Currently, the investigation of Legionella ecology falls into two distinct areas of research activity: (1) that Legionella multiply within water sources by parasitizing amoebic or ciliate hosts or (2) that Legionella grows extracellularly within biofilms. Less focus has been given to the overlaps that may occur between these two areas or the likelihood that Legionella employs multiple survival strategies to persist in water sources. It is likely that Legionella interacts with protozoa, bacteria, algae, fungi, etc., and biofilm components in a more complex fashion than multiplication or death due to the presence or absence of single components of these complex microbial systems. This paper addresses gaps that exist in the understanding of Legionella ecology and serves to pinpoint areas of future research. To assume that only one other class of organism is important to Legionella ecology may limit our understanding of how this bacterium proliferates in heated water sources and also limit our strategies for its control in the built environment.
Reported cases of legionellosis attributable to Legionella longbeachae infection have increased worldwide. In Australia and New Zealand, L. longbeachae has been a known cause of legionellosis since the late 1980s. All cases for which a source was confirmed were associated with potting mixes and composts. Unlike the situation with other Legionella spp., L. longbeachae–contaminated water systems in the built environment that cause disease have not been reported. Spatially and temporally linked outbreaks of legionellosis associated with this organism also have not been reported. Sporadic cases of disease seem to be limited to persons who have had direct contact with potting soil or compost. Long-distance travel of the organism resulting in infection has not been reported. These factors indicate emergence of an agent of legionellosis that differs in etiology from other species and possibly in route of disease transmission.
Campylobacteriosis is infection caused by the bacteria Campylobacter spp. and is considered a major public health concern. Campylobacter spp. have been identified as one of the most common causative agents of bacterial gastroenteritis. They are typically considered a foodborne pathogen and have been shown to colonise the intestinal mucosa of all food-producing animals. Much emphasis has been placed on controlling the foodborne pathway of exposure, particularly within the poultry industry, however, other environmental sources have been identified as important contributors to human infection. This paper aims to review the current literature on the sources of human exposure to Campylobacter spp. and will cover contaminated poultry, red meat, unpasteurised milk, unwashed fruit and vegetables, compost, wild bird faeces, sewage, surface water, ground water and drinking water. A comparison of current Campylobacter spp. identification methods from environmental samples is also presented. The review of literature suggests that there are multiple and diverse sources for Campylobacter infection. Many environmental sources result in direct human exposure but also in contamination of the food processing industry. This review provides useful information for risk assessment.
Cooling water samples from 31 cooling tower systems were cultured for Legionella over a 16-week summer period. The selected systems were known to be colonized by Legionella. Mean Legionella counts and standard deviations were calculated and time series correlograms prepared for each system. The standard deviations of Legionella counts in all the systems were very large, indicating great variability in the systems over the time period. Time series analyses demonstrated that in the majority of cases there was no significant relationship between the Legionella counts in the cooling tower at time of collection and the culture result once it was available. In the majority of systems (25/28), culture results from Legionella samples taken from the same systems 2 weeks apart were not statistically related. The data suggest that determinations of health risks from cooling towers cannot be reliably based upon single or infrequent Legionella tests.
Accurately quantifying Legionella for regulatory purposes to protect public health is essential. Real-time PCR (qPCR) has been proposed as a better method for detecting and enumerating Legionella in samples than conventional culture method. However, since qPCR amplifies any target DNA in the sample, the technique’s inability to discriminate between live and dead cells means that counts are generally significantly overestimated. Propidium monoazide (PMA) has been used successfully in qPCR to aid live/dead discrimination. We tested PMA use as a method to count only live Legionella cells in samples collected from a modified chemostat that generates environmentally comparable samples. Counts from PMA-treated samples that were pretreated with either heat or three types of disinfectants (to kill the cells) were highly variable, with the only consistent trend being the relationship between biofilm mass and numbers of Legionella cells. Two possibilities explain this result: 1. PMA treatment worked and the subsequent muted response of Legionella to disinfection treatment is a factor of biofilm/microbiological effects; although this does not account for the relationship between the amount of biofilm sampled and the viable Legionella count as determined by PMA-qPCR; or 2. PMA treatment did not work, and any measured decrease or increase in detectable Legionella is because of other factors affecting the method. This is the most likely explanation for our results, suggesting that higher concentrations of PMA might be needed to compensate for the presence of other compounds in an environmental sample or that lower amounts of biofilm need to be sampled. As PMA becomes increasingly toxic at higher concentrations and is very expensive, augmenting the method to include higher PMA concentrations is both counterproductive and cost prohibitive. Conversely, if smaller volumes of biofilm are used, the reproducibility of the method is reduced. Our results suggest that using PMA is not an appropriate method for discriminating between live and dead cells to enumerate Legionella for regulatory purposes.
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