bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diagnosis and Management of Human Cytomegalovirus Infection in the Mother, Fetus, and Newborn Infant
Authors: Revello Maria Grazia , Gerna Giuseppe 
Published: October 2002

SUMMARYHuman cytomegalovirus (HCMV) is the leading cause of congenital viral infection and mental retardation. HCMV infection, while causing asymptomatic infections in most immunocompetent subjects, can be transmitted during pregnancy from the mother with primary (and also recurrent) infection to the fetus. Hence, careful diagnosis of primary infection is required in the pregnant woman based on the most sensitive serologic assays (immunoglobulin M [IgM] and IgG avidity assays) and conventional virologic and molecular procedures for virus detection in blood. Maternal prognostic markers of fetal infection are still under investigation. If primary infection is diagnosed in a timely manner, prenatal diagnosis can be offered, including the search for virus and virus components in fetal blood and amniotic fluid, with fetal prognostic markers of HCMV disease still to be defined. However, the final step for definite diagnosis of congenital HCMV infection is detection of virus in the blood or urine in the first 1 to 2 weeks of life. To date, treatment of congenital infection with antiviral drugs is only palliative both prior to and after birth, whereas the only efficacious preventive measure seems to be the development of a safe and immunogenic vaccine, including recombinant, subunit, DNA, and peptide-based vaccines now under investigation. The following controversial issues are discussed in the light of the most recent advances in the field: the actual perception of the problem; universal serologic screening before pregnancy; the impact of correct counseling on decision making by the couple involved; the role of prenatal diagnosis in ascertaining transmission of virus to the fetus; the impact of preconceptional and periconceptional infections on the prevalence of congenital infection; and the prevalence of congenitally infected babies born to mothers who were immune prior to pregnancy compared to the number born to mothers undergoing primary infection during pregnancy.
Clinical and Taxonomic Status of Pathogenic Nonpigmented or Late-Pigmenting Rapidly Growing Mycobacteria
Authors: Brown-Elliott Barbara A. , Wallace Richard J. 
Published: October 2002

SUMMARY
The history, taxonomy, geographic distribution, clinical disease, and therapy of the pathogenic nonpigmented or late-pigmenting rapidly growing mycobacteria (RGM) are reviewed. Community-acquired disease and health care-associated disease are highlighted for each species. The latter grouping includes health care-associated outbreaks and pseudo-outbreaks as well as sporadic disease cases. Treatment recommendations for each species and type of disease are also described. Special emphasis is on the Mycobacterium fortuitum group, including M. fortuitum, M. peregrinum, and the unnamed third biovariant complex with its recent taxonomic changes and newly recognized species (including M. septicum, M. mageritense, and proposed species M. houstonense and M. bonickei). The clinical and taxonomic status of M. chelonae, M. abscessus, and M. mucogenicum is also detailed, along with that of the closely related new species, M. immunogenum. Additionally, newly recognized species, M. wolinskyi and M. goodii, as well as M. smegmatis sensu stricto, are included in a discussion of the M. smegmatis group. Laboratory diagnosis of RGM using phenotypic methods such as biochemical testing and high-performance liquid chromatography and molecular methods of diagnosis are also discussed. The latter includes PCR-restriction fragment length polymorphism analysis, hybridization, ribotyping, and sequence analysis. Susceptibility testing and antibiotic susceptibility patterns of the RGM are also annotated, along with the current recommendations from the National Committee for Clinical Laboratory Standards (NCCLS) for mycobacterial susceptibility testing.
Current Consensus Guidelines for Treatment of Neurocysticercosis
Authors: García Hector H. , Evans Carlton A. W. , Nash Theodore E. , Takayanagui Osvaldo M. , White A. Clinton , Botero David , Rajshekhar Vedantam , Tsang Victor C. W. , Schantz Peter M. , Allan James C. , Flisser Ana , Correa Dolores , Sarti Elsa , Friedland Jon S. , Martinez S. Manuel , Gonzalez Armando E. , Gilman Robert H. , Del Brutto Oscar H. 
Published: October 2002

