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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two pathological patterns of acute poststaphylococcal glomerulonephritis are well defined and include (1) an acute proliferative and exudative glomerulonephritis closely resembling classical acute poststreptococcal glomerulonephritis in patients with Staphylococcus aureus infection and (2) a membranoproliferative glomerulonephritis in patients with Staphylococcus epidermidis infection secondary to ventriculovascular shunts. In this study, we report a novel immunopathologic phenotype of immunoglobulin (Ig) A-dominant acute poststaphylococcal glomerulonephritis occurring in patients with underlying diabetic nephropathy. Five patients with type 2 diabetes presented with acute renal failure occurring after culture-positive staphylococcal infection. Renal biopsy disclosed an atypical pattern of acute endocapillary proliferative and exudative glomerulonephritis with intense deposits of IgA as the sole or dominant immunoglobulin, mimicking IgA nephropathy. The deposits were predominantly mesangial in distribution with few subepithelial humps. All five cases occurred superimposed on well-established diabetic nephropathy. Outcome was poor with irreversible renal failure in four of five (80%) cases. The possible pathophysiological basis of this atypical form of acute poststaphylococcal glomerulonephritis in diabetic patients is explored. Proper recognition of this entity is needed to avoid an erroneous diagnosis of IgA nephropathy, with corresponding therapeutic and prognostic implications.
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PMID:IgA-dominant acute poststaphylococcal glomerulonephritis complicating diabetic nephropathy. 1469 5

Foot and ankle infections are the most common cause of hospitalization among diabetic patients, and Staphylococcus aureus is a major pathogen implicated in these infections. Patients with insulin-resistant (type 2) diabetes are more susceptible to bacterial infections than nondiabetic subjects, but the pathogenesis of these infections is poorly understood. C57BL/6J-Lepr(db)/Lepr(db) (hereafter, db/db) mice develop type 2 diabetes due to a recessive, autosomal mutation in the leptin receptor. We established a S. aureus hind paw infection in diabetic db/db and nondiabetic Lepr(+/+) (+/+) mice to investigate host factors that predispose diabetic mice to infection. Nondiabetic +/+ mice resolved the S. aureus hind paw infection within 10 days, whereas db/db mice with persistent hyperglycemia developed a chronic infection associated with a high bacterial burden. Diabetic db/db mice showed a more robust neutrophil infiltration to the infection site and higher levels of chemokines in the infected tissue than +/+ mice. Blood from +/+ mice killed S. aureus in vitro, whereas db/db blood was defective in bacterial killing. Compared with peripheral blood neutrophils from +/+ mice, db/db neutrophils demonstrated a diminished respiratory burst when stimulated with S. aureus. However, bone marrow-derived neutrophils from +/+ and db/db mice showed comparable phagocytosis and bactericidal activity. Our results indicate that diabetic db/db mice are more susceptible to staphylococcal infection than their nondiabetic littermates and that persistent hyperglycemia modulates innate immunity in the diabetic host.
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PMID:Defects in innate immunity predispose C57BL/6J-Leprdb/Leprdb mice to infection by Staphylococcus aureus. 1910 72

A 74-year-old male with type 2 diabetes, coronary artery disease with history of CABG, hypertension and chronic obstructive pulmonary disease had total left hip replacement in another medical facility five years prior to admission. Since the early postoperative period, he had manifestations of dormant infection and was with empirical antibiotics. On the index admission, his X-ray showed signs of loosening of the prosthetic components with resorption of the bone. Periprosthetic infection was managed by a two-stage surgery. First, the infected prosthesis was removed and replaced with a spacer with antibiotics. One month later, a revision prosthesis, was implanted using cement with antibiotics. Cultures of the excised tissues and materials yielded massive growth of Listeria monocytogenes and scarce growth of Staphylococcus epidermidis. This is the 18th published case of arthroplasty infection caused by Listeria. The presented patient most likely had dormant staphylococcal infection on which Listeria superinfection developed and accelerated the loosening. A literature review suggested several mechanisms that can make conservative management of Listeria infection difficult. They include marked stimulation of the immune system (with resulting resorption of the bone), survival in the macrophages (unavailability to antibiotics susceptible in vitro) and capability to form biofilm as well as settle in biofilms produced by other organisms. Better yield and reliability of microbiological investigations may be achieved by guided intrarticular fluid aspiration from a microincision, prolonged culture and sonification of the extracted material, two-step surgical management and follow-up intraarticular fluid aspiration prior to reimplantation of revision prosthesis.
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PMID:[Listeria infection of a prosthetic hip joint]. 2157 33