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Biomedical subjects

H Connell

Publications and source records attributed to H Connell.

17 recordsLinked to original sources
PubMed1998

Urodynamic factors influence the duration of Escherichia coli bacteriuria in deliberately colonized cases.

PURPOSE: We evaluated the influence of urodynamic factors on the establishment of bacteriuria, after deliberate intravesical inoculation with Escherichia coli. MATERIALS AND METHODS: Nine women and 7 men with recurrent symptomatic urinary tract infections underwent intravesical injection of E. coli 83972. This strain had documented ability to persist in the urinary tract and it lacks expressed virulence factors associated with urinary tract infection. RESULTS: Successful long-term colonization (5 months to 3 years) was achieved in 6 of 12 patients with neurogenic bladder disorder, including normal or high bladder capacity, normal or low detrusor pressure and residual urine. Short-term bacteriuria (13 days) occurred in 1 but long-term bacteriuria was not established in the 4 patients with normal lower urinary tract function. Occasionally urine samples from the colonized patients contained other bacterial strains, which cleared spontaneously except for a Klebsiella strain that became established in 2 and subsequently eliminated E. coli 83972. CONCLUSIONS: E. coli 83972 bacteriuria could only be established in a subset of patients with defective bladder voiding, suggesting that urodynamic defects permit a nonvirulent strain to establish in the urinary tract, but that additional host factors determine if bacteriuria will persist.

Administration, Intravesical↗
PubMed1997

The role of lipopolysaccharide and Shiga-like toxin in a mouse model of Escherichia coli O157:H7 infection.

The role of lipopolysaccharide (LPS) and Shiga-like toxin (SLT) in the pathogenesis of hemolytic uremic syndrome (HUS) was studied in a mouse model. Mice inoculated intragastrically with Escherichia coli O157:H7 developed gastrointestinal, neurologic, and systemic symptoms, necrotic foci in the colon, glomerular and tubular histopathology, and fragmented erythrocytes. LPS-responder (C3H/HeN) mice developed a combination of neurologic and systemic symptoms, whereas LPS-nonresponder (C3H/HeJ) mice had a biphasic course of disease, first developing systemic symptoms and later severe neurologic symptoms. Mice inoculated with SLT-II-positive strains developed severe neurotoxic symptoms and a higher frequency of systemic symptoms and glomerular pathology compared with SLT-II-negative strains. Anti-SLT-II antibodies protected against these symptoms and pathology. These results demonstrate that this model could be used to study aspects of human HUS and that both LPS and SLT are important for disease development.

Animals↗
PubMed1997

Bacterial attachment to uro-epithelial cells: mechanisms and consequences.

Microbial attachment to mucosal surfaces is a first step in mucosal infection. Specific interactions between microbial surface ligands and host receptors influence the distribution of microbes in their sites of infection. Adhesion has often been regarded as a sufficient end point, explaining tissue tropism and bacterial persistence at mucosal sites. Adherence, however, is also a virulence factor through which microbes gain access to host tissues, upset the integrity of the mucosal barrier, and cause disease. The induction of mucosal inflammation is one aspect of this process. Bacterial attachment to mucosal surfaces activates the production of pro-inflammatory cytokines that cause both local and systemic inflammation. Epithelial cells are one source of these cytokines. The binding of fimbrial lectins to epithelial cell receptors triggers transmembrane signaling events that upregulate cytokine-specific mRNA and increase cytokine secretion. P fimbriae that bind the globoseries of glycolipids cause the release of ceramides and activation of the ceramide signaling pathway which contributes to the IL-6 response. Spread of cytokines and other pro-inflammatory mediators from the local site contributes to the symptoms and signs of infection.

Adhesins, Bacterial↗
PubMed1996

Bacterial adherence and mucosal cytokine responses. Receptors and transmembrane signaling.

By attaching to cells or secreted mucosal components, microbes are thought to avoid elimination by the flow of secretions that constantly wash mucosal surfaces. The attached state enhances their ability to trap nutrients and allows the bacteria to multiply more efficiently than do unattached bacterial cells. Attachment is therefore regarded as an end result in itself, and emphasis has been placed on the role of adherence for colonization of mucosal surfaces. Specific adherence was shown to be essential for the tissue tropism that is to guide microbes to their respective sites of colonization/infection. Attachment is not only a mechanism of tissue targeting but also a first step in the pathogenesis of many infections. The attaching bacteria engage in a "cross-talk" with the host cells through the mutual exchange of signals and responses. Enteropathogenic E. coli induce attaching and effacing lesions (Finley et al., this issue). Shigella and Listeria sp. invade the cells and cause actin polymerization (Sansonetti et al., this issue). This review describes the ability of bacteria to trigger mucosal inflammation through activation of cells in the mucosal lining. The results suggest that receptors for bacterial adhesins bind their ligands with a high degree of specificity and that ligand-receptor interactions trigger transmembrane signaling events that cause cell activation. Receptors for microbial ligands thus appear to fulfill also the same criteria as those used to define receptors for other classes of ligands such as hormones, growth factors, and cytokines.

