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Results for “Pathogen diversity”

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At least 343 records · Page 19Linked to original sources

PubMed2000

[Molecular cloning and sequencing of 5' non-coding region of TTV-like mini virus].

OBJECTIVE: To investigate the TTV- like mini virus (TLMV) infection in Chinese patients with non A-G hepatitis and to analyse sequence of 5' non-coding region (5'NCR)of TLMV. METHODS: TLMV DNA was detected by nested - PCR from 53 serum samples of non A-G hepatitis patients without TTV infection. PCR products were cloned and sequenced. RESULTS: TLMV DNA were positive in 37 of 53 patients (69.8%). The sequence of 5' NCR of 8 TLMV isolates was compared with that reported by Takahashi (GenBank Accession No. ab 026930-026931) and showed nucleotide identity between 64% - 83%. CONCLUSIONS: The results of this study indicated that TLMV infection is common in TTV negative patients with non A-G hepatitis. The 5' NCR sequence of TLMV showed a great degree of diversity. The pathogenicity of TLMV and its relationship to non A-G hepatitis need to be confirmed and further study is required.

Adolescent↗

PubMed2001

Analysis of the human periodontal ligament fibroblast response to the cytolethal distending toxin produced by actinobacillus actinomycetemcomitans.

A small number of diverse bacterial pathogens have been found to produce cytolethal distending toxin (CDT). Much evidence has been obtained to show that CDTs cause a variety of eukaryotic cells to become irreversibly blocked in the G2 phase of the cell cycle. Cells which are sensitive to CDT, such as Chinese hamster ovary (CHO) cells, die within a few days after exposure to the toxin. Recent research has shown that CDT is a potential virulence factor for Actinobacillus actinomycetemcomitans, a bacterial species associated with juvenile periodontitis (JP). This research investigates the effects A. actinomycetemcomitans CDT has on human periodontal ligament fibroblasts (HPDLFs). After HPDLFs were exposed to physiologic levels of CDT, cell viability was assessed utilizing an assay that measured the conversion of a tetrazolium compound into a soluble formazan product, which could be read on a spectrophotometer. Cell viability was also measured after exposure to CDT through trypan blue staining and the use of a hemocytometer. CHO cells were utilized as a parallel control to show that the CDT obtained from A. actinomycetemcomitans was active. The results obtained indicate that the HPDLFs are resistant to the cytolethal distending toxin. The possible resistance the HPDLFs have to the CDT may stem from the low turnover rate of the fibroblasts. However, further research must be completed on this topic.

Aggregatibacter actinomycetemcomitans↗

PubMed1991

Suppurative cervical lymphadenitis after Yersinia enterocolitica bacteremia.

Yersinia enterocolitica is increasingly recognized as a pathogen causing diverse complications. We have reported the case of a man with fever, abdominal tenderness, and Y enterocolitica bacteremia. After antibiotic therapy, his condition improved initially, but later, suppurative cervical lymphadenitis developed. This suggests that the hematogenous spread of Y enterocolitica to a distal lymphatic focus of infection is a possible complication of Y enterocolitica bacteremia.

Anti-Bacterial Agents↗

PubMed1991

[Thyroid abcess. Apropos of 5 cases].

Thyroid abcess and acute suppurative thyroiditis are uncommon, representing 0.1 to 0.7% of surgically treated thyroid pathologies. More common in children than in adults, this rarity is associated with poorly indicative clinical symptoms, thus making diagnosis difficult. Five cases reports are presented, 4 of them in adults, illustrating the diagnostic difficulties and the various etiopathological mechanism, thereby explaining the wide diversity of pathogenic agents responsible. Treatment includes surgery (drainage or (partial) thyroidectomy, depending upon the presence or not of an underlying thyroid pathology) and intravenous antibiotics. It is absolutely necessary to eliminate the source of the infection, often a piriform sinus fistula whose total resection effectively prevents a relapse (1 case in this series).

Abscess↗

PubMed1993

Human intestinal intraepithelial lymphocytes are derived from a limited number of T cell clones that utilize multiple V beta T cell receptor genes.

