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BACKGROUND: Interdigestive small bowel motility has a regulatory function on the microflora of the upper small bowel. Here we investigate the effects of ABT-229 and octreotide on morphine-induced dysmotility, the accompanying bacterial overgrowth and bacterial translocation. METHODS: Rats were fitted with jejunal myoelectrodes and a subcutaneous cannula for continuous infusion of saline or morphine. Fasting motility was measured for 6 h on four occasions: one control measurement (day 0) and three measurements on consecutive days (days 1-3) while receiving saline alone (group A), morphine alone (group B), saline + ABT-229 (group C), morphine + ABT-229 (group D), saline + octreotide (group E) or morphine + octreotide (group F). Samples from the mesenteric lymph node complex (MLN), liver, spleen, duodenum and ileum were taken for quantitative microbial culturing on day 4. RESULTS: Neither ABT-229 nor octreotide increased the number of propagated activity fronts during saline infusion. During morphine-induced dysmotility, ABT-229 induced more propagated activity fronts in group D (13.4, 9.8 and 8.8 per 6 h) than in group B (7.0, 4.5, 3.8 per 6 h) on days 1, 2 and 3 (P < 0.05 for all days) Octreotide did not induce more propagated activity fronts. Disruption of small bowel motility by morphine led to bacterial overgrowth in the duodenum. ABT-229 and octreotide did not reduce the bacterial growth levels. The total incidence of bacterial translocation was significantly higher in the morphine-treated animals than in the saline-treated animals. Neither ABT-229 nor octreotide reduced the bacterial translocation incidence. The number of propagated activity fronts on day 3 and duodenal bacterial growth correlated significantly in groups A, E and F. CONCLUSIONS: ABT-229, but not octreotide, reduced morphine induced dysmotility. Small bowel bacterial overgrowth and bacterial translocation were not prevented. Fasting small bowel motility has a regulatory function on the intestinal microflora of the upper small bowel.
A bacterial marker can be used to determine the portion of fecal N that is of bacterial origin, as well as the effect of dietary factors on the bacterial N in feces of the dog. Two experiments were conducted to determine the efficacy of diaminopimelic acid (DAPA) and purines as bacterial markers in dogs. In Exp. 1, five adult female dogs were fed the same commercial diet. In Exp. 2, 50 dogs were fed one of four test diets (as-fed basis): a prebiotic-free control or diets containing either 1% chicory, 1% mannanoligosaccharide (MOS), or 1% chicory plus 1% MOS. Fresh feces were collected in both experiments and used to isolate a bacteria-rich sample (BRS) by differential centrifugation. In Exp. 1, the BRS had a N:purine ratio of 0.66 and N:DAPA ratio of 18.9. The CV for the N:purine ratio (20.7%) was much higher than that for the N:DAPA ratio (6.1%), indicating that DAPA resulted in a less variable estimate of fecal bacterial N. Using either marker, approximately 50% of the fecal N was estimated to be of bacterial origin. In Exp. 2, the N:DAPA ratio of the BRS did not differ (P = 0.14) among treatments. The BRS from dogs fed prebiotic-containing diets had treatment averages for N:DAPA ratios ranging from 16.9 to 18.5, whereas BRS from dogs fed the control diet had a ratio of 15.9. Averaged across all dogs, approximately 46% of fecal N was of bacterial origin. When calculating fecal bacterial concentrations using the average N:DAPA ratio for all dogs, little difference existed in the estimation compared with using individual values. The value resulting from use of the average ratio was approximately 13% higher than when using the individual ratios for dogs fed the control diet, which was due to the lower N:DAPA ratio for dogs fed the control diet compared with dogs fed the other treatments. Based on the consistency of the N:DAPA ratio of the BRS, DAPA seems to be a suitable marker for estimation of bacterial N in the feces of dogs.
