SEARCH · PubMed Health

Results for “Pathogen”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources

PubMed1991

Studies on the relationship between the pathogenicity of Paracoccidioides brasiliensis in mice and its growth rate under different oxygen atmospheres.

We performed comparative studies of the pathogenicity of six strains of Paracoccidioides brasiliensis (Bt-9, Bt-4, Pb-9, Pb-18, Bt-7 and B-1183) for young adult male ddY mice and the growth rate of each strain under different oxygen atmospheres (aerobic, micro-aerobic and anaerobic atmospheres) at 37 degrees C. 10(6) units of yeast cells were intravenously injected into each mouse. The pathogenicity of each isolate was determined by a scoring system based on organ culture and histopathological findings. The growth rates under different oxygen atmospheres were determined by a scoring system in which 300 fungal units per strain were counted. The strain Bt-9 showed the greatest pathogenicity, followed by Bt-4, Pb-9 and Pb-18 had on intermediate rank of pathogenicity. Bt-7 and B-1183 were the least pathogenic of the strains tested. Except for strain Bt-7 all strains showed an excellent growth under an aerobic atmosphere. Bt-4 and Bt-9 also showed excellent growth under a micro-aerobic atmosphere, followed by Pb-9, whereas the growth of Pb-18, Bt-7 and B-1183 was limited. There was a correlation between the growth rate under a micro-aerobic atmosphere and the pathogenicity of a strain. The growth rate of P. brasiliensis under a micro-aerobic atmosphere strongly correlated to its pathogenicity.

Aerobiosis↗

PubMed2003

Evolution of immunological memory and the regulation of competition between pathogens.

Memory is a central characteristic of immune responses. It is defined as an elevated number of specific immune cells that remain after resolution of infection and can protect the host against reinfection. The evolution of immunological memory is subject to debate. The advantages of memory discussed so far include protection from reinfection, control of chronic infection, and the transfer of immune function to the next generation. Mathematical models are used to identify a new force that can drive the evolution of immunological memory: the duration of memory can regulate the degree of competition between different pathogens. While a long duration of memory provides lasting protection against reinfection, it may also allow an inferior pathogen species to persist. This can be detrimental for the host if the inferior pathogen is more virulent. On the other hand, a shorter duration of memory ensures that an inferior pathogen species is excluded. This can be beneficial for the host if the inferior pathogen is more virulent. Thus, while in the absence of pathogen diversity memory is always expected to evolve to a long duration, under specific circumstances, memory can evolve toward shorter durations in the presence of pathogen diversity.

Biological Evolution↗

PubMed2005

Prevalence of blood-borne pathogens in an urban, university-based general surgical practice.

OBJECTIVE: To measure the current prevalence of blood-borne pathogens in an urban, university-based, general surgical practice. SUMMARY BACKGROUND DATA: Human immunodeficiency virus (HIV), hepatitis B, and hepatitis C represent significant occupational hazards to the surgeon. While the incidence of these blood-borne pathogens is increasing in the general population, little is known about the current prevalence of these exposures among patients presenting for surgery. METHODS: We studied 709 consecutive operative cases (July 2003 to June 2004) in a university practice that provides all inpatient, emergency department, and outpatient consultative general surgical services. Trauma cases and bedside procedures were excluded. Data collected included HIV, hepatitis B and C test results, type of operation, age, sex, and history of intravenous drug use. RESULTS: Testing for blood-borne pathogens was performed in 53% (N = 373) of 709 patients based on abnormal liver function tests, neutropenia, history of IV drug use, or patient request. Thirty-eight percent of all operations (142/373) were found to involve a blood-borne pathogen when tested: HIV (26%), hepatitis B (4%), hepatitis C (35%), and coinfection with HIV and hepatitis C (17%). Forty-seven percent of men tested positive for at least 1 blood-borne pathogen. Seventy-three different types of operations were performed, ranging from Whipple procedures to amputations. Soft-tissue abscess procedures 48% (34/71) and lymph node biopsies 67% (10/15) (P < 0.01) were most often associated with blood-borne pathogens. Infections were more common among men (P < 0.01), patients 41 to 50 years of age (P < 0.01), and patients with a history of intravenous drug use (P < 0.01). CONCLUSIONS: HIV and hepatitis C infections are common in an urban university general surgical practice, while hepatitis B is less common. In addition, certain operations are associated with significantly increased exposure rates. Given the high incidence of these infections, strategies such as sharpless surgical techniques should be evaluated and implemented to protect surgeons from blood-borne pathogens.

