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PubMed2005

A model for pathogen population structure with cross-protection depending on the extent of overlap in antigenic variant repertoires.

The persistence of discrete antigenic types among pathogens with multiple immunogenic loci can be explained by the action of immune-mediated competition. It has previously been shown that pathogen populations will self-organize into non-overlapping subsets of antigenic variants if cross-protection between pathogen types sharing any variants is high. Here, we examine the critical question of whether such strain structure will emerge if the degree of immune-mediated competition is dependent on the number of variants shared between pathogen types, rather than in an all-or-nothing manner. Our analysis uncovers a progression from no strain structure through to discrete stable strain structure through intermediate partially structured states. This suggests that the number of loci or epitope regions required to detect linkage disequilibrium (as a manifestation of stable discrete strain structure) in pathogen populations correlates inversely with the strength of immune selection.

Antigenic Variation↗

PubMed2004

The evolution of virulence in pathogens with frequency-dependent transmission.

Frequency-dependent transmission is an important feature of diseases that are sexually transmitted or transmitted by a vector that actively searches for hosts. Here I describe the evolution of virulence in pathogens that have frequency-dependent transmission. I consider two components of virulence--an increase in host mortality due to infection, as is classically described, and a decrease in host fecundity due to infection, because frequency dependence is common among diseases that fully or partially sterilize their hosts. Theoretical predictions pertaining to host-pathogen numerical dynamics can be quite different between pathogens with frequency-dependent transmission and those with density-dependent transmission. In contrast, this study suggests that the principles governing the evolution of virulence that have been established in the context of density-dependent pathogens may also apply (qualitatively) to frequency-dependent pathogens. I examine the evolutionary trajectories of the mortality and sterility components of virulence as well as the role of spatial population structure in the evolution of the sterility component of virulence.

Animals↗

PubMed2004

The effect of treatment on pathogen virulence.

The optimal virulence of a pathogen is determined by a trade-off between maximizing the rate of transmission and maximizing the duration of infectivity. Treatment measures such as curative therapy and case isolation exert selective pressure by reducing the duration of infectivity, reducing the value of duration-increasing strategies to the pathogen and favoring pathogen strategies that maximize the rate of transmission. We extend the trade-off models of previous authors, and represents the reproduction number of the pathogen as a function of the transmissibility, host contact rate, disease-induced mortality, recovery rate, and treatment rate, each of which may be influenced by the virulence. We find that when virulence is subject to a transmissibility-mortality trade-off, treatment can lead to an increase in optimal virulence, but that in other scenarios (such as the activity-recovery trade-off) treatment decreases the optimal virulence. Paradoxically, when levels of treatment rise with pathogen virulence, increasing control efforts may raise predicted levels of optimal virulence. Thus we show that conflict can arise between the epidemiological benefits of treatment and the evolutionary risks of heightened virulence.

Communicable Diseases↗

PubMed2006

Markov chain approach to analyze the dynamics of pathogen fecal shedding--example of Listeria monocytogenes shedding in a herd of dairy cattle.

Fecal shedding is an important mechanism of spreading of a number of human and animal pathogens. Understanding of the dynamics of pathogen fecal shedding is critical to be able to control or prevent the spread of diseases caused by these pathogens. The objective of this study was to develop a model for analysis of the dynamics of pathogen fecal shedding. Fecal shedding of Listeria monocytogenes in dairy cattle was used as a model system. A Markov chain model (MCM) with two states, shedding and non-shedding, has been developed for overall L. monocytogenes fecal shedding (all L. monocytogenes subtypes) and fecal shedding of three L. monocytogenes subtypes (ribotypes 1058A, 1039E and 1042B) using data from one study farm. The matrices of conditional probabilities of transition between shedding and non-shedding states for different sets of covariates have been estimated by application of logistic regression. The covariate-specific matrices of conditional probabilities, describing the presence of different risk factors, were used to estimate (i) the stationary prevalence of dairy cows that shed any L. monocytogenes subtype or ribotypes 1058A, 1039E, and 1042B, (ii) the duration of overall and subtype specific fecal shedding, and (iii) the duration of periods without shedding. A non-homogeneous MCM was constructed to study how the prevalence of fecal shedders changes over time. The model was validated with data from the study farm and published literature. The results of our modeling work indicated that (i) the prevalence of L. monocytogenes fecal shedders varies over time and can be higher than 90%, (ii) L. monocytogenes subtypes exhibit different dynamics of fecal shedding, (iii) the dynamics of L. monocytogenes fecal shedding are highly associated with contamination of silage (fermented feed) and cows' exposure to stress, and (iv) the developed approach can be readily used to study the dynamics of fecal shedding in other pathogen-host-environment systems.