OBJECTIVE: The continuous presence of bacteria or their degraded antigens in the synovium may be involved in the pathogenesis of rheumatoid arthritis (RA). The aim of this study was to determine the presence of bacterial nucleic acids and bacterial cell wall constituents in the joints of patients with RA and other forms of arthritis. METHODS: Joint samples were obtained from patients with RA (n = 26), septic arthritis (n = 2), inflammatory osteoarthritis (n = 5), and gout (n = 6), and joint trauma (n = 1). Universal 16S-ribosomal RNA primers were used to detect the presence of bacterial DNA in these samples, using stringent regimens for sample collection and molecular microbiologic analysis. Automated sequencing and comparative data analysis were performed to identify the species. The presence of bacterial peptidoglycan-polysaccharide complexes in synovial tissue was detected by immunohistologic analysis with a specific antibody. RESULTS: The bacterial species cultured from the synovium could be identified in both of the patients with septic arthritis. DNA amplicons were also detected in the synovial fluid and/or tissue samples from 5 patients with RA and 2 patients with crystal-induced arthritis; these originated from multiple bacterial species. Staining for peptidoglycan-polysaccharide complexes was positive in the synovial tissue of both patients with septic arthritis, 16 with RA, 4 with inflammatory osteoarthritis, 4 with crystal-induced arthropathy, and 1 with joint trauma. The staining was mainly found in cells in the synovial sublining, including macrophages. CONCLUSION: The results indicate that bacterial DNA and bacterial cell wall constituents are retained in the joints of some patients with arthritis, where they might enhance synovial inflammation.
OBJECTIVE: To study the presence of bacterial components in the synovial tissue (ST) of patients with advanced rheumatoid arthritis (RA). METHODS: ST was collected during joint surgery from 41 RA patients. Tissue from 39 patients with osteoarthritis (OA), 4 patients with undifferentiated inflammatory arthritis (UA), and 3 cases of accidental deaths served as controls. The pan-bacterial polymerase chain reaction (PCR) with primers for the 23S ribosomal RNA (rRNA) and 16S rRNA genes was used to detect bacterial DNA. In addition, synovial fluid (SF) samples from patients with chlamydial reactive arthritis (ReA) were also examined by the same method. The positive controls, bacterial DNA or ST spiked with different living bacteria, were analyzed alongside clinical samples. Most of the ST samples were also analyzed by gas chromatography-mass spectrometry (GC-MS) for determining the presence of bacteria-derived muramic acid. Strict precautions were followed in the clinics and the laboratory to prevent contamination. RESULTS: In GC-MS analysis, muramic acid was observed in the ST from 4 of 35 RA patients and from 2 of 14 OA patients, but not in ST from 2 patients with UA and 3 cadavers. Bacterial DNA was not detected by either one of the PCR primers used in ST from 42 patients with RA and 39 patients with OA. However, 5 of 15 SF samples from ReA patients were PCR positive. The sensitivity of GC-MS to detect muramic acid was 2 pg/injected amount (227 pg muramic acid/mg ST), and that of the pan-bacterial PCR was 2-20 bacteria colony forming units/reaction. CONCLUSION: These results indicate that a bacterial component, muramic acid, is detectable by GC-MS in ST from a few patients with advanced RA or OA. However, no bacterial DNA was detectable by PCR.
Patients with bacterial overgrowth of the small intestine developed spontaneous bacterial peritonitis (SBP) more frequently than patients without bacterial overgrowth of the small intestine. The objective of this study was to determine whether the incidences of small intestine dysmotility and bacterial overgrowth are higher in cirrhotic patients with a history of SBP than in cirrhotic patients without SBP. Forty cirrhotic patients were enrolled in this study. There were 20 patients with a history of SBP and 20 patients without a history of SBP. Small intestine bacterial overgrowth was diagnosed by breath hydrogen test. Small intestine motility was recorded, by a 3-channel solid-state manometric catheter, for 24 hours. There were no statistical differences in age or sex between the two groups. The Child-Pugh scores in the SBP group were higher than in the non-SBP group (10.5 +/- 2.1 vs. 8.1 +/- 1.9, P < .01). The incidence of bacterial overgrowth of the small intestine was higher in the SBP group than in the non-SBP group (70% vs. 20%, P < .01). The amplitude and duration of migrating motor complex (MMC) activity fronts, as well as the number of clusters per hour, were similar in both groups. However, the frequency of MMC activity fronts was higher in the non-SBP group than in the SBP group (4.8 +/- 2.3/24 hours vs. 3.5 +/- 1.2/24 hours, P < .05). In addition, the MMC velocity was significantly higher in the non-SBP group (8.3 +/- 2.6 vs. 5.3 +/- 2.1 cm/min, P < .01). The incidence of bacterial overgrowth of the small intestine was higher in cirrhotic patients with history of SBP than in those without SBP. Small intestine motility dysfunction was more severe in cirrhotic patients with history of SBP. Impaired motility of the small intestine, causing bacterial overgrowth of the small intestine, may be one of the explanations for recurrent SBP in cirrhotic patients.
