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Results for “Pathogen diversity”

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PubMed1997

Issues complicating the implementation of postexposure prophylaxis.

Occupational exposures to blood-borne pathogens occur regularly in diverse settings and involve multiple groups of healthcare workers. Current compliance of healthcare workers with behavioral controls is poor, and additional engineering and work-practice controls for exposure prevention are inadequate and/or underutilized. Barriers to effective postexposure management include deficient knowledge and fear and denial among healthcare workers, the diverse risks associated with different exposures, the costs and personnel necessary for providing exposure management 24 hours a day, variable levels of expertise in postexposure prophylaxis strategies, and administrative requirements for standardized policies and procedures. In the current environment, healthcare institutions are largely ill equipped to provide timely and effective postexposure prophylaxis. Widespread worker education, simplified reporting mechanisms, and availability of prompt source and worker testing along with timely, free postexposure prophylaxis is central to an institution's postexposure program. Postexposure management programs should be comprehensive and provide standardized procedures, expand workers' access to postexposure prophylaxis by establishing responsible parties in diverse areas, disseminate program information to all workers, and ensure confidentiality in the care and follow-up of exposed workers. To implement such programs, it may be necessary to merge resources and link local management of exposures with regional expertise to provide up-to-date counseling in a rapidly changing field. Careful surveillance of occupational exposures is essential to evaluate program efficacy, direct prevention efforts, and to determine necessary resources to ensure continued successful delivery of postexposure prophylaxis.

Anti-HIV Agents↗

PubMed2003

Diverse origins of tetracycline resistance in the honey bee bacterial pathogen Paenibacillus larvae.

Paenibacillus larvae is the causative agent of the important honey bee larval disease American Foulbrood (AFB). This pathogen has been treated in bee colonies by a single registered antibiotic, oxytetracycline (OTC), for fifty years. Recently, widespread resistance to OTC has been reported. In this study, the degree of antibiotic resistance was contrasted with DNA sequence variation for 125 P. larvae isolates collected in North America. Resistance was uncorrelated with bacterial haplotype, suggesting either that resistance has evolved multiple times in P. larvae or that resistance involves recent horizontal transfer via a non-genomic (e.g., plasmid or conjugal transposon) route. The recency of OTC resistance in P. larvae across this broad survey area underscores the need to manage foulbrood infections carefully and to monitor populations for resistance.

Animals↗

PubMed1984

Cell-mediated damage to helminths.

Although it is difficult to draw any sweeping conclusions that would be applicable to all helminth infections, the main features that are emphasized in this review may be summarized briefly. Pathogenic helminths, although extremely diverse in structure and behaviour, have one common feature, namely that they present to the host's defenses large, non-phagocytosable surfaces. Because of this, they are susceptible to a range of effector mechanisms differing either quantitatively or qualitatively from those that are active against other parasites or against normal or abnormal host cells. As an extreme example, the various types of cytotoxic lymphocyte, with one interesting exception, are inactive against helminths. Instead, helminth infections are characterized by high IgE responses and increased numbers of circulating eosinophils. Such eosinophils are activated, and show a marked capacity to kill a variety of target helminths in vitro. Further activation may occur in response to mast cell mediators released as a result of IgE-dependent degranulation; and IgE, as well as IgG and complement, can mediate eosinophil attachment and killing. It may therefore be suggested that the eosinophil/IgE/mast cell axis represents a powerful host defense against helminth infections. IgE can also mediate macrophage-dependent killing of several helminths, a process which involves a functional change in the macrophage, resembling activation. Although eosinophil-mediated and IgE-dependent macrophage-mediated effects are particularly potent, other effector cells are not excluded: in certain circumstances, neutrophils and conventionally activated macrophages may be equally or more effective. Neutrophils appear to act solely by oxidative killing mechanisms, whereas degranulation and the release of toxic granule contents is equally or more important in eosinophil-mediated damage. Different stages of different helminths vary in their degree of susceptibility to different mechanisms. Eosinophils appear to be somewhat less active than neutrophils against ensheathed nematodes, whereas trematodes and exsheathed nematodes are highly susceptible to eosinophil attack. In many experimental helminth infections, studies in vivo suggest a role for antibody-dependent cell-mediated immune effector mechanisms. The identity of the effector cell is difficult to establish because of a lack of techniques for specific manipulation of individual cell types, but histological studies frequently point to a strong eosinophil or macrophage involvement. The development and analysis of in vitro assays allows the study of immune effector mechanisms in man.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2002

Treatment of picornavirus infections.

