Predation is a central feature of ecological communities. Most theoretical and empirical studies of predation focus on the consequences of predators consuming their prey. Predators reduce prey population densities through direct consumption (a density‐mediated interaction, DMI), a process that may indirectly affect the prey's resources, competitors, and other predators. However, predators can also affect prey population density by stimulating costly defensive strategies. The costs of these defensive strategies can include reduced energy income, energetic investment in defensive structures, lower mating success, increased vulnerability to other predators, or emigration. Theoretical and empirical studies confirm the existence of these induced costs (trait‐mediated interactions, TMIs); however, the relative importance of intimidation (TMI) and consumption (DMI) effects remains an open question. We conducted a meta‐analysis assessing the magnitude of both TMIs and DMIs in predator–prey interactions. On average, the impact of intimidation on prey demographics was at least as strong as direct consumption (63% and 51% the size of the total predator effect, respectively). This contrast is even more pronounced when we consider the cascading effects of predators on their prey's resources: density effects attenuated through food chains, while TMIs remained strong, rising to 85% of the total predator effect. Predators can thus strongly influence resource density even if they consume few prey items. Finally, intimidation was more important in aquatic than terrestrial ecosystems. Our results suggest that the costs of intimidation, traditionally ignored in predator–prey ecology, may actually be the dominant facet of trophic interactions.

▪ Abstract  Predator-induced phenotypic plasticity is widespread in nature and includes variation in life history, morphology, and behavior. In organisms with complex life histories, predator-induced phenotypic plasticity in the larval period has been widely documented. Several models predict how organisms should alter their size at and time to metamorphosis in response to an increased risk of predation. A survey of empirical studies finds that these theoretical predictions are frequently met. However, no one model performs the best. Additionally, there are several results not predicted by any model. Predator-induced plasticity in metamorphic traits may be related to predator-induced changes in larval morphology and behavior. Predictions of predator effects on larval traits are generally met, except for direct costs of predator-induced morphological phenotypes. Future work should incorporate more detailed studies of growth rate, morphology, and behavior during the larval period, as well as studies of size-specific mortality rates in the presence and absence of predators.

Acinetobacter baumannii is a globally important nosocomial pathogen characterized by an increasing incidence of multidrug resistance. Routes of dissemination and gene flow among health care facilities are poorly resolved and are important for understanding the epidemiology of A. baumannii, minimizing disease transmission, and improving patient outcomes. We used whole-genome sequencing to assess diversity and genome dynamics in 49 isolates from one United States hospital system during one year from 2007 to 2008. Core single-nucleotide-variant-based phylogenetic analysis revealed multiple founder strains and multiple independent strains recovered from the same patient yet was insufficient to fully resolve strain relationships, where gene content and insertion sequence patterns added additional discriminatory power. Gene content comparisons illustrated extensive and redundant antibiotic resistance gene carriage and direct evidence of gene transfer, recombination, gene loss, and mutation. Evidence of barriers to gene flow among hospital components was not found, suggesting complex mixing of strains and a large reservoir of A. baumannii strains capable of colonizing patients.

Background The American Cancer Society, Centers for Disease Control and Prevention, National Cancer Institute, and North American Association of Central Cancer Registries provide annual updates on cancer occurrence and trends by cancer type, sex, race, ethnicity, and age in the United States. This year’s report highlights the cancer burden among men and women age 20–49 years. Methods Incidence data for the years 1999 to 2015 from the Centers for Disease Control and Prevention- and National Cancer Institute–funded population-based cancer registry programs compiled by the North American Association of Central Cancer Registries and death data for the years 1999 to 2016 from the National Vital Statistics System were used. Trends in age-standardized incidence and death rates, estimated by joinpoint, were expressed as average annual percent change. Results Overall cancer incidence rates (per 100 000) for all ages during 2011–2015 were 494.3 among male patients and 420.5 among female patients; during the same time period, incidence rates decreased 2.1% (95% confidence interval [CI] = −2.6% to −1.6%) per year in men and were stable in females. Overall cancer death rates (per 100 000) for all ages during 2012–2016 were 193.1 among male patients and 137.7 among female patients. During 2012–2016, overall cancer death rates for all ages decreased 1.8% (95% CI = −1.8% to −1.8%) per year in male patients and 1.4% (95% CI = −1.4% to −1.4%) per year in females. Important changes in trends were stabilization of thyroid cancer incidence rates in women and rapid declines in death rates for melanoma of the skin (both sexes). Among adults age 20–49 years, overall cancer incidence rates were substantially lower among men (115.3 per 100 000) than among women (203.3 per 100 000); cancers with the highest incidence rates (per 100 000) among men were colon and rectum (13.1), testis (10.7), and melanoma of the skin (9.8), and among women were breast (73.2), thyroid (28.4), and melanoma of the skin (14.1). During 2011 to 2015, the incidence of all invasive cancers combined among adults age 20–49 years decreased −0.7% (95% CI = −1.0% to −0.4%) among men and increased among women (1.3%, 95% CI = 0.7% to 1.9%). The death rate for (per 100 000) adults age 20–49 years for all cancer sites combined during 2012 to 2016 was 22.8 among men and 27.1 among women; during the same time period, death rates decreased 2.3% (95% CI = −2.4% to −2.2%) per year among men and 1.7% (95% CI = −1.8% to −1.6%) per year among women. Conclusions Among people of all ages and ages 20–49 years, favorable as well as unfavorable trends in site-specific cancer incidence were observed, whereas trends in death rates were generally favorable. Characterizing the cancer burden may inform research and cancer-control efforts.