Bacterial vaginosis, Prevotella species, and Bacteroides species have been associated with prematurity and upper genital tract infection. Prevotella (Bacteroides) species and Bacteroides fragilis have also been associated with preterm birth. However, the mechanism by which lower genital tract infection causes upper genital tract disease remains poorly understood. Sialidases (neuraminidases) are enzymes which enhance the ability of microorganisms to invade and destroy tissue. Elevated levels of sialidase activity were detected in 42 (84%) of 50 vaginal fluid specimens from women with bacterial vaginosis and none of 19 vaginal fluids from women without bacterial vaginosis (P less than 0.001). Vaginal fluid from women with bacterial vaginosis had a median specific activity of 9.8 U compared to 2.5 U of sialidase in women without bacterial vaginosis (P less than 0.001). In order to determine the probable source of sialidases in vaginal fluid, the microorganisms recovered from women with bacterial vaginosis before and after treatment were assayed. Of 28 specimens from women with bacterial vaginosis, 27 (96%) yielded sialidase-positive bacteria, at a median concentration of 10(6.5) CFU/ml of vaginal fluid. Prevotella and Bacteroides species accounted for the sialidase activity in 26 of the vaginal fluids, and Gardnerella vaginalis accounted for the sialidase activity in the remaining fluid. After treatment, sialidase was detected in the vaginal fluid of 1 (5%) of 22 women who responded to therapy and in all of 6 women for whom therapy failed. These data suggest that vaginal fluid sialidase is highly correlated with bacterial vaginosis and that the probable sources for this enzyme activity are the Bacteroides and Prevotella species present in the vagina.
Bacterial infection and biofilm formation on the surface of biliary stents is believed to be one of the main factors in stent occlusion. This study explored the role of the new reagent, bismuth dimercaprol, in preventing bacterial adherence and bacterial biofilm formation on the surface of biliary stents. Sterile porcine bile preparations, infected separately with Escherichia coli, Klebsiella pneumoniae, Enterobacter, and Enterococcus, were used as the perfusion media in an in vitro perfusion system. The bacterial growth in the media and the bacterial adherence on the surface of stents were tested when different concentrations of bismuth dimercaprol were used in the perfusion media. BisBAL (5 microM) did not inhibit the growth of any of the tested bacterial species. It did, however, significantly decrease the amount of bacteria adhering to the surface of stents for all bacterial strains except Escherichia coli. Bismuth dimercaprol (20 microM) significantly inhibited the growth of Escherichia coli, Klebsiella pneumoniae, and Enterobacter and, thereby, significantly decreased the amount of these bacteria adhering to the surface of stents. The unique bactericidal and anitbiofilm activities of bismuth thiols might contribute to delaying the process of biliary stent occlusion if the effective concentrations of bismuth thiols could be delivered to the target sites. The feasibility of this application of bismuth thiols deserves further investigation.
Measurements of IgG and IgA antibodies against common gram negative organisms in pre and post prostatic massage urines were investigated. Lower tract urinary localization specimens were obtained in men with chronic bacterial prostatitis, nonbacterial prostatitis, and without evidence of infection. Quantitative cultures were performed on all specimens. A rapid and simple enzyme-linked immunosorbant assay (ELISA) was developed to measure urinary total immunoglobulins and antibodies to common gram negative organisms (mixed antigen-specific antibodies, MASA). Comparison with a previously developed radioimmunoassay yielded a correlation determinant of 0.89 per cent. Almost all patients had post prostatic massage urinary IgA and IgG levels that were higher than the premassage levels, reflecting the presence of prostatic fluid in the postmassage specimens. In only the patients with chronic bacterial prostatitis, however, were levels of IgA or IgG MASA in the postmassage urines higher than those measured in the premassage urines. This same elevation was found in the urinary specimens from men who could not be diagnosed to have bacterial prostatitis by traditional means on a specific occasion because of antibiotic treatment, inadequate specimens, or bacteriuria, but had chronic bacterial prostatitis confirmed traditionally on another occasion. No detectable MASA were measured in either the pre or postmassage urines of men without a history of previous urinary infections. From these data it appears that urinary MASA may be used to diagnose bacterial prostatitis in situations in which quantitative bacteriologic cultures cannot be performed. These measurements may, furthermore, be used to diagnose chronic bacterial prostatic infection in men who cannot be diagnosed to have bacterial prostatitis when prostatic fluid is unobtainable or culture results are uninterpretable.