Intestinal intraepithelial lymphocytes (IEL) are a phenotypically distinct T cell population of unknown function. The majority of human intestinal IEL express the TCR-alpha beta, the CD8 accessory molecule, and the CD45RO Ag, suggesting that they are MHC class I-restricted memory T cells. Recent analyses of the TCR alpha- and beta-chains expressed by these cells have shown marked skewing toward one or several V region genes in individual donors and revealed the presence of clonally expanded cells. In addition, functional data has suggested that the MHC class I-like CD1 molecules may be the target ligands for some human intestinal IEL clones. This report examines in detail the TCR-beta repertoire of human jejunal IEL to determine what fraction of these cells are clonally expanded and to determine whether a particular subset of V beta genes are utilized by the clonally expanded cells. The results demonstrate that the majority of IEL are derived from the expansion of a relatively few T cell clones and that these clones can utilize a large number of different V beta genes. Oligoclonal expansion is also demonstrated among lamina propria lymphocytes (LPL), with overlapping but distinct clones detected in the LPL vs the IEL populations. These results indicate that most intestinal IEL-alpha beta, and a subpopulation of LPL, are specific for a limited number of Ag and place constraints on the possible roles played by IEL in the defense against diverse environmental pathogens or in the generation of oral tolerance.

Amino Acid Sequence↗

PubMed1995

Battling against host phagocytes: the wherefore of the RTX family of toxins?

The RTX family of bacterial exotoxins is a group of related cytolytic proteins produced by a wide variety of gram-negative human and animal pathogens. While diverse in their associated diseases and in their target cell specificities, there remain several themes common to RTX toxins, including genetic organization, structural and functional features, and effects on target cells. In this review, we summarize and discuss the genetics, regulation, epidemiology, structure/function relationships, and in vivo and in vitro activities of the best characterized RTX toxins, and speculate on their roles in pathogenesis and their use in immunotherapy.

Antitoxins↗

PubMed1996

Composition of the Lactobacillus acidophilus complex isolated from vaginal flora.

One hundred and fifty human vaginal samples containing a diversity of pathogens or nonpathogens (Gardnerella vaginalis, Streptococcus sp., Staphylococcus sp., Candida albicans. Mycoplasma sp.) were examined for their content in lactobacilli of the Lactobacillus acidophilus complex. Although all samples contained lactobacilli, strains of the L. acidophilus complex were present in only twenty-nine cases. Isolates were further characterized and compared with type strains or reference strains in an attempt to differentiate by phenotypic means the genospecies of the L. acidophilus complex. Data regarding specific activities of beta-galactosidase (beta-gal) and of phospho-beta-galactosidase (P-beta-gal) provided no specific information at the species level within the L. acidophilus complex. DNA-relatedness differentiates this genospecies. Most lactobacilli isolated from the vaginal flora of symptomatic women were genotypically close to L. gasseri CIP 102991T by the technique of DNA/DNA hybridization.

Anti-Bacterial Agents↗

PubMed1996

Advances in molecular diagnosis.

Approaches to the diagnosis of genetic disease using the tools of molecular genetics are being developed at a rapid pace as efforts to map the human genome progress. Technical challenges remain, however, in devising approaches to permit the wide diversity of pathogenic mutations to be identified in an efficient manner. Moreover, the possibility of population screening for carrier status for gene mutations raises important ethical and social questions. Major progress has been made in both areas and the list of disorders amenable to molecular diagnosis is expanding rapidly.

Ethics, Medical↗

PubMed1998

Genotyping HIV-1 and HCV strains by a combinatorial DNA melting assay (COMA).

BACKGROUND: Human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) strains can be genetically classified into genetic lineages known as genetic types or subtypes according to phylogenetic analyses of complete or partial nucleotide sequences of their genomes. The genetic classification of HIV-1 and HCV strains has important implications for the development of globally effective vaccines and for the management of patients. MATERIALS AND METHODS: A new method, termed combinatorial DNA melting assay (COMA), allows rapid accessing of comparative genetic information between related DNA sequences, making it possible to rapidly and accurately genotype unknown HIV-1 and HCV strains. COMA is mainly based on the differential melting properties of long DNA heteroduplexes. Combinatorial arrays of DNA heteroduplexes are formed when captured PCR-amplified reference DNA with known nucleotide sequences are combined with solution-phase complementary and antigenically labeled DNA with unknown sequences. Genetic divergence between the known and the unknown sequences is inferred as the experimentally derived melting curves of the two strands of the DNA heteroduplexes increasingly diverge. RESULTS: COMA was successfully applied to the genetic classification of HIV-1 and HCV strains into phylogenetic lineages or subtypes. CONCLUSIONS: Use of this assay should accelerate current efforts to understand the global molecular epidemiology of HIV-1 and HCV and may extend to the genetic characterization of other genetically diverse infectious pathogens associated with numerous diseases.

Base Composition↗

PubMed2025

The impacts of chronic infections on shaping cellular senescence.