Animals↗

PubMed2006

Subthreshold and superthreshold coexistence of pathogen variants: the impact of host age-structure.

It is well known that in the most general epidemic models with multiple pathogen variants a competitive exclusion principle is valid, such that the variant with the highest reproduction number eliminates the rest. Mechanisms such as super-infection, coinfection, and cross-immunity can lead to pathogen polymorphism where multiple strains coexist. It is also known that variability of infectivity with host age can destabilize the endemic equilibrium and cause oscillations. In this article we show that the hosts' chronological age can itself lead to coexistence of microparasites in the most basic model where competitive exclusion will occur without the age structure. Moreover, the host age-structure leads to multiple subthreshold dominance equilibria, and both weakly and strongly subthreshold coexistence. We find that the two pathogens cannot cooperate to persist subthreshold if neither one of them can persist subthreshold by itself. If, however, one of them can persist subthreshold by itself, it can cause the two pathogens to coexist in a strongly subthreshold equilibrium. The second strain that persists subthreshold through the mediation of the first always has a lower virulence. Our results show that age structure in infectivity can permit the coexistence of competing pathogens when the incidence is of proportionate mixing type (frequency-dependent transmission) and at least one of the strains is virulent.

Age Factors↗

PubMed2005

The arms race continues: battle strategies between plants and fungal pathogens.

Plants are under constant attack by a vast array of pathogens. To impede their attackers they use both broad-spectrum and pathogen-specific defence mechanisms. The arms race between plants and fungal pathogens is fascinatingly varied, and what might be elicited as a plant defence mechanism against a pathogen could promote or enhance the virulence of other pathogens. Fungi use countermeasures to detoxify plant antimicrobial compounds and to evade host resistance mechanisms. Certain fungal species also manipulate the host hormone balance to create an environment that is beneficial to their survival. Several lines of evidence indicate a co-evolutionary arms race in which both plants and fungi can respond to changes that occur in their opponents.

Antifungal Agents↗

PubMed2006

The regulation of pathogenicity and mutualism in Photorhabdus.

Photorhabdus is a genus of insect-pathogenic bacteria that also maintains a mutualistic interaction with Heterorhabditid nematodes. Bacteria in this genus are members of the family Enterobacteriaceae and are, therefore, closely related to many important mammalian pathogens. This bacteria-nematode complex has been exploited as a biocontrol agent that is active against several insect pests. However, this model system is also uniquely placed to address important fundamental questions about pathogenicity and mutualism. Indeed, recent genetic studies have suggested that there is a significant overlap in the genetic requirements of Photorhabdus for these contrasting interactions. In addition, the identification of key regulators of pathogenicity and symbiosis only serves to highlight the similarities between Photorhabdus, a genus of bacteria that infects invertebrate hosts, and closely related mammalian enteric pathogens.

Animals↗

PubMed2006

Effect of bacterial monoassociation on brush-border enzyme activities in ex-germ-free piglets: comparison of commensal and pathogenic Escherichia coli strains.

This study was designed to investigate the effect of monoassociation of germ-free piglets with Escherichia coli strains on the development of intestinal brush-border enzyme activities. Piglets were delivered by hysterectomy, reared for seven days under germ-free conditions and fed milk formula diet. One group was maintained germ-free, the other four groups were monoassociated on day eight with one of four E. coli strains: non-pathogenic O86 or O83 and G58-1, or pathogenic 933D. The development of brush-border digestive enzyme functions in the small intestine was evaluated after 15 days. Germ-free controls exhibited slower developmental declines of lactase, gamma-glutamyltranspeptidase and alkaline phosphatase, and delayed increases of sucrase and glucoamylase compared to conventionally grown animals. Association of germ-free piglets with the non-pathogenic E. coli strains O86 and O83 resulted in increased enterocyte differentiation along the length of the small intestine, accompanied by declining activities of lactase, gamma-glutamyltranspeptidase and alkaline phosphatase, and elevated activities of maturational markers such as sucrase and glucoamylase. Maturational changes also occurred along the villus-crypt axis, as revealed by histochemical localization of aminopeptidase N on the villi tips in piglets colonized with E. coli O83. Interestingly, colonization with the pathogenic E. coli strain 933D stimulated changes in the main differentiation enzyme markers lactase, sucrase and glucoamylase to an extent comparable with those produced by the non-pathogenic and probiotic E. coli strains. In conclusion, germ-free piglets represent a valuable tool to study the consequences of colonization of the immature sterile gut with defined strains of bacteria.