Adult↗

PubMed2026

Patterns of antimicrobial resistance genes in pathogens across One Health sectors in Ireland: an in silico approach.

As part of a rapid risk assessment, an in silico approach was used to detect antimicrobial resistance (AMR) in pathogenic isolates from humans, animals, and the environment. A total of 11,670 genomic data sets were retrieved from the NCBI Pathogen Detection system for Ireland, which represented 47 pathogenic species, including Salmonella enterica, Escherichia coli/Shigella spp., Staphylococcus aureus, Klebsiella pneumoniae, and Enterococcus faecium. Identifying the most critical pathogenic strains over time is essential, as these organisms significantly contribute to mortality, morbidity, and hospitalization. The analysis identified 799 antimicrobial resistance genes (ARGs), including their allelic diversity, 117 plasmid replicons, and 274 virulence factors. Several critical ARGs, particularly those conferring resistance to beta-lactams, aminoglycosides, quinolones, and colistin, were common across isolates originating from human, animal, and environmental sources, suggesting shared resistance profiles across One Health sectors. Klebsiella pneumoniae, E. coli/Shigella spp., S. enterica, and S. aureus were the dominant hosts of these ARGs and associated mobile genetic elements. Increasing resistance across major antibiotic classes aligned with trends reported across other European countries. This study provides a national-scale in silico comparison of AMR across pathogens and One Health sectors using publicly available genomic data. The findings help reinforce Ireland's AMR surveillance by showing which resistance genes are present and how they spread across critical pathogens in humans, animals, and the environment. These findings highlight the urgent need for improved antibiotic stewardship and integrated One Health surveillance to limit the emergence and spread of AMR.IMPORTANCEAntimicrobial resistance (AMR) is a growing threat to human, animal, and environmental health. This study used publicly available genomic data to identify antimicrobial resistance genes (ARGs) in key bacterial pathogens circulating in Ireland. By analyzing over 11,000 genomes from humans, animals, and the environment, we found that several dangerous resistance genes, including those against last-resort antibiotics, were widespread across different sources. The study highlights which bacteria and resistance genes are most critical and how they may spread between humans, animals, and the environment. These insights provide a national snapshot of AMR, supporting more effective monitoring and prevention strategies. By revealing patterns of resistance and modes of transmission, our findings underscore the importance of coordinated antibiotic stewardship and One Health approaches to slow the emergence and spread of resistant infections, protecting public health and ensuring antibiotics remain effective.

Humans↗

PubMed1998

Pathogenicity of Mycoplasma synoviae in broiler chickens.

