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العنوان
Fusidic Acid Resistance among Staphylococcus aureus Causing Community Acquired Skin
and Soft Tissue Infections
/
المؤلف
Abo Elnour,Safaa Sobhy Mahmoud
هيئة الاعداد
باحث / صفاء صبحي محمود أبوالنور
مشرف / أسامه شمس الدين رسلان
مشرف / ولاء شوقي السيد خاطر
مشرف / مروة كمال أسعد
تاريخ النشر
2016.
عدد الصفحات
168.p;
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب (متفرقات)
تاريخ الإجازة
1/9/2016
مكان الإجازة
جامعة عين شمس - كلية الطب - (Medical Microbiology and Immunology)
الفهرس
Only 14 pages are availabe for public view

from 168

from 168

Abstract

Background: The continued routine use of fusidic acid in clinical practice especially as a topical agent for treatment of Staphylococcus aureus (S. aureus) skin and soft tissue infections (SSTIs) has led to the emergence of resistance to this agent in both methicillin sensitive and resistant S. aureus.
Aim of the work: The current study aimed to detect fusidic acid resistance among methicillin sensitive and methicillin resistant S. aureus isolates causing community associated SSTIs (CA-SSTIs) and to identify the genetic determinants behind this resistance.
Patients and Methods: Pus or skin swabs from suppurative exudates of infected skin and soft tissue lesions were collected from 75 patients with CA-SSTIs. S. aureus isolates were recovered from samples and identified by conventional methods. Methicillin and fusidic acid resistant S. aureus (MRSA and FRSA) isolates were identified by disk diffusion method using cefoxitin (30 μg) and fusidic acid (10 μg) disks. Minimum inhibitory concentration (MIC) to fusidic acid was determined by E-test. Genetic determinants of resistance were investigated in S. aureus isolates using polymerase chain reaction.
Results: S. aureus was isolated from 52 (69.3%) of the patients’ samples. Fusidic acid resistance was detected in 17 (32.7%) isolates while 37 (71.2%) isolates were found resistant to cefoxitin (i.e., MRSA). All FRSA isolates (100%) were noticed to be MRSA (p value < 0.001). PCR showed that fusC gene was present in eight isolates (47.1 %) and fusA L461K mutation was present in five isolates (29.4%). Isolates that harbored fusC gene displayed low level of fusidic acid resistance (MIC range: 12 – 48 μg/ml) while those with fusA L461K mutation displayed high level of resistance (MIC ≥256 μg/ml).
Conclusion: The high rate of fusidic acid resistance among S. aureus is alarming and represents a serious threat that we could be losing a potentially useful agent in the treatment of MRSA SSTIs infections.