Background:The polymyxins including colistin are the "last resort" antibiotics for treatment of infections with carbapenem resistant Enterobacteriaceae. Recently, transferable colistin resistance mediated by the mcr-genes has been described in Enterobacteriaceae. The testing of colistin susceptibility is challenging. The aim of the work is to detect the occurence of mcr-1 and mcr-2 genes in phenotypically colistin-resistant carbapenem resistant Escherichia coli (E. coli) and Klebsiella pneumoniae (K. pneumoniae) isolates using conventional polymerse chain reaction (PCR). Methods: One hundred and sixteen carbapenem-resistant E.coli and K.pneumoniae isolates were collected from patients admitted to different wards of Suez Canal University Hospitals (SCUHs) in Ismailia. Urine, endotracheal aspirates, blood, pus and sputum specimens were collected from different patients. Minimal inhibitory concentration (MIC) by broth microdiluton method was done to assess phenotypic colistin resistance. The colistin resistant E.coli and K.pneumoniae isolates were tested by conventional PCR to detect plasmid mediated mcr-1 and mcr-2 genes. Chi-square test was applied and p-value < 0.05 was considered statistically significant. Results: Forty three isolates out of 116 carbapenem resistant isolates (37.1%) were colistin resistant as shown by MIC by broth microdiluton method. The 43 colistin resistant E.coli and K.pneumoniae isolates were tested by conventional PCR to detect plasmid mediated mcr-1 and mcr-2 genes. Two mcr-2 genes and one mcr-1 gene were detected. Conclusion: Results revealed that the prevalence of colistin resistance among carbapenem-resistant E.coli and K.pneumoniae in SCUHs is concerning; further limiting potential therapeutic options. Plasmid mediated colistin resistance genes mcr-1 and mcr-2 is emerging in SCUHs which refer to a problem in the hospital as by horizontal transfer of this plasmid, the resistance can spread to many isolates in the hospital.

Background: Community acquired methicillin resistant staphylococcus aureus (CA-MRSA) is emerging in hospitals, worldwide. Method: In Suez Canal University Hospitals (SCUH), we documented CA-MRSA causing hospital acquired-(HA-) sepsis, by polymerase chain reaction (PCR) amplification of CA-MRSA major virulence determinant genes, namely: Panton-Valentine leukocidin "pvl", accessory regulator "agr" I and III, and staphylococcal cassette chromosome mec "SCCmec" genes IV and V. Antibiograms were determined by disk diffusion and minimum inhibitory concentration (MIC). Results: Methicillin resistant staphylococcus aureus was detected in 90 hospital acquired infections (HAIs), including bacteremia, pneumonia, osteomyelitis, soft tissue infections, and meningitis. Pvl gene, characterizing CA-MRSA, was detected in 24/90 MRSA strains (26.7%). Pvl+ve strains were subtyped into SCCmec gene type II (8.3%), type IV (75%), type V (8.3%), and 8.3% were non-typeable. They showed only agr group I (62.5%), and III (37.5%). Co-trimoxazole resistance was detected in 41.6% of CA-MRSA. Only 12.5% of CA-MRSA strains were susceptible to all non-beta-lactam drugs. There was no statistical correlation between SCCmec or agr groups, and co-trimoxazole resistance in CA-MRSA; nor between SCCmec types and agr groups. Conclusion: Community aquired-MRSA is emerging in all wards of SCU hospitals, causing HAI, mostly soft tissue infections. The classical antibiogram of CA-MRSA is no longer prevailing. Diagnosis of CA-MRSA should rely upon detection of pvl gene, rather that clinical and antibiogram-profiles. The name "CA-MRSA" is no longer satisfactory to describe such strains in hospital settings; instead, Pvl +ve MRSA is more accurate and reliable term to use.

The most common bacterial agents of atypical pneumonia are Mycoplasma pneumoniae