Six isolates of Mycoplasma synoviae, identified as WVU 1853, K1968, K1858, 92D8034, F10-2AS, and FMT, were compared for pathogenicity in broiler chickens. Specific-pathogen-free chickens were inoculated, in two groups of 20, with each isolate by footpad or eyedrop inoculation at 1 day of age and were examined at necropsy 7, 14, 28, and 42 days postinoculation. Specimens were taken for histopathology, culture, polymerase chain reaction assay, and hemagglutination-inhibition serology. Isolates were grouped according to pathogenicity on the basis of differences in lesion development and tissue distribution in the respiratory system, other viscera, and the skeletal system. K1968 (pathogenic) induced lesions in all sites examined in both the footpad and eyedrop inoculation groups. It was detected in all sites following footpad inoculation and in all sites except viscera following eyedrop inoculation. WVU 1853, K1858, and 92D8034 (moderately pathogenic) induced lesions and were detected in all sites following footpad inoculation. With eyedrop inoculation, lesions were identified only in upper and lower respiratory sites, and organisms were detected only in upper respiratory sites. F10-2AS (moderately pathogenic) was similar; however, footpad inoculation failed to induce visceral lesions or permit organism detection in any site. F10-2AS was detected in upper and lower respiratory tissues following eyedrop inoculation. FMT (mildly pathogenic) induced only upper respiratory lesions when either footpad or eyedrop inoculation was used, and detection was restricted to upper respiratory sites following eyedrop inoculation. These results are useful in comparative evaluations of the virulence of other M. synoviae isolates and form a basis for characterization of virulence factors of M. synoviae.

Air Sacs↗

PubMed2004

Axonal transport and neuronal transcytosis of trophic factors, tracers, and pathogens.

Neurons can specifically internalize macromolecules, such as trophic factors, lectins, toxins, and other pathogens. Upon internalization in terminals, proteins can move retrogradely along axons, or, upon internalization at somatodendritic domains, they can move into an anterograde axonal transport pathway. Release of internalized proteins from neurons after either retrograde or anterograde axonal transport results in transcytosis and trafficking of proteins across multiple synapses. Recent studies of binding properties of several such proteins suggest that pathogens and lectins may utilize existing transport machineries designed for trafficking of trophic factors. Specific pathways may protect trophic factors, pathogens, and toxins from degradation after internalization and may target the trophic or pathogenic cargo for transcytosis after either retrograde or anterograde transport along axons. Elucidating the molecular mechanisms of sorting steps and transport pathways will further our understanding of trophic signaling and could be relevant for an understanding and possible treatment of neurological diseases such as rabies, Alzheimer's disease, and prion encephalopathies. At present, our knowledge is remarkably sparse about the types of receptors used by pathogens for trafficking, the signals that sort trophins or pathogens into recycling or degradation pathways, and the mechanisms that regulate their release from somatodendritic domains or axon terminals. This review intends to draw attention to potential convergences and parallels in trafficking of trophic and pathogenic proteins. It discusses axonal transport/trafficking mechanisms that may help to understand and eventually treat neurological diseases by targeted drug delivery.

Animals↗

PubMed1995

Interdependence of pathogenicity and replicability with potato spindle tuber viroid.

After the unexpected appearance of lethal symptoms on tomato plants infected with the PSTVd strain Intermediate Di, viroids were isolated and sequenced. It was found that a new strain, named RG 1, had been generated spontaneously in our greenhouse. In a different series of plant passages two new strains, named QF A and QF B, were detected which coexisted with the wild-type strain Di. Strains QF A and QF B showed intermediate symptoms when inoculated separately. In order to confirm the working hypothesis that the more pathogenic strain outcompetes the less pathogenic strain but strains of similar pathogenicity might coexist in the host, strains of different pathogenicity were mixed for inoculation in a ratio from 1:1 to 1:100 (more pathogenic:less pathogenic). The concentrations of the individual strains were determined 6 weeks postinfection with the method of nondenaturing polyacrylamide gel electrophoresis, and the working hypothesis was confirmed. The total concentrations of viroids in infected plants were very similar, irrespective of whether severe, intermediate, or mild strains or mixtures of different strains were present. The mutations in all new strains (3 in RG 1, 2 in QF A, 3 in QF B) were located in the so-called virulence-modulating region. The mutations of strain RG 1 influenced dramatically the thermodynamic stability of the native rod-like structure, as determined experimentally by temperature-gradient gel electrophoresis. Since during replication a multihairpin structure is generated transiently which is transformed afterwards into the rod-like structure, a lower thermodynamic stability of the rod-like structure leads to a higher accumulation of the transient structure. It is assumed that the transient structure, which is active in replication as shown earlier, is essential also in pathogenesis. This model explains the experimentally determined interdependence between pathogenicity and replicability of PSTVd strains.

