ABSTRACT
There are oft-quoted studies which advise that between 1% and 10% of healthcare-associated infections (HAIs) present as healthcare-associated outbreaks (HAOs). Examination of these studies showed they lacked validity due to a low sensitivity to detect HAO, and because they pre-date both advanced healthcare systems and the emergence of recent nosocomial pathogen challenges. The accepted inference: that as there are so few HAOs the focus of surveillance programmes should be on endemic and not epidemic infections (outbreaks), is therefore called into question. Current estimates of HAI burden are derived from Point Prevalence Surveys (PPS) which are neither designed to nor are capable of detecting HAOs. We considered the extensive Infection Prevention and Control Team (IPCT) work to prevent and prepare for perennial and novel HAOs and suggest that at present this endeavour is largely unseen, underestimated and undervalued. Any HAI burden estimate needs to comprise a more complete HAI summary than PPS data. This can only be done with a more inclusive surveillance system that has a wider focus than just prevalent infections. There is a real risk of redirection of the IPCT resource from outbreak prevention and preparedness work towards HAI that are counted: such a change could only further increase HAO risks.
ABSTRACT
Cholesterol dependent cytolysins are important in the ability of some bacteria to cause disease in man and animals. Pneumolysin (PLY) plays a key role in the diseases caused by Streptococcus pneumoniae (the pneumococcus). This chapter describes the role of PLY in some of the key process in disease. These include induction of cell death by pore formation and toxin-induced apoptosis as well as more subtle effects on gene expression of host cells including epigenetic effects of the toxin. The use of bacterial mutants that either do not express the toxin or express altered versions in biological systems is described. Use of isolated tissue and whole animal systems to dissect the structure/function relationships of the toxin as well as the role played by different activities in the pathogenesis of infection are described. The role of PLY in meningitis and the associated deafness is discussed as well as the role of the toxin in promoting increased lung permeability and inflammation during pneumococcal pneumonia. Different clinical strains of the pneumococcus produce different forms of PLY and the impact of this on disease caused by these strains is discussed. Finally, the impact of this knowledge on the development of treatment and prevention strategies for pneumococcal disease is discussed.
