Free-living amoebae in water are hosts to many bacterial species living in such an environment. Such an association enables bacteria to select virulence factors and survive in adverse conditions. Waterborne mycobacteria (WBM) are important sources of community-and hospital-acquired outbreaks of nontuberculosis mycobacterial infections. However, the interactions between WBM and free-living amoebae in water have been demonstrated for only few Mycobacterium spp. We investigated the ability of a number (n ‫؍‬ 26) of Mycobacterium spp. to survive in the trophozoites and cysts of Acanthamoeba polyphaga. All the species tested entered the trophozoites of A. polyphaga and survived at this location over a period of 5 days. Moreover, all Mycobacterium spp. survived inside cysts for a period of 15 days. Intracellular Mycobacterium spp. within amoeba cysts survived when exposed to free chlorine (15 mg/liter) for 24 h. These data document the interactions between free-living amoebae and the majority of waterborne Mycobacterium spp. Further studies are required to examine the effects of various germicidal agents on the survival of WBM in an aquatic environment.Mycobacteria are a large group of microorganisms that inhabit a diverse range of natural environments. Environmental mycobacteria are a frequent cause of opportunistic infection in human beings and livestock (23,56,76). There is growing recognition in recent years that water is an important vehicle of transmission of environmental mycobacteria. This is based on the fact that in the recent past contaminated water supply systems have been responsible for several hospital and community outbreaks of mycobacterial infections (16,77,78,79,82,83). These included infections as diverse as life-threatening pneumonia in patients with artificial ventilation, cystic fibrosis (54), and chronic granulomatous disease (79); outbreaks of skin infection following liposuction (51); furunculosis after domestic footbaths (77, 83); mastitis after body piercing (73); and abscess formation in intravenous drug users (26). In one instance (79, 82), workers exposed to contaminated industrial effluents developed pneumonia due to an environmental mycobacterium.In hospital therapy pools, waterborne mycobacteria (WBM) may represent about 33% of the microorganisms present in water and about 80% of those in air in the vicinity of such a contaminated water source (5). WBM include both rapidly and slowly growing Mycobacterium spp., depending on whether they require a week or less for the production of visible colonies in solid medium. Examples of WBM include among other species the Mycobacterium avium complex, Mycobacterium gordonae, Mycobacterium malmoense, Mycobacterium simiae, Mycobacterium marinum, Mycobacterium tusciae, and Mycobacterium lentiflavum, which have been found in natural fresh waters (72,76) . Mycobacterium mucogenicum, Mycobacterium kansasii, M. gordonae, Mycobacterium flavescens, Mycobacterium aurum, Mycobacterium fortuitum, Mycobacterium peregrinum, andMycobacterium chelonae have been ...

Background and Purpose: Brain atrophy can be regarded as an end-organ effect of cumulative cardiovascular risk factors. Accelerated brain atrophy is described following ischemic stroke, but it is not known whether atrophy rates vary over the poststroke period. Examining rates of brain atrophy allows the identification of potential therapeutic windows for interventions to prevent poststroke brain atrophy. Methods: We charted total and regional brain volume and cortical thickness trajectories, comparing atrophy rates over 2 time periods in the first year after ischemic stroke: within 3 months (early period) and between 3 and 12 months (later period). Patients with first-ever or recurrent ischemic stroke were recruited from 3 Melbourne hospitals at 1 of 2 poststroke time points: within 6 weeks (baseline) or 3 months. Whole-brain 3T magnetic resonance imaging was performed at 3 time points: baseline, 3 months, and 12 months. Eighty-six stroke participants completed testing at baseline; 125 at 3 months (76 baseline follow-up plus 49 delayed recruitment); and 113 participants at 12 months. Their data were compared with 40 healthy control participants with identical testing. We examined 5 brain measures: hippocampal volume, thalamic volume, total brain and hemispheric brain volume, and cortical thickness. We tested whether brain atrophy rates differed between time points and groups. A linear mixed-effect model was used to compare brain structural changes, including age, sex, years of education, a composite cerebrovascular risk factor score, and total intracranial volume as covariates. Results: Atrophy rates were greater in stroke than control participants. Ipsilesional hemispheric, hippocampal, and thalamic atrophy rates were 2 to 4 times greater in the early versus later period. Conclusions: Regional atrophy rates vary over the first year after stroke. Rapid brain volume loss in the first 3 months after stroke may represent a potential window for intervention. REGISTRATION: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02205424.