The picornaviruses are a diverse group of viral pathogens that together comprise the most common causes of infections of humans in the developed world. Within the picornavirus family are three well-known groups of human pathogens-the enteroviruses (including polioviruses, coxsackieviruses, and echoviruses), the rhinoviruses, and the hepatoviruses (including hepatitis A). Recently, the parechoviruses (formerly, echoviruses 22 and 23) have been classified as a fourth genus of human picornaviruses. This article will focus on the enteroviruses and rhinoviruses agents, for which substantial effort has been expended and recent successes reported towards the development of safe and effective antiviral therapy.

Aged↗

PubMed2000

The molecular biology of pasteurella multocida.

Pasteurella multocida is an important veterinary and opportunistic human pathogen. The species is diverse and complex with respect to antigenic variation, host predeliction and pathogenesis. Certain serological types are the aetiologic agents of severe pasteurellosis, such as fowl cholera in domestic and wild birds, bovine haemorrhagic septicaemia and porcine atrophic rhinitis. The recent application of molecular methods such as the polymerase chain reaction, restriction endonuclease analysis, ribotyping, pulsed-field gel electrophoresis, gene cloning, characterisation and recombinant protein expression, mutagenesis, plasmid and bacteriophage analysis and genomic mapping, have greatly increased our understanding of P. multocida and has provided researchers with a number of molecular tools to study pathogenesis and epidemiology at a molecular level.

Animals↗

PubMed2001

Distinct levels of genetic diversity of Borrelia burgdorferi are associated with different aspects of pathogenicity.

Different species of pathogenic Borrelia show different symptoms and tick vector specificity. Even within regions where only one species is found, Lyme disease progresses very differently from one patient to another. Since Borrelia shows very little recombination either within or between species, alleles of a gene can be used to mark clones. The ospC gene is highly variable within each species and can be used to define groups of related clones. It has been previously shown that only four out of seventeen ospC groups of Borrelia burgdorferi sensu stricto cause invasive forms of the disease. Other groups cause erythema migrans, a skin rash at the site of the tick bite, but not invasive disease, while still other groups seem to be nonpathogenic to humans. In this study we extend the analysis of the ospC gene to the other pathogenic species, Borrelia garinii and Borrelia afzelii. Only two groups in B. afzelii and four groups in B. garinii cause invasive disease. Thus, only ten out of the 58 defined ospC groups cause invasive and presumably chronic Lyme disease.

Animals↗

PubMed1999

The role of dendritic cells in the induction and regulation of immunity to microbial infection.

Dendritic cells (DCs) play a critical role in the initiation and regulation of immune responses. Recent advances have begun to uncover the nature and diversity of DC-pathogen interactions and the modulation of DC function by microbial stimuli. Antigen pulsed DCs have also been shown in several infection models to induce high levels of protective immunity and to display immunotherapeutic potential. The study of the function of DCs in the response to infection is thus an exciting and rapidly expanding field with important implications for both fundamental and clinical immunology.

Animals↗

PubMed1999

The cytolethal distending toxin family.

Cytolethal distending toxins are produced by a small but diverse group of bacterial pathogens. This newly discovered toxin family can cause a variety of mammalian cells to become irreversibly blocked in the G2 phase of the cell cycle. How this novel effect is accomplished is unknown but the study of these fascinating toxins promises to reveal new methods of host-pathogen interaction.

Aggregatibacter actinomycetemcomitans↗

PubMed2004

Subepidermal blistering disorders: a clinical and histopathologic review.

The subepidermal blistering disorders are comprised of a number of unrelated disorders with a diverse clinical presentation and pathogenic basis that share in common the presence of blister formation beneath the epidermis. Many of the disorders are both debilitating and potentially fatal. Timely and accurate diagnosis facilitates their appropriate management. The etiologic, clinical, and pathologic attributes as well as the treatment of these disorders including bullous pemphigoid, epidermolysis bullosa acquisita, dermatitis herpetiformis, linear IgA dermatosis, cicatricial pemphigold, herpes gestationis,and porphyria cutanea tarda are described.

Humans↗

PubMed1999

Bacterial phospholipases and pathogenesis.

Phospholipases are produced from a diverse group of bacterial pathogens causing very different diseases. In some cases, secreted phospholipases appear to be the major cause of pathophysiological effects. Yet in other cases, phospholipases are key virulence factors, contributing to bacterial survival or dissemination without causing tissue destruction. Perhaps the most intriguing aspect of phospholipases as virulence factors is their potential to interfere with cellular signaling cascades and to modulate the host immune response.

Animals↗

PubMedDate not supplied

S100A8 chemotactic protein is abundantly increased, but only a minor contributor to LPS-induced, steroid resistant neutrophilic lung inflammation in vivo.