Onset of rheumatoid arthritis (RA) is widely believed to be preceded by exposure to some environmental trigger such as bacterial infectious agents. The influence of bacteria on RA disease onset or pathology has to date been controversial, due to inconsistencies between groups in the report of bacterial species isolated from RA disease tissue. Using a modified technique of reverse transcriptase-PCR amplification, we have detected bacterial rRNA in the synovial tissue of late-stage RA and non-RA arthritis controls. This may be suggestive of the presence of live bacteria. Sequencing of cloned complementary rDNA (crDNA) products revealed a number of bacterial sequences in joint tissue from each patient, and from these analyses a comprehensive profile of the organisms present was compiled. This revealed a number of different organisms in each patient, some of which are common to both RA and non-RA controls and are probably opportunistic colonizers of previously diseased tissue and others which are unique species. These latter organisms may be candidates for a specific role in disease pathology and require further investigation to exclude them as causative agents in the complex bacterial millieu. In addition, many of the detected bacterial species have not been identified previously from synovial tissue or fluid from arthritis patients. These may not be easily cultivable, since they were not revealed in previous studies using conventional in vitro bacterial culture methods. In situ hybridization analyses have revealed the joint-associated bacterial rRNA to be both intra- and extracellular. The role of viable bacteria or their nucleic acids as triggers in disease onset or pathology in either RA or non-RA arthritis controls is unclear and requires further investigation.
The use of a broad-range PCR to target conserved sequences in the bacterial ribosome has long been recognized as an approach to investigating idiopathic human diseases for the presence of bacteria. An important example is rheumatoid arthritis where the hypothesis of a bacterial etiology remains viable despite failure of previous methods to identify a causative organism. Practical implementation of this strategy, however, was impeded by requirements unique to the study of these diseases. Hence, an adequately characterized method for achieving this has not appeared. We now describe such a method based on the use of a broadly reactive pair of deoxyinosine-containing primers. Detailed characterization addressing these requirements provided evidence that DNA from at least 96% of potential prokaryotic pathogens would be detected. The sensitivity was shown to approximate that of a single organism per reaction. Importantly, this sensitivity was shown to be maintained among multiple targets and to be unimpaired by a large excess of human DNA. Similar results were obtained with extracts of inflamed human synovial fluid to which as little as 0.01 pg of bacterial DNA or, alternately, a single organism per reaction was added. This method was also shown correctly to detect the causative bacteria in clinically infected synovial fluids, further documenting its applicability to such specimens. Finally, it was converted to an in situ method by which bacterial sequences were histochemically localized to Michaelis-Guttman bodies in tissue sections from a patient with malakoplakia, a poorly understood infectious disease. The broad reactivity and high sensitivity achieved by this approach translate into a high likelihood of detecting an unknown bacterium if present in a clinical specimen. Conversely, if properly controlled, the failure of this method to detect such organisms can provide evidence supporting rejection of the bacterial etiology hypothesis, an important aspect unique to this approach. For those bacterial sequences that are detected, the ability to localize them in situ would help define their histologic context and hence facilitate their pathogenetic interpretation. The present method should therefore be appropriate for use in systematically studying rheumatoid arthritis as well as a number of other important idiopathic disorders where a bacterial etiology is suspect.
