bluuebunny/crossref_metadata_2025_split huggingface dataset:
Use of Immunoglobulin M Cross-Reactions in Differential Diagnosis of Human Flaviviral Encephalitis Infections in the United States
Authors: Martin Denise A. , Biggerstaff Brad J. , Allen Becky , Johnson Alison J. , Lanciotti Robert S. , Roehrig John T. 
Published: July 2002

ABSTRACTTo define the virus specificity of the immunoglobulin M (IgM) antibody-capture enzyme-linked immunosorbent assay (MAC-ELISA) among the medically important members of the Japanese encephalitis (JE) virus serocomplex of flaviviruses, 103 IgM-positive human serum samples from patients with confirmed West Nile (WN) virus, St. Louis encephalitis (SLE) virus, or JE virus infections were assembled and simultaneously tested against all three viral antigens in a standardized MAC-ELISA. Of the serum samples tested, 96 (93%) showed higher positive-to-negative absorbance ratios (P/Ns) with the infecting virus antigen compared to those obtained with the other two virus antigens. Of the seven specimens with higher P/Ns with heterologous virus antigens, six were from patients with SLE virus infections (the serum samples had higher levels of reactivity with WN virus antigen) and one was from a patient with a JE virus infection (this serum sample also had a higher level of reactivity with WN virus antigen). Not surprisingly, similar virus specificity was observed with WN virus-elicited IgM in cerebrospinal fluid. As shown in previous studies, a subset of these specimens was even less reactive in the MAC-ELISA with dengue virus, a member of a different flavivirus serocomplex. The degree of virus cross-reactivity did not appear to be related to days postonset, at least during the first 40 days of infection. Infections with WN virus could be correctly distinguished from infections with SLE virus on the basis of the observed anti-viral IgM cross-reactivities alone 92% of the time. Infections with SLE virus resulted in antibody that was more cross-reactive, so identification of SLE virus as the infecting agent by use of MAC-ELISA cross-reactivity alone was more problematic.
Evaluation of the In Vitro Pyrogen Test System Based on Proinflammatory Cytokine Release from Human Monocytes: Comparison with a Human Whole Blood Culture Test System and with the Rabbit Pyrogen Test
Authors: Nakagawa Yukari , Maeda Hideko , Murai Toshimi 
Published: July 2002

ABSTRACTThe reliability of an in vitro pyrogen test system based on proinflammatory cytokine release from human monocytic cells was assessed by comparison with a test system based on a human whole blood culture as well as with the conventional rabbit pyrogen test. The human cells used as the pyrogen indicator cells were newly selected by subcloning of a human monocytic cell line, Mono-Mac-6. The selected cells, named MM6-CA8, responded to various pyrogens, including endotoxin, peptidoglycan (PG),Staphylococcus aureusCowan 1 (SAC), and poly(I ·  C), with a high sensitivity and produced proinflammatory cytokines, such as interleukin 1 (IL-1), IL-6, and tumor necrosis factor alpha. Among these cytokines, IL-6 was produced most sensitively in response to traces of the pyrogens and detected in the largest quantities in the culture medium. The cytokine-producing responses of MM6-CA8 cells correlated significantly with the responses of cultured human whole blood, which represents an ex vivo culture test system reproducing pyrogen-induced cytokine production in the human body. In terms of cytokine inducibility, the pyrogens were ranked in the order endotoxin > PG > poly (I · C) > SAC in both culture systems, a ranking which almost agreed with the ranking of their pyrogenicity as assessed by the rabbit pyrogen test. These results suggest that the in vitro responsiveness of MM6-CA8 cells to various pyrogens is highly relevant for human pyrogenic reactions. Therefore, the in vitro test system is useful and reliable for detecting the presence of materials that are pyrogenic for humans.
Mycobacterium aviumsubsp.paratuberculosisin Veterinary Medicine
Authors: Harris N. Beth , Barletta Raúl G. 
Published: July 2002