Neutrophilic lung inflammation is an essential component of host defense against diverse eukaryotic and prokaryotic pathogens, but in chronic inflammatory lung diseases, such as chronic obstructive lung disease (COPD), severe asthma, cystic fibrosis, and bronchiolitis, it may damage the host. Glucocorticosteroids are widely used in these conditions and in their infectious exacerbations; however, the clinical efficacy of steroids is disputed. In this study, we used a proteomic approach to identify molecules contributing to neutrophilic inflammation induced by transnasal administration of lipopolysaccharide (LPS) that were also resistant to the potent glucocorticosteroid dexamethasone (Dex). We confirmed that Dex was biologically active at both the transcript (suppression of GM-CSF and TNFalphatranscripts) and protein levels (induction of lipocortin) and used 2D-PAGE/MALDI-TOF to generate global expression profiles, identifying six LPS-induced proteins that were Dex resistant. Of these, S100A8, a candidate neutrophil chemotactic factor, was profiled in detail. Steroid refractory S100A8 expression was highly abundant, transcriptionally regulated, secreted into lung lavage fluid and immunohistochemically localized to tissue infiltrating neutrophils. However, in marked contrast to other vascular beds, neutralizing antibodies to S100A8 had only a weak anti-neutrophil recruitment effect and antibodies against the related S100A9 were ineffective. These data highlight the need for extensive in vivo profiling of proteomically identified candidate molecules and demonstrates that S100A8, despite its abundance, resistance to steroids and known chemotactic activity, is unlikely to be an important determinant of LPS-induced neutrophilic lung inflammation in vivo.

Animals↗

PubMed2006

Primer: mechanisms of immunologic tolerance.

Successful adaptive immunity against a broad range of pathogens depends on the diversity of randomly generated T-lymphocyte and B-lymphocyte receptors. A subset of these receptors will be self-reactive and must be regulated to prevent autoimmunity. The process of immunologic tolerance addresses this problem by either purging autoreactive receptors from the system or tuning down their reactivity sufficiently to prevent disease. Immature lymphocytes generate a novel receptor during development in the thymus or bone marrow. Engagement of self antigens by these nascent receptors leads to their purging, either by the apoptotic death of the lymphocyte or by the initiation of receptor editing, a process in which the autoreactive receptor is replaced. If the lymphocytes mature further, the activation threshold of autoreactive cells can be tuned by the co-expression of inhibitory receptors or negative signaling molecules, allowing the persistence of the receptor without an increased risk of autoimmunity. T-cell and B-cell receptors that escape these checkpoints can still be regulated in the peripheral immune system by both purging and tuning mechanisms. A separate set of mechanisms, mediated by various regulatory cells, also operates to tune peripheral receptors in a cell-extrinsic fashion. The combined action of these processes ensures that the organism does not suffer autoimmune pathology, even if autoreactive receptors are generated and maintained in the immune system.

Autoimmune Diseases↗

PubMed2025

A haplotype-resolved pangenome of the barley wild relative Hordeum bulbosum.

Wild plants can contribute valuable genes to their domesticated relatives1. Fertility barriers and a lack of genomic resources have hindered the effective use of crop-wild introgressions. Decades of research into barley's closest wild relative, Hordeum bulbosum, a grass native to the Mediterranean basin and Western Asia, have yet to manifest themselves in the release of a cultivar bearing alien genes2. Here we construct a pangenome of bulbous barley comprising 10 phased genome sequence assemblies amounting to 32 distinct haplotypes. Autotetraploid cytotypes, among which the donors of resistance-conferring introgressions are found, arose at least twice, and are connected among each other and to diploid forms through gene flow. The differential amplification of transposable elements after barley and H. bulbosum diverged from each other is responsible for genome size differences between them. We illustrate the translational value of our resource by mapping non-host resistance to a viral pathogen to a structurally diverse multigene cluster that has been implicated in diverse immune responses in wheat and barley.

Hordeum↗

PubMed2003

Acyl-homoserine lactone acylase from Ralstonia strain XJ12B represents a novel and potent class of quorum-quenching enzymes.

