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Lipsky B.A.,University of Washington | Peters E.J.G.,VU University Amsterdam | Senneville E.,Gustave Dron Hospital | Berendt A.R.,University of Oxford | And 4 more authors.
Diabetes/Metabolism Research and Reviews | Year: 2012

This update of the International Working Group on the Diabetic Foot incorporates some information from a related review of diabetic foot osteomyelitis (DFO) and a systematic review of the management of infection of the diabetic foot. The pathophysiology of these infections is now well understood, and there is a validated system for classifying the severity of infections based on their clinical findings. Diagnosing osteomyelitis remains difficult, but several recent publications have clarified the role of clinical, laboratory and imaging tests. Magnetic resonance imaging has emerged as the most accurate means of diagnosing bone infection, but bone biopsy for culture and histopathology remains the criterion standard. Determining the organisms responsible for a diabetic foot infection via culture of appropriately collected tissue specimens enables clinicians to make optimal antibiotic choices based on culture and sensitivity results. In addition to culture-directed antibiotic therapy, most infections require some surgical intervention, ranging from minor debridement to major resection, amputation or revascularization. Clinicians must also provide proper wound care to ensure healing of the wound. Various adjunctive therapies may benefit some patients, but the data supporting them are weak. If properly treated, most diabetic foot infections can be cured. Providers practising in developing countries, and their patients, face especially challenging situations. © 2012 John Wiley & Sons, Ltd. Source

Peters E.J.G.,VU University Amsterdam | Lipsky B.A.,University of Washington | Berendt A.R.,University of Oxford | Embil J.M.,University of Manitoba | And 5 more authors.
Diabetes/Metabolism Research and Reviews | Year: 2012

The International Working Group on the Diabetic Foot expert panel on infection conducted a systematic review of the published evidence relating to treatment of foot infection in diabetes. Our search of the literature published prior to August 2010 identified 7517 articles, 29 of which fulfilled predefined criteria for detailed data extraction. Four additional eligible papers were identified from other sources. Of the total of 33 studies, 29 were randomized controlled trials, and four were cohort studies. Among 12 studies comparing different antibiotic regimens in the management of skin and soft-tissue infection, none reported a better response with any particular regimen. Of seven studies that compared antibiotic regimens in patients with infection involving both soft tissue and bone, one reported a better clinical outcome in those treated with cefoxitin compared with ampicillin/sulbactam, but the others reported no differences between treatment regimens. In two health economic analyses, there was a small saving using one regimen versus another. No published data support the superiority of any particular route of delivery of systemic antibiotics or clarify the optimal duration of antibiotic therapy in either soft-tissue infection or osteomyelitis. In one non-randomized cohort study, the outcome of treatment of osteomyelitis was better when the antibiotic choice was based on culture of bone specimens as opposed to wound swabs, but this study was not randomized, and the results may have been affected by confounding factors. Results from two studies suggested that early surgical intervention was associated with a significant reduction in major amputation, but the methodological quality of both was low. In two studies, the use of superoxidized water was associated with a better outcome than soap or povidone iodine, but both had a high risk of bias. Studies using granulocyte-colony stimulating factor reported mixed results. There was no improvement in infection outcomes associated with hyperbaric oxygen therapy. No benefit has been reported with any other intervention, and, overall, there are currently no trial data to justify the adoption of any particular therapeutic approach in diabetic patients with infection of either soft tissue or bone of the foot. © 2012 John Wiley & Sons, Ltd. Source

Bacchus C.,University Pierre and Marie Curie | Bacchus C.,French Institute of Health and Medical Research | Cheret A.,University of Paris Descartes | Avettand-Fenoel V.,University of Paris Descartes | And 18 more authors.
PLoS ONE | Year: 2013

