Pathogenic Characteristics of Staphylococcus aureus Endovascular Infection Isolates from Different Clonal Complexes

Abstract

Staphylococcus aureus is a major cause of bacteremia and, even with appropriate clinical management, causes high morbidity, and mortality due to its involvement in endovascular complications and metastatic infections. Through different pathogenic in vivo and in vitro models we investigated the behavior of S. aureus most relevant clonal complexes (CCs) causing endovascular complications. We analyzed 14 S. aureus strains representing CC5, CC8, CC15, CC30, and CC45 that caused endovascular complications, including methicillin susceptible and resistant isolates and strains with different functionality of the agr global regulator. Their adherence to collagen, interaction with the endothelium, resistance to immune attack, capacity to form biofilm and virulence in the Galleria mellonella model were analyzed. CC30 and CC45 showed greater adhesion to collagen and CC8 showed a trend towards higher rate of intracellular persistence in endothelial cells. All CCs exhibited similar tolerance to neutrophil antimicrobial peptide hNP-1 and were capable of forming biofilms under static conditions. The virulence assay in the G. mellonella model demonstrated that CC15 and CC30 were the most and least virulent, respectively. The analysis of the genomic sequences of the most relevant virulence genes identified some CC15 specific gene patterns (absence of enterotoxins and sak gene) and variants (mainly in leucocidins and proteases), but did not reveal any gene or variant that could be responsible for the increased virulence detected for CC15 strains. Even though all the CCs were capable of causing endovascular complications, our results showed that different CCs are likely to produce these complications through different mechanisms which, if confirmed in more sophisticated models, would indicate the need to more specific management and therapeutic approaches.

Molecular-genetic Method for Fast Direct Detection of Staphylococcus Aureus and Methicillin Resistance in Blood Cultures and Punctures

“…24 The increasing number of hospital-acquired infections, especially BSI due to Staphylococcus spp., in recent years is closely linked to the spread of the mecA gene in strains living in hospital environment, which facilitates their ability to survive there. 4,6 In the present study, mecA was detected in 77.9% of the growth-positive blood cultures with staphylococcal isolates. Accordingly, bacteriemia with staphylococcal etiology is complicated by the emergence of methicillin-resistant pathogens.…”

“…This suggests that there is a difference in the origin of the causative agent -community acquired or hospital acquired, which is more frequently described as a reason for increasing the health care-associated infections in relation to MRSA and MRSCoNS. 6,17,22 MLS resistance that did not correlate with hospital acquired infections. Moreover, a dramatic increase in clindamycin resistance among S. aureus isolates has been described.…”

“…1). 6 Methicillin resistance was determined by detection of mecA with the following primer sequences: F5'-TCC AGA TTA CAA CTT CAC CAG G-3'and R 5'-CCA CTT CAT ATC TTG TAA CG-3' with an amplicon size of 162 bp ( Fig. 1).…”

“…enzymes, hemolysins and other toxins that play a role as virulence factors. [4][5][6] S. aureus has been also detected as one of the common etiological agents of respiratory infections, especially in Bulgarian children over the period from 1998 to 2014. 7 This microorganism has been the one most often isolated from Bulgarian patients with lesions due to chronic venous disease, peripheral arterial occlusive disease of the lower extremities, and advanced diabetic microangiopathy.…”

High persister cell formation by clinical Staphylococcus aureus strains belonging to clonal complex 30

“…Some studies have shown that S. aureus belonging to CC5 and CC30 are able to cause severe infections [16] with CC30 being associated with endocarditis, osteomyelitis and persistent bacteraemia [15]. CC8 strains were shown to be prone to cause persistence in endothelial cells [17]. CC45 strains form the predominant lineage in healthy individuals as well as bloodstream infections, particularly in the USA and Europe [18].…”