Base Sequence↗

PubMed1999

Role of hemagglutinin cleavage for the pathogenicity of influenza virus.

Although human epidemics of influenza occur on nearly an annual basis and result in a significant number of "excess deaths," the viruses responsible are not generally considered highly pathogenic. On occasion, however, an outbreak occurs that demonstrates the potential lethality of influenza viruses. The human pandemic of 1918 spread worldwide and killed millions, and the limited human outbreak of highly pathogenic avian viruses in Hong Kong at the end of 1997 is a warning that this could happen again. In avian species such as chickens and turkeys, several outbreaks of highly pathogenic influenza viruses have been documented. Although the reason for the lethality of the human 1918 viruses remains unclear, the pathogenicity of the avian viruses, including those that caused the human 1997 outbreak, relates primarily to properties of the hemagglutinin glycoprotein (HA). Cleavage of the HA precursor molecule HA0 is required to activate virus infectivity, and the distribution of activating proteases in the host is one of the determinants of tropism and, as such, pathogenicity. The HAs of mammalian and nonpathogenic avian viruses are cleaved extracellularly, which limits their spread in hosts to tissues where the appropriate proteases are encountered. On the other hand, the HAs of pathogenic viruses are cleaved intracellularly by ubiquitously occurring proteases and therefore have the capacity to infect various cell types and cause systemic infections. The x-ray crystal structure of HA0 has been solved recently and shows that the cleavage site forms a loop that extends from the surface of the molecule, and it is the composition and structure of the cleavage loop region that dictate the range of proteases that can potentially activate infectivity. Here influenza virus pathogenicity is discussed, with an emphasis on the role of HA0 cleavage as a determining factor.

Animals↗

PubMed2002

Investigation of Maize streak virus pathogenicity determinants using chimaeric genomes.

Genes and intergenic regions were reciprocally exchanged between a highly pathogenic Maize streak virus (MSV) isolate (MSV-MatA) and three less pathogenic isolates (MSV-Kom, MSV-R2, and MSV-VW) to determine the contribution of individual genome constituents to MSV pathogenicity in maize. Comparison of disease symptoms produced by the 54 resulting chimaeras and parental viruses enabled identification of genome constituents that are primarily responsible for the heightened pathogenicity of MSV-MatA in maize. Whereas pathogenicity determinants were detected in all of the MSV genomic regions examined, generally only chimaeras containing the MSV-MatA long intergenic region, coat protein gene, and/or movement protein gene were more pathogenic than the milder MSV isolates from which most of their genomes were derived. The pathogenicity of chimeras was strongly influenced by the relatedness of their parental viruses and evidence was found of nucleotide sequence-dependent interactions between both coding and intergenic regions.

Chimera↗

PubMed1995

Seasonal distribution of pathogenic free-living amebae in Oklahoma waters.

Pathogenic free-living amebae cause serious human disease, including infection of the eye and the central nervous system. The purpose of this study was to sample aquatic environments in the Tulsa, Oklahoma, area year-round for the presence of these disease-causing amebae. A total of 34 pathogenic isolates were obtained from 2,016 processed water and swab samples. Pathogenicity was determined by the ability of amebae to cause death in mice after intranasal inoculation. Pathogenic amebae were isolated during every month of the year and were identified as Naegleria australiensis (38%), Acanthamoeba species (35%), N. fowleri (18%), and leptomyxid amebae (9%). Pathogenic leptomyxids have not previously been reported from the environment. The greatest percentage of recovery of pathogens occurred during the spring and autumn. The prevalence of pathogenic free-living amebae in the sampled waters was 1 pathogen/3.4 l water.

Acanthamoeba↗

PubMed1991

Causative role of Yersinia and other enteric pathogens in the appendicular syndrome.

