Effects of diabetes on cytokines and oxidative organ injury in a rat model of sepsis.

We aimed to investigate how Diabetes Mellitus (DM) affects myeloperoxidase activity, antioxidant status, and lipid peroxidation using biochemical approaches in heart, liver, and lung and serum cytokine analyses, such as interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) in rat with sepsis induced by a cecal ligation and puncture-induced (CLP) sepsis. The rats were divided into four groups: control group, diabetic group, sepsis group, and diabetic+sepsis group. DM was induced in the male Wistar albino rats by administration of alloxan. Polymicrobial sepsis was induced by cecal ligation and two-hole puncture. After alloxan administration, all groups of rats were allowed to recover for 1 month. CLP model was applied after 1 month recovery to group 3 and 4. IL-6 and TNF-α, were measured. Effects of antioxidant defenses on the DM and/or sepsis process, the antioxidant levels superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) were evaluated in heart, lung and liver tissues. The oxidant levels, such as lipid peroxidation (LPO) and myeloperoxidase (MPO) levels were also evaluated in tissues. We demonstrated DM to augment the level of oxidant and proinflammatory cytokines in lung, liver, and heart and also to exacerbate oxidative injury as assessed by increased LPO and MPO, and decreased GSH and SOD levels in a sepsis model. DM increased levels of proinflammatory cytokines while DM also resulted in significantly increased levels of proinflammatory cytokines following CLP. DM-increased plasma proinflammatory cytokines levels correlated positively with tissue oxidant levels, such as MPO and LPO levels in a rat abdominal sepsis model, based on CLP, which resulted in the exacerbation of oxidative organs injury.

Isolation of pathogenic aerobic bacteria from the blood of septicaemic neonatal calves and the susceptibility of isolates to various antibiotics.

An automated blood culture system (BACTEC 9240) was used for the isolation of aerobic bacteria from the blood of septicaemic neonatal calves. Blood samples were collected from 90 clinically septicaemic and 20 healthy neonatal calves and inoculated into blood culture bottles. There were 89 significant isolates from 90 positive blood cultures using the BACTEC system. Escherichia coli was the most common pathogen detected accounting for 56 (63%) out of 89 isolates. The other pathogens were beta-haemolytic streptococci (15.7%), Staphylococcus aureus (10.1%), Klebsiella sp. (5.6%) and Corynebacterium sp. (5.6%). All isolates showed a susceptibility rate of 100% to enrofloxacin, cefepim, cefoperazone/sulbactam, imipenem and meropenem while some of them were ranged from 75 to 91.7% susceptible to amoxicillin/clavulanic acid, ampicillin/sulbactam, gentamicin and cephalosporins.

Comparison of slime-producing coagulase-negative Staphylococcus colonization rates on vinyl and ceramic tile flooring materials.

This study investigated the colonization of slime-producing coagulase-negative Staphylococcus (CoNS) in 80 patient wards in Turkey (40 vinyl and 40 ceramic tile floors). A total of 480 samples that included 557 CoNS isolates were obtained. Slime production was investigated with the Christensen method and methicillin-susceptibility was tested by the disk-diffusion method. There was a significant difference in the percentage of slime-producing CoNS isolates on vinyl (12.4%) versus ceramic tile flooring (4.4%). From vinyl flooring, the percentage of slime producing methicillin-resistant CoNS (MRCoNS) (8.9%) was significantly higher than for methicillin-sensitive CoNS (MSCoNS) (3.6%), whereas there was no difference from ceramic tile flooring (2.5% MRCoNS versus 1.8% MSCoNS). The most commonly isolated slime-producing CoNS species was S. epidermidis on both types of flooring. It is concluded that vinyl flooring seems to be a more suitable colonization surface for slime-producing CoNS than ceramic tile floors. Further studies are needed to investigate bacterial strains colonized on flooring materials, which are potential pathogens for nosocomial infections.

Serum leptin levels in children with acute viral hepatitis A / Niveles de leptina en plasma en niños con hepatitis viral a aguda

OBJECTIVES: In acute viral hepatitis A (AVH-A), involvement of the liver is through cytotoxic cells and cytokine levels are increased Immune response of the host determines the severity of the disease. Leptin stimulates cytokines, therefore, the authors hypothesized that the relationship between leptin and cellular immunity might cause different clinical presentations of the disease. METHODS: Twenty-eight children with AVH-A and 10 healthy children formed the basis of the study. Serum leptin, C-reactive protein (CRP) and alpha-1-antitrypsin (A1AT) levels were determined RESULTS: There was significant positive correlation between body mass index (BMI) and leptin levels both in patients and controls (p = 0.003 and p = 0.001 respectively). No significant difference in serum leptin, CRP or A1AT levels between patients and controls was detected (p > 0.05). Presence of icterus or fulminant hepatic failure (FHF) did not affect serum leptin level (p > 0.05). Mean A1AT level was significantly higher in children with FHF (p < 0.05). On the 30th day of admission, mean BMI, weight and leptin levels increased (p < 0.01, p < 0.01 and p < 0.05 respectively) and mean A1AT level decreased (p < 0.01). CONCLUSION: Leptin levels are not altered in children with AVH-A. In the convalescence period, leptin increased parallel to BMI. It is suggested that expected increment in leptin due to inflammation might be balanced with the decrease due to loss of appetite during acute illness or it might be entirely due to loss of production.

Serum leptin levels in children with acute viral hepatitis A.

