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BACKGROUND: Intracavity medical devices (ICMDs) are used in a wide variety of healthcare settings. The approach to their decontamination and the resources available also differ widely. Their potential for infection transmission is considerable. AIM: To produce a comprehensive risk assessment-based approach to the decontamination of ICMDs, accompanied by an adaptable audit tool.

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BACKGROUND: In December 2011 and early 2012 four neonates died from Pseudomonas aeruginosa bacteraemia in hospitals in Northern Ireland. AIM: To assess whether P. aeruginosa was associated with the neonatal unit taps and whether waterborne isolates were consistent with patient isolates. METHODS: Thirty taps and eight flow straighteners from the relevant hospitals were categorized and dismantled into 494 components and assessed for aerobic colony and P. aeruginosa counts using non-selective and selective agars. P. aeruginosa isolates were typed by variable number tandem repeat (VNTR) analysis. Selected tap components were subjected to epifluorescence and scanning electron microscopy to visualize biofilm. FINDINGS: The highest P. aeruginosa counts were from the flow straighteners, metal support collars and the tap bodies surrounding these two components. Complex flow straighteners had a significantly higher P. aeruginosa count than other types of flow straighteners (P < 0.05). Highest aerobic colony counts were associated with integrated mixers and solenoids (P < 0.05), but there was not a strong correlation (r = 0.33) between the aerobic colony counts and P. aeruginosa counts. Representative P. aeruginosa tap isolates from two hospital neonatal units had VNTR profiles consistent with strains from the tap water and infected neonates. CONCLUSION: P. aeruginosa was predominantly found in biofilms in flow straighteners and associated components in the tap outlets and was a possible source of the infections observed. Healthcare providers should be aware that water outlets can be a source of P. aeruginosa contamination and should take steps to reduce such contamination, monitor it and have strategies to minimize risk to susceptible patients.

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BACKGROUND: Routine screening of premature newborns for haemolytic streptococci, Staphylococcus aureus and enteric Gram-negative bacteria done at birth using umbilical swabs identified clustering of babies colonized with Bacillus cereus in summers of 2009 and 2010 at a 400-bedded UK general hospital. AIM: To determine the source of this organism by focusing on the clinical environment. METHODS: Umbilical swab screening was extended to all newborns and the labour ward environment, including construction-related dust, was sampled for B. cereus. FINDINGS: During the summer of 2009, 65% of newborns had umbilical swabs which were culture positive for B. cereus. Blood agar and B. cereus selective agar impression plates of unused labour ward linen, and freshly received linen from the hospital's external laundry, gave mainly confluent growth of B. cereus in >85% of items sampled. In-use and exposed healthcare products including liquid handwashing agents, paper hand-towels, vaginal lubricants, labour ward dust and air were culture negative. Linen contamination and umbilical swab culture positivity both approached zero in autumn. B. cereus colonization of newborn umbilici recurred in summer 2010 and unused laundered linen was again found to be as contaminated. Washing linen at the laundry in a washer-extractor, with higher dilution than the continuous tunnel washer normally used, coincided with lowering of detectable B. cereus numbers in unused washed linen and no clustering in newborns the following summer (2011). CONCLUSION: Freshly laundered linen can be contaminated with B. cereus with subsequent spread and colonization of newborns. This contamination appears to be associated with low-dilution washing and high ambient temperatures.

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Decontamination of surfaces and medical equipment is integral to the control of Clostridium difficile transmission, and many products claim to inactivate this bacterium effectively. Thirty-two disinfectants were tested against spores of C. difficile in a suspension test based on European Standard BS EN 13704:2002, with contact times of 1 and 60 min in simulations of clean (0.3% albumin) and dirty (3% albumin) conditions. The addition of a 1-min contact time was chosen as a more realistic simulation of probable real-life exposures in the situation being modelled than the 60 min specified by the Standard. The manufacturer's lowest recommended concentrations for use were tested. Sixteen products achieved >10(3) reduction in viability after 60 min (the pass criterion for the Standard) under both clean and dirty conditions. However, only eight products achieved >10(3) reduction in viability within 1 min under dirty conditions. Three products failed to reduce the viability of the C. difficile spores by a factor of 10(3) in any of the test conditions. This study highlights that the application of disinfectants claiming to be sporicidal is not, in itself, a panacea in the environmental control of C. difficile, but that carefully chosen environmental disinfectants could form part of a wider raft of control measures that include a range of selected cleaning strategies.

