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PubMed2004

Characterisation and differentiation of pathogenic and non-pathogenic Acanthamoeba strains by their protein and antigen profiles.

Free-living amoebae of the genus Acanthamoeba are the causative agents of Acanthamoeba keratitis (AK) and granulomatous amoebic encephalitis. Acanthamoebae occur ubiquitously in the environment and are thus a constant cause of antigenic stimulation. In a previous study we have shown that compared to control sera, AK patients exhibit markedly lower immunoreactivities to whole cell antigen of Acanthamoeba spp. As the pathogenicity of acanthamoebae primarily relies on the excretion of proteins, it was the aim of the present study to investigate the immunoreactivity of metabolic antigen from different Acanthamoeba strains of varying pathogenicity. Three Acanthamoeba strains, one highly pathogenic, one non-pathogenic but thermophilic and one non-thermophilic non-pathogenic, were used for antigen extraction. The antigen was harvested before and after contact with human cells and all strains were tested with AK sera and with sera from healthy individuals. It was shown that the somatic protein profiles of the Acanthamoeba strains correlated to the morphological groups, and that within morphological group II-the group associated with AK-the profiles of the metabolic antigens correlated to strain pathogenicity. Moreover, it was shown that the control sera showed markedly higher immunoreactivities than the sera of the AK patients and that this immunoreactivity was generally higher to the non-pathogenic strains than to the pathogenic strain. Altogether our results once again raise the question of whether there is an immunological predisposition in AK. To our knowledge this is the first study on the immunoreactivity of metabolic antigen of acanthamoebae.

Acanthamoeba↗
PubMed1986

Cell-cell recognition of host surfaces by pathogens. The adsorption of maize (Zea mays) root mucilage by surfaces of pathogenic fungi.

The adsorption of radioactive mucilage by pathogenic fungi was shown to be dependent upon time, the composition of mucilage, the type of fungal surface (conidia, hyphae, hyphal apices), fungal species, pH and bivalent cations. All fungal adhesins were inactivated by either proteinase or polysaccharase treatments. Adsorption was not inhibited by the numberous mono-, di- and oligo-saccharides that were tested individually, but it was inhibited absolutely by several polysaccharides. This suggested that adsorption of mucilage by pathogens involved conformational and ionic interactions between plant and fungal polymers but not fungal lectins bound to sugar residues of mucilage. Several fractionation schemes showed that pathogens bound only the most acidic of the variety of polymers that comprise mucilage. There was not any absolute distinction between ability to bind radioactive mucilage and type of pathogen or non-pathogen. However, there were notable differences in characteristics of adsorption between two types of pathogen. Differences were revealed by comparison of the adsorption capacities of conidia and germinant conidia and chromatography of radioactive mucilage on germinant conidia. An ectotrophic root-infecting fungus (a highly specialized pathogen) bound a greater proportion of mucilage than did a vascular-wilt fungus (of catholic host and tissue range) with more than one class of site for adsorption. In contrast with the vascular-wilt fungus, sites for adsorption on the specialized pathogen were present solely on surfaces formed by germination.

Adsorption↗
PubMed1990

Pathogenic and non-pathogenic zymodemes of Entamoeba histolytica in a rural area of Mexico. Concordance with serology.

OBJECTIVES: a) to describe the frequency of pathogenic and nonpathogenic zymodemes of E. histolytica in asymptomatic carriers in rural Mexico, b) to identify the isoenzymatic pattern of the zymodemes and c) to measure the concordance of pathogenic zymodemes and positive serology. DESIGN: Descriptive cross-sectional survey. Reference population: rural communities of the mexican highlands. STUDY UNITS: 2048 individuals from 341 families of 5 rural communities. METHODS: From the local census of each community, 70 to 100 families were selected by random sampling. All members of each family were studied. After obtaining the consent the following activities were done: a) filling of a questionnaire about housing and sanitary condition and structure of the family; age, sex, literacy and digestive symptoms and illness during the previous 4 weeks, in each individual; b) a blood sample for serology (CEIP and IHA) and c) a stool sample for coproparasitoscopic analysis (CPS) and zymodemes identification, in each individual. Statistical evaluation was done by kappa index and receiving operating curves (ROC). MAIN RESULTS: there were 122/1730 (7.1%) CPS studies positive to E histolytica cysts, 100/1730 (5.8%) zymodemes isolated and 137/1886 (7.3%) positive serologic studies. Of the 100 zymodemes 30 had a pathogenic pattern, three had a mixture (pathogenic/nonpathogenic) and 67 had a non-pathogenic patterns. There were two (XVII, XVIII) patterns described for the first time in Mexico. Concordance between pathogenic zymodemes and positive serology (IHA greater than 1:128) was very low, Kappa = 0.05. ROC curves for IHA in pathogenic and non-pathogenic zymodemes showed little relationship between positive serology and pathogenic pattern. CONCLUSIONS: Although the frequency of positive serology, coproparasitoscopic studies and zymodemes identification was similar, the concordance between serology and the coprologic studies was very low. This disagrees with other reports, and deserves further investigation using methodologic standards in design.