SUMMARY
Taenia solium neurocysticercosis is a common cause of epileptic seizures and other neurological morbidity in most developing countries. It is also an increasingly common diagnosis in industrialized countries because of immigration from areas where it is endemic. Its clinical manifestations are highly variable and depend on the number, stage, and size of the lesions and the host's immune response. In part due to this variability, major discrepancies exist in the treatment of neurocysticercosis. A panel of experts in taeniasis/cysticercosis discussed the evidence on treatment of neurocysticercosis for each clinical presentation, and we present the panel's consensus and areas of disagreement. Overall, four general recommendations were made: (i) individualize therapeutic decisions, including whether to use antiparasitic drugs, based on the number, location, and viability of the parasites within the nervous system; (ii) actively manage growing cysticerci either with antiparasitic drugs or surgical excision; (iii) prioritize the management of intracranial hypertension secondary to neurocysticercosis before considering any other form of therapy; and (iv) manage seizures as done for seizures due to other causes of secondary seizures (remote symptomatic seizures) because they are due to an organic focus that has been present for a long time.
Effects of Global Climate on Infectious Disease: the Cholera Model
Authors: Lipp Erin K. , Huq Anwar , Colwell Rita R. 
Published: October 2002

SUMMARY

Recently, the role of the environment and climate in disease dynamics has become a subject of increasing interest to microbiologists, clinicians, epidemiologists, and ecologists. Much of the interest has been stimulated by the growing problems of antibiotic resistance among pathogens, emergence and/or reemergence of infectious diseases worldwide, the potential of bioterrorism, and the debate concerning climate change. Cholera, caused by
Vibrio cholerae
, lends itself to analyses of the role of climate in infectious disease, coupled to population dynamics of pathogenic microorganisms, for several reasons. First, the disease has a historical context linking it to specific seasons and biogeographical zones. In addition, the population dynamics of
V. cholerae
in the environment are strongly controlled by environmental factors, such as water temperature, salinity, and the presence of copepods, which are, in turn, controlled by larger-scale climate variability. In this review, the association between plankton and
V. cholerae
that has been documented over the last 20 years is discussed in support of the hypothesis that cholera shares properties of a vector-borne disease. In addition, a model for environmental transmission of cholera to humans in the context of climate variability is presented. The cholera model provides a template for future research on climate-sensitive diseases, allowing definition of critical parameters and offering a means of developing more sophisticated methods for prediction of disease outbreaks.
Toll-Like Receptor 4 (TLR4)-Deficient Murine Macrophage Cell Line as an In Vitro Assay System To Show TLR4-Independent Signaling ofBacteroides fragilisLipopolysaccharide
Authors: Lorenz Eva , Patel Dhavalkumar D. , Hartung Thomas , Schwartz David A. 
Published: October 2002

ABSTRACTBacterial lipopolysaccharides (LPS) activate cells of innate immunity, such as macrophages, by stimulating signaling through toll-like receptor 4 (TLR4). We and others have hypothesized that LPS derived from different bacterial species may function through TLR4-independent mechanisms. To test this hypothesis, we have generated using a nonviral transformation procedure a bone marrow-derived macrophage cell line called 10ScNCr/23 from mouse strain C57BL/10ScNCr. This mouse strain has a deletion of the TLR4 locus, causing the mouse strain to be nonresponsive to stimulation by LPS fromEscherichia coliwhile responding normally to other bacterial substrates, such as lipoteichoic acid (LTA) fromStaphylococcus aureus, which signal TLR4 independently. Stimulation with LTA induces five- and sixfold increases in 10ScNCr/23 cell line tumor necrosis factor alpha and macrophage inflammatory protein-2 (MIP-2) secretion, but no increases in either cytokine were found when cells were stimulated withE. coliLPS.Bacteroides fragilis-derived LPS, however, can effectively stimulate MIP-2 expression in the absence of functional TLR4 in the 10ScNCr/23 cell line. This gives rise to the notion that LPS from some bacterial species will utilize alternative receptors to stimulate the innate immune response.
Control of Mycobacterial Replication in Human Macrophages: Roles of Extracellular Signal-Regulated Kinases 1 and 2 and p38 Mitogen-Activated Protein Kinase Pathways
Authors: Blumenthal Antje , Ehlers Stefan , Ernst Martin , Flad Hans-Dieter , Reiling Norbert 
Published: October 2002