SUMMARYMycobacterium avium subsp. paratuberculosis (basonym M. paratuberculosis) is the etiologic agent of a severe gastroenteritis in ruminants known as Johne's disease. Economic losses to the cattle industry in the United States are staggering, reaching $1.5 billion annually. A potential pathogenic role in humans in the etiology of Crohn's disease is under investigation. In this article, we review the epidemiology, pathogenesis, diagnostics, and disease control measures of this important veterinary pathogen. We emphasize molecular genetic aspects including the description of markers used for strain identification, diagnostics, and phylogenetic analysis. Recent important advances in the development of animal models and genetic systems to study M. paratuberculosis virulence determinants are also discussed. We conclude with proposals for the applications of these models and recombinant technology to the development of diagnostic, control, and therapeutic measures.
Moraxella catarrhalis: from Emerging to Established Pathogen
Authors: Verduin Cees M. , Hol Cees , Fleer André , van Dijk Hans , van Belkum Alex 
Published: July 2002

SUMMARYMoraxella catarrhalis (formerly known as Branhamella catarrhalis) has emerged as a significant bacterial pathogen of humans over the past two decades. During this period, microbiological and molecular diagnostic techniques have been developed and improved for M. catarrhalis, allowing the adequate determination and taxonomic positioning of this pathogen. Over the same period, studies have revealed its involvement in respiratory (e.g., sinusitis, otitis media, bronchitis, and pneumonia) and ocular infections in children and in laryngitis, bronchitis, and pneumonia in adults. The development of (molecular) epidemiological tools has enabled the national and international distribution of M. catarrhalis strains to be established, and has allowed the monitoring of nosocomial infections and the dynamics of carriage. Indeed, such monitoring has revealed an increasing number of Β-lactamase-positive M. catarrhalis isolates (now well above 90%), underscoring the pathogenic potential of this organism. Although a number of putative M. catarrhalis virulence factors have been identified and described in detail, their relationship to actual bacterial adhesion, invasion, complement resistance, etc. (and ultimately their role in infection and immunity), has been established in a only few cases. In the past 10 years, various animal models for the study of M. catarrhalis pathogenicity have been described, although not all of these models are equally suitable for the study of human infection. Techniques involving the molecular manipulation of M. catarrhalis genes and antigens are also advancing our knowledge of the host response to and pathogenesis of this bacterial species in humans, as well as providing insights into possible vaccine candidates. This review aims to outline our current knowledge of M. catarrhalis, an organism that has evolved from an emerging to a well-established human pathogen.
Biofilms: Survival Mechanisms of Clinically Relevant Microorganisms
Authors: Donlan Rodney M. , Costerton J. William 
Published: July 2002

SUMMARYThough biofilms were first described by Antonie van Leeuwenhoek, the theory describing the biofilm process was not developed until 1978. We now understand that biofilms are universal, occurring in aquatic and industrial water systems as well as a large number of environments and medical devices relevant for public health. Using tools such as the scanning electron microscope and, more recently, the confocal laser scanning microscope, biofilm researchers now understand that biofilms are not unstructured, homogeneous deposits of cells and accumulated slime, but complex communities of surface-associated cells enclosed in a polymer matrix containing open water channels. Further studies have shown that the biofilm phenotype can be described in terms of the genes expressed by biofilm-associated cells. Microorganisms growing in a biofilm are highly resistant to antimicrobial agents by one or more mechanisms. Biofilm-associated microorganisms have been shown to be associated with several human diseases, such as native valve endocarditis and cystic fibrosis, and to colonize a wide variety of medical devices. Though epidemiologic evidence points to biofilms as a source of several infectious diseases, the exact mechanisms by which biofilm-associated microorganisms elicit disease are poorly understood. Detachment of cells or cell aggregates, production of endotoxin, increased resistance to the host immune system, and provision of a niche for the generation of resistant organisms are all biofilm processes which could initiate the disease process. Effective strategies to prevent or control biofilms on medical devices must take into consideration the unique and tenacious nature of biofilms. Current intervention strategies are designed to prevent initial device colonization, minimize microbial cell attachment to the device, penetrate the biofilm matrix and kill the associated cells, or remove the device from the patient. In the future, treatments may be based on inhibition of genes involved in cell attachment and biofilm formation.
Aggregation Substance Increases Adherence and Internalization, but Not Translocation, of
Enterococcus faecalis
through Different Intestinal Epithelial Cells In Vitro
Authors: Sartingen S. , Rozdzinski E. , Muscholl-Silberhorn A. , Marre R. 
Published: July 2002

ABSTRACT

The aggregation substance of
Enterococcus faecalis
increased bacterial adherence to and internalization by epithelial cells originating from the colon and duodenum but not by cells derived from the ileum. However, enterococcal translocation through monolayers of intestinal epithelium was not observed.
Vibrio cholerae
Requires
rpoS
for Efficient Intestinal Colonization
Authors: Merrell D. Scott , Tischler Anna D. , Lee Sang Ho , Camilli Andrew 
Published: July 2002