In 2,861 consecutive patients undergoing appendicectomy for clinically suspected appendicitis an enteric pathogen was isolated from the appendix in almost 7% using an optimal combination of culture media. The pathogenic Yersinia enterocolitica serotypes 03 and 09 predominated (3.6%), followed by Campylobacter and nontyphoid Salmonella. The same pathogen was isolated from the stool in 72.5% of patients with a culture-positive appendix and in 84.1% of those positive for a pathogenic Yersinia. Conversely, no pathogenic Yersinia were isolated in 326 gynaecologic control patients, in whom a normal appendix was removed. No frank appendicitis but mesenteric adenitis and/or terminal ileitis were found in 62.3% of 138 patients with a culture positive appendix, and in 74.6% of those positive for a pathogenic Yersinia. Histologic findings available in 135 patients showed acute suppurative appendicitis in only six (4.5%) patients, and in only one of 73 (1.4%) positive for a pathogenic Yersinia. In contrast, 46.8% of a group of 345 culture-negative appendices showed acute inflammation. A positive stool culture in a patient with suspected appendicitis, if consistent with sonographic and clinical findings, should be taken as strong evidence against the presence of true appendicitis.

Adolescent↗

PubMed2003

Actin-related defense mechanism to reject penetration attempt by a non-pathogen is maintained in tobacco BY-2 cells.

The actin cytoskeleton is a key player in defense responses during early stages of infection by fungal pathogens. To investigate molecular mechanisms of actin-related defense responses, a cultured tobacco ( Nicotiana tabacum L.) BY-2 cell system was devised. When conidia were directly deposited on BY-2 cells, neither a pathogen, Erysiphe cichoracearum, nor a non-pathogen, Erysiphe pisi, was able to form appressoria or haustoria on BY-2 cells. On the other hand, conidia of the powdery mildews formed appressoria on BY-2 cells if they were covered with a thin hydrophobic membrane of Formvar. Percentages of appressoria formation of the powdery mildews on the Formvar-covered BY-2 cells were mostly the same as those on leaf epidermal cells. The pathogen successfully penetrated through the membrane into BY-2 cells and formed haustoria, whereas penetration attempts of the non-pathogen were completely rejected by the BY-2 cells similar to attempts on leaf epidermal cells. On the other hand, when BY-2 cells were treated with actin cytoskeleton-depolymerizing agents, cytochalasins, the non-pathogen became able to penetrate and form haustoria in BY-2 cells. Simultaneously, cytochalasin inhibited callose deposition at penetration sites of the non-pathogen. These results demonstrated that the actin cytoskeleton plays an important role in defense mechanisms against fungal penetration, even in the dedifferentiated cultured cells. The newly devised Formvar-covered cultured cell system will be a useful tool for molecular dissection of signal perception and defense mechanisms of plant cells during the early stage of fungal attack.

Actins↗

PubMed2002

Pathogenic hantaviruses selectively inhibit beta3 integrin directed endothelial cell migration.

Hantaviruses cause two diseases of man, hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Pathogenic and non-pathogenic hantaviruses use beta3 and beta1 integrins, respectively, to enter endothelial cells. Beta3 integrins were recently reported to bind receptors that regulate vascular permeability suggesting that hantavirus beta3 integrin interactions may regulate endothelial cell function and contribute to viral pathogenesis. In this study we investigated the ability of pathogenic and non-pathogenic hantaviruses to regulate beta3 and beta1 integrin directed endothelial cell functions. We found that pathogenic NY-1, SNV, HTN, SEO and PUU viruses blocked endothelial cell migration on beta3, but not beta1, integrin ligands. Migration is similarly inhibited by antibodies to beta3 integrins which selectively block vitronectin directed endothelial cell migration. As a result, the ability of endothelial cells to migrate on integrin ligands was selectively inhibited by only pathogenic hantaviruses. Infection by NY-1 virus inhibited endothelial cell migration as early as 24-48 h post-infection. In contrast, non-pathogenic PH and TUL viruses had no effect on the ability of endothelial cells to migrate on either beta3 or beta1 integrin ligands from 1 to 5 days post-infection. These findings indicate that only hantaviruses which use beta3 integrins, and are associated with HPS and HFRS diseases, functionally dysregulate endothelial cell migration. These findings further demonstrate that hantaviruses regulate only beta3 integrin directed endothelial cell functions and have no effect on beta1 integrin functions. Since beta3 integrins are linked to changes in vascular permeability and the maintenance of vascular integrity, these findings suggest a means by which hantavirus usage and regulation of beta3 integrins may contribute to hantavirus pathogenesis.

