Causative Agent Of Osteomyelitis Research Articles

Comparative analysis of resistance of main etiological agents of chronic osteomyelitis isolated from association and in monoculture

Introduction. To date, a significant number of works have been published devoted to the analysis of the sensitivity of the leading causative agents of osteomyelitis to modern drugs, however, in the available literature there are no data on a comparative analysis of the antibiotic resistance of bacteria isolated from the osteomyelitis focus from the association and in monoculture. Purpose of the work: to compare the resistance profiles of the leading causative agents of osteomyelitis, depending on the bacterial composition of the focus of infection.Materials and methods. The study included 216 clinical isolates, of which 114 were isolated as part of two-component associations, 102 – in a monoculture from pathological material in patients with chronic osteomyelitis who were treated in the purulent department of National Medical Scientific Centre of Traumatology and Orthopedics n.a. academician G.E. Ilizarov (Kurgan, Russia) from 2018 to 2020. To analyze the resistance profiles, depending on the type of microorganism, modern drugs used in the clinic for the treatment of osteomyelitis were taken into account.Results and its discussion. Effective drugs against P. aeruginosa strains isolated from the association were polymyxin and meropenem, and in monoculture–polymyxin, piperacillin/tazobactam, tobramycin; in relation to strains of K. pneumoniae isolated from the association, it was imipenem, in monoculture – amikacin. S. aureus strains isolated both from the association and in monoculture were highly susceptible to antibacterial drugs.Conclusion. The analysis of the sensitivity of the leading causative agents of osteomyelitis, isolated in monoculture and from the association, to the antibacterial drugs used in the clinic, showed significant differences in the resistance profiles between the groups: for S. aureus strains, 4 antibiotics tested out of 13, for P. aeruginosa strains – 7 out of 13, for K. pneumoniae strains – 12 out of 16. The tested antibacterial drugs were less active against P. aeruginosa and S. aureus strains isolated from associations. In contrast, the percentage of resistant strains of K. pneumoniae was higher among monocultures.

Staphylococcus prettenkoferi – biochemical properties, methods of species identification and clinical significance

Staphylococcus pettenkoferi was first isolated from blood culture a 25-years-old patient with fever of unknown etiology. Based on the literature analysis, it was found that it is an opportunistic microorganism. It causes blood stream infections and was an causative agent of osteomyelitis. Staphylococcus pettenkoferi is a component of the human microbiome, was found in a hospital environment and was also isolated from animals and their surroundings.

Acute hematogenous osteomyelitis due to Salmonella in a pediatric patient: a case report

Acute hematogenous osteomyelitis is an inflammatory process in the bone tissue. It’s usually of bacterial etiology, caused by a contiguous infection focus. In pediatric patients, the main isolated pathogen is Staphylococcus aureus. Salmonella spp. as a causative agent of osteomyelitis is infrequent; it can be found in less than 1% of the casesand it is generally associated with risk factors. We analyze the case of a 4 years old male patient known to be healthy, who enters the emergency service with a 2 weeks of increasing fever and difficulty when walking. Upon physical examination, he presented acute pain, edema and a local increased temperature in the right ankle. He was hospitalized for suspicion of septic arthritis and he was treated empirically with clindamycin. Positive cultures were reported for Salmonella spp, isolated from blood and a tibia’s secretion sample. The betalactambased approach, specifically third-generation cephalosporins, is recommended in international treatment guidelines, so the success of the use of ampicillin was expected. Thus, identifying the etiological agent of the infectious process is determinant in the success of antibiotic therapy, as well as the joint approach of the medical personnel and the laboratory service.

Optimizing the treatment of osteomyelitis with antimicrobial drugs: current concepts

The success of osteomyelitis treatment, particularly in cases related to implants, depends on extensive surgical debridement and adequate and effective antibiotic therapy. Direct administration of antimicrobial agents through their incorporation into orthopaedic cement is an important adjuvant therapy. The capacity for biofilm to form by causative agents of osteomyelitis is an obstacle to antimicrobial treatment of these infections. Bacteria present in biofilm usually has greater bacterial resistance and higher expression of virulence factors than sessile bacteria, as well as mechanisms to escape the host immune response. The ability of causative agents of infection, particularly Staphylococcus aureus, to form small colony variants (SCV), a phenotype capable of invading and infecting osteoblasts, is another important mechanism that contributes to exacerbation of osteomyelitis to a chronic state. To optimize the antimicrobial treatment of osteomyelitis and improve patients’ prognosis, it is fundamental to consider these complicating factors, as well as the antimicrobial susceptibility profile of the causative microorganisms. Rifampicin should always be considered as part of the therapeutic regimen because it presents good bone concentration and has proven capacity to act on strains present in biofilm and in SCV.

Apoptosis-associated uncoupling of bone formation and resorption in osteomyelitis

The mechanisms underlying the destruction of bone tissue in osteomyelitis are only now being elucidated. While some of the tissue damage associated with osteomyelitis likely results from the direct actions of bacteria and infiltrating leukocytes, perhaps exacerbated by bacterial manipulation of leukocyte survival pathways, infection-induced bone loss predominantly results from an uncoupling of the activities of osteoblasts and osteoclasts. Bacteria or their products can directly increase osteoclast formation and activity, and the inflammatory milieu at sites of infection can further promote bone resorption. In addition, osteoclast activity is critically regulated by osteoblasts that can respond to bacterial pathogens and foster both inflammation and osteoclastogenesis. Importantly, bone loss during osteomyelitis is also brought about by a decline in new bone deposition due to decreased bone matrix synthesis and by increased rates of osteoblast apoptosis. Extracellular bacterial components may be sufficient to reduce osteoblast viability, but the causative agents of osteomyelitis are also capable of inducing continuous apoptosis of these cells by activating intrinsic and extrinsic cell death pathways to further uncouple bone formation and resorption. Interestingly, bacterial internalization appears to be required for maximal osteoblast apoptosis, and cytosolic inflammasome activation may act in concert with autocrine/paracrine death receptor-ligand signaling to induce cell death. The manipulation of apoptotic pathways in infected bone cells could be an attractive new means to limit inflammatory damage in osteomyelitis. However, the mechanism that is the most important in bacterium-induced bone loss has not yet been identified. Furthermore, it remains to be determined whether the host would be best served by preventing osteoblast cell death or by promoting apoptosis in infected cells.