Animals↗
PubMed1992

Computer analysis of the amino acid sequences in gp41 of apathogenic African green monkey (AGM) virus, less pathogenic HIV-2 and highly pathogenic SIV and HIV-1 lentiviruses.

The bestfit computer program was used to compare the amino acid sequence of the gp160 envelope glycoprotein of an apathogenic AGM and the pathogenic SIVAGM monkey lentiviruses. It was found that the gp120 envelope glycoproteins of these viruses resembled each other in their functional domains. However, an insert of 40 amino acids was found in the gp41 envelope glycoproteins of the pathogenic SIVAGM virus in the amino acid sequence between the membrane anchoring sequence and the carboxyterminus. The insert introduced a new "RRIR" proteolytic cleavage signal into gp41. Comparing HIV-1 gp41 to that of the pathogenic SIVAGM virus revealed that the HIV-1 sequence contains an "RR" sequence that also serves as a signal for proteolytic cleavage. Comparing HIV-2 gp41 to the apathogenic and pathogenic simian immunodeficiency viruses revealed that HIV-2 gp41 lacks the above proteolytic cleavage signal. It is hypothesized that the pathogenic human and simian immunodeficiency lentiviruses can be proteolytically cleaved at the carboxyterminus of gp41, releasing two peptides: a) an "immunodeficiency" 58 amino acid peptide and b) an IL-2-like peptide. The apathogenic AGM virus and the less pathogenic HIV-2 lack one proteolytic cleavage signal in the gp41 amino acid sequence and therefore can release only the IL-2-like peptide but not the "immunodeficiency" peptide. If indeed the pathogenic SIVAGM and HIV-1 do release an "immunodeficiency" peptide, then such a peptide can be regarded as a toxin. Immunization of healthy individuals or HIV-1 patients against the toxic effect of the viral gp41 toxic peptide might prevent damage to the immune system when the virus reactivation leads to ARC and AIDS in infected individuals. Synthetic peptides modeled according to the immunodeficiency peptide (the toxin) can be used to produce anti-toxin antibodies in healthy HIV-1 infected individuals. Such anti-toxin antibodies can be used for passive immunization of AIDS patients or for active immunization of HIV-1 positive individuals prior to ARC or AIDS.

Amino Acid Sequence↗
PubMed2000

Chromosome structure and sequence organization between pathogenic and non-pathogenic Leishmania spp.

We have used a chromosome fragmentation strategy based on systematic genomic insertions of the rare cutting yeast I-SceI endonuclease to assess structure and sequence organization of homologous chromosomes between evolutionary divergent pathogenic and non-pathogenic Leishmania species. This method was combined to physical mapping and hybridization studies using a number of specific chromosomal markers as probes. Our studies have concentrated on two different chromosomes of Leishmania major (L. major), L. donovani and L. infantum and of the non-pathogenic species L. tarentolae. Specific chromosome fragmentation events at the level of multiple I-SccI genomic integrations indicated that very similar distances separated internal genomic sequences between homologous chromosomes and that distances from chromosome ends were more variable. The order and orientation of genes along the homologous chromosomes were also conserved between species. With only few exceptions, genome organization between pathogenic and non-pathogenic Leishmania species was found to be highly conserved. Genomic comparison of pathogenic and non-pathogenic species may be useful for depicting regions involved in species-specific related pathologies.

