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Biology subjects

Pilcher, D.

Publications and source records attributed to Pilcher, D..

2 recordsLinked to original sources

Changes in body size with age do not follow the temperature-size rule

The temperature size-rule is often described as a reduction in ectothermic body size with warming. This coincides with the expectation that faster growth under warming would lead to larger sizes early in life but smaller sizes later in life. Here, we use > 99,000 observations of weight-at-age of four commercially-important fishes over 25 years to ask whether changes in size and growth can be explained by temperature. We also examine whether oxygen, a key part of a proposed mechanism behind the temperature size-rule, explains patterns of weight-at-age better than temperature. Changes in weight-at-age over time were more related to temperature than oxygen but the effect of temperature on weight was small and did not vary by age, counter to the temperature size-rule. Importantly, these results were sensitive to how the relationship between weight-at-age and temperature was modeled. While the functional form (linear or polynomial) mattered little, how space was included in the model led to different conclusions regarding how temperature affects size and growth. Assuming that spatial and spatiotemporal random effects - those that account for the higher degree of similarity between observations collected closer in space and time - are shared across ages led to different results compared to allowing these effects to vary by age. Models with shared effects suggested weight for younger ages had positive relationships with temperature and negative relationships for older ages. However, these models provided spurious support for the temperature size-rule as they had less statistical support than models that allowed spatial effects to vary by age. Overall, our work highlights that relationships among size, growth, temperature, and oxygen may not be as straightforward as theory suggests and illustrates that modeling decisions can have a large effect on tests of ecological theory, and more broadly, our ability to understand biological responses to climate change.

ecology↗

Gastrointestinal carriage is a major reservoir of K. pneumoniae infection in intensive care patients

BackgroundKlebsiella pneumoniae is an opportunistic pathogen and a leading cause of hospital-associated (HA) infections. Patients in intensive care units (ICUs) are particularly at risk, and outbreaks are frequently reported in ICUs. K. pneumoniae is also part of the healthy human microbiome, providing a potential reservoir for HA infection. However, the frequency of K. pneumoniae gut colonization and its contribution to HA infections are not well characterized.\n\nMethodsWe conducted one-year prospective cohort study of ICU patients. Participants (n=498) were screened for rectal and throat carriage of K. pneumoniae shortly after admission, and clinical information was extracted from hospital records.K. pneumoniae isolated from screening swabs and clinical diagnostic samples were characterized using whole genome sequencing. Genomic and epidemiological data were combined to identify likely transmission events.\n\nResults and ConclusionsK. pneumoniae carriage frequencies were estimated at 6% (95% CI, 3%-8%) amongst ICU patients admitted direct from the community, and 19% (95% CI, 14% - 51%) amongst those who had recent contact with healthcare. Gut colonisation on admission was significantly associated with subsequent K. pneumoniae infection (infection risk 16% vs 3%, OR=6.9, p<0.001), and genome data indicated a match between carriage and infection isolates in most patients. Five likely transmission chains were identified, resulting in six infections (12% of K. pneumoniae infections in ICU). In contrast, 49% of K. pneumoniae infections were caused by a strain that was unique to the patient, and 48% of patients with K. pneumoniae infections who participated in screening were positive for prior colonisation. These data confirm K. pneumoniae colonisation is a significant risk factor for subsequent infection in ICU, and indicate that half of all K. pneumoniae infections result from patients own microbiota. Screening for colonisation on admission could limit risk of infection in the colonised patient and others.

microbiology↗