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The incidence of urinary tract infection (UTI) after kidney transplantation (KT) caused by multidrug-resistant (MDR) bacteria is growing. The aim of this study was to analyze the impact of UTI caused by carbapenem-resistant Gram-negative bacteria (CR-GNB) in the survival of graft and recipients following KT. This was a retrospective cohort study involving patients who underwent KT between 2013 and 2016. Patients were followed since the day of the KT until loss of graft, death or end of the follow-up period (31th December 2016). The outcomes measured were UTI by MDR following KT and graft and patient survival. Analyses were performed using Cox regression; for the graft and patient survival analysis, we used a propensity score for UTI by CR-GNB to matching a control group. UTI was diagnosed in 178 (23.9%) of 781 patients, who developed 352 UTI episodes. 44.6% of the UTI cases were caused by MDR bacteria. Identified risk factors for UTI by MDR bacteria were DM, urologic disease as the cause of end-stage renal failure, insertion of ureteral stent, carbapenem use, and delayed graft function (DGF). Risk factors for death during the follow-up period were female gender, patients over 60 years old at the time of KT, DM, body mass index over 31.8, UTI caused by CR-GNB. In conclusion, UTIs caused by CR-GNB have great impact on patients' survival after KT., (© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Teeth are colonized by oral bacteria from saliva containing more than 700 different bacterial species. If removed regularly, the dental biofilm mainly comprises oral streptococci and is regarded as resident microflora. But if left undisturbed, a complex biofilm containing up to 100 bacterial species at a site will build up and may eventually cause development of disease. Depending on local ecological factors, the composition of the dental biofilm may vary considerably. With access to excess carbohydrates, the dental biofilm will be dominated by mainly gram-positive carbohydrate-fermenting bacteria causing demineralization of teeth, dental caries, which may further lead to inflammation and necrosis in the pulp and periapical region, i.e., pulpitis and periapical periodontitis. In supra- and subgingival biofilms, predominantly gram-negative, anaerobic proteolytic bacteria will colonize and cause gingival inflammation and breakdown of supporting periodontal fibers and bone and ultimately tooth loss, i.e., gingivitis, chronic or aggressive periodontitis, and around dental implants, peri-implantitis. Furthermore, bacteria from the dental biofilm may spread to other parts of the body by bacteremia and cause systemic disease. Basically, prevention and treatment of dental biofilm infections are achieved by regular personal and professional removal of the dental biofilm., (© 2017 APMIS. Published by John Wiley & Sons Ltd.)

Background: Infections are the leading cause of hospitalization and mortality in transplant recipients. Nigeria has a growing number of renal transplant recipients. The aim of this study was to determine the pattern of infections in renal allograft recipients in one of the major renal transplant centers in Nigeria., Methods: All case records of renal allograft recipients on follow-up were retrieved. Those that had infection at any time after transplantation were selected. Demographic and clinical information was collected and analyzed., Results: Thirty-three case records were analyzed, out of which 24/33 (72.7%) were males, with a mean age of 42.3 years (± 7.38). The median duration of developing infection post transplant was 270 days (range 2-2190). Most of the infections occurred after 6 months in 15/33 (45.5%). Urinary tract infection was the most common infection, noted in 13/33 (39.4%), followed by pneumonia, which was seen in 12 (33.3%), 9/12 (75%) of which were culture-positive. There were 2 cases (5.6%) of tuberculosis and 1 case (2.8%) of cytomegalovirus colitis. Out of the 9 culture-positive pneumonia cases, 6 (66.7%) were caused by gram-negative pathogens, with Pseudomonas aeruginosa being the most common isolate seen in 3/9 (33.3%) of the patients. Among those with urinary tract infection, Escherichia coli and Klebsiella species were isolated with equal proportion in 3/13 (23.1%), while Enterococcus faecalis was the most common isolate in 4/13 (30.8%). Overall infection-related mortality was 10/33 (30.3%), out of which 5/10 (50%) of deaths were from pneumonia., Conclusion: Post-transplant infection surveillance must be strengthened. The role of multidrug-resistant gram-negative bacteria in post-renal transplant infection in Nigeria needs to be evaluated., (© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Introduction: The human immunodeficiency virus (HIV) can integrate into T cells, macrophages and dendritic cells resulting in a latent infection. Reports have also demonstrated that various microbial and host cell factors can trigger HIV reactivation leading to HIV recrudescence, potentially undermining highly active antiretroviral therapies., Methods: This study evaluated the capacity of oral bacteria associated with chronic periodontal infections to stimulate HIV promoter activation in various cell models of HIV latency., Results: T cells (1G5) challenged with oral bacteria demonstrated a dose-response of HIV promoter activation with a subset of the bacteria, as well as kinetics that were generally similar irrespective of the stimuli. Direct bacterial challenge of the T cells resulted in increased activation of approximately 1.5- to 7-fold over controls. Challenge of macrophages (BF24) indicated different kinetics for individual bacteria and resulted in consistent increases in promoter activation of five fold to six fold over basal levels for all bacteria except Streptococcus mutans. Dendritic cells showed increases in HIV reactivation of 7- to 34-fold specific for individual species of bacteria., Conclusion: These results suggested that oral bacteria have the capability to reactivate HIV from latently infected cells, showing a relationship of mature dendritic cells > immature dendritic cells > macrophages > or = T cells. Expression of various pattern recognition receptors on these various cell types may provide insight into the primary receptors/signaling pathways used for reactivation by the bacteria.

