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PubMed2005

Engulfed pathogen-induced apoptosis in haemocytes of giant freshwater prawn, Macrobrachium rosenbergii.

Haemocytes of the giant freshwater prawn, Macrobrachium rosenbergii, were investigated for the induction of apoptosis after phagocytosis of pathogenic yeasts, bacteria and non-pathogenic latex beads in vitro. Isolated haemocytes of M. rosenbergii were cultured at a ratio of 1:50 haemocytes to pathogen with the yeast Debaryomyces hansenii, the bacteria Aeromonas hydrophila or Enterococcus faecium, or with latex beads at 25 degrees C for 2 h, followed by washing to remove free particles. At least 200 haemocytes were counted to determine the phagocytosis rate, and the results showed that haemocytes engulfed latex beads at a higher rate than the aquatic pathogens. By transmission electron microscopy, the yeast- or bacterium-engulfing haemocytes displayed morphological changes characteristic of apoptosis, including formation of cytoplasmic vacuoles, chromatin condensation and fragmentation of nuclei. This pathogen-induced apoptosis was further confirmed by DNA laddering and TUNEL (terminal deoxynucleotidyl transferase-mediated deoxy-UTP nick-end-labelling) assays. Neither haemocytes treated with latex beads nor uninfected haemocytes (control group) showed signs of apoptosis after 48 h in culture.

Aeromonas hydrophila↗
PubMed1993

A pleiotropic reduced virulence (Rvi-) mutant of Erwinia carotovora subspecies atroseptica is defective in flagella assembly proteins that are conserved in plant and animal bacterial pathogens.

Erwinia carotovora subsp. atroseptica was mutagenized and assayed for virulence in planta. Those mutants which exhibited reduced virulence (Rvi-) were assayed for growth rate, auxotrophy and extracellular enzyme secretion and seven mutants were found to be wild type for all of these phenotypes. When screened for other phenotypes, two were found to be non-motile. One mutant was complemented for motility by a heterologous gene library. A 2.7kb XmaIII-ClaI complementing fragment was sequenced and the gene products were found to have similarity to flagella biosynthesis gene products from several bacteria. Further similarity was found to a pathogenicity protein from the plant pathogen Xanthomonas campestris pv. glycines and to the Spa pathogenicity proteins of the human pathogen Shigella flexneri, which are involved in the surface presentation of antigens. These studies highlight the emergence of common themes in the molecular strategies employed by both plant and animal bacterial pathogens for the targeting of proteins involved in the elaboration of disease.

Amino Acid Sequence↗
PubMed2005

Who's talking to whom? Epithelial-bacterial pathogen interactions.

Our perception that host-bacterial interactions lead to disease comes from rare, unsuccessful interactions resulting in the development of detectable symptoms. In contrast, the majority of host-bacterial interactions go unnoticed as the host and bacteria perceive each other to be no threat. In July 2004, a focused international symposium on epithelial-bacterial pathogen interactions was held in Newcastle upon Tyne (UK). The symposium concentrated on recent advances in our understanding of bacterial interactions at respiratory and gastrointestinal mucosal epithelial layers. For the host these epithelial tissues represent a first line of defence against invading bacterial pathogens. Through the discovery that the innate immune system plays a pivotal role during host-bacterial interactions, it has become clear that epithelia are being utilized by the host to monitor or communicate with both pathogenic and commensal bacteria. Interest in understanding the bacterial perspective of these interactions has lead researchers to realize that the bacteria utilize the same factors associated with disease to establish successful long-term interactions. Here we discuss several common themes and concepts that emerged from recent studies that have allowed physiologists and microbiologists to interact at a common interface similar to their counterparts -- epithelia and bacterial pathogens. These studies highlight the need for further multidisciplinary studies into how the host differentiates between pathogenic and commensal bacteria.

Bacteria↗
PubMed2005

The origin and evolution of human pathogens.

What are the genetic origins of human pathogens? An international group of scientists discussed this topic at a workshop that took place in late October 2004 in Baeza (Spain). Focusing primarily on bacterial pathogens, they examined the role that pathogenicity islands and bacteriophages play on determining the virulence properties that distinguish closely related members of a given species, such as host range and tissue specificity. They also discussed an instance in which closely related bacterial species differ in the production of a cell surface modification mediating resistance to an antibiotic as a result of the disparate regulation of homologous genes. In certain pathogens, genes normally carrying out housekeeping functions may adopt new functions, whereas in other organisms, genes that respond to stresses associated with non-host environments are silenced during infection to prevent the expression of products that interfere with the normal colonization process. The adaptive behaviour of certain pathogens relies on gene variation at certain loci that by virtue of containing polymeric repeats in regulatory or coding regions, can generate variants that may or may not express products that modify the cell surface of the organism. The meeting also addressed the properties of ORFan genes, which have no homologues in the sequence databases, as well as the creation of genes de novo by duplication and divergence.