Selective intestinal decontamination with norfloxacin is useful in preventing spontaneous bacterial peritonitis in cirrhotic patients and also in cirrhotic rats. The emergence of norfloxacin-resistant infections in these patients warrants a search for alternative therapies. The aim of this study was to evaluate the effect of long-term trimethoprim-sulfamethoxazole administration on carbon tetrachloride (CCl4) -induced cirrhosis in rats with specific attention to intestinal flora, bacterial translocation, spontaneous bacterial peritonitis (SBP), and survival. Male Sprague-Dawley rats received CCl4 administered weekly by gavage. After eight weeks of CCl4 administration rats were randomly allocated into two groups. Group I received daily overnight trimethoprim-sulfamethoxazole diluted in phenobarbital water during follow-up and group II did not. The rats were killed when gravely ill, and a laparotomy was performed to culture samples of cecal stool, mesenteric lymph nodes, and portal and inferior vena caval blood. There was a trend toward a reduction in the incidence of bacterial translocation (8/17 vs 11/14, respectively) and SBP (5/17 vs 7/14, respectively) in treated rats that were killed just before death compared to untreated rats. A decrease in the incidence of bacterial translocation caused by gram-negative bacilli was observed in group I (17.6% vs 78.6%, P < 0.01). The development of ascites was delayed in group I (P < 0.05) and survival was prolonged in group I (P < 0.05), despite a higher CCl4 dose in this group (P < 0.05). In conclusion, long-term prophylactic trimethoprim-sulfamethoxazole administration in CCl4-induced cirrhosis in rats delayed the development of ascites, prolonged survival, and reduced the incidence of gram-negative bacterial translocation but not of SBP, without increasing gram-positive episodes. These data suggest that trimethoprim-sulfamethoxazole might be a good alternative to norfloxacin for preventing gram-negative bacterial translocation.
While bacterial antigen detection (BAD) tests have been used on cerebrospinal fluid (CSF) with success in the diagnosis of bacterial infection in developing countries, their value in the developed world has been recently questioned. In Darwin, Northern Territory (NT), there are good diagnostic resources but high rates of infectious disease, so it was unclear which findings were applicable to our own population. This study aimed to determine the utility of the BAD tests in detection of bacterial meningitis from CSF in patients studied at Darwin, using a retrospective review of hospital case records and microbiology laboratory reports, over a 19 month period, and utilising a clinical component in the case definition of bacterial meningitis. The sensitivity of the BAD test in the diagnosis of acute bacterial meningitis was 28.6%, with a specificity of 98.7% and a positive predictive value of 85.7%. The cost per positive test was computed at $240. No cases of bacterial meningitis which were positive on the BAD test were missed on Gram's stain of CSF. We conclude that in our setting BAD tests alone are not sensitive enough to confidently diagnose bacterial meningitis. BAD tests are more costly and offer no advantage in speed of diagnosis or in antibiotic pre-treated patients, compared to routine Gram's stain.
OBJECTIVE: To investigate the changes in the bacterial ecology and to analyze the bacterial resistance to antibiotics in a burn ward in Nanning district during the past 15 years, so as to provide reference to the clinical management of burn infection under subtropical climate. METHODS: Five thousand eight hundred and fifty-five strains of bacteria were isolated from the wounds and blood of 2269 burn patients admitted to our hospital from April of 1989 to March of 2004. Kiry-Bauer method was employed for the detection of antibiotic sensitivity test. The bacterial examination and bacterial resistance were analyzed in spans of every five years. RESULTS: Burn patients in our district were mainly infected by the gram negative bacilli (3559 strains, accounting for 60.79%), among which Pseudomonas aeruginosa, Enterobacter cloacae and Nitrate negative bacilli were major ones in every period. Gram positive cocci accounted for 33.99% (1990 strains), which ranked the second, among which Staphylococcus aureus, Staphylococcus epidermidis, and Coagulase negative staphylococci (MRCNS) were the most predominant ones. The bacterial resistance to multiple antibiotics, such as Gentamicin, third generation of Cephalosporin, and Norfloxacin showed a tendency of increase or maintained at high level while the incidence of resistance to Imipenem and Vancomycin was very low. CONCLUSION: The climate and the way of using antibiotics exerted direct effects on the status of the bacterial ecology and change in bacterial resistance to various antibiotics.