Alkaline Phosphatase↗

PubMed2026

Synergistic transcriptional modules in Trichoderma asperellum enhance glutathione detoxification to counteract fungal pathogen toxins.

Trichoderma fungi are potent biocontrol agents. However, their defence mechanisms against pathogen-derived toxins remain poorly understood. We identified two synergistic transcription factor modules in T. asperellum that orchestrate the detoxification of cytotoxic secondary metabolites from the poplar blight pathogen Alternaria alternata. Overexpression of the central regulator TasMYB46 reduced disease lesion area by approximately 22% and was associated with decreased pathogen-induced reactive oxygen species (ROS) accumulation. Mechanistically, TasMYB46 directly activates the glutathione S-transferases TasGST61.1 and TasGST56.1 through distinct promoter binding sites (G-box/as-1/MBS), forming dedicated detoxification modules. Crucially, we identified urolithin C as the most abundant phytotoxin in A. alternata metabolites, which is efficiently detoxified through the TasMYB46-TasGST61.1 module. The transcription enhancer TasbHLH53.8 amplifies this system by binding to TasMYB46, boosting TasGST expression and enhancing glutathione-dependent detoxification capacity. This coordinated response elevates glutathione pools and antioxidant enzyme activities (GST/GPx), conferring increased oxidative stress resistance. This study reveals a novel defence mechanism in Trichoderma in which MYB-bHLH-GST modules enable biocontrol agents to neutralise pathogen-derived toxins. Given that Alternaria toxins threaten crops globally (tomatoes, potatoes, citrus), the discovered regulatory synergy represents a strategic advance in developing next-generation biocontrol solutions against toxin-producing plant pathogens.

Alternaria↗

PubMed2004

Plant perception systems for pathogen recognition and defence.

Recognition of and defence against microbial infections are universal adaptations of multicellular organisms. Plants express a sophisticated molecular system for recognition of and response to potentially pathogenic microorganism. Although the environments of plant and animal cells are vastly different and present unique challenges to invading pathogens, the molecular basis of the innate immune response shows remarkable evolutionary conservation in both kingdoms. Even if more cellular components are continually being identified in plants, the mechanism, interactions and responses are only partly understood. Furthermore, most of this research has been performed in the model plant Arabidopsis thaliana and a significant effort will be needed to understand the above processes in crop species and in natural populations. In this review I will describe examples of the best characterized recognition systems in plants, that mediate pathogen perception either through the perception of highly variable and non-essential pathogen molecules or via conserved microbial structures called pathogen associated molecular patterns (PAMPs).

Arabidopsis↗

PubMed2005

Innate immune recognition of the extracellular mucosal pathogen, Helicobacter pylori.

Toll-like receptor (TLR) molecules play a frontline role in the defence of the host against infection by microbial pathogens. These molecules, together with the recently described Nod family proteins, have been shown to trigger innate immune responses in host cells via the recognition of highly conserved microbial structures. TLR4, which is the best-characterised of these "pathogen-recognition molecules" (PRMs), was the first to be shown to recognise a specific microbial component: the lipopolysaccharide (LPS) from Gram-negative bacteria. The molecular specificities of the remaining PRMs have, in nearly all cases, now also been elucidated. Host cells belonging to the myeloid cell lineage are known to be particularly responsive to these microbial constituents. Conversely, other cell types such as epithelial cells, were generally thought to be hypo-responsive to stimulation by such molecules. New evidence suggests that these cells are in fact likely to play a fundamental role in host defence against pathogenic micro-organisms. Indeed, epithelial cells afford an initial barrier against the host microflora, and appear to be able to differentiate between pathogenic and commensal micro-organisms. This review article will discuss current knowledge regarding innate immune responses in epithelial and myeloid cells to the model non-invasive pathogen, Helicobacter pylori, which is a major cause of upper gastrointestinal tract disease in humans.