Optimizing therapeutic strategies for an HIV cure requires better understanding the characteristics of early HIV-1 spread among resting CD4+ cells within the first month of primary HIV-1 infection (PHI). We studied the immune distribution, diversity, and inducibility of total HIV-DNA among the following cell subsets: monocytes, peripheral blood activated and resting CD4 T cells, long-lived (naive [TN] and central-memory [TCM]) and short-lived (transitional-memory [TTM] and effector-memory cells [TEM]) resting CD4+T cells from 12 acutely-infected individuals recruited at a median 36 days from infection. Cells were sorted for total HIV-DNA quantification, phylogenetic analysis and inducibility, all studied in relation to activation status and cell signaling. One month post-infection, a single CCR5-restricted viral cluster was massively distributed in all resting CD4+ subsets from 88% subjects, while one subject showed a slight diversity. High levels of total HIV-DNA were measured among TN (median 3.4 log copies/million cells), although 10-fold less (p = 0.0005) than in equally infected TCM (4.5), TTM (4.7) and TEM (4.6) cells. CD3-CD4+ monocytes harbored a low viral burden (median 2.3 log copies/million cells), unlike equally infected resting and activated CD4+ T cells (4.5 log copies/million cells). The skewed repartition of resting CD4 subsets influenced their contribution to the pool of resting infected CD4+T cells, two thirds of which consisted of short-lived TTM and TEM subsets, whereas long-lived TN and TCM subsets contributed the balance. Each resting CD4 subset produced HIV in vitro after stimulation with anti-CD3/anti-CD28+IL-2 with kinetics and magnitude varying according to subset differentiation, while IL-7 preferentially induced virus production from long-lived resting TN cells. In conclusion, within a month of infection, a clonal HIV-1 cluster is massively distributed among resting CD4 T-cell subsets with a flexible inducibility, suggesting that subset activation and skewed immune homeostasis determine the conditions of viral dissemination and early establishment of the HIV reservoir. © 2013 Bacchus et al. Source

Lipsky B.A.,University of Geneva | Lipsky B.A.,University of Oxford | Aragon-Sanchez J.,La Paloma Hospital | Diggle M.,University of Nottingham | And 7 more authors.
Diabetes/Metabolism Research and Reviews | Year: 2016