Animals↗
PubMed2002

Do plant and human pathogens have a common pathogenicity strategy?

Recently, a novel 'two-step' model of pathogenicity has been described that suggests host-cell-derived vasculoproliferative factors play a crucial role in the pathogenesis of bacillary angiomatosis, a disease caused by the human pathogenic bacterium Bartonella henselae. The resulting proliferation of endothelial cells could be interpreted as bacterial pathogens triggering the promotion of their own habitat: the host cell. Similar disease mechanisms are well known in the plant pathogen Agrobacterium tumefaciens, which causes crown gall disease. There are notable similarities between the pathogenicity of A. tumefaciens leading to tumourous disease in plants and to the B. henselae-triggered proliferation of endothelial cells in humans. Here, we hypothesize that this pathogenicity strategy might be common to several bacterial species in different hosts owing to shared pathogenicity factors.

Agrobacterium tumefaciens↗
PubMed2002

Host-pathogen interactions: Host resistance factor Nramp1 up-regulates the expression of Salmonella pathogenicity island-2 virulence genes.

Nramp1 (Natural resistance-associated macrophage protein-1; also known as Slc11a1) is a host resistance gene that provides protection against several intracellular pathogens, including Salmonella enterica serovar Typhimurium. Little is known about the dynamic interplay that occurs between mammalian host resistance determinants such as Nramp1 and pathogens during infection. To explore these interactions, we examined the effect of Nramp1 on expression of Salmonella typhimurium (STM) virulence factors. We demonstrate that Salmonella pathogenicity island 2 (SPI2) is essential for replication of STM in spleens of infected Nramp1(+/+) mice. Furthermore, the presence of Nramp1 in transfected cell lines and congenic knockout mice resulted in the up-regulation of STM SPI2-associated virulence genes critical for intramacrophage survival. This Nramp1-dependent up-regulation of SPI2 was mimicked in vitro by chelation of iron, demonstrating the iron-responsive nature of expression of STM SPI2-associated virulence genes. We propose that acquisition of SPI2 by S. enterica not only enabled this bacterium to become an effective intracellular pathogen but also allowed the bacterium to withstand the effects of macrophage defense mechanisms such as Nramp1 early in the evolution of its pathogenic character. These dynamic Nramp1-pathogen interactions may be essential for regulating the course of an infection. This study demonstrates the presence of a previously undescribed direct influence of a mammalian innate host resistance locus on a pathogen at the genetic level.

2,2'-Dipyridyl↗
PubMed2000

Protective immune responses induced by a non-pathogenic simian/human immunodeficiency virus (SHIV) against a challenge of a pathogenic SHIV in monkeys.

A simian/human immunodeficiency virus (SHIV)-NM3n containing the human nef, but not the monkey nef, and vpr genes of SIV was inoculated into two cynomolgus monkeys, resulting in systemic infection with a minimum level of transient virus load. In order to study the nature of immune responses associated with the prevention of a pathogenic SHIV, the SHIV-NM3n-inoculated monkeys and three naive monkeys were intravenously challenged with a pathogenic SHIV containing the envelope gene of HIV-1 89.6. After the heterologous virus challenge, all of the SHIV-NM3n-inoculated animals completely avoided the loss of CD4+ T lymphocytes in PBMC as well as lymphoid tissues compared to pathogenic SHIV-injected control animals. The inhibition of CD4+ cell depletion was associated with maintaining the proliferative response of helper T-cells against SIV p27 in the previously nonpathogenic virus-inoculated animals following the pathogenic virus challenge. Furthermore, the decline of CD28+ cells, the increase in CD95+ cells, and the enhancement of in vitro apoptosis in PBMC were inhibited in the non-pathogenic virus-inoculated animals. These results suggest that nonpathogenic SHIV-NM3n infection induces the protection of monkeys from heterologous pathogenic viruses that may be associated with blocking the change in immune responses and the cell loss induced by a pathogenic virus.

AIDS Vaccines↗
PubMed1996

Pathogenicity islands and the evolution of bacterial pathogens.