ABSTRACTIntracellular persistence of mycobacteria may result from an intricate balance between bacterial replication and signaling events leading to antimicrobial macrophage activities. Using human monocyte-derived macrophages, we investigated the relevance of mitogen-activated protein kinase activation for the growth control ofMycobacterium aviumisolates differing in their abilities to multiply intracellularly. The highly replicative smooth transparent morphotype ofM. aviumstrain 2151 induced significantly less p38 and extracellular signal-regulated kinases 1 and 2 (ERK1/2) phosphorylation than the smooth opaque morphotype of the same strain, which was gradually eliminated from macrophage cultures. Inhibition of the p38 pathway by highly specific inhibitors did not significantly affect mycobacterial replication within macrophages, regardless of the in vitro virulence of theM. aviumstrain. However, repression of the ERK1/2 pathway further enhanced intracellular growth of highly replicativeM. aviumstrains, although it did not increase survival of the poorly replicatingM. aviumisolate. Inhibition of the ERK1/2 pathway resulted in decreased tumor necrosis alpha (TNF-α) secretion irrespective of the virulence of theM. aviumisolate used for infection, revealing that TNF-α could have been only partially responsible for the control of intracellularM. aviumgrowth. In conclusion, ERK1/2- and TNF-α-independent pathways are sufficient to limit intramacrophage growth of less-virulentM. aviumstrains, but early ERK1/2 activation in infected macrophages is critically involved in controlling the growth of highly replicativeM. aviumstrains.
Tolerance to Self Gangliosides Is the Major Factor Restricting the Antibody Response to Lipopolysaccharide Core Oligosaccharides inCampylobacter jejuniStrains Associated with Guillain-Barré Syndrome
Authors: Bowes Tyrone , Wagner Eric R. , Boffey Judith , Nicholl Dawn , Cochrane Lynne , Benboubetra Mustapha , Conner Joe , Furukawa Keiko , Furukawa Koichi , Willison Hugh J. 
Published: October 2002

ABSTRACTGuillain-Barré syndrome followingCampylobacter jejuniinfection is frequently associated with anti-ganglioside autoantibodies mediated by molecular mimicry with ganglioside-like oligosaccharides on bacterial lipopolysaccharide (LPS). The regulation of antibody responses to these T-cell-independent antigens is poorly understood, and only a minority ofCampylobacter-infected individuals develop anti-ganglioside antibodies. This study investigates the response to gangliosides and LPS in strains of mice by using a range of immunization strategies. In normal mice following intraperitoneal immunization, antibody responses to gangliosides and LPS are low level but can be enhanced by the antigen format or coadministration of protein to recruit T-cell help. Class switching from the predominant immunoglobulin M (IgM) response to IgG3 occurs at low levels, suggesting B1-cell involvement. Systemic immunization results in poor responses. In GalNAc transferase knockout mice that lack all complex gangliosides and instead express high levels of GM3 and GD3, generation of anti-ganglioside antibodies upon immunization with either complex gangliosides or ganglioside-mimicking LPS is greatly enhanced and exhibits class switching to T-cell-dependent IgG isotypes and immunological memory, indicating that tolerance to self gangliosides is a major regulatory factor. Responses to GD3 are suppressed in knockout mice compared with wild-type mice, in which responses to GD3 are induced specifically by GD3 and as a result of polyclonal B-cell activation by LPS. The anti-ganglioside response generated in response to LPS is also dependent on the epitope density of the ganglioside mimicked and can be further manipulated by providing secondary signals via lipid A and CD40 ligation.
Immunogenicity in a Mouse Model of a Conjugate Vaccine Made with a Synthetic Single Repeating Unit of Type 14 Pneumococcal Polysaccharide Coupled to CRM197
Authors: Mawas Fatme , Niggemann Jutta , Jones Christopher , Corbel Michael J. , Kamerling Johannis P. , Vliegenthart Johannes F. G. 
Published: October 2002

ABSTRACTOligosaccharides (OSs) related to the pneumococcal type 14 capsular polysaccharide (Pn14PS) were studied for their ability to inhibit the binding between anti-PS14 antisera and native PS14. A synthetic tetrasaccharide corresponding to the repeating unit of the Pn14PS, a hexasaccharide mimic, and an octasaccharide fragment obtained by Pn14PS depolymerization were good inhibitors. CRM197 conjugates of the tetrasaccharide and an octasaccharide mimic were prepared by using either adipic acid diester or diethyl squarate linkers. The conjugate with the tetrasaccharide chains induced anti-Pn14PS antibodies when injected subcutaneously into mice, as determined by an enzyme-linked immunosorbent assay, and antibody titers increased with oligosaccharide loading. The adipic acid-linked tetrasaccharide conjugates elicited higher antibody titers than those prepared with a squarate spacer. The lower anti-Pn14PS antibody response of the octasaccharide mimic conjugate indicates the importance of the backbone galactose residue for an appropriate antibody response. The OS-CRM197 conjugate prepared from a single repeat unit of the Pn14PS is a potential vaccine candidate.
Effects of Ageing on the Immunoregulation of Parasitic Infection
Authors: Humphreys Neil E. , Grencis Richard K. 
Published: October 2002