N-acylhomoserine lactones (AHLs) are used as signal molecules by many quorum-sensing Proteobacteria. Diverse plant and animal pathogens use AHLs to regulate infection and virulence functions. These signals are subject to biological inactivation by AHL-lactonases and AHL-acylases. Previously, little was known about the molecular details underlying the latter mechanism. An AHL signal-inactivating bacterium, identified as a Ralstonia sp., was isolated from a mixed-species biofilm. The signal inactivation encoding gene from this organism, which we call aiiD, was cloned and successfully expressed in Escherichia coli and inactivated three AHLs tested. The predicted 794-amino-acid polypeptide was most similar to the aculeacin A acylase (AAC) from Actinoplanes utahensis and also shared significant similarities with cephalosporin acylases and other N-terminal (Ntn) hydrolases. However, the most similar homologues of AiiD are deduced proteins of undemonstrated function from available Ralstonia, Deinococcus and Pseudomonas genomes. LC-MS analyses demonstrated that AiiD hydrolyses the AHL amide, releasing homoserine lactone and the corresponding fatty acid. Expression of AiiD in Pseudomonas aeruginosa PAO1 quenched quorum sensing by this bacterium, decreasing its ability to swarm, produce elastase and pyocyanin and to paralyze nematodes. Thus, AHL-acylases have fundamental implications and hold biotechnological promise in quenching quorum sensing.

4-Butyrolactone↗

PubMed2000

Cluster analysis of AP-PCR generated DNA fingerprints of Vibrio vulnificus isolates from patients fatally infected after consumption of raw oysters.

Arbitrarily-primed-polymerase chain reaction (AP-PCR) DNA fingerprints were generated for 10 Vibrio vulnificus strains isolated from patients who became infected and died between 1993 and 1996 as a result of consuming raw oysters. Analysis of the DNA fingerprints with gel imaging and cluster analysis software revealed significant genetic heterogeneity among these strains, suggesting that V. vulnificus has a high degree of variation in its genomic organization, and that multiple pathogenic strains with greatly diverse genomic arrangements, rather than a single type of infective strain or serogroup, caused these infections.

Animals↗

PubMed2002

Human immunedeficiency virus type 1 (HIV-1) disease progression may be due to defects in the expression of the TCR/CD3 complex as well as to a T CD4+ cell deficit.

The loss of T CD4+ cells leading to impairment of the immune system is the major cause of disease progression during HIV infection. More recently, the use of highly active anti-retroviral therapy (HAART) has raised important questions regarding the immune system restoration. Idiopathic CD4+ T lymphocytopenia syndrome (ICL) is similar to AIDS, except for the presence of HIV. Despite this similarity, ICL patients have a longer survival time than AIDS cases without HAART. The impairment of TCR/CD3-directed CD4+ T cell immune responses may be responsible for HIV disease progression. We think that the reduction of opportunistic infections which lead to death after HAART, is due to the ability of these memory clones to restore enough clones of the TCR/CD3 complex with fair capacity and diversity to confront frequent pathogens.

CD3 Complex↗

PubMed2006

Pathogen relatedness affects the prevalence of within-host competition.

Although the evolutionary consequences of within-host competition among pathogens have been examined extensively, there exists a critical gap in our understanding of factors determining the prevalence of multiple infections. Here we examine the effects of relatedness among strains of the anther-smut pathogen Microbotryum violaceum on the probability of multiple infection in its host, Silene latifolia, after sequential inoculations. We found a significantly higher probability of multiple infection when interacting strains were more closely related, suggesting mechanisms of competitive exclusion that are conditional on genotypic characteristics of the strains involved. Pathogen relatedness therefore determines the prevalence of multiple infection in addition to its outcome, with important consequences for our understanding of virulence evolution and pathogen population structure and diversity.

Basidiomycota↗

PubMed2003

Pseudomonas type III effector AvrPtoB induces plant disease susceptibility by inhibition of host programmed cell death.

The AvrPtoB type III effector protein is conserved among diverse genera of plant pathogens suggesting it plays an important role in pathogenesis. Here we report that Pseudomonas AvrPtoB acts inside the plant cell to inhibit programmed cell death (PCD) initiated by the Pto and Cf9 disease resistance proteins and, remarkably, the pro-apoptotic mouse protein Bax. AvrPtoB also suppressed PCD in yeast, demonstrating that AvrPtoB functions as a cell death inhibitor across kingdoms. Using truncated AvrPtoB proteins, we identified distinct N- and C-terminal domains of AvrPtoB that are sufficient for host recognition and PCD inhibition, respectively. We also identified a novel resistance phenotype, Rsb, that is triggered by an AvrPtoB truncation disrupted in the anti-PCD domain. A Pseudomonas syringae pv. tomato DC3000 strain with a chromosomal mutation in the AvrPtoB C-terminus elicited Rsb-mediated immunity in previously susceptible tomato plants and disease was restored when full-length AvrPtoB was expressed in trans. Thus, our results indicate that a type III effector can induce plant susceptibility to bacterial infection by inhibiting host PCD.

Animals↗