Host- and Tissue-Specific Pathogenic Traits of Staphylococcus aureus

Abstract

Comparative genomics were used to assess genetic differences between Staphylococcus aureus strains derived from infected animals versus colonized or infected humans. A total of 77 veterinary isolates were genetically characterized by high-throughput amplified fragment length polymorphism (AFLP). Bacterial genotypes were introduced in a large AFLP database containing similar information for 1,056 human S. aureus strains. All S. aureus strains isolated from animals in close contact with humans (e.g., pet animals) were predominantly classified in one of the five main clusters of the AFLP database (cluster I). In essence, mastitis-associated strains from animals were categorized separately (cluster IVa) and cosegregated with bacteremia-associated strains from humans. Distribution of only 2 out of 10 different virulence genes differed across the clusters. The gene encoding the toxic shock syndrome protein (tst) was more often encountered among veterinary strains (P < 0.0001) and even more in the mastitis-related strains (P<0.0001) compared to human isolate results. The gene encoding the collagen binding protein (cna) was rarely detected among invasive human strains. The virulence potential, as indicated by the number of virulence genes per strain, did not differ significantly between the human-and animal-related strains. Our data show that invasive infections in pets and humans are usually due to S. aureus strains with the same genetic background. Mastitis-associated S. aureus isolated in diverse farm animal species form a distinct genetic cluster, characterized by an overrepresentation of the toxic shock syndrome toxin superantigen-encoding gene.

Escherichia coli, but notStaphylococcus aureustriggers an early increased expression of factors contributing to the innate immune defense in the udder of the cow

“…However, it is well known that different strains of the same bacterial pathogen species may differ vastly in their genome [20,53]. Indeed, we wanted to establish a model for subclinical mastitis.…”

Methicillin-Resistant and -SusceptibleStaphylococcus aureusSequence Type 398 in Pigs and Humans

“…Spa gene sequencing (13) showed heterogeneity in the ST398 MRSA lineage with types t011 and t108, Figure 1. A) Meta-analysis of the amplifi ed fragment length polymorphism data obtained for the pig-associated methicillin-resistant Staphylococcus aureus sequence type 398 (ST398 MRSA) and its closely related methicillin-susceptible S. aureus (MSSA) strains, carriage MSSA isolates from healthy children and elderly persons, invasive MSSA from hospitalized children and elderly persons, and invasive animal S. aureus isolates (including 2 MRSA isolates) (10,11). Green and red represent 161,700 binary outcomes generated by high throughput restriction fragment length polymorphism with 147 marker fragments.…”

“…We embedded the genetic fi ngerprints of the 46 pigrelated MRSA isolates in the population structure of S. aureus as obtained before (10,11). These studies include high throughput AFLP fi ngerprints of 829 nonclinical S. aureus human carriage isolates and 146 and 77 (including 2 MRSA isolates) clinical isolates of human and animal origin, respectively.…”

“…ST398 MSSA nasal carriage isolates were also identifi ed in several pig farmers in a study by ArmandLefevre et al (1). We describe the population genetic analysis of Dutch community-based and nosocomial MSSA isolates in comparison with pig-and pig farmer-derived ST398 MRSA isolates, performed by spa-sequencing and amplifi ed fragment length polymorphism (AFLP) analysis (10,11).…”

Mapping the genetic diversity within major clonal complexes of meticillin-resistant Staphylococcus aureus utilizing genome-wide fluorescent amplified fragment length polymorphism markers

“…Moreover, whilst FAFLP probably underestimates the level of genetic diversity in accessory regions, it does sample such variable regions and can help facilitate our understanding of the micro-evolution of S. aureus (Melles et al, 2004;van Leeuwen et al, 2005). Existing molecular typing techniques for MRSA may not detect minor variations throughout the genome.…”