The term pathogenicity island has been used to refer to large chromosomal regions in pathogenic bacteria that encode virulence genes. This article reviews the recent history of this term and considers what characteristics define a pathogenicity island. It appears that pathogenicity islands can confer complex virulence phenotypes and were acquired by bacteria from unrelated organisms, leading to interesting hypotheses about how bacterial pathogens evolved. It is likely that mechanisms that generate pathogenicity islands continue to operate and may contribute to the emergence of bacterial pathogens with new virulence properties.

Bacteria↗
PubMed2026

Dynamics of antibiotic resistance genes co-occurrence with pathogenic and non-pathogenic bacteria throughout wastewater treatment processes.

Wastewater treatment plants (WWTPs) are recognized hotspots for antibiotic resistance genes (ARGs) and pathogenic bacteria. Despite advancements in treatment technologies, the persistence of ARGs and pathogenic bacteria remains a concern. In this study, we analyzed the dynamic changes in ARGs and bacterial communities throughout the treatment processes within an anaerobic-anoxic-oxic (AAO) WWTP over one week by using HT-qPCR coupled with 16S rRNA gene amplicon sequencing. The connectedness index, based on network analysis, showed that the dynamics of ARGs and mobile genetic elements (MGEs) were more strongly associated with potentially pathogenic bacteria than with non-pathogenic bacteria, suggesting that ARG immigration and dissemination in the WWTP were likely driven by potentially pathogenic taxa. The AAO treatment significantly reduced ARGs in final effluent (EF) (∼64 %) and residual sludge (RS) (∼81 %); however, potential hosts of ARGs such as Comamonas testosteroni and Clostridioides difficile persisted with minimal changes in relative abundance and remained detectable in EF and RS. Notably, the abundance of ARGs was lower in RS than in EF, and source tracking analysis identified influent as the primary source of ARGs and potentially pathogenic taxa in EF, underscoring the greater health risks associated with effluent discharge.

Wastewater↗
PubMed2003

Host plant-dependent phenotypic reversion of Ralstonia solanacearum from non-pathogenic to pathogenic forms via alterations in the phcA gene.

Ralstonia solanacearum is a plant pathogenic bacterium that undergoes a spontaneous phenotypic conversion (PC) from a wild-type pathogenic to a non-pathogenic form. PC is often associated with mutations in phcA, which is a key virulence regulatory gene. Until now, reversion to the wild-type pathogenic form has not been observed for PC variants and the biological significance of PC has been questioned. In this study, we characterized various alterations in phcA (eight IS element insertions, three tandem duplications, seven deletions and a base substitution) in 19 PC mutants from the model strain GMI1000. In five of these variants, reversion to the pathogenic form was observed in planta, while no reversion was ever noticed in vitro whatever culture media used. However, reversion was observed for a 64 bp tandem duplication in vitro in the presence of tomato root exudate. This is the first report showing a complete cycle of phenotypic conversion/reversion in a plant pathogenic bacterium.

Bacterial Proteins↗
PubMed1998

Prevalence of the "high-pathogenicity island" of Yersinia species among Escherichia coli strains that are pathogenic to humans.

The fyuA-irp gene cluster contributes to the virulence of highly pathogenic Yersinia (Yersinia pestis, Yersinia pseudotuberculosis, and Yersinia enterocolitica 1B). The cluster encodes an iron uptake system mediated by the siderophore yersiniabactin and reveals features of a pathogenicity island. Two evolutionary lineages of this "high pathogenicity island" (HPI) can be distinguished on the basis of DNA sequence comparison: a Y. pestis group and a Y. enterocolitica group. In this study we demonstrate that the HPI of the Y. pestis evolutionary group is disseminated among species of the family Enterobacteriaceae which are pathogenic to humans. It prevails in enteroaggregative Escherichia coli and in E. coli blood culture isolates (93 and 80%, respectively), but is rarely found in enteropathogenic E. coli, enteroinvasive E. coli, and enterotoxigenic E. coli isolates. In contrast, the HPI was absent from enterohemorrhagic E. coli, Shigella, and Salmonella enterica strains investigated. Polypeptides encoded by the fyuA, irp1, and irp2 genes located on the HPI could be detected in E. coli strains pathogenic to humans. However, these E. coli strains showed a reduced sensitivity to the bacteriocin pesticin, whose uptake is mediated by the FyuA receptor. Escherichia strains do not possess the hms gene locus thought to be a part of the HPI of Y. pestis. Deletions of the juA-irp gene cluster affecting solely the fyuA part of the HPI were identified in 3% of the E. coli strains tested. These results suggest horizontal transfer of the HPI between Y. pestis and some pathogenic E. coli strains.

