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Pseudomonas aeruginosa: new insights into pathogenesis and host defenses Shaan L. Gellatly & Robert E.W. Hancock Centre for Microbial Diseases and Immunity Research, University of British Columbia, Vancouver, BC, Canada This review about Pseudomonas aeruginosa acute and chronic virulence is timely and extremely well presented. Nosa has an array of innate and acquired immune factors that enable it to surmount host defenses and establish infection. Quorum Sensing and Biofilms P. Aeruginosa expresses several virulence factors that promote the establishment and persistence of infection. Many of these factors are believed to be regulated by cell density–dependent.

All protein virulence factors are chromosomally-encoded, and their gene sequences and positions are well known from the P. Aeruginosa PAO1 strain (earlier called “Pseudomonas aeruginosa strain 1”) genome sequence 12. The co-existence of antimicrobials resistance determinants and virulence factors in P. Aeruginosa isolates is an alarming. A multitude of virulence factors are produced by Pseudomonas aeruginosa. Flagella and type 4 pili are the main adhesins, capable of binding to host epithelial gangliosides, asialoGM1 and asialoGM2. Along with lipopolysaccharide, these surface appendages are also highly inflammatory.

Geerlings, Peter (2013)Studies of Pseudomonas aeruginosa and its virulence factors in a mouse model of dermal infection. PhD thesis, Murdoch University.

Abstract

Pseudomonas aeruginosa is an opportunistic pathogen of hosts with impaired immune function or concurrent disease, most notably patients with Cystic Fibrosis and those who have been severely burned. It has an extensive array of virulence factors (VFs) which enable it to colonise and penetrate host tissue. It is responsible for a high percentage of nosocomial infections and is becoming increasingly antibiotic resistant, so there is an immediate need for novel treatments of severe P. aeruginosa infections. Following severe traumatic injury to the skin, the dermis and epidermis may be destroyed, leaving the fascia and endothelium of the vasculature as the final structural barriers protecting the circulation and preventing bacteraemia. Little has been reported on the mechanisms used by P. aeruginosa to penetrate the fascia and enter the circulation, because conventional animal models of dermal injury do not allow for quantitative study of bacterial pathogenesis and host responses. To address this, a novel transdermal chamber was designed, manufactured and implanted into mice allowing for repeated sampling and quantitative analysis of bacterial replication, VFs, and host responses. Despite the bacterial load in the chamber exudate being similar to normal control mice, mice immunosuppressed using cyclophosphamide (CP) had significantly higher levels of Exotoxin A (ETA), P. aeruginosa elastase (PAE) and Phospholipase C (PLC), and developed fatal bacteraemia when compared to immunocompetent mice.

Download Virulence Factors Of Pseudomonas Aeruginosa Pdf Ppt

It was hypothesised that raised levels of ETA and PAE contributed to the pathogenesis of P. aeruginosa in CP treated mice by increasing the permeability of the fascia and endothelium allowing bacteria to enter the circulation. To test this, purified ETA and PAE were added to the chambers of immunocompetent mice, followed by fluorescently labelled dextran to assess efflux measured as a change in dextran concentration in the chamber exudate over time. ETA caused sustained local depletion of leukocytes and fibroblasts, reduction in exudate volume and weight loss, but did not change the dextran concentration in the chamber exudate compared to control mice. PAE was proinflammatory, increased exudate volume, damaged fascial tissue, induced local haemorrhage, and resulted in a decrease in dextran concentration in the chamber compared to controls. Combining ETA and PAE in the chamber resulted in increased weight loss, haemoglobinaemia and increased accumulation of dextran in the local draining lymph nodes.

Preliminary trials using ovine anti-sera to P. aeruginosa antigens in infected chambers of CP-treated mice increased their survival. Collectively, these results show that the increased concentration of VFs, not bacterial load, facilitated bacterial translocation across the fascia and endothelium, and uncovers the underlying significance of the superficial fascia as a defensive barrier against infectious agents. Furthermore, this study suggests that neutrophils are crucial to reducing VF concentration, and that topically applied heterologous anti-P. aeruginosa antibodies may be useful in preventing fatal bacteraemia in severe dermal infections of susceptible patients.

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