ABSTRACT

Vibrio cholerae
is a facultative intestinal pathogen that lives in aquatic environments, often in association with planktonic species. In the suckling mouse, oral inoculation with
V. cholerae
leads to intestinal colonization and symptoms of diarrheal disease. Results reported here indicate a role for the alternative sigma factor, RpoS, in intestinal colonization in this model of cholera. We constructed within
rpoS
multiple independent mutations which consistently resulted in a fivefold decrease in colonization ability as assessed by competition assays. These mutations had no detectable effect on the in vitro growth of
V. cholerae
in a rich medium. The occurrence of spontaneous suppressor mutations potentially required for viability of
rpoS
strains was ruled out by determination of the frequency of insertional inactivation of
rpoS
in comparison to two other nonessential loci. Finally, both the in vitro and in vivo mutant phenotypes of
rpoS
strains were fully complemented by providing
rpoS
in
trans
or by allelic reversion, indicating that the observed decrease in colonization fitness was indeed due to the loss of functional RpoS.
A Major Cell Surface Antigen of
Coccidioides immitis
Which Elicits Both Humoral and Cellular Immune Responses
Authors: Hung Chiung-Yu , Ampel Neil M. , Christian Lara , Seshan Kalpathi R. , Cole Garry T. 
Published: July 2002

ABSTRACT

Multinucleate parasitic cells (spherules) of
Coccidioides immitis
isolates produce a membranous outer wall component (SOW) in vitro which has been reported to be reactive with antibody from patients with coccidioidal infection, elicits a potent proliferative response of murine immune T cells, and has immunoprotective capacity in a murine model of coccidioidomycosis. To identify the antigenic components of SOW, the crude wall material was first subjected to Triton X-114 extraction, and a water-soluble fraction derived from this treatment was examined for protein composition and reactivity in humoral and cellular immunoassays. Protein electrophoresis revealed that the aqueous fraction of three different isolates of
C. immitis
each contained one or two major glycoproteins (SOWgps), distinguished by their molecular sizes, which ranged from 58 to 82 kDa. The SOWgps, however, showed identical N-terminal amino acid sequences, and each was recognized by sera from patients with
C. immitis
infection. Antibody raised against the purified 58-kDa glycoprotein (SOWgp58) of the Silveira isolate was used for Western blot and immunolocalization analyses. Expression of SOWgp was shown to be parasitic phase specific, and the antigen was localized to the membranous SOW. The water-soluble fraction of SOW and the purified SOWgp58 were tested for the ability to stimulate proliferation of human peripheral monocytic cells (PBMC). The latter were obtained from healthy volunteers with positive skin test reaction to spherulin, a parasitic-phase antigen of
C. immitis
, and from volunteers who showed no skin test reaction to the same antigen. The SOW preparations stimulated proliferation of PBMC from skin test-positive but not skin test-negative donors, and the activated cells secreted gamma interferon, which is indicative of a T helper 1 pathway of immune response. Results of this study suggest that SOWgp is a major parasitic cell surface-expressed antigen that elicits both humoral and cellular immune responses in patients with coccidioidal infection.
Helicobacter felisInfection Is Associated with Lymphoid Follicular Hyperplasia and Mild Gastritis but Normal Gastric Secretory Function in Cats
Authors: Simpson Kenneth W. , Strauss-Ayali Dalit , Scanziani Eugenio , Straubinger Reinhard K. , McDonough Patrick L. , Straubinger Alix F. , Chang Yung-Fu , Domeneghini Cynzia , Arebi Naila , Calam John 
Published: July 2002