Animals↗

PubMed2006

In vitro pathogenicity assay for the ergot fungus Claviceps purpurea.

The pathogenic development of the biotrophic ergot fungus Claviceps purpurea is strictly limited to the ovary of grasses. Early colonization stages occur within a defined spatio-temporal course of events, including the directed growth to the vascular tissue for nutrient supply. To characterize mutant strains with putative defects in pathogenicity, the close observation of the infection pathway is therefore indispensable. Here, we describe the establishment of a new pathogenicity assay, based on the in vitro cultivation of isolated rye ovaries. The pathogenic development of a wild-type strain of C. purpurea was compared with the infection of mature rye flowers on whole plants. Up to the sixth day post inoculation, the route of infection within the isolated ovaries was maintained and temporally equal to that seen in mature flowers. Therefore, the in vitro pathogenicity assay is an effective alternative to the whole-plant infection tests, and suitable for detailed infection studies and screening high numbers of mutants for defects in early pathogenesis.

Aniline Compounds↗

PubMed2006

Show and tell: cell biology of pathogen invasion.

Because the initial stages of pathogen invasion are often confined to a limited number of host cells, measures of host responses that are averaged over attacked and non-attacked cells provide an unsatisfactory view of these events. To identify the earliest and often transient responses to pathogen attack, there is considerable interest in monitoring the subcellular events that occur specifically in living host cells. Recent improvements in live-cell imaging using fluorescent-tagged markers have expanded the scope of the experiments that can be performed. Changes in the subcellular distribution of organelles and of fluorescently tagged proteins can be monitored in real time in living tissues during pathogen attack, and the dynamic nature of such changes across space and over time can be determined. The application of these sensitive imaging methods has extended earlier observations, made with Nomarski microscopy or inferred from static transmission electron micrographs, about the focal accumulation of subcellular organelles at sites of pathogen attack. In addition, recent experiments have demonstrated the focused accumulation and interaction of specific plant proteins at penetration sites, opening a new window on early host responses and raising questions about the underlying plant processes that sense and direct this marshalling of host resources to block pathogen entry.

Fungi↗

PubMed2005

Diffuse and point pollution impacts on the pathogen indicator organism level in the Geum River, Korea.

The pathogens originating from diffuse pollution have raised much concern recently. In many countries, pathogen levels are monitored in surface water by measuring the pathogen indicator organism level, which indicates the concentration of pathogen associated microorganisms to determine contamination. Among indicator organisms, total coliform, fecal coliform, and Escherichia coli were selected for study, and their concentration as well as their flow rate were monitored at monitoring stations from October, 2001 to April, 2003. Monitoring stations include six sampling stations in the Geum River, two small watersheds used for forestry and agricultural land, one large wastewater treatment plant, one separate sewer overflow site, and one separate sewer overflow site in the Geum River basin. The coliform concentration of the combined sewer overflow was the highest, followed by the runoff from agricultural land use, the separate sewer overflow, and the runoff from forestry land use. The Pearson correlation coefficient for flow rate against total coliform concentration was 0.71 and was significant at 0.01 level, while the Pearson coefficient for other water quality constituents showed weak correlation (-0.36 to +0.37) against flow rate. Coliform concentration showed higher correlation against suspended solid concentration or flow rate during storm flow condition than during low flow condition. Two different relationship lines could explain the relationships between the flow rate and coliform loadings. Load duration curve technique was presented to assess the relative contributions of diffuse and point source pollution to the pathogen level at monitoring sites in the Geum River.

Colony Count, Microbial↗

PubMed2003

Pathogenicity islands and phages in Vibrio cholerae evolution.