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A systematic search and quality assessment of published literature was conducted to establish current knowledge on the role of healthcare workers uniforms' as vehicles for the transfer of healthcare-associated infections. This review comprised a systematic search of national and international guidance, published literature and data on recent advances in laundry technology and processes. We found only a small number of relevant studies that provided limited evidence directly related to the decontamination of uniforms. Studies concerning domestic laundry processes are small scale and largely observational. Current practice and guidance for laundering uniforms is extrapolated from studies of industrial hospital linen processing. Healthcare workers' uniforms, including white coats, become progressively contaminated in use with bacteria of low pathogenicity from the wearer and of mixed pathogenicity from the clinical environment and patients. The hypothesis that uniforms/clothing could be a vehicle for the transmission of infections is not supported by existing evidence. All components of the laundering process contribute to the removal or killing of micro-organisms on fabric. There is no robust evidence of a difference in efficacy of decontamination of uniforms/clothing between industrial and domestic laundry processes, or that the home laundering of uniforms provides inadequate decontamination.

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Two aminoglycoside-resistant strains of Klebsiella pneumoniae caused an outbreak on the neonatal unit at St Thomas' Hospital. One, which affected 18 patients, was capsular type K18 and resistant to newer cephalosporins by the production of the extended-spectrum beta-lactamase SHV-2; the other, which colonized four patients, was capsular non-typeable and did not produce extended-spectrum beta-lactamase. Both strains were probably brought into the unit by carrier patients; the probable carrier of the non-typeable strain was transferred from another hospital but was negative on a single admission screen; the probable carrier of the K18 strain was not screened on admission because he had been born at St Thomas', but his mother had been transferred from another hospital. Despite intensive efforts to control the outbreak by standard methods of hand washing, screening, patient isolation and environmental cleaning, a total of 22 neonates on the unit eventually became colonized or infected. One of three patients with bacteraemia died. A small proportion of samples of expressed breast milk, electronic thermometers and oxygen saturation probes were contaminated by the K18 strain and may have contributed to some of the cross-infection, but this did not explain the extent of the outbreak. The outbreak was controlled only by opening a temporary ward for colonized neonates and another for newly born babies, which allowed the closure and cleaning of the main neonatal unit. Multiply antibiotic resistant klebsiellas may be highly epidemic and cause serious, difficult-to-control outbreaks on neonatal units. All patients, regardless of their admission history, should be screened on admission for carriage of multiply resistant enterobacteria by a sensitive method, and units should have plans for temporary ward closure should outbreaks occur.

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Jet injectors are needleless injectors that penetrate skin with high-pressure fluid. They have potential advantages over needles and syringes in mass immunisation programs, but concerns over their capacity to transfer blood-borne viruses have been a barrier to acceptance. Hepatitis B infection can transmit in 10 pl of blood; detection of such low volumes presents severe difficulties to such assessments. A model to assess jet injector safety was developed using injection of an inert buffer into calves and assaying the next injector discharge, representing the next dose of vaccine, for blood using a highly sensitive ELISA. Four injectors were tested: two with reusable heads and direct skin contact, one with single-use injector heads and one where the injector head discharged at a distance from the skin. All injectors tested transmitted significant (over 10 pl) volumes of blood; the volumes and frequency of contamination varied with injector. The source of the contamination was consistent with contamination by efflux of injected fluid and blood from the pressurised pocket in tissue that is formed during injection. This insight should inform the design of safe jet injectors.

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Tuberculosis infection control in hospitals has received renewed interest after decades of low prominence following the occurrence of multiply drug-resistant strains in populations of patients with immune systems affected by HIV. This paper examines the history of tuberculosis infection control in hospitals and how recent outbreaks have influenced contemporary measures. The principal infection control measure must always be early recognition and isolation of patients in HIV-care situations who may be dispersing Mycobacterium tuberculosis, in both ward and outpatient areas. If there is either a high degree of suspicion or proven TB, patients should be housed in negative pressure isolation rooms whilst undergoing treatment and investigation. Procedures which may generate infectious aerosols should be carried out in similarly ventilated rooms. The quality assurance in such infection control is through the administrative systems put in place, staff training and the engineering controls of isolation room ventilation.

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Superoxide dismutase 1 (SOD1), a ubiquitously expressed enzyme, detoxifies superoxide radicals and participates in copper homeostasis. Mutations in this enzyme have been linked to a subset of autosomal dominant cases of familial amyotrophic lateral sclerosis (FALS), a disorder characterized by selective degeneration of motor neurons. Transgenic mice expressing FALS mutant human (Hu) SOD1 at high levels develop a motor neuron disease, indicating that mutant Hu SOD1 gains properties that are particularly toxic to motor neurons. In this report, we demonstrate that transgenic mice expressing Hu SOD1 with the G37R FALS mutation, but not mice expressing wild-type enzyme, develop focal increases in immunoreactivity in the proximal axons of spinal motor neurons. This SOD1 immunoreactivity and immunoreactivity to hypophosphorylated neurofilament H epitopes are found adjacent to small vacuoles in axons. Using metabolic radiolabeling methods, we show that mutant G37R HuSOD1 as well as endogenous mouse SOD1 are transported anterograde in slow component b in motor and sensory axons of the sciatic nerve. Together, these findings suggest that anterogradely transported mutant SOD1 may act locally to damage motor axons.