Introduction: Periodontal disease is an inflammatory condition caused by periodontal microorganisms. Viruses such as human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) are associated with certain types of periodontal disease, but their roles in promoting the disease are unclear. Because both viruses infect human macrophages, cells which play key roles in the clearance of pathogenic bacteria, it is likely that the viruses alter the functional capacity of macrophages by inhibiting their defense mechanisms against invading pathogens., Methods: Macrophages preinfected with HCMV or EBV were evaluated following stimulation by selected oral bacteria. Bacteria-induced macrophage activation was assayed by measuring the levels of tumor necrosis factor-alpha (TNF-alpha) produced in the media, and phagocytic activity was analysed by a phagocytosis assay with fluorescein isothiocyanate-labeled bacteria. The virus-infected macrophages were also subjected to semi-quantitative polymerase chain reaction to measure the expression of toll-like receptor 9, which is involved in the activation of phagocytosis-related pathways., Results: Both HCMV and EBV significantly diminished the TNF-alpha production typically induced by oral bacteria, inhibited the phagocytic activity of macrophages, and downregulated the expression of toll-like receptor 9., Conclusion: Infection by HCMV or EBV inhibits the functional ability of macrophages to respond to bacterial challenge, thereby suggesting their pathogenic role in the development of periodontal disease.

Background/aims: The oral cavity harbors a diverse and complex microbial community. Bacteria accumulate on both the hard and soft oral tissues in sessile biofilms and engage the host in an intricate cellular dialog, which normally constrains the bacteria to a state of commensal harmony. Dendritic cells (DCs) are likely to balance tolerance and active immunity to commensal microorganisms as part of chronic inflammatory responses. While the role played by DCs in maintaining intestinal homeostasis has been investigated extensively, relatively little is known about DC responses to oral bacteria., Methods: In this study, we pulsed human monocyte-derived immature DCs (iDCs) with cell wall extracts from pathogenic and commensal gram-positive or gram-negative oral bacteria., Results: Although all bacterial extracts tested induced iDCs to mature and produce cytokines/chemokines including interleukin-12p40, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 (MCP-1), the most important factor for programming DCs by oral bacteria was whether they were gram-positive or gram-negative, not whether they were commensal or pathogenic. In general, gram-negative oral bacteria, except for periodontopathic Porphyromonas gingivalis, stimulated DC maturation and cytokine production at lower concentrations than gram-positive oral bacteria. The threshold of bacteria needed to stimulate chemokine production was 100-fold to 1000-fold lower than that needed to induce cytokines. In addition, very low doses of oral commensal bacteria triggered monocytes to migrate toward DC-derived MCP-1., Conclusion: Oral commensal and pathogenic bacteria do not differ qualitatively in how they program DCs. DC-derived MCP-1 induced in response to oral commensal bacteria may play a role, at least in part, in the maintenance of oral tissue integrity by attracting monocytes.