ABSTRACTThe plethora of changes associated with immunosenescence radically alters virtually all aspects of immune responsiveness. How this transformation effects resolution of an infectious challenge is addressed in this study. A well-established infection model was used;Trichuris muris, a cecum-dwelling helminth, is natural to mice, and infection in different strains results in clearly polarized responses. A dominating T helper 2 (Th2) response orchestrates immunity, whereas a Th1 response will result in susceptibility. Mice between 19 and 28 months old were more susceptible to infection, whereas 3-month-old mice of the same strain demonstrated the resistant phenotype. The cytokine response made by these aged mice was clearly altered at the site of infection, and within the local draining lymph nodes higher Th1 and lower Th2 cytokine levels were found, both at the protein and RNA level. Confirming these changes, aged mice also showed a delayed parasite-specific immunoglobulin G1 response and intestinal mastocytosis, both of which are driven by Th2 cytokines. To address possible causes of the observed immune deviation, purified CD4 cells from both young and aged mice were stimulated in vitro. Cells from aged mice did not respond to stimulation via CD28 and in vitro were less able to proliferate and polarize into Th2 cells; Th1 polarization was found to be normal. Together these data suggest that changes in cytokine phenotype, particularly CD4 cells, contribute to the observed age-associated switch fromT. murisresistance to susceptibility.
Susceptibility of Nontypeable
Haemophilus influenzae
to Human β-Defensins Is Influenced by Lipooligosaccharide Acylation
Authors: Starner Timothy D. , Swords W. Edward , Apicella Michael A. , McCray Paul B. 
Published: October 2002

ABSTRACT

Nontypeable
Haemophilus influenzae
(NTHI) lipooligosaccharide
htrB
mutants exhibited greater than 45-fold-increased sensitivity to human β-defensin 2 (HBD-2) compared to the wild type. Complementation by
htrB in trans
to acylation competence reversed this increased sensitivity. In contrast, NTHI was more susceptible to HBD-3 and showed no changes in sensitivity as a result of lipooligosaccharide mutations in oligosaccharide and lipid A biosynthesis genes.
Cluster IIcheGenes fromPseudomonas aeruginosaAre Required for an Optimal Chemotactic Response
Authors: Ferrández Abel , Hawkins Andrew C. , Summerfield Douglas T. , Harwood Caroline S. 
Published: October 2002

ABSTRACTPseudomonas aeruginosa, a γ-proteobacterium, is motile by means of a single polar flagellum and is chemotactic to a variety of organic compounds and phosphate.P. aeruginosahas multiple homologues ofEscherichia colichemotaxis genes that are organized into five gene clusters. Previously, it was demonstrated that genes in cluster I and cluster V are essential for chemotaxis. A third cluster (cluster II) contains a complete set ofchegenes, as well as two genes,mcpAandmcpB, encoding methyl-accepting chemotaxis proteins. Mutations were constructed in several of the cluster IIchegenes and in themcpgenes to examine their possible contributions toP. aeruginosachemotaxis. AcheB2mutant was partially impaired in chemotaxis in soft-agar swarm plate assays. ProvidingcheB2intranscomplemented this defect. Further, overexpression of CheB2 restored chemotaxis to a completely nonchemotactic, cluster I,cheB-deficient strain to near wild-type levels. AnmcpAmutant was defective in chemotaxis in media that were low in magnesium. The defect could be relieved by the addition of magnesium to the swarm plate medium. AnmcpBmutant was defective in chemotaxis when assayed in dilute rich soft-agar swarm medium or in minimal-medium swarm plates containing any 1 of 60 chemoattractants. The mutant phenotype could be complemented by the addition ofmcpBintrans. Overexpression of either McpA or McpB inP. aeruginosaorEscherichia coliresulted in impairment of chemotaxis, and these cells had smooth-swimming phenotypes when observed under the microscope. Expression ofP. aeruginosa cheA2,cheB2, orcheW2inE. coliK-12 completely disrupted wild-type chemotaxis, while expression ofcheY2had no effect. These results indicate thatchecluster II genes are expressed inP. aeruginosaand are required for an optimal chemotactic response.
N
-Acyl-Homoserine Lactone Inhibition of Rhizobial Growth Is Mediated by Two Quorum-Sensing Genes That Regulate Plasmid Transfer
Authors: Wilkinson A. , Danino V. , Wisniewski-Dyé F. , Lithgow J. K. , Downie J. A. 
Published: October 2002