Bacteria↗
PubMed2005

Frp1 is a Fusarium oxysporum F-box protein required for pathogenicity on tomato.

Fusarium oxysporum f. sp. lycopersici is the causal agent of tomato wilt disease. In order to identify genes involved in its pathogenicity, we performed insertional mutagenesis. Mutant N40 had lost its pathogenicity completely, when tested in bioassays with tomato seedlings. Molecular characterization of mutant N40 revealed that the plasmid insertion had occurred in a gene that codes for a 60.2 kDa protein containing an F-box motif. The gene was therefore designated as FRP1 (F-box protein required for pathogenicity). Targeted FRP1 disruptants had lost their pathogenicity completely, and became fully virulent again upon re-introduction of the FRP1 gene. This confirmed that the FRP1 gene is required for pathogenesis. In a yeast two-hybrid assay Frp1 interacts with Skp1, suggesting involvement of an SCF ubiquitin ligase complex in pathogenicity. FRP1 is constitutively expressed during infection and under different culture conditions. Although growth, spore formation and germination on artificial media were not impaired, confocal laser scanning microscopy of a GFP-marked mutant N40 and a GFP-marked targeted FRP1 disruptant revealed that they were unable to colonize the roots.

Amino Acid Sequence↗
PubMed1993

Induction of complement resistance in cloned pathogenic Entamoeba histolytica.

The lytic effect of complement activated through the alternative pathway (AP) was studied on pathogenic and nonpathogenic Entamoeba histolytica recently isolated from stool samples. Recent nonpathogenic isolates were nearly unaffected by exposure to AP whereas recent pathogenic stool isolates were highly susceptible to AP dependent complement-mediated lysis. Complement susceptible pathogenic stool isolates developed complement resistance in vivo during hamster liver passage and in vitro during cultivation in the presence of increasing concentrations of normal human serum (NHS). Since a clone of pathogenic HM-1:IMSS which initially was highly susceptible also acquired complement resistance during cultivation in the presence of NHS, it is concluded that complement resistance was caused by induction rather than by selection alone. Because cultivation in the presence of heat-inactivated NHS did not affect complement susceptibility of the cloned HM-1:IMSS, complement activation itself might induce complement resistance in pathogenic E. histolytica.

Animals↗
PubMed2006

The immunomodulatory factors of arthropod saliva and the potential for these factors to serve as vaccine targets to prevent pathogen transmission.

In general, attempts to develop vaccines for pathogens transmitted by arthropods have met with little or no success. It has been widely observed that the saliva of arthropods that transmit disease enhances the infectivity of pathogens the arthropod transmits to the vertebrate host. Indeed, it has been observed that vaccinating against components of the saliva of arthropods or against antigens expressed in the gut of arthropods can protect the host from infection and decrease the viability of the arthropod. These results suggest that multi-subunit vaccines that target the pathogen itself as well as arthropod salivary gland components and arthropod gut antigens may be the most effective at controlling arthropod-borne pathogens as these vaccines would target several facets of the lifecycle of the pathogen. This review covers known immunomodulators in arthropod salivary glands, instances when arthropod saliva has been shown to enhance infection and a limited number of examples of antiarthropod vaccines, with emphasis on three arthropods: sandflies, mosquitoes and hard ticks.

Animals↗
PubMed2004

Beta-amino-butyric acid-induced resistance against necrotrophic pathogens is based on ABA-dependent priming for callose.