Ecological and evolutionary processes are affected by forces acting at both local and regional scales, yet our understanding of how these scales interact has remained limited. These processes are fundamentally linked through individuals that develop as juve niles in one environment and then either remain in the natal habitat or disperse to new environments. Empirical studies in a diverse range of organisms have demonstrated that the conditions experienced in the natal habitat can have profound effects on the adult phenotype. This environmentally induced phenotypic variation can in turn affect the probability that an individual will disperse to a new environment and the ecological and evolutionary impact of that individual in the new environment. We synthesize the literature on this process and propose a framework for exploring the linkage between local devel opmental environment and dispersal. We then discuss the ecological and evolutionary implications of dispersal asymmetries generated by the effects of natal habitat conditions on individual phenotypes. Our review indicates that the influence of natal habitat conditions on adult phenotypes may be a highly general mechanism affecting the flow of individuals between populations. The wealth of information already gathered on how local conditions affect adult phenotype can and should be integrated into the study of dispersal as a critical force in ecology and evolution.

Environmental contaminants and disease may synergistically contribute to amphibian population declines. Sub-lethal levels of contaminants can suppress amphibian immune defenses and, thereby, may facilitate disease outbreaks. We conducted laboratory experiments on newly metamorphosed foothill yellow-legged frogs (Rana boylii) to determine whether sublethal exposure to the pesticide carbaryl would increase susceptibility to the pathogenic chytrid fungus Batrachochytrium dendrobatidis that is widely associated with amphibian declines. We examined the effect of carbaryl alone, chytrid alone, and interactions of the two on individual survival, growth, and antimicrobial skin defenses. We found no effect of chytrid, carbaryl, or their interaction on survival. However, chytrid infection reduced growth by approximately one-half. This is the first report of suppressed growth in post-metamorphic amphibians due to infection with chytrid. Rana boylii skin peptides strongly inhibited chytrid growth in vitro, which may explain why chytrid exposure did not result in significant mortality. Skin peptide defenses were significantly reduced after exposure to carbaryl suggesting that pesticides may inhibit this innate immune defense and increase susceptibility to disease.

Ecological and evolutionary processes are affected by forces acting at both local and regional scales, yet our understanding of how these scales interact has remained limited. These processes are fundamentally linked through individuals that develop as juve niles in one environment and then either remain in the natal habitat or disperse to new environments. Empirical studies in a diverse range of organisms have demonstrated that the conditions experienced in the natal habitat can have profound effects on the adult phenotype. This environmentally induced phenotypic variation can in turn affect the probability that an individual will disperse to a new environment and the ecological and evolutionary impact of that individual in the new environment. We synthesize the literature on this process and propose a framework for exploring the linkage between local devel opmental environment and dispersal. We then discuss the ecological and evolutionary implications of dispersal asymmetries generated by the effects of natal habitat conditions on individual phenotypes. Our review indicates that the influence of natal habitat conditions on adult phenotypes may be a highly general mechanism affecting the flow of individuals between populations. The wealth of information already gathered on how local conditions affect adult phenotype can and should be integrated into the study of dispersal as a critical force in ecology and evolution.

Induced defenses are widespread in nature, and in amphibian larvae they are often expressed as altered behavior and changes in tail shape, color, and size. Theory predicts that induced defenses should be costly in the absence of a predator threat. No costs have been found for these defenses after metamorphosis. In this study, we tested for induced defenses in western toads, Bufo boreas, and measured larval and postmetamorphic consequences of these responses. Larvae were raised in either the presence or absence of nonlethal predator cues. Defense responses to these larval treatments were measured during the larval stage and shortly after metamorphosis using both predator bioassays and quantification of the putative chemical defense common in toads, bufadienolides. We found no differences in larval morphology, growth rate, or development rate between the predator and control treatments. In the larval bioassays, some types of invertebrate predators consumed significantly fewer of the B. boreas larvae that were reared with predator cues compared to the control treatments. Bufadienolides were not present in B. boreas larvae. In the postmetamorphic bioassays, tiger salamanders (Ambystoma tigrinum) had longer handling times when consuming B. boreas that had developed in larval environments without predator cues compared to predator‐treatment B. boreas. However, postmetamorphic B. boreas from predator cue larval environments had significantly higher concentrations of bufadienolides than did those from larval environments without predators, suggesting that these defenses are ineffective against tiger salamanders. Our results demonstrate that there is plasticity in the chemical defenses of toads and suggest that induced larval defenses may incur costs that are only apparent after metamorphosis. Corresponding Editor: D. W. Pfennig.