Bacterial Adhesion↗
PubMed1996

Linker insertion analysis of the FimH adhesin of type 1 fimbriae in an Escherichia coli fimH-null background.

The gene encoding the Escherichia coli FimH adhesin of type 1 fimbriae has been subjected to linker insertion mutagenesis. Amino acid changes were introduced at a number of positions spanning the entire sequence in order to probe the structure-function relationship of the FimH protein. The effect of these mutations on the ability of bacteria to express a D-mannose binding phenotype was assessed in a fimH null mutant (MS4) constructed by allelic exchange in the E. coli K-12 strain PC31. Mutations mapping at amino acid residues 36, 58 and 279 of the mature FimH protein were shown to completely abolish binding to D-mannose receptors. Differences in the level of fimbriation were also observed as a result of some of the mutations in the fimH gene. These mutants may prove useful in dissecting receptor-ligand interactions by defining regions of the FimH protein that are important in erythrocyte binding.

Adhesins, Bacterial↗
PubMed1996

Decreased expression of mannose-specific adhesins by Escherichia coli in the colonic microflora of immunoglobulin A-deficient individuals.

Most Escherichia coli isolates can express type 1 fimbriae with mannose-specific adhesins. These adhesins bind to the oligosaccharide chains of secretory immunoglobulin A (IgA). Thus, in addition to specific antibody activity, secretory IgA possesses a broad reactivity with bacteria expressing type 1 fimbriae. The absence of secretory IgA in colonic secretions, as seen in IgA deficiency, might therefore alter the ability of type 1-fimbriated E. coli to colonize the large intestines of these individuals. In the present study, 10 E. coli isolates from each of 17 IgA-deficient and 17 age-matched control individuals were assessed for the carriage of the fim gene cluster by DNA-DNA hybridization and for the expression of type 1 fimbriae by hemagglutination of guinea pig erythrocytes. The contribution of type 1-fimbria-mediated adherence to HT-29 colonic cells was also analyzed. The proportion of fim+ E. coli isolates was lower in IgA-deficient than in control individuals (74 versus 94%, P < 0.05), as was the proportion of isolates expressing type 1 fimbriae in vitro (69% versus 85%, P < 0.05). The median mannose-sensitive adherence to HT-29 cells was lower for isolates from IgA-deficient individuals than from the controls (9 versus 26 bacteria per cell, P < 0.05). Isolates expressing type 1 fimbriae showed lower adherence to HT-29 cells when they were derived from IgA-deficient individuals than when they were derived from control individuals (15 versus 27 bacteria per cell, P < 0.05). The results suggest that the interaction of type 1 fimbriae with secretory IgA contributes to the large intestinal colonization by these bacteria.

Adhesins, Bacterial↗
PubMed1995

Intestinal carriage of P fimbriated Escherichia coli and the susceptibility to urinary tract infection in young children.

This prospective study analyzed the intestinal carriage of P fimbriated Escherichia coli as a host susceptibility factor in urinary tract infection (UTI). P fimbriation was defined by the pap and G adhesin (papG1A2, prsGJ96) genotypes. Children with UTI carried pap+ E. coli in the fecal flora more often than healthy controls both at diagnosis (86% vs. 29%) and during infection-free intervals (approximately 40%; P < .01). P1 blood group-positive children carried pap+ E. coli in the fecal flora more often (88%) than those with P2 blood group (40%; P < .05). A pap+ E. coli strain caused UTI in 53 of 55 patients who carried both pap+ and pap- strains in their fecal flora. These results suggest that persons who develop UTI have an increased tendency to carry pap+ E. coli in the large intestine and that these pap+ E. coli cause UTI more often than pap E. coli strains in the fecal flora of the same host.

Adhesins, Escherichia coli↗
PubMed1994

Molecular characterization of a plasmid-borne (pGT633) erythromycin resistance determinant (ermGT) from Lactobacillus reuteri 100-63.

