Human Pathogen Shown to Cause Disease in the Threatened Eklhorn Coral Acropora palmata

Coral reefs are in severe decline. Infections by the human pathogen Serratia marcescens have contributed to precipitous losses in the common Caribbean elkhorn coral, Acropora palmata, culminating in its listing under the United States Endangered Species Act. During a 2003 outbreak of this coral disease, called acroporid serratiosis (APS), a unique strain of the pathogen, Serratia marcescens strain PDR60, was identified from diseased A. palmata, human wastewater, the non-host coral Siderastrea siderea and the corallivorous snail Coralliophila abbreviata. In order to examine humans as a source and other marine invertebrates as vectors and/or reservoirs of the APS pathogen, challenge experiments were conducted with A. palmata maintained in closed aquaria to determine infectivity of strain PDR60 from reef and wastewater sources. Strain PDR60 from wastewater and diseased A. palmata caused disease signs in elkhorn coral in as little as four and five days, respectively, demonstrating that wastewater is a definitive source of APS and identifying human strain PDR60 as a coral pathogen through fulfillment of Koch's postulates. A. palmata inoculated with strain PDR60 from C. abbreviata showed limited virulence, with one of three inoculated fragments developing APS signs within 13 days. Strain PDR60 from non-host coral S. siderea showed a delayed pathogenic effect, with disease signs developing within an average of 20 days. These results suggest that C. abbreviata and non-host corals may function as reservoirs or vectors of the APS pathogen. Our results provide the first example of a marine “reverse zoonosis” involving the transmission of a human pathogen (S. marcescens) to a marine invertebrate (A. palmata). These findings underscore the interaction between public health practices and environmental health indices such as coral reef survival

Analysis of VanA vancomycin-resistant Enterococcus faecium isolates from Saudi Arabian hospitals reveals the presence of clonal cluster 17 and two new Tn 1546 lineage types

Objectives; The aim of this study was to characterize 34 vancomycin-resistant VanA Enterococcus faecium isolates obtained from two hospitals in Saudi Arabia and to assess Tn 1546 variation within these isolates. Methods: PFGE and multilocus sequence typing (MLST) genotypes, antibiotic susceptibility patterns, the presence of enterococcal surface protein (esp) and hyaluronidase (hyl) genes and conjugation frequencies were determined. In addition, Tn 1546 elements were characterized. Results: PFGE and MLST analysis revealed the presence of 31 and 6 different genotypes, respectively. Further, three new ST types were discovered. Ninety-seven percent (33/34) of the isolates were associated with clonal complex 17 (CC17), with all isolates but one being resistant to ampicillin and all isolates being susceptible to linezolid. The esp and hyl genes were found in 44% (15/34) and 53% (18/34) of the isolates, respectively. Tn 1546 analysis revealed that the isolates belonged to five different groups, including two new lineages. The IS-element insertions described did not abolish the transfer of VanA resistance. Conclusions: VanA vancomycin-resistant E. faecium isolates obtained from Saudi Arabian hospitals include CC17 MLST types, a clonal cluster associated with E. faecium nosocomial infection worldwide. Novel E. faecium MLST types are circulating in Saudi Arabia, as well as novel Tn 1546 types. It seems likely that CC17 E. faecium isolates may be distributed throughout the Middle East as well as Europe, America, Africa and Australia

Host- and Tissue-Specific Pathogenic Traits of Staphylococcus aureus

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