Bacterial Outer Membrane Proteins↗
PubMed2002

Animal health and foodborne pathogens: enterohaemorrhagic O157:H7 strains and other pathogenic Escherichia coli virotypes (EPEC, ETEC, EIEC, EHEC).

The majority of interactions between microorganisms and animals are based on convenient relations for both of them. Symbiotic microorganisms, like intestinal microbiota, produce important vitamins for animals and protects them from putative pathogens. In general, for monogastric animals, the main contribution of intestinal microorganisms is to supply with growth factors the animal diet, and in some cases they are responsible for providing essential vitamins (e.g. vitamin K). Some particular and relatively few microbes like viruses, bacteria, fungi, protozoa and algae are responsible for animal illness. Because microorganisms are easily dispersed, display physiological diversity, and tolerate extreme conditions, they are ubiquitous and may contaminate and grow in many products, including food and raw materials. Foodborne diseases are caused by consumption of contaminated food or beverages. Many different disease-causing pathogens can contaminate food, so there are many different foodborne infections. In addition, poisonous chemicals and biological toxins can cause disease if they are present in food. To know how a particular disease is spreading is an important matter to take appropriate steps to stop it. For example Escherichia coli O157:H7 infections can spread through contaminated food (meat, vegetables, cheese, etc.), contaminated drinking water or juices, contaminated swimming water and from person to person. Among foodborne pathogens, the most frequently detected are bacteria, but also parasitic protozoa and worms, viruses, natural toxins and other pathogenic agents like prions are important agents for foodborne diseases. Particular pathogenic types of E. coli, classified by their specific pathogenic mechanisms (toxins, adhesins, invasiveness, etc.) are actually known as E. coli virotypes. Enterohaemorrhagic E. coli (EHEC), which constitute the main part of this review, were also named verotoxigenic E. coli (VTEC) or Shiga toxigenic E. coli (STEC). EHEC strains cause haemorrhagic colitis (HC), haemolytic uremic syndrome (HUS) and thrombotic thrombocytopaenic purpura (TP) in humans. They synthetize shigatoxins (verotoxins) which are potent cytotoxic substances, adherence factors and enterohaemolysin. EHEC are responsible for many outbreaks of bloody diarrhoea caused by contaminated foods: beef, milk, fruits, juice, water, etc. The most important serogroups among EHEC are O26, O111 and O157, being O157:H7 the most relevant serotype in foodborne outbreaks. The normal intestinal microflora of cattle was found to be the most relevant reservoir of EHEC strains.

Animals↗
PubMed1988

Effect of naturally occurring intramammary infections by minor pathogens on new infections by major pathogens in cattle.

New mammary infections were recorded in 3 dairy herds during a lactation period by bacteriologic examination of milk samples at 3-week intervals. Influences of the infection status of quarters at the time of new infection and of microorganisms responsible for bacterial invasion were analyzed. The new infection rate in uninfected quarters was about 3 times the rate in quarters already harboring bacterial considered minor pathogens (coagulase-negative staphylococci and Corynebacterium bovis) or major pathogens (Staphylococcus aureus, streptococci). The frequency of new infections with major pathogens was almost halved by preexisting infections with minor pathogens (P = 0.05), mainly because of coagulase-negative staphylococci (P = 0.05) and, to a lesser extent, C bovis (P = 0.19). New infections by minor pathogens also were less frequent in quarters harboring a major pathogen (P less than 0.05), indicating that the competition or antagonism between mammary infections was a general phenomenon.

Animals↗
PubMed1985

In vivo interference between pathogenic and non-pathogenic viruses.

