Infection In Diabetes Mellitus Research Articles

A Case of Isolated Pulmonary Mucormycosis in an Immunocompetent Host

Mucormycosis is a rare fungal disease that holds a fatal opportunistic fungal infection in diabetes mellitus, hematological malignancy, and immunocompromised host. Isolated pulmonary mucormycosis is extremely rare. Optimal therapy is a combined medical-surgical approach and a management of the patient's underlying disease. Herein, we report a case-study of isolated pulmonary mucormycosis which was being presented as multiple lung nodules in a patient with no underlying risk factors. Considering that the patient had poor pulmonary functions, we treated him with only antifungal agent rather than a combined medical-surgical approach. After treatment with antifungal agent for six months, the nodules of pulmonary mucormycosis were improved with the prominent reductions of size on the computed tomography.

Association Between Helicobacter pylori Colonization and Glycated Hemoglobin Levels: Is This Another Reason to Eradicate H. pylori in Adulthood?

Helicobacter pylori infection is acquired in early childhood and becomes a chronic infection if left untreated [1]. The majority of infected people remain asymptomatic, and only a small portion develop illness, usually in adulthood [2]. Helicobacter pylori infection causes gastric and duodenal ulcers. It also increases the risk of gastric cancer [2, 3]; the bacterium was classified by the International Agency for Research on Cancer as a group 1 (definite) carcinogen in gastric carcinoma [4]. Helicobacter pylori also increases the likelihood of gastric lymphoma [5]. Moreover, positive associations between H. pylori infection and extragastric manifestations, such as iron deficiency anemia [6] and idiopathic thrombocytopenic purpura, also have been reported [7]. Many of the above-mentioned diseases and conditions are associated with the primary H. pylori virulence factors, cytotoxin-associated gene A (cagA) and vacuolating-associated gene A (vacA). Chronic H. pylori infection causes a continuous activation of the immune system, with a skewed T-helper 1 response [8, 9]. This response has been proposed as a possible mechanism responsible for some potential beneficial effects of H. pylori infection, such as protection against diarrheal diseases [10] and asthma [11]. Type 2 diabetes is an emerging pandemic, with estimates of 3.8 million deaths attributed to the disease in adults globally [12]. Lifestyle (eg, diet, obesity, physical activity), genetic, and socioeconomic factors are among the risk factors for the disease [13, 14]. There are conflicting reports concerning the association between H. pylori infection and the various clinical manifestations of the metabolic or insulin-resistance syndrome [15]. The roles of H. pylori infection in cardiovascular disease and its risk factors [16–18] and in type 2 diabetes are not clear. Although no association was found between H. pylori immunoglobulin G seropositivity and diabetes mellitus [19], a significantly higher prevalence of H. pylori gastritis was reported in patients with type 2 diabetes, compared with age-matched healthy controls (80% vs 56%; P5 .03) [20]. A recent systematic review summarized the epidemiological evidence concerning the association between H. pylori infection and quantitative indexes of insulin resistance and indicated that such an association may exist. The authors of the review concluded, however, that further studies are needed to determine whether this is a causal association [15]. Studying biomarkers of diabetes mellitus, such as glycated hemoglobin levels (HbA1c) and insulin resistance, can contribute substantially to an understanding of the etiologic role of H. pylori infection in diabetes mellitus. In this issue of the Journal, Chen and Blaser report findings of a seroepidemiological study in which they examined the association between seroprevalence of H. pylori infection and the mean levels of HbA1c in 2 large national surveys: the National Health and Nutrition Examination Survey (NHANES) III and NHANES 1999–2000. They report that H. pylori seropositivity, and especially H. pylori cagA positivity, was associated with higher mean HbA1c levels, an association that persisted after excluding individuals with a history of diabetes mellitus and controlling for potential confounders. The association was evident mainly in adults aged .18 years. Chen and Blaser also show a synergistic effect of H. pylori and body mass index (BMI) on increased levels of HbA1c in that higher levels were found in H. pylori–infected subjects with BMI $25 but not in those with lower Received and accepted 4 January 2012. Correspondence: Dani Cohen, MPH, PhD, Department of Epidemiology and Preventive Medicine, School of Public Health, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, 69978, Israel (dancohen@post.tau.ac.il). The Journal of Infectious Diseases The Author 2012. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@ oup.com DOI: 10.1093/infdis/jis110