ABSTRACT

The growth of some strains of
Rhizobium leguminosarum
bv. viciae is inhibited by
N
-(3-hydroxy-7-
cis
tetradecenoyl)-
l
-homoserine lactone (3OH-C
14:1
-HSL), which was previously known as the
small
bacteriocin before its characterization as an
N
-acyl homoserine lactone (AHL). Tn
5
-induced mutants of
R. leguminosarum
bv. viciae resistant to 3OH-C
14:1
-HSL were isolated, and mutations in two genes were identified. These genes,
bisR
and
triR
, which both encode LuxR-type regulators required for plasmid transfer, were found downstream of an operon containing
trb
genes involved in the transfer of the symbiotic plasmid pRL1JI. The first gene in this operon is
traI
, which encodes an AHL synthase, and the
trbBCDEJKLFGHI
genes were found between
traI
and
bisR
. Mutations in
bisR
,
triR
,
traI
, or
trbL
blocked plasmid transfer. Using gene fusions, it was demonstrated that
bisR
regulates
triR
in response to the presence of 3OH-C
14:1
-HSL. In turn,
triR
is then required for the induction of the
traI-trb
operon required for plasmid transfer.
bisR
also represses expression of
cinI
, which is chromosomally located and determines the level of production of 3OH-C
14:1
-HSL. The cloned
bisR
and
triR
genes conferred 3OH-C
14:1
-HSL sensitivity to strains of
R. leguminosarum
bv. viciae normally resistant to this AHL. Furthermore,
bisR
and
triR
made
Agrobacterium tumefaciens
sensitive to
R. leguminosarum
bv. viciae strains producing 3OH-C
14:1
-HSL. Analysis of patterns of growth inhibition using mutant strains and synthetic AHLs revealed that maximal growth inhibition required, in addition to 3OH-C
14:1
-HSL, the presence of other AHLs such as
N
-octanoyl
-l-
homoserine lactone and/or
N
-(3-oxo-octanoyl)
-l-
homoserine lactone. In an attempt to identify the causes of growth inhibition, a strain of
R. leguminosarum
bv. viciae carrying cloned
bisR
and
triR
was treated with an AHL extract containing 3OH-C
14:1
-HSL. N-terminal sequencing of induced proteins revealed one with significant similarity to the protein translation factor Ef-Ts.
Genome-Scale Metabolic Model of
Helicobacter pylori
26695
Authors: Schilling Christophe H. , Covert Markus W. , Famili Iman , Church George M. , Edwards Jeremy S. , Palsson Bernhard O. 
Published: October 2002

ABSTRACT

A genome-scale metabolic model of
Helicobacter pylori
26695 was constructed from genome sequence annotation, biochemical, and physiological data. This represents an in silico model largely derived from genomic information for an organism for which there is substantially less biochemical information available relative to previously modeled organisms such as
Escherichia coli
. The reconstructed metabolic network contains 388 enzymatic and transport reactions and accounts for 291 open reading frames. Within the paradigm of constraint-based modeling, extreme-pathway analysis and flux balance analysis were used to explore the metabolic capabilities of the in silico model. General network properties were analyzed and compared to similar results previously generated for
Haemophilus influenzae
. A minimal medium required by the model to generate required biomass constituents was calculated, indicating the requirement of eight amino acids, six of which correspond to essential human amino acids. In addition a list of potential substrates capable of fulfilling the bulk carbon requirements of
H. pylori
were identified. A deletion study was performed wherein reactions and associated genes in central metabolism were deleted and their effects were simulated under a variety of substrate availability conditions, yielding a number of reactions that are deemed essential. Deletion results were compared to recently published in vitro essentiality determinations for 17 genes. The in silico model accurately predicted 10 of 17 deletion cases, with partial support for additional cases. Collectively, the results presented herein suggest an effective strategy of combining in silico modeling with experimental technologies to enhance biological discovery for less characterized organisms and their genomes.
The NorR Protein of
Escherichia coli
Activates Expression of the Flavorubredoxin Gene
norV
in Response to Reactive Nitrogen Species
Authors: Hutchings Matthew I. , Mandhana Neeraj , Spiro Stephen 
Published: October 2002

ABSTRACT

The
Escherichia coli norVW
genes encode a flavorubredoxin and NADH:(flavo)rubredoxin reductase, respectively, which are involved in nitric oxide detoxification under anaerobic growth conditions. Here it is shown that the
norVW
genes also have a role in protection against reactive nitrogen intermediates generated from nitroprusside. Transcription from the
norV
promoter is activated by the presence of nitroprusside in the growth medium; activation requires the product of a divergently transcribed regulatory gene,
norR
.