Cell Movement↗

PubMed1991

Optimal growth schedule of pathogens within a host: switching between lytic and latent cycles.

We have studied the optimal growth schedule of a pathogen, which maximizes the total number of transmissions from an infected host to other individuals until host death or recovery. It is assumed that both transmission rate f(N) and host mortality increase with the number of pathogens, N. The model predicts that the optimal growth schedule of pathogens strongly depends on the curvature of f(N): If f(N) increases faster than linearly with N, the pathogens should always reproduce at the maximum speed. By contrast, if f(N) saturates with N, the optimal schedule is composed of (1) a brief initial stage of infection, in which the pathogens proliferate at the maximum speed (productive cycle), (2) followed by the long latent period with the "stationary infection level," N* (latent cycle), (3) which may end when the pathogens start rapid proliferation triggered either by the host's senescence ("programmed break") or by the sudden rise in the host's mortality ("incidental break"). The latter may be caused by the double infection of another strain. We also examine the Nash equilibrium schedule of pathogen growth in the presence of multiple infections.

Age Factors↗

PubMed1994

Evaluation of the role of exogenous pathogens on the incidence of embryo loss during early pregnancy in mice.

The mating of CBA/j female mice (H2k) by DBA/2j male mice (H2d) typically results in an elevated incidence of spontaneous embryo loss thus providing an ideal genetically controlled laboratory model for the study of the factors causing early embryo loss during pregnancy. There is now considerable data on the cells and factors involved in fetal resorption but little is known about the events which activate this process. While the activation of the maternal response to the fetal implant could have endogenous or genetic origins, a role for exogenous factors including microbial pathogens could also be involved. In order to investigate these possibilities, the reproductive success of CBA/j female x DBA/2j male matings in a conventional animal care facility were compared with matings in a specific pathogen free (SPF) animal facility. All animals housed under these conditions were routinely screened by immunoassay and culture, for the presence of a number of viral and bacterial pathogens of mice. The incidence of spontaneous embryo loss in specific pathogen free CBA female mice mated by DBA and other male strains was found to be virtually identical to that of CBA female mice infected with multiple viral pathogens and housed under otherwise identical conditions (non-SPF). However, the numbers of implantation per pregnancy was significantly greater in an SPF facility. Therefore, exposure of mating mice to exogenous viral and bacterial pathogens did not appear to alter the overall incidence of spontaneous embryo resorption. It was concluded that the immunomodulatory effects of infection by common murine pathogens neither augmented nor reduced post-implantation embryo losses.

Abortion, Veterinary↗

PubMedDate not supplied

The antigen-specific cell-mediated immune response in mice is suppressed by infection with pathogenic lyssaviruses.