Diversity and complexity of urinary tract infection in diabetes mellitus

Urinary tract infections (UTIs) are a common burden in patients with diabetes mellitus. Cystitis, ascending infections leading to pyelonephritis, emphysematous complications and renal and perinephric abscesses are well recognised in this group of patients especially if glycaemic control is poor. Despite the clinical significance of UTI in diabetes, it is inadequately understood and management regimens are mostly not evidence based. Anticipation of potential complications and earlier interventions are vital to reduce serious adverse outcomes. Herein we discuss the aetiology, pathogenesis and management of UTI and its local and more remote complications.

Neutrophil function and metabolism in individuals with diabetes mellitus

Neutrophils act as first-line-of-defense cells and the reduction of their functional activity contributes to the high susceptibility to and severity of infections in diabetes mellitus. Clinical investigations in diabetic patients and experimental studies in diabetic rats and mice clearly demonstrated consistent defects of neutrophil chemotactic, phagocytic and microbicidal activities. Other alterations that have been reported to occur during inflammation in diabetes mellitus include: decreased microvascular responses to inflammatory mediators such as histamine and bradykinin, reduced protein leakage and edema formation, reduced mast cell degranulation, impairment of neutrophil adhesion to the endothelium and migration to the site of inflammation, production of reactive oxygen species and reduced release of cytokines and prostaglandin by neutrophils, increased leukocyte apoptosis, and reduction in lymph node retention capacity. Since neutrophil function requires energy, metabolic changes (i.e., glycolytic and glutaminolytic pathways) may be involved in the reduction of neutrophil function observed in diabetic states. Metabolic routes by which hyperglycemia is linked to neutrophil dysfunction include the advanced protein glycosylation reaction, the polyol pathway, oxygen-free radical formation, the nitric oxide-cyclic guanosine-3'-5'monophosphate pathway, and the glycolytic and glutaminolytic pathways. Lowering of blood glucose levels by insulin treatment of diabetic patients or experimental animals has been reported to have significant correlation with improvement of neutrophil functional activity. Therefore, changes might be primarily linked to a continuing insulin deficiency or to secondary hyperglycemia occurring in the diabetic individual. Accordingly, effective control with insulin treatment is likely to be relevant during infection in diabetic patients.

Impairment of Type III Group B Streptococcus-Stimulated Superoxide Production and Opsonophagocytosis by Neutrophils in Diabetes

The effect of hyperglycemia upon susceptibility to bacterial infection in diabetes mellitus is incompletely elucidated. The present experiments assessed the effect of hyperglycemia upon neutrophil-mediated phagocytosis of type III group B Streptococcus (GBS). Type III GBS was chosen for study because the incidence of invasive GBS disease is substantially increased in type 2 diabetic compared with nondiabetic subjects. The hypothesis tested was that severe hyperglycemia would alter neutrophil metabolism by diverting NADPH from superoxide production into the aldose reductase-dependent polyol pathway that converts glucose into sorbitol and thus would impair opsonophagocytosis (OP) of type III GBS. Neutrophils from 10 adults with type 2 diabetes had no intrinsic phagocytic defect under baseline glycemic conditions. After equilibration in 60 or 120 mM glucose or in 60 mM choline chloride, OP activity was reduced significantly (P ≤ 0.03). Neutrophil superoxide production correlated with glucose concentration and also was significantly reduced during hyperglycemia (P < 0.05). Addition of III GBS capsular polysaccharide-specific IgG in a sufficient concentration supported efficient OP, even during hyperglycemia. Alrestatin, an aldose reductase inhibitor, increased superoxide production and significantly improved OP of type III GBS (P = 0.03). Thus, diversion of NADPH into the polyol pathway is one mechanism by which OP of GBS III is impaired during hyperglycemia, and this effect is mitigated when levels of capsular polysaccharide-specific IgG are sufficient.

