ABSTRACT
Purpose: Different studies show consistent predictable bacterial profiles in wound infections, antibiotic resistance and capacity to adapt to a changing environment, which render the pathogens a matter of concern in hospital acquired infections. Therefore, periodical monitoring of bacterial profile and their antibiotic susceptibility pattern is essential. The objective of this study is to determine the commonly encountered pathogens in pus samples along with their antibiotic susceptibility patterns. Methodology: Pus samples received for diagnostic microbiology were processed and identified by standard protocols at the research lab of SZABIST Biosciences Department. Antibiotic susceptibility testing was done by Kirby-Bauer Disc Diffusion method. MS Excel has been used for data compiling and analysis. Standard Deviation has been applied for the results analysis. Results: Among the isolated organisms from pus specimens, Staphylococcus aureus (50%) was the most common followed by Escherichia coli (25%), Klebsiella pneumonia (9%), Pseudomonas aeruginosa (8%), Proteus species (5%) and Acinetobacter species (3%). Quinolones (76.4%), Cephalosporins (66.4%) and Aminoglycosides (41.6%) were found to be the most effective antimicrobials in vitro, whereas Amoxicillin (17.4%), Minocycline (14.6%) and Trimethoprim-sulphamethaxazole (3%) were least effective. The resistance of organisms to antibiotics is increasing steadily as they are becoming more resistant to newer antibiotics, such as quinolones. Conclusion: Doctors and nurses need to spread awareness of antibiotic resistance, and it is their duty to keep themselves updated with the latest antibiograms of commonly encountered pathogens, so that appropriate antibiotics may be provided for the treatment of infections.
ABSTRACT
The outer leaflet of Gram-negative bacterial membrane contains a great amount of lipopolysaccharides, also known as endotoxins, which play a central role in the pathogenesis of sepsis and ultimately septic shock. Lipopolysaccharide (LPS) is potent inducer of acute sepsis or chronic inflammation. Sepsis can strike anyone, but is most likely to develop from infection associated with events such as pneumonia, trauma, surgery, and burns, or serious illnesses such as cancer and AIDS. In fact, people whose deaths are ascribed to complications of cancer, AIDS, or pneumonia, often actually die as a direct result of sepsis. Sepsis involves a complex interaction between bacterial toxins and the host immune system. LPS stimulates Toll-like receptor (TLR)-4 which leads to the formation and release of range of proinflammatory mediators which are essential for the potent immune response. The massive host response to this single bacterial pattern recognition molecule is sufficient to generate diffuse endothelial injury, tissue hypoperfusion, disseminated intravascular coagulation and refractory shock. LPS recognition involves LPS binding protein (LBP), CD14 ending up in TLR4/MD-2/LPS complex. The complex leads to activation of TLR4 and subsequent signaling cascade via two pathways i. e., myeloid differentiation protein 88 (MyD88)-dependent and TRIF-dependent. Here is a brief review of TLR4 signaling and LPS recognition biology with its impact if any on downstream pathways.