USA300 is an epidemic community-acquired methicillin-resistant Staphylococcus aureus (C-MRSA) clone in the USA, whereas the European C-MRSA clone ST80-IV has mainly a sporadic diffusion in Europe. The prevalence of European clone ST80-IV in Algeria is poorly documented. We prospectively studied S. aureus infections at Mustapha Bacha hospital in Algiers over a 20-month period. S. aureus nasal colonization was studied during a further 6-month period. The European clone ST80-IV was responsible for more than one-third of both community infections (35.7%) and hospital infections (35.8%). Panton-Valentine leukocidin (PVL)-positive MRSA isolated from hospital inpatients were resistant to multiple antibiotics, including fluoroquinolones in 44.9% of cases. The PVL-positive MRSA nasal carriage rate was high among patients and staff in the dermatology unit (8.7% and 18.5%, respectively), but low (2.7%) among patients attending the outpatient clinic. The European PVL-positive C-MRSA clone ST80-IV is widespread in the Algiers hospital and community settings.
Many toxins are expressed in vivo and recognized by the immune system during staphylococcal infections, suggesting their involvement in S. aureus pathogenesis.
Staphylococcus aureus strains producing Panton-Valentine leukocidin (PVL) have been epidemiologically linked to specific human infections. To evaluate immunological tests that may be used to diagnose infections with PVL-producing strains, we prospectively collected pus, respiratory tract specimens, and joint fluid specimens from which S. aureus had been isolated in clinical laboratories in six countries. An enzyme-linked immunosorbent assay (ELISA) and an immunochromatographic test (ICT) targeting LukS-PV were performed directly with clinical samples for the detection of PVL. The same tests were applied to S. aureus culture supernatants. The corresponding S. aureus isolates were characterized by PCR for the presence of the PVL locus (lukS-PV and lukF-PV) and the mecA gene. A total of 185 samples from 144 skin infections, 23 bone and joint infections, and 18 lower respiratory tract infections were analyzed. By PCR, 72/185 S. aureus isolates were PVL locus positive (PVL ؉ ); 28 of these were also mecA positive. PVL was detected in the supernatants of all PVL ؉ strains by both ELISA and an ICT, while no signal was observed with PVL-negative strains. The PVL concentrations in human clinical samples that grew PVL ؉ strains ranged from 0 to 399 g/ml by ELISA. By the use of 0.015 g/ml of PVL as a cutoff value, PVL was detected in 65/72 (90%) of the clinical samples by ELISA. The sensitivity and specificity of the ELISA test were 90% and 100%, respectively. By the ICT, PVL was detected in 57/72 (79%) of the samples, and the sensitivity and specificity of ICT were 79% and 100%, respectively. PVL is expressed by S. aureus during human infection, and a PVL-specific ELISA and ICT could be reliable tests for the diagnosis of infections caused by PVL-producing strains.
SHV-12, QnrS1, QnrB1 and QnrB4 were reported for the first time in Algeria. This study also described a co-expression of qnrS1 and qnrB4 by an SHV-12 producer isolate.
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