Nucleotide Sequence and Expression of Rat β-Defensin-1: Its Significance in Diabetic Rodent Models

β-Defensins are epithelium-derived antimicrobial peptides that function in the host’s innate defense. We identified the first member of the rat β-defensin family, β-defensin-1 (BD-1), in the kidney and determined its nucleotide sequence. It was predicted to be a 37-amino-acid peptide. Rat BD-1 mRNA was expressed most abundantly in the kidney, next in skin, tongue, esophagus, and uterus, followed (at low levels) by brain, trachea, stomach, urinary bladder, and ovary. BD-1 gene expression in rat kidney was not increased by lipopolysaccharide administration. BD-1 gene expressions in the kidneys of diabetic rodent models, cholecystokinin-insensitive Otsuka Long-Evans Tokushima Fatty rats, leptin-insensitive obese (fa/fa) Wistar rats, and db/db mice, were significantly lower than those of their lean littermates. BD-1 reduction may be in part responsible for the high incidence of urinary tract infections in diabetes mellitus.

Deep foot infections in diabetes mellitus - costs topical

Deep foot infections in diabetes mellitus - costs topical

Impairment of endotoxin-induced macrophage inflammatory protein 2 gene expression in alveolar macrophages in streptozotocin-induced diabetes in mice.

To elucidate the mechanism of the high incidence of lower respiratory tract infections in patients with diabetes mellitus, we investigated the kinetics of production of macrophage inflammatory protein 2 (MIP-2), an important mediator of lung neutrophil recruitment, using mice with streptozotocin-induced diabetes. Intratracheal challenge with 1 mg of lipopolysaccharide (LPS), an endotoxin, per kg of body weight resulted in a time-dependent increase in the levels of MIP-2 protein in bronchoalveolar lavage (BAL) fluid, with the peak concentration (49.4 +/- 13 ng/ml) occurring at 3 h and significant neutrophil accumulation becoming apparent by 3 h in normal mice. In diabetic mice, the peak level of MIP-2 protein in BAL fluid did not occur until 6 h and was reduced to 21.9 +/- 10 ng/ml. Immunohistochemical studies using anti-MIP-2 antibody confirmed that the main cellular source of MIP-2 in the lung after LPS challenge was alveolar macrophages (AMs) in normal mice. The lungs in diabetic mice, however, showed no AMs staining for MIP-2 within 3 h after LPS challenge. PCR analysis using whole-lung RNA showed a time-dependent increase in MIP-2 mRNA levels after LPS instillation. The level of MIP-2 mRNA in diabetic mice was markedly decreased compared to that in normal mice. Our results indicate that impairment of MIP-2 mRNA expression in the AMs in diabetic mice resulted in delayed neutrophil recruitment in the lungs, and this may explain the development and progression of pulmonary infection in diabetes mellitus.

Insulin-Dependent Reduction in Hepatic and Splenic Contents of Interleukin-1 Beta in Expermental Diabetes

Interleukin-1 beta (IL-1 beta) is a polypeptide produced by a variety of cells of hematological, dermal and neural origin. We have investigated the effect of type I diabetes mellitus and insulin treatment on tissue levels of IL-1 beta using streptozotocin (STZ)-treated mouse as an animal model. Diabetes affected IL-1 beta in a tissue specific manner. For example, IL-1 beta levels (as measured by ELISA) were markedly decreased in the liver and spleen of the STZ diabetic mice. In contrast, the levels of this cytokine remained unalatered in other tissues including kidney, testis, hippocampus and pituitary. Insulin treatment restored the diabetes-related decreases in liver and spleen IL-1 beta levels. Overall, the present data suggest that the abnormalities in hepatic and splenic IL-1 beta levels may contribute, at least in part, to the immunodeficiency and increased susceptibility to infection in diabetes mellitus.