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beta-Tubulin is encoded by a family of genes that produces at least five distinct polypeptide isotypes in neurons. Two of these isotypes (i.e., classes II and III) preferentially accumulate in axons, and the expression of one of them (i.e., class II) correlates closely with axonal outgrowth during development and regeneration. In dorsal root ganglion (DRG) neurons, expression of the class II isotype declines to relatively low levels during early postnatal development, and increases dramatically in mature neurons during axon regeneration (i.e., to a level comparable to that in developing neurons). In contrast, expression of the class III isotype, which rises slightly during postnatal development, increases much less than the class II isotype during regeneration. We now document that these changes in gene expression are associated with an increase in the relative amount of class II as compared to class III beta-tubulin delivered to regenerating sensory axons of rat sciatic nerve by slow axonal transport. In this study, the tubulin transported in sensory axons was labeled by injecting [35S]methionine into the L5 DRG either 7 or 14 days after crushing the sciatic nerve; pulse-labeled class II and class III beta-tubulin were identified using immunoprecipitation. This change in the isotype composition of beta-tubulin transported in regenerating axons may influence outgrowth by altering the assembly and dynamic properties of axonal microtubules.

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To examine the mechanism through which neurofilaments regulate the caliber of myelinated axons and to test how aberrant accumulations of neurofilaments cause motor neuron disease, mice have been constructed that express wild-type mouse NF-H up to 4.5 times the normal level. Small increases in NF-H expression lead to increased total neurofilament content and larger myelinated axons, whereas larger increases in NF-H decrease total neurofilament content and strongly inhibit radial growth. Increasing NF-H expression selectively slow neurofilament transport into and along axons, resulting in severe perikaryal accumulation of neurofilaments and proximal axonal swellings in motor neurons. Unlike the situation in transgenic mice expressing modest levels of human NF-H (Cote, F., J.F. Collard, and J.P. Julien. 1993. Cell. 73:35-46), even 4.5 times the normal level of wild-type mouse NF-H does not result in any overt phenotype or enhanced motor neuron degeneration or loss. Rather, motor neurons are extraordinarily tolerant of wild-type murine NF-H, whereas wild-type human NF-H, which differs from the mouse homolog at > 160 residue positions, mediates motor neuron disease in mice by acting as an aberrant, mutant subunit.

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Inhalation of aerosols contaminated with gram-negative bacteria generated from home-use nebulizers used by cystic fibrosis (CF) patients may be a primary route for bacterial colonization of the lung. Burkholderia cepacia was isolated from 3 of [corrected] 35 home-use nebulizers, and Stenotrophomonas maltophilia was isolated from 4 of 35 home-use nebulizers. Sputum cultures for two patients whose nebulizers were contaminated with B. cepacia did not yield the organism. However, DNA macrorestriction analysis by pulsed-field gel electrophoresis confirmed that one of two strains of B. cepacia recovered from the nebulizer of a third patient was also present in the sputum of that patient. Although Pseudomonas aeruginosa was isolated from 34 patients, none of the nebulizers were positive for the organism. Sixty-nine percent of nebulizers were contaminated, and up to 16 different environmental colistin-resistant, gram-negative species were identified. The heaviest contamination was found beneath the chamber atomizer. A questionnaire survey showed that the majority of patients (28 of 34) were receiving nebulized colistin and/or gentamicin. Patients who followed recommended instructions for good nebulizer hygienic practice and paid particular attention to drying had minimal or no contamination of their nebulizers.

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We have analyzed the axonal transport of beta III-tubulin in the central (dorsal root) and peripheral (sciatic nerve) branches of sensory axons after injury of the sciatic nerve. Our finding that the relative amount of beta III-tubulin transported in slow component b (SCb) is increased in both axonal branches does not support the generally accepted hypothesis that the transport of cytoskeletal proteins is altered in the peripheral, but not the central branch after injury of the sciatic nerve.

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The phenotypes of many neurological diseases, including motor neuron disease (amyotrophic lateral sclerosis; ALS) and Alzheimer's disease (AD), are determined by the vulnerabilities of populations of nerve cells and the character/ evolution of cellular abnormalities. Because different cell types respond selectively to individual trophic factors, these factors may be useful in ameliorating pathology in cells that express their cognate receptors. To test therapies for ALS and AD, investigators require model systems. Although there are a variety of models of ALS, two models are particularly attractive: transgenic mice that express human superoxide dismutase 1 (SOD-1) mutations linked to familial ALS develop paralysis associated with a gain of adverse property of the mutant SOD; and axotomy of facial axons in neonatal rats, a manipulation that causes retrograde cell degeneration, which can be ameliorated by several trophic factors.

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