Responsiveness of T cells (RTC) was studied in BALB/c mice intramuscularly infected with various lyssaviruses. After infection by this peripheral route, two types of viruses could be classified according to their effects: 1) pathogenic viruses, including fixed rabies Pasteur virus (serogenotype 1) and wild viruses belonging to serogenotype 1 (from a rabid fox in France and from a cow infected by a vampire bat in Brazil) or to serogenotype 5 (European bat lyssavirus 1); and 2) non-pathogenic viruses, including Mokola virus (serogenotype 3). RTC was tested by analysing in vitro the capacity of splenic T cells from infected BALB/c mice to produce cytokines after antigenic (purified lyssavirus antigens) or polyclonal stimulation (concanavalin A). Cytokine production was followed by assaying the biological activity of interleukin-2 and by testing for interleukin-2, interleukin-4 and interferon-gamma (IL2, IL4 and IFN gamma ) messenger RNAs (mRNA) by transcription into complementary DNA and amplification by the polymerase chain reaction. The initial biologically active IL2 and cytokine mRNA production was observed in mice infected with pathogenic or non-pathogenic lyssaviruses. Only mice with symptoms (infected with pathogenic viruses) lost the capacity to produce cytokines in vitro after antigen-specific stimulation. No such loss was observed after polyclonal stimulation. In mice peripherally infected with non-pathogenic viruses, no loss was observed after stimulation with lyssavirus antigens. Thus, infection with pathogenic lyssaviruses by the peripheral route induces in BALB/c mice a loss of T-cell responsiveness after antigen activation, but not after polyclonal activation.

Animals↗

PubMed2006

Multiple detection of food-borne pathogenic bacteria using a novel 16S rDNA-based oligonucleotide signature chip.

There have been many attempts to develop sensitive and accurate techniques for the detection and diagnosis of pathogenic bacteria using nucleic acid-based technology. To achieve efficient multiple detection of seven selected food-borne pathogens, we assessed the respective 16S rDNA pathogen specific sequences using an oligonucleotide-based signature array. Strategic optimal design of specific capture probes was achieved by using the characteristic first variable region. To assess the specificity of this pathogen detection system, we employed a two-step experimental strategy. Under conditions established through experiments with chemically synthesized model targets comprising both conserved and variable regions of 16S rDNA, we confirmed the validity of this system using real 16S rDNA targets. Detection with real targets was successfully performed using our system, and better specificity was obtained compared to experiments with model targets. Moreover, the subtypes of Vibrio pathogens were successfully classified. We developed a two-dimensional visualization plot tool for positive control and specific spots, which allowed facile and minute differentiation between spot intensities. Repeated array formats were employed to ensure experimental uniformity, and included the statistical p-value criterion for pathogen discrimination. The present results thus indicate that our novel oligonucleotide-based signature chip detection system can be employed for the effective detection of multiple pathogens.

Bacteria↗

PubMed2005

Sclerotinia sclerotiorum: when "to be or not to be" a pathogen?

Sclerotinia sclerotiorum is unusual among necrotrophic pathogens in its requirement for senescent tissues to establish an infection and to complete the life cycle. A model for the infection process has emerged whereby the pathogenic phase is bounded by saprophytic phases; the distinction being that the dead tissues in the latter are generated by the actions of the pathogen. Initial colonization of dead tissue provides nutrients for pathogen establishment and resources to infect healthy plant tissue. The early pathogenicity stage involves production of oxalic acid and the expression of cell wall degrading enzymes, such as specific isoforms of polygalacturonase (SSPG1) and protease (ASPS), at the expanding edge of the lesion. Such activities release small molecules (oligo-galacturonides and peptides) that serve to induce the expression of a second wave of degradative enzymes that collectively bring about the total dissolution of the plant tissue. Oxalic acid and other metabolites and enzymes suppress host defences during the pathogenic phase, while other components initiate host cell death responses leading to the formation of necrotic tissue. The pathogenic phase is followed by a second saprophytic phase, the transition to which is effected by declining cAMP levels as glucose becomes available and further hydrolytic enzyme synthesis is repressed. Low cAMP levels and an acidic environment generated by the secretion of oxalic acid promote sclerotial development and completion of the life cycle. This review brings together histological, biochemical and molecular information gathered over the past several decades to develop this tri-phasic model for infection. In several instances, studies with Botrytis species are drawn upon for supplemental and supportive evidence for this model. In this process, we attempt to outline how the interplay between glucose levels, cAMP and ambient pH serves to coordinate the transition between these phases and dictate the biochemical and developmental events that define them.

Ascomycota↗