Cellular senescence is a fundamental biological process characterized by stable cell cycle arrest, genomic instability, and the acquisition of a proinflammatory secretory phenotype. While senescence is traditionally associated with aging, growing evidence reveals that chronic infections such as viral, bacterial, and protozoan parasites can serve as powerful inducers of senescence, contributing to premature aging and long-term tissue damage. This review explores the diverse mechanisms by which persistent pathogens trigger or sustain senescence in host cells. We highlight how these chronic infections manipulate host DNA repair, mitochondrial dynamics, telomere maintenance, oxidative stress, and immune function to promote senescence and immunosenescence. Emerging findings also reveal how pathogens hijack the host cellular machinery to induce senescence across various tissue types. In many cases, senescence not only enables pathogen persistence but also drives pathological outcomes such as fibrosis, neurodegeneration, cardiomyopathy, and immune exhaustion. Collectively, this emerging evidence highlights a unifying strategy among diverse pathogens: the exploitation of cellular senescence to support chronic infection and promote disease. Understanding how infectious agents drive senescence offers new insights into age-related pathologies and highlights potential therapeutic targets, such as senolytic and senomorphic agents, to mitigate the long-term impacts of chronic infections.

Bacterial infection↗

PubMed2004

Ecology drives the worldwide distribution of human diseases.

Identifying the factors underlying the origin and maintenance of the latitudinal diversity gradient is a central problem in ecology, but no consensus has emerged on which processes might generate this broad pattern. Interestingly, the vast majority of studies exploring the gradient have focused on free-living organisms, ignoring parasitic and infectious disease (PID) species. Here, we address the influence of environmental factors on the biological diversity of human pathogens and their global spatial organization. Using generalized linear multivariate models and Monte Carlo simulations, we conducted a series of comparative analyses to test the hypothesis that human PIDs exhibit the same global patterns of distribution as other taxonomic groups. We found a significant negative relationship between latitude and PID species richness, and a nested spatial organization, i.e., the accumulation of PID species with latitude, over large spatial scales. Additionally, our results show that climatic factors are of primary importance in explaining the link between latitude and the spatial pattern of human pathogens. Based on our findings, we propose that the global latitudinal species diversity gradient might be generated in large part by biotic interactions, providing strong support for the idea that current estimates of species diversity are substantially underestimated. When parasites and pathogens are included, estimates of total species diversity may increase by more than an order of magnitude.

Biodiversity↗

PubMed2006

Intraspecific mitochondrial DNA polymorphism within the emerging filamentous fungal pathogen Trichoderma longibrachiatum.

The genetic diversity of the emerging fungal pathogen Trichoderma longibrachiatum was examined at the level of mitochondrial DNA. The 17 investigated strains, comprising nine clinical and eight non-clinical isolates, exhibited seven and ten different mitochondrial DNA profiles by using the restriction enzymes BsuRI and Hin6I, respectively. The sizes of mitochondrial DNAs varied from 34.9 to 39.5 kb. The discriminatory power of the method was higher than that of internal transcribed spacer sequence analysis and therefore should be more suitable for identification and epidemiological investigations. However, clinical and non-clinical isolates did not form separate clusters on the resulting dendrogram and thus there was no indication of a correlation between genetic structure and pathogenicity of the isolates.

DNA, Mitochondrial↗

PubMed1992

Molecular evolution of the fungi: human pathogens.

The morphological, ecological, and clinical diversity among ascomycete fungi that are pathogenic to humans suggest that the potential for pathogenicity may have arisen multiple times within these higher fungi. We have obtained 18S ribosomal DNA sequences from a diverse group of human pathogenic fungi in order to determine their evolutionary origins. The fungi studied include a skin pathogen that is confined to humans (Trichophyton rubrum) and three systemic, facultative parasites that cause histoplasmosis (Histoplasma capsulatum), blastomycosis (Blastomyces dermatitidis) and coccidioidomycosis (Coccidioides immitis) in humans and other higher animals. Also included in our analysis are representatives of non-pathogenic fungi, as well as two opportunistic pathogens, Pneumocystis carinii and Candida albicans, that cause severe disease in immunocompromised individuals, especially those with AIDS. Two of the fungi we sequenced, T. rubrum and C. immitis, are limited to asexual modes of reproduction and therefore lack the sexual structures that are most useful for evolutionary comparison as well as being essential for classification among the higher fungi. Coccidioides immitis is particularly problematic owing to its contradictory and confusing asexual morphologies, which have caused it to be placed in three fungal classes and the protista. Our analysis shows that the specialized, superficial parasite and the systemic, facultative parasites, including C. immitis, are closely related ascomycetes, which clearly demonstrates the power of molecular characters to compensate for missing or confusing reproductive morphology. Analysis also shows that the opportunistic pathogens are more distantly related, with the likely explanation that pathogenicity has arisen more than once within the Ascomycetes.