Introduction: The purpose of this study was to utilize an in vitro biofilm model of subgingival plaque to investigate resistances in subgingival biofilm communities to antibiotics commonly used as adjuncts to periodontal therapy., Methods: Biofilms were grown on saliva-coated hydroxyapatite supports in trypticase-soy broth for 4 h-10 days and then exposed for 48 h to either increasing twofold concentrations of tetracycline, amoxicillin, clindamycin, and erythromycin or therapeutically achievable concentrations of tetracycline, doxycycline, minocycline, amoxicillin, metronidazole, amoxicillin/clavulanate, and amoxicillin/metronidazole., Results: Concentrations necessary to inhibit bacterial strains in steady-state biofilms were up to 250 times greater than the concentrations needed to inhibit the same strains grown planktonically. In the presence of therapeutically available antibiotic concentrations, significantly higher proportions of the biofilms remained viable as the biofilms reached steady-state growth. The combinations of amoxicillin/clavulanate and amoxicillin/metronidazole were the most effective in suppressing growth. These combinations were particularly effective against biofilms up to and including 7 days of age and inhibited 90% or more of the bacteria present relative to untreated controls. As the biofilms approached steady state, these combinations were less effective with 50-60% of the bacteria retaining viability., Conclusion: Most, but not all, species of subgingival bacteria are considerably more resistant in biofilms than in planktonic cultures. Resistance appeared to be age-related because biofilms demonstrated progressive antibiotic resistance as they matured with maximum resistance coinciding with the steady-state phase of biofilm growth.

Serious systemic infections may occur during cancer chemotherapy due to disturbances in the oropharyngeal and gastrointestinal microflora, impaired mucosal barrier functions and immunosuppression. Bacteria may spread from the gastrointestinal tract to the regional lymph nodes. The routes for bacterial spread from the oral cavity are less well known. In the present study we investigated changes in the oral and intestinal microfloras in rats given 50 mg/kg 5-fluorouracil (5-FU) i.v. for 6 days. Bacterial dissemination to the lymph nodes draining the oral cavity and the lymph nodes draining the gastrointestinal tract was examined. Effects of adding the probiotic strain Lactobacillus plantarum 299v in the drinking water to the rats were measured. 5-FU treatment caused an increase in the number of facultative and strictly anaerobic bacteria in biopsies from the oral cavity and an increase in the number of facultative anaerobes in the large intestine. The proportion of facultative gram-negative rods increased in both the oral cavity and intestine. Bacteria translocated to both the cervical and mesenteric lymph nodes in untreated animals and increased in numbers after 5-FU treatment due to an increase in the number of facultative gram-negative rods. Treatment with L. plantarum 299v improved food intake and body weight in 5-FU-treated rats. It also reduced the 5-FU-induced raise in the total numbers of facultative anaerobes in the intestine, but did not reduce translocation and did not prevent diarrhea. This study reinforces the oral cavity, along with the gastrointestinal tract, as a source for bacterial dissemination. The use of probiotic bacteria may reduce some side effects of 5-FU treatment.

A total of eight bacterial isolates belonging to six species, and a select group of 12 oral Candida albicans isolates, were used to study the effect of bacteria on germ-tube formation. Briefly, each bacterial suspension (10(5-6) cells/ml) was mixed with a C. albicans suspension (10(7) cells/ml) and incubated at 37 degrees C for 90 min with bovine serum, and the percentage germ-tube-positive Candida cells was quantified using a haemocytometer, under light microscopy. In general, out of eight bacteria, Streptococcus sanguis SK21A, Streptococcus salivarius SK56, Escherichia coli ATCC 25922, and S. salivarius OBU3 suppressed germ-tube formation to varying degrees, with different C albicans isolates. Porphyromonas gingivalis Pg 50, Lactobacillus casei ATCC 7469 and Prevotella intermedia OBU4 elicited significant enhancement of germ-tube formation, whereas S. sanguis OBU 2 had no effect. E. coli ATCC 25922 was the only organism to show statistically significant suppression of germ-tube formation (p=0.0312). A significant increase in the germ tube production of C. albicans isolated from HIV-infected compared with HIV-free individuals was also noted. The current results tend to suggest that commensal and transient oral bacterial populations may selectively influence the differential expression of germ-tube-forming ability of C. albicans isolates.