OBJECTIVES: In acute viral hepatitis A (AVH-A), involvement of the liver is through cytotoxic cells and cytokine levels are increased Immune response of the host determines the severity of the disease. Leptin stimulates cytokines, therefore, the authors hypothesized that the relationship between leptin and cellular immunity might cause different clinical presentations of the disease. METHODS: Twenty-eight children with AVH-A and 10 healthy children formed the basis of the study. Serum leptin, C-reactive protein (CRP) and alpha-1-antitrypsin (A1AT) levels were determined RESULTS: There was significant positive correlation between body mass index (BMI) and leptin levels both in patients and controls (p = 0.003 and p = 0.001 respectively). No significant difference in serum leptin, CRP or A1AT levels between patients and controls was detected (p > 0.05). Presence of icterus or fulminant hepatic failure (FHF) did not affect serum leptin level (p > 0.05). Mean A1AT level was significantly higher in children with FHF (p < 0.05). On the 30th day of admission, mean BMI, weight and leptin levels increased (p < 0.01, p < 0.01 and p < 0.05 respectively) and mean A1AT level decreased (p < 0.01). CONCLUSION: Leptin levels are not altered in children with AVH-A. In the convalescence period, leptin increased parallel to BMI. It is suggested that expected increment in leptin due to inflammation might be balanced with the decrease due to loss of appetite during acute illness or it might be entirely due to loss of production.

Infestation of the human intestine by the millipede, Nopoiulus kochii.

Specimens of the millipede, Nopoiulus kochii (Gervais) were seen in faeces and vomit of a 14-year-old boy residing in Oltu, Erzurum, Turkey. The patient complained of a burning sensation in his throat and stomach-ache. Physical examination revealed no pathological findings, and how the patient became infected was unknown. Anti-parasitic drugs (niclosamide, albendazole), which he had been taking intermittently for 2 years by the prescription of a physician, had not resolved the problem.

Nasopharyngeal carriage rate of Haemophilus influenzae in children aged 7-12 years in Turkey.

This study was undertaken to determine the nasopharyngeal carriage prevalence of Haemophilus spp. in children aged 7-12 years in Erzurum, Turkey. Three hundred randomly selected students from three regions with different socioeconomic properties were included in the study. Nasopharyngeal swabs taken from the students were streaked into selective media for Haemophilus spp. Isolated colonies were identified by macroscopic and microscopic examination and their X and V factor needs determined. Those identified as H. influenzae were serotyped by specific capsule antisera. Haemophilus spp. were recovered from 51 (17.0%), nine (3.0%) of which were H. influenzae type b (Hib), 30 (10.0%) H. influenzae non-type b, and 12 (4.0%) H. parainfluenzae. Results were evaluated by several risk factors such as age, gender, number of siblings, siblings attending a nursery, family smoking habits and family economic status.

A comparison of high-level aminoglycoside resistance in vancomycin-sensitive and vancomycin-resistant Enterococcus species.

The aim of this study was to investigate whether there was a significant difference in high-level aminoglycoside resistance (HLAR) between vancomycin-sensitive enterococci (VSE) and vancomycin-resistant enterococci (VRE). Vancomycin resistance was determined in 116 Enterococcus isolates using brain-heart infusion agar containing 6 micrograms/ml vancomycin. HLAR was determined by both standard agar screening and disk diffusion methods. Streptomycin and gentamicin were used as predictors of HLAR. Vancomycin resistance and HLAR were found in 17 (14.7%) and 41 (35.3%) of the Enterococcus strains, respectively. HLAR was found in 11 of 17 VRE and 30 of 98 VSE strains. HLAR in VRE strains was significantly higher than in VSE. More enterococcal strains were found to be resistant to both gentamicin and streptomycin (29) than to gentamicin (one) or streptomycin (11) alone. The HLAR rate in VRE was two-fold higher than in VSE. The synergistic bactericidal effect of aminoglycosides and beta-lactam or glycopeptide antibiotics is lost if there is high-level resistance to aminoglycosides.

Demonstration of in vitro antagonism between fusidic acid and quinolones.

Fusidic acid is an antibiotic active against staphylococci and other bacterial pathogens. It is used in the treatment of staphylococcal infections usually in combination with other antibacterial agents. Reports of the clinical effects of antimicrobial combinations containing fusidic acid have been somewhat inconsistent. The aim of this study was to investigate the in vitro antagonism of fusidic acid and quinolones. Twenty-six staphylococci strains isolated from various clinical samples were tested. After detecting the diameter of the zone of inhibition around fusidic acid, levofloxacin, ciprofloxacin, ofloxacin and moxifloxacin for each strain, in vitro antagonism between fusidic acid and each quinolone was investigated using disk approximation. In all 26 strains, quinolones and fusidic acid were antagonist in vitro. The reason for this antagonistic effect and its clinical implications are not known. However, care should be exercised in prescribing quinolones and fusidic acid in combination.

Detection of antimicrobial resistance and extended-spectrum beta-lactamase production in Klebsiella pneumoniae strains from infected neonates.

The present study was designed to determine the antimicrobial resistance and extended-spectrum beta-lactamase (ESBL) activities of Klebsiella pneumoniae strains isolated from the neonatal intensive care unit of Atatürk University Hospital, Erzurum, Turkey. Antibiotic susceptibility of 40 isolates was detected by the standard disk diffusion method according to the National Committee for Clinical Laboratory Standards Guidelines. The double-disk synergy method was used to determine ESBL activity, which is associated with resistance to beta-lactam antibiotics. Twenty-four (60%) of 40 K. pneumoniae strains were found to produce ESBL. Of the antibiotics tested, meropenem was found to be the most effective (100%), and ampicillin the least effective (0%). With the increasing incidence of antimicrobial resistance, which poses a clinically significant risk to vulnerable patients, it is important that clinical microbiology laboratories have accurate and timely information concerning the strains of bacteria present to enable them to predict which antibiotics are likely to be effective in treating the infections they may cause.