In order to clarify the role of PlPMI3 resistance gene in sunflower differential lines D4 for differentiation the pathogenicity in Plasmopara halstedii (sunflower downy mildew), analyses were carried out in two groups including four pathotypes which overcome and do not overcome PlPMI3 (Pl gene has still not been mapped) resistance gene. Based on the reaction for the P. halstedii isolates to sunflower hybrids varying only in Pl resistance genes, there were no virulence differences for the two groups. Index of aggressiveness was calculated for pathogen isolates and revealed the presence of significant differences between isolates of races 304 and 314; however, there were no aggressiveness differences for 7xx races. Regarding the life-history trait and the genetic architecture of the pathogen: there were morphological and genetic variations for the four P. halstedii isolates without a correlation with pathogenic diversity. The importance of the PlPMI3 resistance gene to differentiate the pathogenicity in sunflower downy mildew was discussed.
Phenotypic groups including pathogenic, morphological and genetic characteristics for 50 Plasmopara halstedii (downy mildew) isolates belonging to seven races based on interactions with sunflower plants were revealed. Pathogenicity for pathogen isolates were analysed in sunflower plants showing different levels of resistance. Based on the reaction for the P. halstedii isolates to sunflower hybrids varying only in Pl resistance genes, there were three identified groups based on virulence reaction. Index of aggressiveness was calculated for pathogen isolates and revealed the presence of significant differences between isolates of 100 and 3xx races (more aggressive) and isolates of 710 and 7xx races (less aggressive). Morphological analyses were carried out on zoosporangia and sporangiophores for P. halstedii isolates produced on the surface of cotyledons in sunflower plants infected thought roots. There were no groups based on the morphology of zoosporangia and sporangiophores for pathogen isolates. Genetic relationships were detected between pathogen isolates using 12 EST-derived markers. There was no intra-race genetic variation, but five genetically-identified groups were detected among pathogen isolates of all races. Combining data of pathogen’s variation with variability in sunflower to arrive at durable resistance against P. halstedii was discussed.
biofilm-forming genes and the biofilm phenotype of MR-CoNS isolates were observed. The study also suggests that periodical monitoring of the association and co-occurrence of biofilm forming genes in inducing virulence among clinical isolates in order to
, are important in the pathogenesis of the organism [ 13 ]. In the same way that other pathogenicity islands are necessary for bacterial virulence in a particular animal, Salmonella pathogenicity islands (SPIs) represent substantial gene cassettes in
Enterotoxigenic E. coli (ETEC) bacteria frequently cause watery diarrhoea in newborn and weaned pigs. Plasmids carrying genes of different enterotoxins and fimbrial adhesins, as well as plasmids conferring antimicrobial resistance are of prime importance in the epidemiology and pathogenesis of ETEC. Recent studies have revealed the significance of the porcine ETEC plasmid pTC, carrying tetracycline resistance gene tet(B) with enterotoxin genes. In contrast, the role of tet(A) plasmids in transferring resistance of porcine ETEC is less understood. The objective of the present study was to provide a comparative analysis of antimicrobial resistance and virulence gene profiles of porcine post-weaning ETEC strains representing pork-producing areas in Central Europe and in the USA, with special attention to plasmids carrying the tet(A) gene. Antimicrobial resistance phenotypes and genotypes of 87 porcine ETEC strains isolated from cases of post-weaning diarrhoea in Austria, the Czech Republic, Hungary and the Midwest USA was determined by disk diffusion and by PCR. Central European strains carrying tet(A) or tet(B) were further subjected to molecular characterisation of their tet plasmids. Results indicated that > 90% of the ETEC strains shared a common multidrug resistant (MDR) pattern of sulphamethoxazole (91%), tetracycline (84%) and streptomycin (80%) resistance. Tetracycline resistance was most frequently determined by the tet(B) gene (38%), while tet(A) was identified in 26% of all isolates with wide ranges for both tet gene types between some countries and with class 1 integrons and resistance genes co-transferred by conjugation. The virulence gene profiles included enterotoxin genes (lt, sta and/or stb), as well as adhesin genes (k88/f4, f18). Characterisation of two representative tet(A) plasmids of porcine F18+ ETEC from Central Europe revealed that the IncF plasmid (pES11732) of the Czech strain (~120 kb) carried tet(A) in association with catA1 for chloramphenicol resistance. The IncI1 plasmid (pES2172) of the Hungarian strain (~138 kb) carried tet(A) gene and a class 1 integron with an unusual variable region of 2,735 bp composed by two gene cassettes: estX-aadA1 encoding for streptothricin-spectinomycin/streptomycin resistance exemplifying simultaneous recruitment, assembly and transfer of multidrug resistance genes by the tet(A) plasmid of porcine ETEC. By this we provide the first description of IncF and IncI1 type plasmids of F18+ porcine enterotoxigenic E. coli responsible for cotransfer of the tet(A) gene with multidrug resistance. Additionally, the unusual determinant estX, encoding for streptothricin resistance, is first reported here in porcine enterotoxigenic E. coli.
Serratia marcescens, a Gram-negative bacillus that belongs to the family Enterobacteriaceae, is a human opportunistic pathogen bacterium that causes many diseases, such as urinary tract infections, respiratory tract infections, bacteremia, conjunctivitis, endocarditis, meningitis and wound infections. Many plasmides that confers multi-drug resistance were discovered, such as virulence factors, like cytotoxins that damage epithelial cells. The main topic of this paper presents a review about the molecular traits evolved in the pathogenic processes mediated by Serratia and its mechanism of resistance to drugs.
genes, iv) the emergence of a biofilm specific phenotype [ 9 ]. Biofilm also plays an essential role in increasing the expression of virulence genes, leading to the worsening of the disease [ 10 ]. Additionally, to antibiotic resistance and resistance
The fast evolution of Plasmopara halstedii (downy mildew) remains a major risk for sunflower crop, as new races of the pathogen are bypassing the resistance of sunflower hybrids. In order to understand the processes which led a new virulence to appear in a local P. halstedii population, the genetic relationships were studied using 12 EST (Expressed Sequence Tag)-derived markers between five progeny isolates of races 300, 304, 314, 704 and 714 and two parental ones of races 100 and 710. All genetic analyses were carried out using five single zoosporangium isolates per P. halstedii isolate. There was no intra-isolate genetic variation among the seven pathogen isolates and five multilocus genotypes (MLG) were identified among the 35 P. halstedii single zoosporangium isolates. The single zoosporangium isolates of races 314, 704 and 714 had an intermediary genetic position between the single zoosporangium isolates of two parental isolates. The single zoosporangium isolates of three isolates of races 100, 300 and 304 were localized in the same genetic clade. Two genetic mechanisms could explain the emergence of new virulence in P. halstedii as a recombination between races and mutations in a clonal lineage.