The interference among viruses is a well-documented biological phenomenon, both in animals and tissue culture systems. In two of our previous in vivo experiments and in four independent animal experiments, which are described in this presentation, interferences were successfully used to influence the outcomes of viral diseases by using non-pathogenic viruses. In this study, four pathogenic viruses were studied in their natural hosts, and against these viruses, in different combinations, 15 non-pathogenic viruses were tested. There was great variation in mutual effects among pathogenic and non-pathogenic viruses. In our four experiments, the viruses were either simultaneously inoculated or the non-pathogenic viruses were preinoculated. Newcastle disease vaccine (Strain H) had remarkable effects in the development of mouse ascites-associated lymphoma virus. The 50% mortality rate in mice caused by a vaccine strain of rabies virus was reduced to 15% using avian encephalitis virus. The clinical manifestations of rabbit myxoma virus effects were significantly delayed by Newcastle disease vaccine (Strain H). The 72% mortality rate due to Rous sarcoma virus in chickens was decreased to 33.3% when the animals were preinoculated with avian bursa virus vaccine.

Animals↗
PubMed2003

DNA microarray for discrimination between pathogenic 0157:H7 EDL933 and non-pathogenic Escherichia coli strains.

The primary technique currently used to detect biological agents is based on immunoassays. Although sensitive and specific, currently employed immunoassays generally rely on the detection of a single epitope, and therefore often cannot discriminate subtle strain-specific differences. Since DNA microarrays can hybridize hundreds to thousands of genomic targets simultaneously and do not rely on phenotypic expression of these genetic features for identification purposes, they have enormous potential to provide inexpensive, flexible and specific strain-specific detection and identification of pathogens. In this study, pathogenic Escherichia coli O157:H7-specific genes, non-pathogenic K12-specific genes, common E. coli genes, and negative control genes were polymerase chain reaction-amplified and spotted onto the surface of treated glass slides. After labeled bacterial cDNA samples were hybridized with probes on the microarray, specific fluorescence patterns were obtained, enabling identification of pathogenic E. coli O157:H7 and non-pathogenic E. coli K12. To test the utility of this microarray device to detect genetically engineered bacteria, E. coli BL21 (a B strain derivative with antibiotic resistance gene, ampR) and E. coli JM107 (a K12 strain derivative lacking the gene ompT) were also employed. The array successfully confirmed the strain genotypes and demonstrated that antibiotic resistance can also be detected. The ability to assess multiple data points makes this array method more efficient and accurate than a typical immunoassay, which detects a single protein product.

Colony Count, Microbial↗
PubMed2003

Three pathogen-inducible genes encoding lipid transfer protein from pepper are differentially activated by pathogens, abiotic, and environmental stresses.

The three cDNA clones, CALTPI, CALTPII, and CALTPIII, corresponding to pepper lipid transfer protein (LTP) genes were isolated from a pepper (Capsicum annuum) cDNA library from hypersensitive response (HR) lesions of leaves infected with Xanthomonas campestris pv. vesicatoria. The CALTP genes are well conserved in their coding region with 57-72% identity at the amino acid level, but display 72-83% identity at the nucleotide sequence level. The transcripts of the three CALTP genes differentially accumulated in pepper leaf, stem, and fruit tissues infected by X. campestris pv. vesicatoria, Phytophthora capsici and Colletotrichum gloeosporioides. The CALTP genes were also strongly induced in the systemic, upper leaves after immunization on lower leaves by either pathogenic or non-pathogenic bacteria. In situ hybridization results showed that the CALTPI mRNA was localized in phloem cells of vascular tissues in pepper leaf, stem and fruit tissues after pathogen infection. CALTPI and CALTPIII genes were predominantly expressed in various pepper tissues infected by pathogens, while infection by P. capsici and C. gloeosporioides did not induce the transcription of the CALTPII gene. Ethylene, methyl jasmonate and abscisic acid induced CALTPI and III gene expression in pepper leaves. Drought, high salinity, low temperature and wounding stresses also induced the expression of the CALTPI and CALTPIII genes in a similar manner. In contrast, only high salinity induced the CALTPII expression that was not generally affected by abiotic and other environmental stimuli. When compared with each other and with LTPs from other plants, CALTPI is more distantly related than CALTPII and CALTPIII sequences, indicating that the three pepper CALTP genes represent two different classes. These results thus show that CALTPI and CALTPIII genes, although different in sequence structure, are transcriptionally activated in pepper tissues by pathogen infection as well as abiotic and environmental stresses.

Journal Article↗