Group B streptococcus cystitis presenting in a diabetic patient with a massive abdominopelvic abscess: a case report

INTRODUCTION: Streptococcus agalactiae or group B streptococcus is a Gram-positive pathogen that is typically associated with neonatal disease and infection in pregnant women. Group B streptococcus also causes invasive infections in non-pregnant adults including urinary tract infections. The spectrum of urinary tract infections caused by group B streptococcus includes cystitis, pyelonephritis, urosepsis and asymptomatic bacteriuria, which is particularly common among elderly individuals. A rare form of invasive group B streptococcus infection in adults is secondary abscess. Here, we present the first reported case of a patient who developed an unusual, massive abdominopelvic abscess secondary to acute group B streptococcus urinary tract infection. CASE PRESENTATION: A 46-year-old African-American woman presented to the University Emergency Department complaining of urinary tract infection symptoms and severe abdominal pain. Diagnostic imaging by transvaginal ultrasound and computed tomography revealed a massive peripherally-enhancing, low-attenuating fluid collection within her pelvis. The patient’s abdominopelvic abscess was drained by ultrasound-guided drainage and this yielded a septic aspirate that was culture positive for abundant S. agalactiae. A recent history of urinary tract infection symptoms in the patient suggested that her abscess developed secondary to cystitis. Complete resolution of the abscess as a favorable outcome was achieved in this case following surgical drainage and appropriate antimicrobial therapy. CONCLUSION: Acute bacterial urinary tract infection leading to an abdominopelvic abscess has not previously been reported in the literature. This case report defines a new disease etiology associated with acute streptococcal cystitis and it will be of interest in cases of urinary tract infections where there is an association with abdominal and/or pelvic pain. A brief review of the literature on unusual secondary abscesses due to group B streptococcus is provided alongside this case to highlight the clinical significance and prognoses of these rare infections. Finally, this case emphasizes the requirement to distinguish unusual etiologies of pyogenic abscesses in order to guide successful clinical management and to treat patients with antibiotics active against the causal organism

Thermal-Expansion and Fracture Toughness Properties ofParts made from Liquid Crystal Stereolithography Resins

Liquid crystal (LC) resins are a new kind ofstereolithography material that can produce parts with structured or ordered morphologies instead ofthe amorphous morphologies that result from standard resins. The LC molecules can be aligned before cure resulting in an anisotropic crosslinked network when the laser induced polymerization "locks-in" the alignment. Previous papers have explored liquid crystal orientation dynamics [1], the effects of orientation on viscoelastic and mechanical properties [2,3], and the processing ofLC resins by stereolithography [4]. This paper considers the effects ofmorphology on fracture toughness and thermal-expansion properties. Both toughness and thermal-stability continue to be important issues for stereolithography parts. The use ofLC resins may provide a way to significantly improve performance in both ofthese areas, and in addition result in parts with high upper use . temperatures.Mechanical Engineerin

Genome-wide mapping of cystitis due to Streptococcus agalactiae and Escherichia coli in mice identifies a unique bladder transcriptome that signifies pathogen-specific antimicrobial defense against urinary tract infection

The most common causes of urinary tract infections (UTIs) are Gram-negative pathogens such as Escherichia coli; however, Gram-positive organisms, including Streptococcus agalactiae, or group B streptococcus (GBS), also cause UTI. In GBS infection, UTI progresses to cystitis once the bacteria colonize the bladder, but the host responses triggered in the bladder immediately following infection are largely unknown. Here, we used genome-wide expression profiling to map the bladder transcriptome of GBS UTI in mice infected transurethrally with uropathogenic GBS that was cultured from a 35-year-old women with cystitis. RNA from bladders was applied to Affymetrix Gene-1.0ST microarrays; quantitative reverse transcriptase PCR (qRT-PCR) was used to analyze selected gene responses identified in array data sets. A surprisingly small significant-gene list of 172 genes was identified at 24 h; this compared to 2,507 genes identified in a side-by-side comparison with uropathogenic E. coli (UPEC). No genes exhibited significantly altered expression at 2 h in GBS-infected mice according to arrays despite high bladder bacterial loads at this early time point. The absence of a marked early host response to GBS juxtaposed with broad-based bladder responses activated by UPEC at 2 h. Bioinformatics analyses, including integrative system-level network mapping, revealed multiple activated biological pathways in the GBS bladder transcriptome that regulate leukocyte activation, inflammation, apoptosis, and cytokine-chemokine biosynthesis. These findings define a novel, minimalistic type of bladder host response triggered by GBS UTI, which comprises collective antimicrobial pathways that differ dramatically from those activated by UPEC. Overall, this study emphasizes the unique nature of bladder immune activation mechanisms triggered by distinct uropathogens