Treatment of purulent wounds in diabetic patients with low-frequency ultrasound combined with helium-neon laser

Acute surgical infection in diabetes mellitus is still one of the difficult problems of practical medicine and requires more in-depth research.&#x0D; The aim of this work was to determine the effectiveness of treatment of acute pyo-inflammatory diseases of soft tissues in diabetic patients with ultrasound treatment of wounds with low-frequency ultrasound and subsequent stimulation of reparative processes in them by radiation of low-intensity helium-neon-based laser.

Pneumococcal Vaccination in Diabetes

To the Editor.— The COMMENTARY by James M. Moss, MD (1980;243:2301), entitled Pneumococcus Infection in Diabetes Mellitus: Is This a Justification for Immunization? concluded that diabetes is not a valid indication for pneumococcal vaccination because excess risk for development of the disease among diabetics has not been established. I do not think that this conclusion is warranted for several reasons. First, direct extrapolation of animal data to humans is problematical. Citation of the study of Dolkart et al1examining antibody response among alloxan diabetic mice as proof of the contention that there is no measureable decrease in antibody response among diabetic humans may or may not be accurate. Richardson2studied diabetic patients and reported that antibody response to typhoid vaccine was impaired. However, we recently found that these patients do respond as well as control subjects to pneumococcal polysaccharide vaccine.3There are little or no data available

Diabetes Mellitus and the Pneumococcus

THE COMMENTARY on Pneumococcus Infection in Diabetes Mellitus: Is This a Justification for Immunization?1 raises an interesting issue. It may indeed be true that the attack rate of pneumococcal pneumonia in well-regulated diabetics is no higher than that in the nondiabetic population, although data to confirm or to refute this view are lacking. The view set forth by the author that diabetic ketoacidosis is precipitated by is widely held by those knowledgeable about diabetes mellitus. The cited COMMENTARY also states that vascular changes in the course of diabetes may affect a number of organs, including the kidneys and heart, the ultimate failure of which would be a detriment to resistance to pneumococcal infection. Value of Prophylaxis The question of the value of prophylaxis for pneumococcal infection may be approached from several points of view. One is to look at the incidence of such infection and to make a judgment

Pneumococcus infection in diabetes mellitus. Is this a justification for immunization?

Pneumococcus infection in diabetes mellitus. Is this a justification for immunization?

Bacterial infections in diabetes mellitus

British Journal of DermatologyVolume 91, Issue 4 p. 481-487 Bacterial infections in diabetes mellitus J. A. Savin, J. A. Savin Department of Dermatology, Royal Infirmary, EdinburghSearch for more papers by this author J. A. Savin, J. A. Savin Department of Dermatology, Royal Infirmary, EdinburghSearch for more papers by this author First published: October 1974 https://doi.org/10.1111/j.1365-2133.1974.tb13096.xCitations: 41AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume91, Issue4October 1974Pages 481-487 RelatedInformation

End-vessel reactivity and capillary clearance in diabetes mellitus

Capillary clearance and end-vessel reactivity to pressor substances may be factors that could modify wound healing and the response to infection in diabetes mellitus. Angiotensin and saline were injected intradermally in control, diabetic, and atherosclerotic patients to evaluate this hypothesis. Capillary clearance of saline and end-vessel reactivity to angiotensin were both prolonged in the diabetic patient when compared with the control and atherosclerotic patients. Reduced end-vessel perfusion and delayed capillary clearance could combine with the metabolic abnormalities of diabetes mellitus to facilitate the development of infection and to interfere with wound healing.