Fusobacterium nucleatum has been identified as significantly associated with sites with active periodontal disease and, as a group, the oral fusobacteria coaggregate with members of all oral bacteria genera tested. Monoclonal antibodies were prepared and used in conjunction with other potential inhibitors, such as simple sugars and amino acids, to characterize coaggregation interactions, of F. nucleatum PK1594. Four unique monoclonal antibodies, 5H11, 14C7, 19F2 and 29C12, were obtained by their ability to inhibit coaggregation of F. nucleatum PK1594 with Actinomyces israelii PK16. They were also capable of inhibiting other coaggregations including Streptococcus oralis H1, S. oralis J22, Capnocytophaga ochracea ATCC33596, Prevotella denticola PK1277 and Prevotella intermedia PK1511. All of these interactions were completely inhibited by N-acetylneuraminic acid. Neither N-acetylneuraminic acid nor monoclonal antibody 5H11 had any inhibitory effect on other F. nucleatum PK1594 interactions, including all galactose-inhibitable coaggregations. The results indicate that F. nucleatum PK1594 expresses upon its surface a distinct type of adhesin that mediates coaggregation interactions that are inhibited by N-acetylneuraminic acid.

The adherence of lipopolysaccharides (LPSs) from periodontal disease-associated bacteria to saliva-coated hydroxyapatite (S-HA) and serum-coated HA beads was examined by chromogenic Limulus activity (toxicolor test). Phenol-water extracted LPS preparations from Bacteroides intermedius, Fusobacterium nucleatum, Actinobacillus actinomycetemcomitans, Eikenella corrodens, and rough-type LPS from Escherichia coli adhered to S-HA and serum-coated beads and agglutinated human erythrocytes. The adhered LPSs to S-HA and serum-coated HA beads were not removed by vigorous washing with distilled water. LPSs from Bacteroides (Porphyromonas) gingivalis strains and wild-type E. coli did not adhere to S-HA, serum-coated HA beads or show hemagglutinating activity. SDS-PAGE patterns stained with silver stain showed that LPSs adhered to S-HA, and serum-coated HA beads and erythrocytes possessed a distinct fast-migrating band similar to rough-type LPS. B. gingivalis LPSs possessed slow-migrating and repeating ladder bands similar to wild-type LPS.

Some R-mutant Escherichia coli and Salmonella heavily adhered to murine lymphoma cells of B cell and T cell lineages. This adhesion was primarily mediated by membrane-localized proteins on tumor cells, which bind the polymyxin B-reactive hydrophilic structure of lipis A on bacteria. SDS-PAGE analysis of tumor cell membranes showed that proteins or glycoproteins of MW = around 45Kd, 25-35Kd and around 15Kd preferentially bind lipid A. Various lymphoma cell lines binding the bacteria at different levels possessed lipid A-binding proteins of slightly different compositions. We conclude that lymphoma cells carry not a single but a group of lipid A-binding proteins in their membranes.

Bacterial endotoxins are known to be an important cause of cholestasis, yet not all organisms that cause cholestasis produce endotoxins. In order to determine whether bacterial products other than endotoxins may be involved in the cholestasis process, 14C-taurocholate (TC) uptake by isolated rat hepatocytes was measured in the presence of mid-log, stationary and mid-death phase bacterial broth supernatants from eight common bacterial pathogens. The results were then correlated with a quantitative assessment of endotoxin production by each organism. Supernatants from Haemophilus influenzae, Pseudomonas aeruginosa and Klebsiella pneumonia demonstrated a striking inhibitory effect on bile salt uptake (77.2 +/- 6.7, 46.9 +/- 6.5 and 32.9 +/- 7.1% maximum inhibition of 14C-TC uptake, respectively) when compared to sterile broth controls. Streptococcus faecalis (Enterococcus), Escherichia coli, Staphylococcus aureus and Bacteroides fragilis products, on the other hand, had relatively minor effects (12.3 +/- 5.2, 12.0 +/- 7.5, 8.4 +/- 6.7 and less than 5.0% inhibition respectively), while those from Proteus mirabilis had an intermediate effect (18.5 +/- 8.3% inhibition). Bile salt efflux rates (16.0 +/- 2.7 and 25.1 +/- 4.2 nmol/min/10(6) hepatocytes, mean +/- SEM) were similar in bacteria demonstrating marked uptake inhibition (Haemophilus influenzae, Pseudomonas aeruginosa) when compared to those with only minor inhibitory effects (Staphylococcus aureus, Bacteroides fragilis) (14.3 +/- 1.1 and 18.4 +/- 2.6 nmol/min/10(6) hepatocytes, respectively, p greater than 0.05). 14C-TC uptake inhibition did not correlate with the amount of endotoxin produced by each organism (r = 0.251). The results of this study indicate that bacteria produce a factor other than endotoxin that significantly inhibits bile salt uptake by isolated rat hepatocytes.(ABSTRACT TRUNCATED AT 250 WORDS)