The non-protein amino acid beta-amino-butyric acid (BABA) protects plants against a wide range of pathogens. We have examined the effectiveness and mode of action of BABA on resistance against two necrotrophic pathogens. Treatment of Arabidopsis with BABA induced resistance against Alternaria brassicicola and Plectosphaerella cucumerina to a similar level by jasmonic acid (JA). Conversely, treatment with benzothiadiazole (BTH), a functional analogue of salicylic acid (SA), had no significant effect on the resistance against both pathogens. BABA-induced resistance against A. brassicicola and P. cucumerina was unaffected in the JA-insensitive mutant coi1-1 and the camalexin-deficient mutant pad3-1. Moreover, the expression of BABA-induced resistance was not associated with enhanced accumulation of camalexin or enhanced transcription of the JA-inducible PDF1.2 gene. The expression of BABA-induced resistance against P. cucumerina was unaffected in mutants impaired in ethylene (ET) and SA signalling, but was blocked in the abscisic acid (ABA)-deficient mutant aba1-5, the ABA-insensitive mutant abi4-1 and the callose-deficient mutant pmr4-1. Upon infection by both pathogens, BABA-treated plants showed an earlier and more pronounced accumulation of callose. Treatment with the callose-inhibitor 2-deoxy-D-glucose (2-DDG) reversed the BABA-induced resistance against A. brassicicola. Furthermore, primed callose deposition was absent in BABA-treated abi4-1 and pmr4-1 plants upon infection by P. cucumerina. Although the expression of BABA-induced resistance was not associated with enhanced transcription of the ABA-inducible RAB18 gene, application of ABA mimicked the effect of BABA on the level of callose accumulation and resistance. Hence, BABA-induced resistance against necrotrophic pathogens is based on primed callose accumulation, which is controlled by an ABA-dependent defence pathway.

Abscisic Acid↗
PubMed2007

Early events in the pathogenicity of Pseudomonas syringae on Nicotiana benthamiana.

Conserved microbial molecules known as PAMPs (pathogen-associated molecular patterns) elicit defence responses in plants through extracellular receptor proteins. One important PAMP is the flagellin protein derived from motile bacteria. We show here that the solanaceous species Nicotiana benthamiana perceives the flagellin proteins of both pathogenic and non-host species of Pseudomonas syringae. The response to flagellin required a gene closely related to that encoding the Arabidopsis thaliana flagellin receptor that we designated NbFls2. In addition, silencing of NbFls2 led to increased growth of compatible, non-host and non-pathogenic strains of P. syringae. Thus, flagellin perception restricts growth of P. syringae strains on N. benthamiana. Pathogenic bacteria secrete effector proteins into the plant cell to enhance virulence. We tested the ability of several unrelated effectors to suppress PAMP-mediated defences. The effector proteins AvrPto and AvrPtoB, but not AvrRps4, suppressed all responses tested including the hypersensitive response induced by non-host flagellins and the oomycete elicitor INF1. Strikingly, transient expression of avrPto or avrPtoB stimulated the growth of non-pathogenic Agrobacterium tumefaciensin planta, suggesting that multiplication of this species is also restricted by PAMP perception. Unexpectedly, AvrPtoB but not AvrPto required the defence-associated genes Rar1, Sgt1 and Eds1 for suppression. This observation separates the respective mechanisms of the two effectors, and suggests that AvrPtoB may target the defence machinery directly for its suppressive effect.

Bacterial Proteins↗
PubMed2005

Spatial scale of local adaptation in a plant-pathogen metapopulation.

The rate and scale of gene flow can strongly affect patterns of local adaptation in host-parasite interactions. I used data on regional pathogen occurrence to infer the scale of pathogen dispersal and to identify pathogen metapopulations in the interaction between Plantago lanceolata and its specialist phytopathogen, Podosphaera plantaginis. Frequent extinctions and colonizations were recorded in the metapopulations, suggesting substantial gene flow at this spatial scale. The level of pathogen local adaptation was assessed in a laboratory inoculation experiment at three different scales: in sympatric host populations, in sympatric host metapopulations and in allopatric host metapopulations. I found evidence for adaptation to sympatric host populations, as well as evidence indicating that local adaptation may extend to the scale of the sympatric host metapopulation. There was also variation among the metapopulations in the degree of pathogen local adaptation. This may be explained by regional differences in the rate of migration.

Adaptation, Physiological↗
PubMed2006

Differential sensitivities of pathogens in red cell concentrates to Tri-P(4)-photoinactivation.