The identification of accessory genetic elements (plasmids, phages and chromosomal 'pathogenicity islands') encoding virulence-associated genes has facilitated our efforts to understand the origination of pathogenic microorganisms. Toxigenic Vibrio cholerae, the etiologic agent of cholera, represents a paradigm for this process in that this organism evolved from environmental nonpathogenic V. cholerae by acquisition of virulence genes. The major virulence genes in V. cholerae, which are clustered in several chromosomal regions, appear to have been recently acquired from phages or through undefined horizontal gene transfer events. Evidence is accumulating that the interactions of phages with each other can also influence the emergence of pathogenic clones of V. cholerae. Therefore, to track the evolution of pathogens from their nonpathogenic progenitors, it is also crucial to identify and characterize secondary genetic elements that mediate lateral transfer of virulence genes in trans. Understanding the evolutionary events that lead to the emergence of pathogenic clones might provide new approaches to the control of cholera and other infectious diseases.

Biological Evolution↗

PubMed2006

Plant-mediated effects in insect-pathogen interactions.

Interactions between insect herbivores and their pathogens can be modulated by host plants. Inter- and intraspecific differences in plant chemistry and structure can alter the susceptibility of insects to infection and the production and environmental persistence of pathogens. Whether plants can manipulate insect pathogens to act as "bodyguards" and increase their own fitness remains to be shown. Reduced insect performance owing to poor plant quality can enhance the susceptibility of an insect to disease while these same phytochemicals can also reduce the effectiveness of entomopathogens in killing the host. As we discuss here, plants have an important role in the evolution of insect-pathogen relationships and a tritrophic perspective should thus be incorporated into the study of insects and their pathogens.

Animals↗

PubMed2005

Aerosol-, but not intradermal-immunization with the live vaccine strain of Francisella tularensis protects mice against subsequent aerosol challenge with a highly virulent type A strain of the pathogen by an alphabeta T cell- and interferon gamma- dependent mechanism.

Francisella tularensis is an extremely virulent facultative intracellular bacterial pathogen of many mammalian species including mice and humans in which it causes a spectrum of disease collectively called tularemia. In humans, intradermal or inhaled inocula of 10cfu or less of the most virulent strains of the pathogen are sufficient to cause severe infection and possible death; in mice similar inocula are routinely lethal. An attenuated live vaccine strain, F. tularensis LVS, was developed almost 50 years ago, and remains the sole prophylactic against virulent strains of the pathogen. Using F. tularensis LVS as a model vaccine, we recently showed that it was possible to systemically immunize various mouse strains and protect them against subsequent massive (2000 cfu) intradermal (i.d.) challenge, but not against low dose (approximately 10 cfu) aerosol challenge, with virulent strains of the pathogen. This is troubling because the latter route is considered an important means of deliberately disseminating F. tularensis in a bioterrorist attack. Others have previously shown that administering LVS to humans, guinea pigs and monkeys as an aerosol enhanced protection against subsequent aerosol challenge with virulent F. tularensis. In the present study, we show the same phenomenon in BALB/c and C3H/HeN mice. In this model, interferon gamma (IFNgamma) and CD4+ and CD8+ T cells are essential for the expression of anti-Francisella immunity in the lungs. Combined this immune response operates by limiting dissemination of the pathogen to susceptible internal organs. Further, understanding of how inhaled LVS elicits local cell-mediated protective immunity will be critical for devising improved vaccines against pulmonary tularemia.

Administration, Inhalation↗

PubMed2006

An emerging avian influenza A virus H5N7 is a genetic reassortant of highly pathogenic genes.

We full genome characterised the newly discovered avian influenza virus H5N7 subtype combination isolated from a stock of Danish game ducks to investigate the composition of the genome and possible features of high pathogenicity. It was found that the haemagglutinin and the acidic polymerase genes were closely related to a low pathogenic H5 strain (A/Duck/Denmark/65047/04 H5N2). The neuraminidase and the non-structural genes were closely related to the highly pathogenic H7N7 strains from The Netherlands 2003. The basic polymerase genes 1 and 2 were shared between the Danish H5N7 and H5N2 and the H7N7 from The Netherlands. The nucleoprotein and the matrix genes were closely related to H6 strains. Thus, the new H5N7 subtype share genes with H5, H7 and H6 subtypes and possesses internal genes originating from highly pathogenic strains. The findings emphasize the need for surveillance presumed low pathogenic avian influenza A viruses.

Animals↗