Background and Objective: Diabetic foot ulceration is a multifactorial process involving various intrinsic complications of diabetes mellitus which cause injury to the foot at risk. The diabetic foot ulcer infections are polymicrobial in nature. Failure to recognize and control of the infectious process may have devastating consequences of limb amputation, sepsis, and mortality. Hence, the study was undertaken to determine the bacterial and clinical profile of diabetic foot ulcer using optimal culture techniques and the antimicrobial sensitivity pattern of the isolates. Materials and Methods: A total of 100 patients with diabetic foot ulcer of Wagner's grade I and above were included in the study. Pus and tissue biopsy were collected for bacteriological study. The specimen was processed in the microbiology laboratory for Gram stain, aerobic culture, and anaerobic culture. The organisms isolated were identified by standard procedures and antimicrobial susceptibility was done by Kirby-Bauer disc diffusion method. Results: A total of 187 organisms were isolated, with an average of 1.87 organisms per specimen. Pseudomonas sp, 36 (21.9%), was the most common aerobic organisms isolated followed by Klebsiella sp, 32 (19.4%). Anaerobic organisms isolated were 22 (11.77%). The predominant anaerobic organisms isolated were Peptostreptococcus sp, 10 (45.5%). All the aerobic Gram-negative organisms were sensitive to imipenem (100%). Gram-positive organism was 100% sensitive to vancomycin. Methicillin resistant staphylococcus aureus (MRSA) was seen in 66.7%. All the anaerobes were sensitive to metronidazole, clindamycin, cefoxitin, and penicillin G. Conclusion: Pseudomonas was the most common organism isolated in our study. MRSA was seen in 66.7% of the isolate.

Fatty acids (FAs) are important as metabolic substrates and as structural components of biological membranes. However, they also function as signalling molecules. Recently, a series of G protein-coupled receptors (GPRs) for FAs has been described and characterized. These receptors have differing specificities for FAs of differing chain length and degree of saturation, for FA derivatives such as oleoylethanolamide, and for oxidized FAs. They are a critical component of the body's nutrient sensing apparatus, and small molecule agonists and antagonists of these receptors show considerable promise in the management of diabetes and its complications. Agonists of the long-chain free fatty acid receptors FFAR1 and GPR119 act as insulin secretagogues, both directly and by increasing incretins. Although, drugs acting at short-chain FFA receptors (FFAR2 and FFAR3) have not yet been developed, they are attractive targets as they regulate nutrient balance through effects in the intestine and adipose tissue. These include regulation of the secretion of cholecystokinin, peptide YY and leptin. Finally, GPR132 is a receptor for oxidized FAs, which may be a sensor of lipid overload and oxidative stress, and which is involved in atherosclerosis. Regulation of its signalling pathways with drugs may decrease the macrovascular risk experienced by diabetic patients. In summary, FA receptors are emerging drug targets that are involved in the regulation of nutrient status and carbohydrate tolerance, and modulators of these receptors may well figure prominently in the next generation of antidiabetic drugs.

We conclude that GPR132 is an independent monocyte activation marker in diabetes, but does not contribute to PPAR-γ-mediated induction of FABP4 by HODEs.

Macrophage apoptosis, a key process in atherogenesis, is regulated by oxidation products, including hydroxyoctadecadienoic acids (HODEs). These stable oxidation products of linoleic acid (LA) are abundant in atherosclerotic plaque and activate PPARc and GPR132. We investigated the mechanisms through which HODEs regulate apoptosis. The effect of HODEs on THP-1 monocytes and adherent THP-1 cells were compared with other C18 fatty acids, LA and a-linolenic acid (ALA). The number of cells was reduced within 24 hours following treatment with 9-HODE (p \ 0.01, 30 lM) and 13 HODE (p \ 0.01, 30 lM), and the equivalent cell viability was also decreased (p \ 0.001). Both 9-HODE and 13-HODE (but not LA or ALA) markedly increased caspase-3/7 activity (p \ 0.001) in both monocytes and adherent THP-1 cells, with 9-HODE the more potent. In addition, 9-HODE and 13-HODE both increased Annexin-V labelling of cells (p \ 0.001). There was no effect of LA, ALA, or the PPARc agonist rosiglitazone (1lM), but the effect of HODEs was replicated with apoptosis-inducer camptothecin (10lM). Only 9-HODE increased DNA fragmentation. The pro-apoptotic effect of HODEs was blocked by the caspase inhibitor DEVD-CHO. The PPARc antagonist T0070907 further increased apoptosis, suggestive of the PPARc-regulated apoptotic effects induced by 9-HODE. The use of siRNA for GPR132 showed no evidence that the effect of HODEs was mediated through this receptor. 9-HODE and 13-HODE are potent-and specific-regulators of apoptosis in THP-1 cells. Their action is PPARcdependent and independent of GPR132. Further studies to identify the signalling pathways through which HODEs increase apoptosis in macrophages may reveal novel therapeutic targets for atherosclerosis.

Primary amoebic meningoencephalitis (PAM) caused by free-living amebae Naegleria fowleri is a rare and fatal condition. A fatal case of primary amoebic meningoencephalitis was diagnosed in a 5-month-old infant who presented with the history of decrease breast feeding, fever, vomiting, and abnormal body movements. Trophozoites of Naegleria fowleri were detected in the direct microscopic examination of CSF and infant was put on amphotericin B and ceftazidime. Patient condition deteriorated, and he was discharged against medical advice and subsequently expired. We also reviewed previously reported 8 Indian cases of primary amoebic meningoencephalitis (PAM) and observed that for the last 5 years, none of the patients responded to amphotericin B. Has an era of amphotericin B-resistant Naegleria fowleri been emerged? Management strategy of PAM needs to be reviewed further.

Tellapragada et al.: Lower genital tract infections during pregnancy and adverse pregnancy outcomes: a hospital based observational cohort study. BMC Infectious Diseases 2014 14(Suppl 3):E35.

Background: Children with cleft lip and cleft palate come across lot of impediment, hurdles in society. There are several social factors which hinders the proper nourishment of CL only, CP or CLP children, so majority of them tend to suffer malnutrition due to lack of standard care especially from their parents and society. Due to even low socio-economic status, impact on growth of these children is vexatious. However potential risk of malnutrition is particularly more during early childhood. Moreover, till date there are not much significant data on malnutrition in CL only, CP or CLP children. The aim of the study was to assess the prevalence of malnutrition in non syndromic CL only, CP or CLP in south India.Methods: Anthropometric parameters weight for age z score (WAZ), height for age z score (HAZ), of children with CLP were compared with age matched controls.Results: Prevalence of PEM and stunting for cleft group were 40% and 21.3% respectively compared to 33.33% and 17.33% for the control. Differences in the underweight, and stunting between the two groups were not statistically significant (χ2=2.83, p value=0.58, and χ2=1.48, p value=0.69 respectively).Conclusions: There is no statistically significant difference in the occurrence of malnutrition in children with non- syndromic cleft lip and Palate compared with control.

No abstract