ABSTRACTThe relationship ofHelicobacter felis, a bacterium observed in the stomachs of cats, to gastric disease is unclear. The objective of this study was to determine ifH. felisinfection alters gastric histopathology, proinflammatory cytokine expression, and secretory function and evokes a humoral immune response in cats. Five specific-pathogen-free (SPF)Helicobacter-free cats were studied before and for 1 year after oral inoculation withH. felis(ATCC 49179). Four SPFH. felis-uninfected cats served as controls. The stomachs of all fiveH. felis-inoculated cats became colonized, as determined by urease activity, histopathology, PCR, culture, and transmission electron microscopy of serial gastric biopsies at 0, 3, 5, 8, and 12 months. Uninoculated cats remainedHelicobacterfree. Lymphoid follicular hyperplasia, atrophy, and fibrosis were observed primarily in the pylorus of infected cats. Mild mononuclear inflammation was detected in both infected and uninfected cats, but was more extensive in infected cats, with pangastric inflammation, eosinophilic infiltrates, and cardia gastritis observed only in infected cats. No upregulation of antral mucosal interleukin 1α (IL-1α), IL-1β, or tumor necrosis factor alpha was detected by reverse transcription-PCR in any cat. The gastric secretory axes, assessed by fasting plasma gastrin, antral mucosal gastrin and somatostatin immunoreactivity, and pentagastrin-stimulated gastric acid secretion, were similar in both infected and uninfected cats. Gradual seroconversion (immunoglobulin G) was observed in four of five infected cats, with enzyme-linked immunosorbent assay values reaching 4× to 12× baseline 12 months postinfection. These findings indicate thatH. felisinfection in cats induces lymphoid follicular hyperplasia, mild gastritis, and seroconversion, but is associated with normal gastric secretory function.
Immunity Reduces Reservoir Host Competence ofPeromyscus leucopusforEhrlichia phagocytophila
Authors: Levin Michael L. , Fish Durland 
Published: July 2002

ABSTRACTInfection withEhrlichia phagocytophilain white-footed mice is transient and followed by a strong immune response. We investigated whether the presence of acquired immunity againstE. phagocytophilaprecludes white-footed mice from further maintenance of this agent in nature. Mice were infected withE. phagocytophilavia tick bite and challenged either 12 or 16 weeks later byIxodes scapularisnymphs infected with the same agent. Xenodiagnostic larvae fed upon each mouse simultaneously with challenging nymphs and 1 week thereafter. Ticks were tested for the agent by PCR, and the prevalence of infection was compared to that in ticks that fed upon nonimmune control mice. Only 30% of immunized mice sustained cofeeding transmission ofE. phagocytophilabetween simultaneously feeding infected and uninfected ticks, compared to 100% of control mice. An average of 6.3% of xenodiagnostic ticks acquiredEhrlichiafrom previously immunized mice when fed 1 week after the challenge, compared to 82.5% infection in the control group. Although an immune response to a single infection withE. phagocytophilain white-footed mice provided only partial protection against reinfection with the same agent, the majority of mice were rendered reservoir incompetent for at least 12 to 16 weeks. Immunity acquired by mice duringI. scapularisnymphal activity in early summer may exclude a large proportion of the mouse population from maintainingE. phagocytophiladuring the period of larval activity later in the season.
Role of
Bordetella bronchiseptica
Fimbriae in Tracheal Colonization and Development of a Humoral Immune Response
Authors: Mattoo Seema , Miller Jeff F. , Cotter Peggy A. 
Published: July 2002

ABSTRACT

Fimbriae are filamentous, cell surface structures which have been proposed to mediate attachment of
Bordetella
species to respiratory epithelium.
Bordetella bronchiseptica
has four known fimbrial genes:
fim2
,
fim3
,
fimX
, and
fimA
. While these genes are unlinked on the chromosome, their protein products are assembled and secreted by a single apparatus encoded by the
fimBCD
locus. The
fimBCD
locus is embedded within the
fha
operon, whose genes encode another putative adhesin, filamentous hemagglutinin (FHA). We have constructed a Fim
−
B. bronchiseptica
strain, RB63, by introducing an in-frame deletion extending from
fimB
through
fimD
. Western blot analysis showed that RB63 is unable to synthesize fimbriae but is unaffected for FHA expression. Using this mutant, we assessed the role of fimbriae in pathogenesis in vitro and in vivo in natural animal hosts. Although RB63 was not significantly defective in its ability to adhere to various tissue culture cell lines, including human laryngeal HEp-2 cells, it was considerably altered in its ability to cause respiratory tract infections in rats. The number of Δ
fimBCD
bacteria recovered from the rat trachea at 10 days postinoculation was significantly decreased compared to that of wild-type
B. bronchiseptica
and was below the limit of detection at 30 and 60 days postinoculation. The number of bacteria recovered from the nasal cavity and larynx was not significantly different between RB63 and the wild-type strain at any time point. The ability of fimbriae to mediate initial attachment to tracheal tissue was tested in an intratracheal inoculation assay. Significantly fewer RB63 than wild-type bacteria were recovered from the tracheas at 24 h after intratracheal inoculation. These results demonstrate that fimbriae are involved in enhancing the ability of
B. bronchiseptica
to establish tracheal colonization and are essential for persistent colonization at this site. Interestingly, anti-
Bordetella
serum immunoglobulin M (IgM) levels were significantly lower in animals infected with RB63 than in animals infected with wild-type
B. bronchiseptica
at 10 days postinoculation. Even at 30 days postinoculation, RB63-infected animals had lower serum anti-
Bordetella
antibody titers in general. This disparity in antibody profiles suggests that fimbriae are also important for the induction of a humoral immune response.
Identification of Regions of the
Escherichia coli
Chromosome Specific for Neonatal Meningitis-Associated Strains
Authors: Bonacorsi Stéphane Pierre Paul , Clermont Olivier , Tinsley Colin , Le Gall Isabelle , Beaudoin Jean-Christophe , Elion Jacques , Nassif Xavier , Bingen Edouard 
Published: July 2002