Lactobacillus reuteri 100-63 contains a 9.8 kb plasmid (pGT633) encoding resistance to the macrolide-lincosamide-streptogramin (MLS) type B antibiotics. The restriction endonucleases AccI, BamHI, BclI, EcoRI, EcoRV, HhaI, HindII, HpaI, KpnI, SalI, and SspI were employed to establish a physical map of pGT633. Next, genetic transfer experiments were conducted to establish the host range of pGT633. The results revealed that pGT633 replicated autonomously and encoded constitutive resistance to erythromycin in a variety of bacterial hosts, including Bacillus subtilis BD170, Streptococcus sanguis DL1, Staphylococcus aureus RN4220, and Enterococcus faecalis 19433, as well as several Lactobacillus spp. A 2.2 kb BamHI fragment of pGT633 containing the genetic determinant (ermGT) encoding resistance to erythromycin was cloned into Escherichia coli. Determination of the nucleotide sequence of ermGT revealed a methylase gene 731 bp in length that was highly related (ca. 81% nucleotide and ca. 78% amino acid identity) to the ermC gene from S. aureus plasmid pE194. The leader sequences of ermGT and ermC were identical except for a single base change at nt 51.

Amino Acid Sequence↗
PubMed1994

Suppressed antibody and interleukin-6 responses to acute pyelonephritis in pregnancy.

This study examined the effect of pregnancy on the host response to acute pyelonephritis. Urine and serum samples were obtained at the time of diagnosis and after two weeks, from non-pregnant and pregnant women with acute pyelonephritis. The samples were analyzed for interleukin-6 (IL-6) and specific antibody activity to antigens extracted from the Escherichia coli strain infecting each patient. The host response to infection was further quantitated as fever, C-reactive protein, and renal concentrating capacity. Acute pyelonephritis in non-pregnant and pregnant women was accompanied by a significant serum and urine antibody response. The serum antibody response was significantly lower in the pregnant group. The IL-6 levels in serum and urine at diagnosis were significantly higher in the non-pregnant compared to the pregnant women. These results demonstrate that the immunosuppression of pregnancy includes the mucosal IL-6 and specific antibody responses to acute pyelonephritis caused by E. coli.

Acute Disease↗
PubMed1993

Lack of association between hemolysin production and acute inflammation in human urinary tract infection.

Hemolysins are cytolytic proteins which have been extensively characterized at the molecular level, however, their in vivo functions remain unclear. This study analyzed the association of hemolysin production with the inflammatory response in patients with urinary tract infection (UTI). Infants and children with their first episode of UTI (n = 644) were followed prospectively. The body temperature, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), urinary leucocyte count and renal concentrating capacity were used as measures of the inflammatory response. The hemolytic genotype (hly) of the Escherichia coli strain from each UTI episode was defined by DNA-DNA hybridization, and the phenotype by hemolysis in blood agar. There was no significant increase in the level of fever, CRP, ESR, or decrease in renal concentrating capacity during UTI episodes caused by hly positive compared to hly negative E. coli. Multiple regression analysis did not demonstrate significant associations of hly with elevated fever, CRP, ESR or reduced renal concentrating capacity. In contrast, patients infected with P fimbriated E. coli strains had higher fever, CRP, ESR and lower renal concentrating capacity than those infected with other strains. This association was not influenced by the hly genotype of the P fimbriated strains. The frequency of hly+ strains was not significantly higher in the subset of patients assigned a diagnosis of acute pyelonephritis compared to asymptomatic bacteriuria. This was in contrast to P fimbriae, which were accumulated in acute pyelonephritis. The results suggested that the acute inflammatory response to E. coli UTI is independent of hemolysin production. The inflammatogenic potential of uropathogenic E. coli clones was better described by the presence or absence of P-fimbriae than by hemolysin.

Child, Preschool↗
PubMed1990

Study of the possible interaction between fentanyl and propofol using a computer-controlled infusion of propofol.

A computer-controlled infusion of propofol designed to achieve a target blood concentration of propofol 3 microgram ml-1 was used to investigate the possibility of an interaction between propofol and fentanyl in 32 patients undergoing body surface surgery. In 16 patients who were not receiving a neuromuscular blocker during maintenance anaesthesia with 67% nitrous oxide, there were no significant differences in blood concentrations of propofol between eight patients who received fentanyl 5 micrograms kg-1 before induction of anaesthesia, and eight patients who did not. In a further 16 patients who received vecuronium during maintenance anaesthesia with 67% nitrous oxide, there were no significant differences in blood propofol concentrations between eight patients who received fentanyl 5 micrograms kg-1 before induction of anaesthesia, and eight patients who did not. Fentanyl administered i.v. immediately before a computer-controlled infusion of propofol resulted in more satisfactory anaesthetic conditions than when fentanyl was not used, but did not significantly prolong the recovery time.

Adult↗
PubMed1987

General anaesthesia in mothers with severe pre-eclampsia/eclampsia.

Twenty patients with severe pregnancy induced (PIH) or pregnancy aggravated (PAH) hypertension, undergoing general anaesthesia for Caesarean section were studied. All patients received a standard anaesthetic technique designed to control the potentially dangerous, reflex cardiovascular instability associated with laryngoscopy. The average increase in systolic arterial pressure (SAP) was 56.4 mm Hg following laryngoscopy and tracheal intubation.

Adolescent↗