Airborne transmission is known to be the route of infection for diseases such as tuberculosis and aspergillosis. It has also been implicated in nosocomial outbreaks of MRSA, Acinetobacter spp. and Pseudomonas spp. Despite this there is much scepticism about the role that airborne transmission plays in nosocomial outbreaks. This paper investigates the airborne spread of infection in hospital buildings, and evaluates the extent to which it is a problem. It is concluded that although contact-spread is the principle route of transmission for most infections, the contribution of airborne micro-organisms to the spread of infection is likely to be greater than is currently recognised. This is partly because many airborne micro-organisms remain viable while being non-culturable, with the result that they are not detected, and also because some infections arising from contact transmission involve the airborne transportation of micro-organisms onto inanimate surfaces.

Biological decontamination using a nonthermal gas discharge at atmospheric pressure in air is the subject of significant research effort at this time. The mechanism for bacterial deactivation undergoes a lot of speculation, particularly with regard to the role of ions and reactive gas species. Two mechanisms have been proposed: electrostatic disruption of cell membranes and lethal oxidation of membrane or cytoplasmic components. Results show that death is accompanied by cell lysis and fragmentation in Gram-negative bacteria but not Gram-positive species, although cytoplasmic leakage is generally observed. Gas discharges can be a source of charged particles, ions, reactive gas species, radicals, and radiation (ultraviolet, infrared, and visible), many of which have documented biocidal properties. The individual roles played by these in decontamination are not well understood or quantified. However, the reactions of some species with biomolecules are documented otherwise in the literature. Oxidative stress is relatively well studied, and it is likely that exposure to gas discharges in air causes extreme oxidative challenge. In this paper, a review is presented of the major reactive species generated by nonthermal plasma at atmospheric pressure and the known reactions of these with biological molecules. Understanding these mechanisms becomes increasingly important as plasma-based decontamination and sterilization devices come closer to a wide-scale application in medical, healthcare, food processing, and air purification applications. Approaches are proposed to elucidate the relative importance of reactive species.

Venous abnormalities contribute to the pathophysiology of several neurological conditions. This paper reviews the literature regarding venous abnormalities in multiple sclerosis (MS), leukoaraiosis, and normal-pressure hydrocephalus (NPH). The review is supplemented with hydrodynamic analysis to assess the effects on cerebrospinal fluid (CSF) dynamics and cerebral blood flow (CBF) of venous hypertension in general, and chronic cerebrospinal venous insufficiency (CCSVI) in particular.CCSVI-like venous anomalies seem unlikely to account for reduced CBF in patients with MS, thus other mechanisms must be at work, which increase the hydraulic resistance of the cerebral vascular bed in MS. Similarly, hydrodynamic changes appear to be responsible for reduced CBF in leukoaraiosis. The hydrodynamic properties of the periventricular veins make these vessels particularly vulnerable to ischemia and plaque formation.Venous hypertension in the dural sinuses can alter intracranial compliance. Consequently, venous hypertension may change the CSF dynamics, affecting the intracranial windkessel mechanism. MS and NPH appear to share some similar characteristics, with both conditions exhibiting increased CSF pulsatility in the aqueduct of Sylvius.CCSVI appears to be a real phenomenon associated with MS, which causes venous hypertension in the dural sinuses. However, the role of CCSVI in the pathophysiology of MS remains unclear.

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Background: Clostridium difficile-associated diarrhoea (CDAD) is a frequently occurring healthcare-associated infection, which is responsible for significant morbidity and mortality amongst elderly patients in healthcare facilities. Environmental contamination is known to play an important contributory role in the spread of CDAD and it is suspected that contamination might be occurring as a result of aerial dissemination of C. difficile spores. However previous studies have failed to isolate C. difficile from air in hospitals. In an attempt to clarify this issue we undertook a short controlled pilot study in an elderly care ward with the aim of culturing C. difficile from the air.

Background: In recent years there has been renewed interest in the use of air ionisers to control of the spread of airborne infection. One characteristic of air ions which has been widely reported is their apparent biocidal action. However, whilst the body of evidence suggests a biocidal effect in the presence of air ions the physical and biological mechanisms involved remain unclear. In particular, it is not clear which of several possible mechanisms of electrical origin (i.e. the action of the ions, the production of ozone, or the action of the electric field) are responsible for cell death. A study was therefore undertaken to clarify this issue and to determine the physical mechanisms associated with microbial cell death.

Purpose: To investigate cerebrospinal fluid (CSF) dynamics in the aqueduct of Sylvius in multiple sclerosis (MS) patients and healthy controls (HC) using cine phase contrast imaging. Materials and Methods:In all, 67 MS patients (48 relapsing-remitting [RR] and 19 secondary-progressive [SP]), nine patients with clinically isolated syndrome (CIS), and 35 age-and sex-matched HC were examined. CSF flow and velocity measures were quantified using a semiautomated method and compared with clinical and magnetic resonance imaging (MRI) disease outcomes.Results: Significantly decreased CSF net flow was detected in MS patients compared to HC (À3.7 vs. À7.1 mL/beat, P ¼ 0.005). There was a trend for increased net positive flow between SP, RR, and CIS patients. Altered CSF flow and velocity measures were associated with more severe T1 and T2 lesion volumes, lateral and fourth ventricular volumes, and third ventricular width in MS and CIS patients (P < 0.01 for all). In CIS patients, conversion to clinically definite MS in the following year was related to decreased CSF net flow (P ¼ 0.007). There was a trend between increased annual relapse rate and altered CSF flow/velocity measures in RRMS patients (P < 0.05).Conclusion: CSF flow dynamics are altered in MS patients. More severe clinical and MRI outcomes in RRMS and CIS patients relate to altered CSF flow and velocity measures.