Recommendations: Classification/diagnosis: Diabetic foot infection must be diagnosed clinically, based on the presence of local or systemic signs or symptoms of inflammation (strong; low). Assess the severity of any diabetic foot infection using the Infectious Diseases Society of America/International Working Group on the Diabetic Foot classification scheme (strong; moderate). Osteomyelitis: For an infected open wound, perform a probe-to-bone test; in a patient at low risk for osteomyelitis, a negative test largely rules out the diagnosis, while in a high-risk patient, a positive test is largely diagnostic (strong; high). Markedly elevated serum inflammatory markers, especially erythrocyte sedimentation rate, are suggestive of osteomyelitis in suspected cases (weak; moderate). A definite diagnosis of bone infection usually requires positive results on microbiological (and, optimally, histological) examinations of an aseptically obtained bone sample, but this is usually required only when the diagnosis is in doubt or determining the causative pathogen's antibiotic susceptibility is crucial (strong; moderate). A probable diagnosis of bone infection is reasonable if there are positive results on a combination of diagnostic tests, such as probe-to-bone, serum inflammatory markers, plain X-ray, magnetic resonance imaging (MRI) or radionuclide scanning (strong; weak). Avoid using results of soft tissue or sinus tract specimens for selecting antibiotic therapy for osteomyelitis as they do not accurately reflect bone culture results (strong; moderate). Obtain plain X-rays of the foot in all cases of non-superficial diabetic foot infection (strong; low). Use MRI when an advanced imaging test is needed for diagnosing diabetic foot osteomyelitis (strong; moderate). When MRI is not available or contraindicated, consider a white blood cell-labelled radionuclide scan, or possibly single-photon emission computed tomography (CT) and CT (SPECT/CT) or fluorine-18-fluorodeoxyglucose positron emission tomography/CT scans (weak; moderate). Assessing severity: At initial evaluation of any infected foot, obtain vital signs and appropriate blood tests, debride the wound and probe and assess the depth and extent of the infection to establish its severity (strong; moderate). At initial evaluation, assess arterial perfusion and decide whether and when further vascular assessment or revascularization is needed (strong; low). Microbiological considerations: Obtain cultures, preferably of a tissue specimen rather than a swab, of infected wounds to determine the causative microorganisms and their antibiotic sensitivity (strong; high). Do not obtain repeat cultures unless the patient is not clinically responding to treatment, or occasionally for infection control surveillance of resistant pathogens (strong; low). Send collected specimens to the microbiology laboratory promptly, in sterile transport containers, accompanied by clinical information on the type of specimen and location of the wound (strong; low). Surgical treatment: Consult a surgical specialist in selected cases of moderate, and all cases of severe, diabetic foot infection (weak; low). Perform urgent surgical interventions in cases of deep abscesses, compartment syndrome and virtually all necrotizing soft tissue infections (strong; low). Consider surgical intervention in cases of osteomyelitis accompanied by spreading soft tissue infection, destroyed soft tissue envelope, progressive bone destruction on X-ray or bone protruding through the ulcer (strong; low). Antimicrobial therapy: While virtually all clinically infected diabetic foot wounds require antimicrobial therapy, do not treat clinically uninfected wounds with antimicrobial therapy (Strong; Low) Select specific antibiotic agents for treatment based on the likely or proven causative pathogens, their antibiotic susceptibilities, the clinical severity of the infection, evidence of efficacy of the agent for diabetic foot infection and costs (strong; moderate). A course of antibiotic therapy of 1-2 weeks is usually adequate for most mild and moderate infections (strong; high). Administer parenteral therapy initially for most severe infections and some moderate infections, with a switch to oral therapy when the infection is responding (strong; low). Do not select a specific type of dressing for a diabetic foot infection with the aim of preventing an infection or improving its outcome (strong; high). For diabetic foot osteomyelitis, we recommend 6 weeks of antibiotic therapy for patients who do not undergo resection of infected bone and no more than a week of antibiotic treatment if all infected bone is resected (strong; moderate). We suggest not using any adjunctive treatments for diabetic foot infection (weak; low). When treating a diabetic foot infection, assess for use of traditional remedies and previous antibiotic use and consider local bacterial pathogens and their susceptibility profile (strong; low). © 2016 John Wiley & Sons, Ltd. Source

Lolli V.,Erasmus University College Brussels | Molinari F.,Gustave Dron Hospital | Pruvo J.-P.,Roger Salengro Hospital | Soto Ares G.,Roger Salengro Hospital
Journal of Neuroradiology | Year: 2016

Background and purpose: Cerebral sinovenous thrombosis (CSVT) represents an increasingly recognized cause of pediatric stroke. Our purpose was to assess gender and age differences in the etiology, clinical presentation, and imaging features of CSVT in neonates and older children. Methods: Subjects aged newborn to 18 years diagnosed with CSVT at the Lille university hospital between 2011 and 2014 were included. Results: Eleven neonates and 16 non-neonates constituted the study population. The incidence of CSVT was significantly higher in male newborns. Clinical presentation did not vary significantly between the groups. Risk factors were age-dependent, with acute systemic illnesses significantly predominating in neonates (54%), whereas local infections, prothrombotic conditions, and trauma were more common in older children (36, 27, and 27% respectively). No predisposing factor could be identified in 36% of the neonates as compared to less than 5% of the non-neonates. Thrombosis of the deep venous structures was documented in 73% of the neonates whereas involvement of the superficial sinuses was significantly more frequent in the non-neonates group. Venous infarctions and extraparenchymal hemorrhages were significantly more frequent in the neonates group. Conclusion: Male patients are at higher risk for CSVT than females. In neonates, involvement of the deep venous structures is significantly more common. Brain parenchymal and extraparenchymal changes occur more frequently in this age group than in older children. © 2016 Elsevier Masson SAS. Source

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