Microbiological profile of diabetic foot ulcers and its antibiotic susceptibility pattern in a teaching hospital, Gujarat

Background: Diabetic foot lesions are a major medical, social and economic problem and are the leading cause of hospitalization for patients with diabetes worldwide. Infection sometimes leads to amputation of the infected foot if not treated promptly. The present study was conducted to isolate and identify the bacterial pathogens associated with diabetic foot ulcer and to find out its antibiotic susceptibility pattern to reduce the risk of complications.Methods: Total 100 pus samples were collected from patients having diabetic foot ulcer, during July to October 2012. Samples were processed as per standard guidelines.Results: Out of 100 pus samples, 73 (73%) yielded growth of organisms making total of 92 isolates. Out of 92 bacterial isolates, 72 were gram negative and 20 were gram positive. Pseudomonas aeruginosa 25 (27%) was most common isolate causing diabetic foot infections followed by 20 (22%) Klebsiella sp., 17 (19%) E. coli, 15 (17%) S. aureus, 6 (7%) Proteus sp. and 4(3%) Enterococci, 2 (2%) Acinetobacter sp. and 2(2%) CONS and 1(1%) Providencia. Out of 72 GNB, 50 (69.4%) were extended spectrum β lactamase (ESBL) producer. Most gram negative isolates were resistant to levofloxacin, gentamicin, ampicillin-sulbactam and gatifloxacin. All GNB were sensitive to imipenem. Out of 15 S. aureus, 9 (60%) were Methicillin Resistant Staphylococcus aureus (MRSA) and were sensitive to vancomycin and linezolid.Conclusions: Pseudomonas sp. was the most common cause of infections.  Most isolates were multi drug resistance

Bacteriological profile and antibiogram of blood culture isolates from patients of rural tertiary care hospital

Microbial invasion of blood stream is associated with significant mortality and morbidity. Identification of bacterial isolates and antibiotic susceptibility of bacteria isolated from blood culture would guide the antibiotics treatment for patients with bacteremia. 1) To determine age – wise blood culture positivity rate in bacteremia 2) To identify age – wise common bacterial species isolates in bacteremia 3) To determine Antibiotic sensitivity pattern of the bacterial isolates. Atotal of 247 blood culture samples received from various clinical departments of rural teaching hospital from August 2013 to September 2015 were included in the study. Samples were collected in brain heart infusion broth. Identification of isolates and antimicrobial susceptibility was done as per standard microbiological methods. Out of 247 specimens bacteria sp. was isolated from 46 (18.62%) samples. Blood culture positivity was noted highest among neonates age group (38.71%). Lowest rate was observed among elders (4.55%). Klebsiella pneumoniae, Coagulase negative staphylococcus (CONs), and S. aureus were common blood culture isolates. In neonates Klebsiella pneumoniae was the most common isolate. Out of 27 gram negative bacilli, 14 (51.85%) were extended spectrum betalactamases (ESBL) positive. High resistance was noted against amoxycillin and amoxicillin/clavulanic acid and third generation cephalosporins in all gram negative organisms except, S. typhi. Out of 12 Staphylococcus sp., none of these were methicillin resistant. Routine antibiotic susceptibility surveillance helps in choice of antibiotics for treatment, identification of resistance and control of its spread. Published by the International journal of Microbiology and Mycology (IJMM

PPARδ Activation Acts Cooperatively with 3-Phosphoinositide-Dependent Protein Kinase-1 to Enhance Mammary Tumorigenesis

Peroxisome proliferator-activated receptorδ (PPARδ) is a transcription factor that is associated with metabolic gene regulation and inflammation. It has been implicated in tumor promotion and in the regulation of 3-phosphoinositide-dependent kinase-1 (PDK1). PDK1 is a key regulator of the AGC protein kinase family, which includes the proto-oncogene AKT/PKB implicated in several malignancies, including breast cancer. To assess the role of PDK1 in mammary tumorigenesis and its interaction with PPARδ, transgenic mice were generated in which PDK1 was expressed in mammary epithelium under the control of the MMTV enhancer/promoter region. Transgene expression increased pT308AKT and pS9GSK3β, but did not alter phosphorylation of mTOR, 4EBP1, ribosomal protein S6 and PKCα. The transgenic mammary gland also expressed higher levels of PPARδ and a gene expression profile resembling wild-type mice maintained on a diet containing the PPARδ agonist, GW501516. Both wild-type and transgenic mice treated with GW501516 exhibited accelerated rates of tumor formation that were more pronounced in transgenic animals. GW501516 treatment was accompanied by a distinct metabolic gene expression and metabolomic signature that was not present in untreated animals. GW501516-treated transgenic mice expressed higher levels of fatty acid and phospholipid metabolites than treated wild-type mice, suggesting the involvement of PDK1 in enhancing PPARδ-driven energy metabolism. These results reveal that PPARδ activation elicits a distinct metabolic and metabolomic profile in tumors that is in part related to PDK1 and AKT signaling

Peripheral Disruption of the Grb10 Gene Enhances Insulin Signaling and Sensitivity In Vivo▿

Grb10 is a pleckstrin homology and Src homology 2 domain-containing protein that interacts with a number of phosphorylated receptor tyrosine kinases, including the insulin receptor. In mice, Grb10 gene expression is imprinted with maternal expression in all tissues except the brain. While the interaction between Grb10 and the insulin receptor has been extensively investigated in cultured cells, whether this adaptor protein plays a positive or negative role in insulin signaling and action remains controversial. In order to investigate the in vivo role of Grb10 in insulin signaling and action in the periphery, we generated Grb10 knockout mice by the gene trap technique and analyzed mice with maternal inheritance of the knockout allele. Disruption of Grb10 gene expression in peripheral tissues had no significant effect on fasting glucose and insulin levels. On the other hand, peripheral-tissue-specific knockout of Grb10 led to significant overgrowth of the mice, consistent with a role for endogenous Grb10 as a growth suppressor. Loss of Grb10 expression in insulin target tissues, such as skeletal muscle and fat, resulted in enhanced insulin-stimulated Akt and mitogen-activated protein kinase phosphorylation. Hyperinsulinemic-euglycemic clamp studies revealed that disruption of Grb10 gene expression in peripheral tissues led to increased insulin sensitivity. Taken together, our results provide strong evidence that Grb10 is a negative regulator of insulin signaling and action in vivo