Résumé
Background: staphylococcus Aureus [S.aureus] skin infections are a global problem affecting all age groups from infancy to elderly, mainly because of emerging resistance against widely used antibiotics and presence of specific virulence determinants Panton-Valentine Leukocidin [PVL]. Nasal colonization with methicillin-resistant S, aureus [MRSA] is believed to precede skin diseases, therefore it is reasonable to expect that testing for 'nasal MRSA colonization could provide guidance in the choice of empirical therapy for skin infections. Better control of MRSA within the community setting is necessary to prevent dissemination of epidemic and or multi resistant MRSA clones among outpatients. Combined phenotypic and molecular tests for rapid identification and discrimination of the Staphylococcus genus from others, with simultaneous discrimination of methicillin-resistant from susceptible staphylococcal strains and concomitant detection of PVL genes are of great values
Aim of the study: this study was designed to assess the role of nasal colonization of MRSA and identify the link between PVL toxin gene expression in recurrent skin infections as treatable risk factors to reduce infection-related morbidity and mortality. This may help in prevention, optimal treatment and even to control spread of resistance
Patients and methods: this study was carried out on 30 patients attending dermatology outpatient clinics [OPDs] with a history of repeated skin infections. Twenty apparently healthy participants were taken as a control group. All patients and control were subjected to full history and complete clinical examination as well as laboratory investigations including complete blood count [CBC], erythrocyte sedimentation rate [ESR] and C-reactive proteins [CRP]. All skin and nasal S. aureus bacteriological swabs were selected and detection of MRSA isolates were done by oxacillin [OX] and cefoxitin [FOX] disc diffusion tests. Confirmation of resistance was carried out by detection of mecA gene by polymerase chain reaction [PCR]. Antibiotic susceptibility patterns of MRSA isolates recovered from the skin lesions were compared with that of the nasal isolates .Screening for PVL toxin genes in skin MRSA isolates was done using PCR technique
Results: out of 30 patients with recurrent skin infection, 26 [86.6%] had S. aureus positive skin culture; 42.3% of these isolates were MSSA while the remaining [57.7%] isolates were MRSA. Concerning the S.aureus nasal frequency in the two studied groups, a statistically significant difference was revealed [P < 0.05] where the S. aureus frequency in nasal isolates of recurrent skin infection group was [63.3%]; [42.1 %] were MSSA and [57.9%] were MRSA .Meanwhile its ,frequency in healthy controls was [25%]; [40%] were MSSA and [60%] were MRSA . The MRSA antimicrobial susceptibility pattern did not express a statistically significant difference in skin and nasal isolates in patients group [P>O.OS] for antimicrobial tested except for fusidic acid [Pc0.05]. There was 100% concordance of susceptibilities for nasal and skin isolates of patients for vancomycin and rifampicin. It was found that PVL was detected only in 5 MRSA skin isolates [38.4 %]; 4 isolates were from patients with furuncles while the remaining isolate was from patient with cellulitis. The 5 detected PVL producers were, found to be among patients with more frequent episodes of skin infections
Conclusion: among patients with skin infections, nasal carriers of MRSA are at higher risk for recurrent skin infection than non-carriers; thus, screening these susceptible patients should be served as a health priority. PVL producing MRSA was found to be among isolates from patients with more frequent episodes of skin infections, including furuncles and abscesses, so importance of surveillance for detection of PVL producers arises from the urgent need for specific antibiotic therapy
Résumé
Background: macrophage migration inhibitory factor [MIF] has a regulator role of host responses to infection and stress. It is now emerging as a key integrator of the immunoneuroendocrine interface and has capacity to counter-regulate the effects of glucocorticoids on immune cells. Functional promoter polymorphisms of the human A4IF gene single-nucleotide polymorphism [SNP] at position 173 *G/C altered level of MIF gene transcription and contribute to increase susceptibility for early onset, severity and poor outcome of Atopic Dermatitis [AD]
Objective: to evaluate values of human MIF gene single nucleotide polymorphism [SNP], immunohistochemically study of MIF expression in biopsies from the skin lesions [as it mirrors serum MIF levels] versus serum cortisol levels and their relation to different degrees of severity in early onset AD
Patients and Method: this study was carried out on twenty four Participants. Fourteen with AD, 11 females and 3 males, their ages ranged from 3-12ys with mean+/- sd [7.6+/-3.03] [group l]. Ten healthy participant's age and sex matched were taken as controls, their ages ranged from 4-llys with mean+/-sd [6.15+1.53] [group2].Group 1 after that were subdivided for immunohistochemically staining into group A and Group B. They were selected from dermatology outpatient clinic at Al-Zahraa University Hospital after taking informed consent from their parents, and they were subjected to full history, clinical and dermatological examinations; measuring CEC, ESR, morning serum cortisol levels; Genetic study for human MIF gene single-nucleotide polymorphism [SNP] [MIF-173*G/C], and immunohistochemically study of MIF expression in skin biopsies
Results: five out of Fourteen patients were moderate AD [Objective SCORAD index]. They had been associated with SNP of human MIF at 173 *C [35.71%]. There was strong and moderate positive expressions of MIF in skin biopsies from moderate AD patients with SNP, while mild or no expressions of MlF in mild AD skin lesions by immunohistochemically staining. No significant difference in morning serum cortisol in group1 and 2; mean +/- SD was [10.67+/-3.73], [12.34+/-3.58], and also between cases with MIF gene SNP [group B] and without [group A], mean +/- SD was [11.64+/-2.68]. [10.13+/-4.26] respectively p>0.05
Concision: potent association was found between human MIF gene [SNP], Tissue expression of MIF and severity of AD. Anti MIF antibodies can be used in management of different forms of AD. Higher doses of steroid therapy may be required in some cases to antagonize elevated MIF level and possibility of subclinical hypo function of adrenal gland