Ordered and ushered; the assembly and translocation of the adhesive Type I and P Pili

Type I and P pili are chaperone-usher pili of uropathogenic Escherichia coli, which allow bacteria to adhere to host cell receptors. Pilus formation and secretion are orchestrated by two accessory proteins, a chaperone, which catalyses pilus subunit folding and maintains them in a polymerization-competent state, and an outer membrane-spanning nanomachine, the usher, which choreographs their assembly into a pilus and drives their secretion through the membrane. In this review, recent structures and kinetic studies are combined to examine the mechanism of type I and P pili assembly, as it is currently known. We also investigate how the knowledge of pilus biogenesis mechanisms has been exploited to design selective inhibitors of the process

Spiritual wellbeing in the healing process

Spiritual wellbeing in the healing proces

Uropathogenic Escherichia coli virulence and innate immune responses during urinary tract infection

Urinary tract infections (UTI) are among the most common infectious diseases of humans and are the most common nosocomial infections in the developed world. It is estimated that 40-50% of women and 5% of men will develop a UTI in their lifetime, and UTI accounts for more than 1 million hospitalizations and $1.6 billion in medical expenses each year in the USA. Uropathogenic Escherichia coli (UPEC) is the primary cause of UTI. This review presents an overview of recent discoveries related to the primary virulence factors of UPEC and major innate immune responses to infection of the lower urinary tract. New and emerging themes in UPEC research are discussed in the context of the interface between host and pathogen

The co-transcriptome of uropathogenic Escherichia coli-infected mouse macrophages reveals new insights into host-pathogen interactions

© 2014 The Authors. Cellular Microbiology published by John Wiley & Sons Ltd. Urinary tract infections (UTI) are among the most common infections in humans. Uropathogenic Escherichia coli (UPEC) can invade and replicate within bladder epithelial cells, and some UPEC strains can also survive within macrophages. To understand the UPEC transcriptional programme associated with intramacrophage survival, we performed host-pathogen co-transcriptome analyses using RNA sequencing. Mouse bone marrow-derived macrophages (BMMs) were challenged over a 24h time course with two UPEC reference strains that possess contrasting intramacrophage phenotypes: UTI89, which survives in BMMs, and 83972, which is killed by BMMs. Neither of these strains caused significant BMM cell death at the low multiplicity of infection that was used in this study. We developed an effective computational framework that simultaneously separated, annotated and quantified the mammalian and bacterial transcriptomes. Bone marrow-derived macrophages responded to the two UPEC strains with a broadly similar gene expression programme. In contrast, the transcriptional responses of the UPEC strains diverged markedly from each other. We identified UTI89 genes up-regulated at 24h post-infection, and hypothesized that some may contribute to intramacrophage survival. Indeed, we showed that deletion of one such gene (pspA) significantly reduced UTI89 survival within BMMs. Our study provides a technological framework for simultaneously capturing global changes at the transcriptional level in co-cultures, and has generated new insights into the mechanisms that UPEC use to persist within the intramacrophage environment

Comprehensive analysis of type 1 fimbriae regulation in fimB -null strains from the multidrug resistant Escherichia coli ST131 clone

