Rheumatoid arthritis (RA) is a chronic disease associated with many factors, such as urinary tract infection (UTI), and the complicated type of UTI bacteria is Proteus mirabilis. Accordingly, 67 RA patients with UTI and 45 healthy controls from Baghdad regions were included in this study. Proteus mirabilis isolates were obtained from the urine of patients with RA and identified in 11.9% by biochemical tests and 16sRNA gene sequencing. ABO blood types, serum TNF-α level, serum rheumatoid factor (RF), C-reactive protein, and anti-bacterial antibody level of RA patients were compared to healthy controls. The study indicated that there is a correlation between blood type O, serum TNF-α level, rheumatoid factor (RF), C-reactive protein, and anti-bacterial antibody level of RA patients. The significant result was the increased serum level of TNF-α of RA patients who were infected with urease-produced bacteria, this might be due to the enzyme structure's role in evoking the disease.

No abstract

Staphylococcus epidermidis is the most significant nosocomial pathogen related to people with vulnerable frameworks such as malignant growth patients, neonates, and foreign body embedded materials such as heart valves. A few virulence factors in S. epidermidis can cause host damage in comparison to Staphylococcus aureus. In spite of that, the key roles of S. epidermidis virulency rely on biofilm formation, bacterial biofilm is essential for the pathogenesis by encouraging microorganisms to consist shape networks of assurance rather than free planktonic cells, hence resistance to antibacterial agents, and medically uninsured problems by colonizing medical indwelling, making the disease long span, and difficult to treat. The National Institute of Health (NIH) reported 65-80% of bacterial illnesses are biofilm formed, thus making numerous passing wellbeing additional costs. Therefore, the biofilms establishing on the susceptible hosts' tissues demonstrate; preventing antibiotics efficient treatment, protecting against host defense mechanisms, and announce the bacteria virulence determinants manifesting.

No abstract

No abstract