp-resistant R plasmids ranged from 157 to 67 kb and 8 R plasmids were classified to incompatibilty group IncFI or IncFII ranging from 120 to 83 kb. Three and two R plasmids belonged to IncFII showed similar molecular weight, resistance pattern, and reaction site by southern hybridization with DHFR I probe. Twenty-five plasmids specifically responded on various EcoRI endonuclease fragments to DHFR I probe but not to DHFR II or DHFR III probe. These findings suggest that most of Tp- resistant R plasmids from urine isolates of E. coli were derived from various sources but some plasmids including IncFII R plasmids were probably originated from same or similar sources.
Aminoglycosides
;
Carbenicillin
;
Cephalosporins
;
Deoxyribonuclease EcoRI
;
DNA
;
Drug Resistance, Multiple
;
Escherichia coli*
;
Escherichia*
;
Microbial Sensitivity Tests
;
Molecular Weight
;
Penicillins
;
Plasmids
;
R Factors
;
Sulfisoxazole
;
Trimethoprim Resistance*
;
Trimethoprim*
;
Urinary Tract Infections