Summary\ud \ud Uropathogenic Escherichia coli (UPEC) of sequence type 131 (ST131) are a pandemic multidrug resistant clone associated with urinary tract and bloodstream infections. Type 1 fimbriae, a major UPEC virulence factor, are essential for ST131 bladder colonization. The globally dominant sub-lineage of ST131 strains, clade C/H30-R, possess an ISEc55 insertion in the fimB gene that controls phase-variable type 1 fimbriae expression via the invertible fimS promoter. We report that inactivation of fimB in these strains causes altered regulation of type 1 fimbriae expression. Using a novel read-mapping approach based on Illumina sequencing, we demonstrate that ‘off’ to ‘on’ fimS inversion is reduced in these strains and controlled by recombinases encoded by the fimE and fimX genes. Unlike typical UPEC strains, the nucleoid-associated H-NS protein does not strongly repress fimE transcription in clade C ST131 strains. Using a genetic screen to identify novel regulators of fimE and fimX in the clade C ST131 strain EC958, we defined a new role for the guaB gene in the regulation of type 1 fimbriae and in colonisation of the mouse bladder. Our results provide a comprehensive analysis of type 1 fimbriae regulation in ST131, and highlight important differences in its control compared to non-ST131 UPEC

Contribution of siderophore systems to growth and urinary tract colonization of asymptomatic bacteriuria Escherichia coli

The molecular mechanisms that define asymptomatic bacteriuria (ABU) E. coli colonization of the human urinary tract remain to be properly elucidated. Here we utilize ABU E. coli strain 83972 as a model to dissect the contribution of siderophores to iron acquisition, growth, fitness and colonization of the urinary tract. We show that E. coli 83972 produces enterobactin, salmochelin, aerobactin and yersiniabactin, and examine the role of these systems using mutants defective in siderophore biosynthesis and uptake. Enterobactin and aerobactin contributed most to total siderophore activity and growth in defined iron-deficient media. No siderophores were detected in an 83972 quadruple mutant deficient in all four siderophore biosynthesis pathways; this mutant did not grow in defined iron-deficient media but grew in iron-limited pooled human urine due to iron uptake via the FecA ferric citrate receptor. In a mixed 1:1 growth assay with 83972 there was no fitness disadvantage of the 83972 quadruple biosynthetic mutant, demonstrating its capacity to act as a ‘cheater’ and utilize siderophores produced by the wild-type strain for iron uptake. An 83972 enterobactin/salmochelin double receptor mutant was outcompeted by 83972 in human urine and the mouse urinary tract, indicating a role for catecholate receptors in urinary tract colonization

Diversity of group B streptococcus serotypes causing urinary tract infection in adults

Serotypes of group B streptococcus (GBS) that cause urinary tract infection (UTI) are poorly characterized. We conducted a prospective study of GBS UTI in adults to define the clinical and microbiological characteristics of these infections, including which serotypes cause disease. Patients who had GBS cultured from urine over a 1-year period were grouped according to symptoms, bacteriuria, and urinalysis. Demographic data were obtained by reviewing medical records. Isolates were serotyped by latex agglutination and multiplex PCRreverse line blotting (mPCR/RLB). Antibiotic susceptibilities were determined by disc diffusion. GBS was cultured from 387/34,367 consecutive urine samples (1.1%): 62 patients had bacteriuria of >10 7 CFU/liter and at least one UTI symptom; of these patients, 31 had urinary leukocyte esterase and pyuria (others not tested), 50 (81%) had symptoms consistent with cystitis, and 12 (19%) had symptoms of pyelonephritis. Compared with controls (who had GBS isolated without symptoms), a prior history of UTI was an independent risk factor for disease. Increased age was also significantly associated with acute infection. Serotyping results were consistent between latex agglutination and mPCR/RLB for 331/387 (85.5%) isolates; 22 (5.7%) and 7 (1.8%) isolates were nontypeable with antisera and by mPCR/RLB, respectively; and 45/56 (80.4%) isolates with discrepant results were typed by mPCR/RLB as belonging to serotype V. Serotypes V, Ia, and III caused the most UTIs; serotypes II, Ib, and IV were less common. Nontypeable GBS was not associated with UTI. Erythromycin (39.5%) and clindamycin (26.4%) resistance was common. We conclude that a more diverse spectrum of GBS serotypes causes UTI than previously recognized, with the exception of nontypeable GBS