Background: Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease. Conflicting reports are available about the association between human parvovirus B19 (B19) infection and RA. Most studies were done in European and Asian countries, but only few studies were performed in Africa. Objectives: This study aimed to investigate the seroprevalence of parvovirus B19 infection in RA patients compared with healthy controls and to search for possible association of B19 viremia with disease activity and severity. Methodology: This case-control study was conducted on 50 RA patients who fulfilled the 2010 American College of Rheumatology/European League against Rheumatism classification criteria for rheumatoid arthritis and 30 matched healthy controls. All participants were examined for parvovirus B19 infection by serological detection of anti-B19 IgM and IgG by ELISA and B19 DNA by nested PCR. Results: Parvovirus B19 DNA was detected in 17 (34%) of patients While controls were (6.7%) with a significant difference (0.005). There was significant difference between patients and controls (P=0.007) regarding IgG anti-B19 antibody but not anti-B19 IgM (P =0.59). There was a significant association between B19 viremia and all activity parameters. B19 positive patients had higher levels of ESR and CRP, higher DAS28 scores and more affected joints than B19 negative patients with statistically significant differences. B19 positive patients had significantly higher levels of RF and anti-CCP. Furthermore, B19 positive patients were more likely to have joint erosion. Conclusion: This study revealed that parvovirus B19 infection may play a role in the aetiopathogenesis of RA.

Background: Staphylococcus aureus is a leading cause of burn wound infection. Vancomycin resistance among methicillin-resistant Staphylococcus aureus (MRSA) is becoming a worldwide growing threat. Objectives: to detect the prevalence of MRSA in burn patients and its antibiotic susceptibility patterns. In addition, the resistance patterns of MRSA to vancomycin and the prevalence of vanA gene among MRSA isolates were investigated. Methodology: A total 250 clinical samples were obtained from patients admitted to Burn Unit in Menoufia University Hospitals. Identification and antimicrobial susceptibility testing of S. aureus isolates were performed. Cefoxitin disk diffusion method was used to identify MRSA strains. Vancomycin resistance was determined by agar dilution method. Detection of mecA and vanA genes by multiplex PCR was done. Results: Staphylococcus aureus represented 43.3% of all isolates. By cefoxitin disc diffusion method, 94% (79/84) of isolated S. aureus were MRSA that showed a high resistance to most antimicrobials used with rates ranged from 40.5 % to 100%. Phenotypically among MRSA isolates, vancomycin sensitive S. aureus (VSSA), vancomycin-intermediate S. aureus (VISA) and vancomycin-resistant S. aureus (VRSA) were 59.5%, 15.2%, 25.3% respectively. Among MRSA isolates, 17 (21.5%) isolates had vanA gene by PCR (16 isolates were VRSA and one isolate was VSSA).Conclusion: This study is considered as an alarm demonstrating that implementation of proper infection control measures is mandatory to control spread of such resistant strains in our hospital.

Background: Acinetobacter baumannii (A. baumannii) is one of the most important nosocomial pathogen. With the introduction of colistin as a last resort in treatment of A. baumannii, resistant strains. Using combined antibiotics could increase the success of treatment and reduce resistance. Objectives: To assess potential in-vitro synergistic activity of colistin when combined with (vancomycin, teicoplanin, rifampicin, tigecycline, meropenem, amikacin, and ceftazidime) against colistin resistant A. baumannii (CRAB). Also, to screen the prevalence of plasmid mediated colistin resistance (mcr) genes (mcr-1 to mcr-5) in colistin resistant isolates. Methodology: A. baumannii strains were isolated from different microbial specimens. Antibiotic susceptibility testing was done for all isolates by disk diffusion method while broth micro dilution (BMD) was performed to determine colistin minimum inhibitory concentration (MIC). Genotypic detection of mcr genes was done using multiplex PCR. Checkerboard method was done to detect potential synergistic activities between colistin and other tested antibiotics against CRAB. Results: A total of 94 A. baumannii strains were isolated from 373 different clinical samples. Colistin resistance was detected in 44/94 (46.8%) of isolated A. baumannii. Only 2 out of 44 CRAB (4.5%) carried mcr-1 gene and neither of other mcr genes could be detected. All isolated CRAB were resistant to 7 tested antibiotics by BMD. But when colistin was included in a checkerboard pattern, colistin-based combinations with vancomycin, meropenem, rifampicin, teicoplanin and ceftazidime showed synergy in 93. 2%, 90.9%, 88.7%, 86.4% and 79.5% of isolated CRAB respectively. For both tigecyclin and amikacin more than 90% of CRAB showed indifference in combination with colistin. Conclusion: Further studies are needed to determine the ability of colistin based antimicrobial combinations as an alternative therapy to treat CRAB infections and confirm that synergy.

Background: SLE is an autoimmune disease with complex etiology. Genetic aberrations disrupting the immune regulatory mechanisms may initiate autoimmune disease development. As CTLA-4 is a negative regulator of T-cell immune response and IL-1β is a potential pro-inflammatory cytokine, their allelic polymorphisms might have an impact on SLE susceptibility. Objectives: To investigate a possible association between the polymorphisms of interleukin-1β (IL-1β) and cytotoxic T lymphocyte associated antigen-4 (CTLA-4) genes and increased susceptibility and activity of systemic lupus erythematosus (SLE). Methodology: This study was conducted on 50 SLE patients and 25 age-and sex-matched healthy individuals. All patients were subjected to full clinical evaluation and laboratory investigations. The studied groups were genotyped for CTLA-4 -318 C/T and IL-1β -31 T/C polymorphisms by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Results: The TT genotype and T allele frequencies of the IL-1β -31 T/C polymorphism were significantly (P <0.05) higher in SLE patients than controls. In SLE patients, significant (P <0.05) association of IL-1β -31 T/C polymorphism and SLE activity was observed in TT genotype. There was an increased frequency of TT genotype of IL-1β -31 T/C polymorphism in SLE patients with arthritis and vasculitis compared to those without these manifestations. SLE patients with TT genotype had higher SLEDAI score, anti-dsDNA titer and ESR compared to those with C/T or CC genotypes. On the other hand, the disease susceptibility and activity, demographic characters, clinical data, SLEDAI score, clinical manifestations, autoantibody profile and laboratory characteristics had insignificant association with different genotypes of CTLA-4 -318 C/T polymorphism (P >0.05). Conclusion: IL-1β -31 T/C but not CTLA-4 -318 C/T polymorphisms are associated with increased SLE susceptibility and activity.