BACKGROUND AND OBJECTIVES: Photodynamic treatment (PDT) with the cationic porphyrin, mono-phenyl-tri-(N-methyl-4-pyridyl)-porphyrin chloride [Tri-P(4)], has previously been shown to be effective at inactivating vesicle stomatitis virus (VSV) in red cell concentrates (RCC) with limited damage to red blood cells (RBC). The aim of this study was to determine the pathogen-inactivating capacity of PDT with Tri-P(4) for a broader range of pathogens and to establish the associated effect on in vitro RBC quality. MATERIALS AND METHODS: A series of viruses and bacteria was spiked into 60% RCC. Pathogen inactivation was determined after PDT with 25 microm Tri-P(4) and red light up to 360 kJ/m2. Human immunodeficiency virus (HIV)-infected cells were evaluated for cell death induction, and RCC were analysed for the induction of haemolysis and ATP content. RESULTS: For the lipid-enveloped viruses bovine viral diarrhoea virus, HIV and pseudorabies virus, and for the Gram positive bacterium, Staphylococcus aureus, and the Gram-negative bacteria, Pseudomonas aeruginosa and Yersinia enterolitica, inactivation of > or = 5 log10 was measured after 60 min of PDT with Tri-P(4). The required treatment time to achieve this level of inactivation was four times longer than required for VSV. For cell-associated HIV, only 1.7 log10 of inactivation was found, despite clear induction of cell death of HIV-infected cells. The non-enveloped virus, canine parvovirus, was completely resistant to the treatment. PDT of RCC with Tri-P(4) for 60 min, and subsequent storage in AS-3, resulted in 4% haemolysis after 35 days of storage. The ATP content of untreated and treated RBC declined with similar kinetics during storage. CONCLUSION: PDT of RCC with Tri-P(4) for 60 min inactivates a wide range of pathogens, but not cell-associated HIV and a non-enveloped virus, and compromises RBC quality. This reduces the suitability of PDT with Tri-P(4) for red cell sterilization. Therefore, further improvements in the treatment procedures to potentiate pathogen inactivation and to preserve RBC integrity will be required to generate an effective treatment for sterilizing RCC.

Anti-Bacterial Agents↗
PubMedDate not supplied

Pathogenicity of yeasts and algae isolated from bovine mastitis secretions in a murine model.

The pathogenicity of strains of yeasts and algae isolated from bovine mastitis secretions was evaluated in immunosuppressed mice. Strains of Candida tropicalis (n = 3) were the most pathogenic, but all strains of Geotrichum capitatum (n = 5) and the colourless alga Prototheca zopfii (n = 5) were also lethal to mice at the highest dose of 1 x 10(7) CFU per mouse. Reisolation of the inoculated micro-organisms and the occurrence of histopathological lesions within organs of mice challenged with 1 x 10(3) to 1 x 10(7) CFU per animal revealed strains of C. krusei (n = 17), C. kefyr (n = 6) and C. rugosa (n = 6) to have a moderate pathogenicity, whereas strains of C. valida (n = 1) and C. catenulata (n = 2) were weakly pathogenic and non-pathogenic respectively.

Animals↗
PubMed1996

[Are there pathogenicity factors in fungi?].

Since many years so-called pathogenicity or virulence factors of pathogenic bacteria have been studied intensively. Whereas these factors are produced especially by obligate but also facultative pathogenic bacteria, their presence and function in pathogenic fungi is still a matter of debate. In this minireview we summarize some data about possible pathogenicity factors of Cryptococcus neoformans, Aspergillus fumigatus and Candida albicans. The production of adhesins, proteases and capsules contributes to the virulence of these fungi. As fungal infections usually affect immunocompromised patients, the immune status of the host plays a decisive role in addition to the virulence factors produced by fungi.

AIDS-Related Opportunistic Infections↗
PubMed2005

The causative pathogens of onychomycosis in southern Taiwan.

Selecting an appropriate antimycotic targeting the pathogens are among the most important factors for successfully treating onychomycosis. The aim of this study was to investigate the pathogens of onychomycosis in southern Taiwan and analyse the association between various factors and the distribution of pathogens. A total of 375 patients with onychomycosis were enrolled. Histopathological examination and fungus culture of nail specimens were performed. The pathogens were dermatophytes in 227 patients (60.5%), Candida in 118 (31.5%) and moulds in 30 (8%). Compared to patients with toenail involvement, the odds ratio (OR) for those with fingernail involvement to have non-dermatophytic onychomycosis (NDO), i.e. onychomycosis caused by Candida and moulds, was 5.04 [95% confidence interval (CI): 2.21-11.15], and the OR for those with fingernail and toenail involvement to have NDO was 2.66 (95% CI: 1.61-4.34). The F/M OR to have NDO was 2.36 (95% CI: 1.51-3.61), and 9.80 for diabetics (95% CI: 1.01-106.85). The OR for patients with paronychia to have NDO was 10.33 (95% CI: 5.61-18.88) compared to those without paronychia. Compared to patients with a non-wet occupation, the OR for those with a wet occupation to have NDO was 4.76 (95% CI: 2.01-11.16). The distribution of pathogens significantly varies with the involved sites, patients' gender and occupation, and presence of diabetes mellitus or paronychia. In contrast to temperate western countries, NDO is more prevalent in the tropics and subtropics including southern Taiwan.