ABSTRACT

Specific virulence factors associated with the pathogenesis of
Escherichia coli
strains causing neonatal meningitis (ECNM), such as the K1 capsular polysaccharide, the S fimbriae, and the Ibe10 protein, have been previously identified. However, some other yet unidentified factors are likely to be involved in the pathogenesis of ECNM. To identify specialized unique DNA regions associated with ECNM virulence, we used the representational difference analysis technique. The genomes of two strains belonging to nonpathogenic phylogenetic group A of the ECOR reference collection were subtracted from
E. coli
strain C5, isolated from a case of neonatal meningitis. Strain C5 belongs to the phylogenetic group B2 as do the majority of ECNM. We have isolated and mapped 64 DNA fragments which are specific for strain C5 and not found in nonpathogenic strains. Of these clones, 44 were clustered in six distinct regions on the chromosome. The
sfa
and
ibe10
genes were located in regions 2 and 6, respectively. A group of genes (
cnf1
,
hra
,
hly
, and
prs
) known to be present in a pathogenicity island of the uropathogenic strain
E. coli
J96 colocalized with region 6. The occurrence of these DNA regions was tested in a set of meningitis-associated strains and in a control group composed of non-meningitis-associated strains belonging to the same B2 group. Regions 1, 3, and 4 were present in 91, 82, and 81%, respectively, of the meningitis strains and in 40, 13, and 47% of the control strains. Together, these data suggest that regions 1, 3, and 4 code for factors associated with the ability of
E. coli
to invade the meninges of neonates.
Four Different Genes Responsible for Nonimmune Immunoglobulin-Binding Activities within a Single Strain of
Escherichia coli
Authors: Sandt Carol H. , Hill Charles W. 
Published: July 2002

ABSTRACT

Certain
Escherichia coli
strains bind the Fc fragment of immunoglobulin G (IgG) at the bacterial cell surface. Previous work established that this nonimmune Ig binding depends on several large proteins with apparent molecular masses that can exceed 200 kDa. For
E. coli
strain ECOR-9, four distinct genes (designated
eibA
,
eibC
,
eibD
, and
eibE
) are responsible for Ig binding. Two
eib
genes are linked to
eaa
genes, which are homologous to genes for the autotransporter family of secreted proteins. With reference to the
E. coli
K-12 chromosome, the
eibA-eaaA
cluster is adjacent to
trpA
(min 28.3) while the
eibC-eaaC
cluster is adjacent to
aspS
(min 42.0). Sequence adjacent to the
eibA-eaaA
cluster converges with that of strain K-12 precisely as observed for the Atlas family of prophages, suggesting that
eibA
is part of one of these. All four
eib
genes, when cloned into plasmid vectors, impart IgG binding to
E. coli
K-12 strains, and three impart IgA binding also. The IgG binding occurs at the bacterial cell surface, and its expression increases survival in serum by up to 3 orders of magnitude. The
eib
sequences predict a C-terminal peptide motif that is characteristic of outer membrane proteins, and the protein sequences show significant similarity near the C terminus to both the YadA virulence factor of
Yersinia
species and the universal surface protein A II of
Moraxella catarrhalis
. The sizes predicted for Eib proteins from DNA sequence are much smaller than their apparent sizes on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, possibly reflecting stable oligomerization.