In order to evaluate the effect of surface modification of biomaterials on bacterial adherence and bacterial translocation after intraperitoneal biomaterial implantation, phosphatidylcholine- or phosphatidylinositol-impregnated rubber drain pieces, which had been intraperitoneally implanted in the rat for 2 and 7 days, or unimplanted, were incubated in vitro with 3H-labelled Escherichia coli and Enterobacter cloacae. As compared with unimpregnated pieces, the adherence of bacteria significantly decreased to phosphatidylcholine- and phosphatidylinositol-impregnated rubber drain pieces that were either unimplanted or implanted for 2 days, but not for 7 days. The supplementation of albumin in the medium reduced the adherence of bacteria to the unimplanted, unimpregnated drain pieces, but did not further decrease adherence of bacteria to the unimplanted, phospholipid-impregnated brain pieces. Bacterial growth was inhibited after incubation in nutrient broth supplemented with phospholipids. The incidence of enteric bacterial translocation induced by intraperitoneal drain implantation did not differ between phospholipid-impregnated and unimpregnated drain pieces. Scanning electron microscopy revealed a large amount of biofilm and fibrous deposition on the surface of the implanted, phospholipid-impregnated rubber drain pieces. Thus, phospholipid impregnation of rubber drains reduces bacterial adherence and inhibits bacterial growth, without influencing the incidence of bacterial translocation.
A central feature of Salmonella pathogenicity is the bacterium's ability to enter into non-phagocytic cells. Bacterial internalization is the consequence of cellular responses characterized by Cdc42- and Rac-dependent actin cytoskeleton rearrangements. These responses are triggered by the co-ordinated function of bacterial proteins delivered into the host cell by a specialized protein secretion system termed type III. We report here that SopB, a Salmonella inositol polyphosphatase delivered to the host cell by this secretion system, mediates actin cytoskeleton rearrangements and bacterial entry in a Cdc42-dependent manner. SopB exhibits overlapping functions with two other effectors of bacterial entry, the Rho family GTPase exchange factors SopE and SopE2. Thus, Salmonella strains deficient in any one of these proteins can enter into cells at high efficiency, whereas a strain lacking all three effectors is completely defective for entry. Consistent with an important role for inositol phosphate metabolism in Salmonella-induced cellular responses, a catalytically defective mutant of SopB failed to stimulate actin cytoskeleton rearrangements and bacterial entry. Furthermore, bacterial infection of intestinal cells resulted in a marked increase in Ins(1,4,5,6)P4, a consumption of InsP5 and the activation of phospholipase C. In agreement with the in vivo findings, purified SopB specifically dephosphorylated InsP5 to Ins(1,4,5,6)P4 in vitro. Surprisingly, the inositol phosphate fluxes induced by Salmonella were not caused exclusively by SopB. We show that the SopB-independent inositol phosphate fluxes are the consequence of the SopE-dependent activation of an endogenous inositol phosphatase. The ability of Salmonella to stimulate Rho GTPases signalling and inositol phosphate metabolism through alternative mechanisms is an example of the remarkable ability of this bacterial pathogen to manipulate host cellular functions.
CD36 and LIMPII analog 1, CLA-1, and its splicing variant, CLA-2 (SR-BI and SR-BII in rodents), are human high density lipoprotein receptors with an identical extracellular domain which binds a spectrum of ligands including bacterial cell wall components. In this study, CLA-1- and CLA-2-stably transfected HeLa and HEK293 cells demonstrated several-fold increases in the uptake of various bacteria over mock-transfected cells. All bacteria tested, including both Gram-negatives (Escherichia coli K12, K1 and Salmonella typhimurium) and Gram-positives (Staphylococcus aureus and Listeria monocytogenes), demonstrated various degrees of lower uptake in control cells. This result is consistent with the presence of high-density lipoprotein-receptor-independent bacterial uptake that is enhanced by CLA-1/CLA-2 overexpression. Bacterial lipopolysaccharides, lipoteichoic acid, and synthetic amphipathic helical peptides (L-37pA and D-37pA) competed with E. coli K12 for CLA-1 and CLA-2 binding. Transmission electron microscopy and confocal microscopy revealed cytosolic accumulation of bacteria in CLA-1/CLA-2-overexpressing HeLa cells. The antibiotic protection assay confirmed that E. coli K12 was able to survive and replicate intracellularly in CLA-1- and CLA-2-overexpressing HeLa, but both L-37pA and D-37pA prevented E. coli K12 invasion. Peritoneal macrophages isolated from SR-BI/BII-knockout mice demonstrated a 30% decrease in bacterial uptake when compared with macrophages from normal mice. Knockout macrophages were also characterized by decreased bacterial cytosolic invasion, ubiquitination, and proteasome mobilization while retaining bacterial lysosomal accumulation. These results indicate that, by facilitating bacterial adhesion and cytosolic invasion, CLA-1 and CLA-2 may play an important role in infection and sepsis.