Adult↗
PubMed2005

The rhizosphere as a reservoir for opportunistic human pathogenic bacteria.

During the last years, the number of human infections caused by opportunistic pathogens has increased dramatically. One natural reservoir of opportunistic pathogens is the rhizosphere, the zone around roots that is influenced by the plant. Due to a high content of nutrients, this habitat is a 'microbial hot-spot', where bacterial abundances including those with strong antagonistic traits are enhanced. Various bacterial genera, including Burkholderia, Enterobacter, Herbaspirillum, Ochrobactrum, Pseudomonas, Ralstonia, Staphylococcus and Stenotrophomonas, contain root-associated strains that can encounter bivalent interactions with both plant and human hosts. Mechanisms responsible for colonization of the rhizosphere and antagonistic activity against plant pathogens are similar to those responsible for colonization of human organs and tissues, and pathogenicity. Multiple resistances against antibiotics are not only found with clinical strains but also with strains isolated from the rhizosphere. High competition, the occurrence of diverse antibiotics in the rhizosphere, and enhanced horizontal gene transfer rates in this microenvironment appear to contribute to the high levels of natural resistances. While opportunistic bacteria from the rhizosphere have some properties in common, each of these emerging pathogens has its own features, which are discussed in detail for Burkholderia, Ochrobactrum and Stenotrophomonas.

Bacteria↗
PubMed2004

The role and regulation of programmed cell death in plant-pathogen interactions.

It is commonly known that animal pathogens often target and suppress programmed cell death (pcd) pathway components to manipulate their hosts. In contrast, plant pathogens often trigger pcd. In cases in which plant pcd accompanies disease resistance, an event called the hypersensitive response, the plant surveillance system has learned to detect pathogen-secreted molecules in order to mount a defence response. In plants without genetic disease resistance, these secreted molecules serve as virulence factors that act through largely unknown mechanisms. Recent studies suggest that plant bacterial pathogens also secrete antiapoptotic proteins to promote their virulence. In contrast, a number of fungal pathogens secrete pcd-promoting molecules that are critical virulence factors. Here, we review recent progress in determining the role and regulation of plant pcd responses that accompany both resistance and susceptible interactions. We also review progress in discerning the mechanisms by which plant pcd occurs during these different interactions.

Apoptosis↗
PubMed2004

Simultaneous analysis of host and pathogen interactions during an in vivo infection reveals local induction of host acute phase response proteins, a novel bacterial stress response, and evidence of a host-imposed metal ion limited environment.

A fundamental goal in the study of infections is to understand the dynamic interplay between host and pathogen; however, direct in vivo interrogation of this disease process via transcriptional profiling has been lacking. Here we describe the development and application of novel bacterial RNA amplification technology to simultaneously identify key elements of both host and pathogen responses in a murine infection model. On the bacterial side, we found induction of an unusual pattern of stress response genes, a response to host-induced metal ion limitation, and a failure to achieve stationary phase in vivo. On the mammalian side, we observed the surprising induction of several genes encoding acute phase response proteins including hepcidin, haptoglobin, complement C3 and metallothionein 1 at the site of infection, as well as other mediators of innate immunity. Thus, our results reveal host-pathogen cross-talk not predicted by previous in vitro analyses and provide the framework to eavesdrop on a broad array of host-pathogen interactions in vivo. As described here, the comprehensive examination of host-pathogen interactions during an infection is critical to the discovery of novel approaches for intervention not predicted by current models.

Acute-Phase Proteins↗
PubMed2006

Role of the dual interaction of fungal pathogens with pattern recognition receptors in the activation and modulation of host defence.

Recognition of pathogen-associated molecular patterns (PAMPs) of microorganisms by pathogen recognition receptors induces signals responsible for the activation of genes important for an effective host defence, especially those of pro-inflammatory cytokines. Toll-like receptors (TLRs) and lectin-like receptors are the most important classes of pattern-recognition receptors. In addition to their effects on the activation of host defence, recent studies suggest that pathogenic fungi can modulate or interfere with the pattern recognition mechanisms of innate immunity, and can use pattern recognition receptors as mechanisms of escape from host defence. Two major recognition receptor-mediated escape mechanisms have been identified during infection with fungal pathogens: immunosuppression induced by activation of certain pattern recognition receptors, especially induction of IL-10 release through TLR2; and the blockade of TLR recognition by antigen modification during the germination of yeasts into hyphae. Thus, signals mediated by recognition receptors are not only beneficial to the host, but in certain situations can be used by pathogenic fungi to escape immune recognition and promote infection.

Animals↗