Base Sequence↗

PubMed2001

Yersinia HPI in septicemic Escherichia coli strains isolated from diverse hosts.

High pathogenicity islands (HPIs), first identified in various Yersinia species, encode an iron uptake system. We have studied the occurrence of HPIs in septicemic strains of Escherichia coli isolated from a variety of hosts. The results presented in this communication indicate that most septicemic strains tested contained HPI sequences even though they already have the aerobactin encoding genes. We have also observed two types of HPI deletions, suggesting genetic instability of this element. Notable exceptions are several strains isolated from septicemia in sheep that lacked both iron acquisition systems.

Animals↗

PubMed2024

Beyond water and soil: Air emerges as a major reservoir of human pathogens.

Assessing the risk of human pathogens in the environment is crucial for controlling the spread of diseases and safeguarding human health. However, conducting a thorough assessment of low-abundance pathogens in highly complex environmental microbial communities remains challenging. This study compiled a comprehensive catalog of 247 human-pathogenic bacterial taxa from global biosafety agencies and identified more than 78 million genome-specific markers (GSMs) from their 17,470 sequenced genomes. Subsequently, we analyzed these pathogens' types, abundance, and diversity within 474 shotgun metagenomic sequences obtained from diverse environmental sources. The results revealed that among the four habitats studied (air, water, soil, and sediment), the detection rate, diversity, and abundance of detectable pathogens in the air all exceeded those in the other three habitats. Air, sediment, and water environments exhibited identical dominant taxa, indicating that these human pathogens may have unique environmental vectors for their transmission or survival. Furthermore, we observed the impact of human activities on the environmental risk posed by these pathogens, where greater amounts of human activities significantly increased the abundance of human pathogenic bacteria, especially in water and air. These findings have remarkable implications for the environmental risk assessment of human pathogens, providing valuable insights into their presence and distribution across different habitats.

Humans↗

PubMed1997

Comparative sensitivity of 13 species of pathogenic bacteria to seven chemical germicides.

BACKGROUND: The relative resistance of diverse human bacterial pathogens to commonly used germicidal agents has not been established. METHODS: We measured by titration the survival of thirteen different bacteria after exposure to glutaraldehyde, formaldehyde, hydrogen peroxide, peracetic acid, cupric ascorbate, sodium hypochlorite, or phenol. RESULTS: Our comparative experiments allowed classification of the organisms' survival into four groups: (a) Pseudomonas aeruginosa and Staphylococcus aureus showed the most resistance, (b) Clostridium perfringens, Salmonella typhimurium, Staphylococcus epidermidis, and Escherichia coli O157:H7 showed intermediate resistance, (c) Listeria monocytogenes, Shigella sonnei, and Vibrio parahaemolyticus survived some treatments with chemical agents only in the presence of protecting protein (serum albumin), and (d) Vibrio cholerae, Vibrio vulnificus, Bacillus cereus, and Yersinia enterocolitica did not survive any of the treatments applied. CONCLUSION: We found species that more frequently survived exposure to germicidal agents were also those most commonly reported in association with hospital infections. Our findings suggest that resistance to disinfectants may be more important than pathogenicity in determining the relative prominence of an organism as an agent responsible for nosocomial infections.

Bacteria↗

PubMed1996

Cross-talk between bacterial pathogens and their host cells.

A taxonomically diverse group of bacterial pathogens have evolved a variety of strategies to subvert host-cellular functions to their advantage. This often involves two-way biochemical interactions leading to responses in both the pathogen and host cell. Central to this interaction is the function of a specialized protein secretion system that directs the export and/or translocation into the host cells of a number of bacterial proteins that can induce or interfere with host-cell signal transduction pathways. The understanding of these bacterial/host-cell interactions will not only lead to novel therapeutic approaches but will also result in a better understanding of a variety of basic aspects of cell physiology and immunology.

Animals↗

PubMed2002

Bacterial avoidance of phagocytosis.

Phagocytosis constitutes the primary line of host innate and adaptive defence against incoming microbial pathogens, providing an efficient means for their removal and destruction. However, several virulent bacteria that do not function as intracellular pathogens have evolved mechanisms to avoid and prevent phagocytosis that constitute an essential part of their pathogenic capacity. Some of these mechanisms include preventing recognition by phagocytic receptors or blocking uptake by professional phagocytes. Recently, the molecular mechanisms of such antiphagocytic properties have been elucidated for some pathogens. Such mechanisms illustrate the diversity of mechanisms bacterial pathogens use to avoid phagocytic uptake.

Antigens, Bacterial↗