Resilience of Coral-Associated Bacterial Communities Exposed to Fish Farm Effluent

10.1371/journal.pone.0007319PLoS ONE410

Cellular Responses in Sea Fan Corals: Granular Amoebocytes React to Pathogen and Climate Stressors

BACKGROUND: Climate warming is causing environmental change making both marine and terrestrial organisms, and even humans, more susceptible to emerging diseases. Coral reefs are among the most impacted ecosystems by climate stress, and immunity of corals, the most ancient of metazoans, is poorly known. Although coral mortality due to infectious diseases and temperature-related stress is on the rise, the immune effector mechanisms that contribute to the resistance of corals to such events remain elusive. In the Caribbean sea fan corals (Anthozoa, Alcyonacea: Gorgoniidae), the cell-based immune defenses are granular acidophilic amoebocytes, which are known to be involved in wound repair and histocompatibility. METHODOLOGY/PRINCIPAL FINDINGS: We demonstrate for the first time in corals that these cells are involved in the organismal response to pathogenic and temperature stress. In sea fans with both naturally occurring infections and experimental inoculations with the fungal pathogen Aspergillus sydowii, an inflammatory response, characterized by a massive increase of amoebocytes, was evident near infections. Melanosomes were detected in amoebocytes adjacent to protective melanin bands in infected sea fans; neither was present in uninfected fans. In naturally infected sea fans a concurrent increase in prophenoloxidase activity was detected in infected tissues with dense amoebocytes. Sea fans sampled in the field during the 2005 Caribbean Bleaching Event (a once-in-hundred-year climate event) responded to heat stress with a systemic increase in amoebocytes and amoebocyte densities were also increased by elevated temperature stress in lab experiments. CONCLUSIONS/SIGNIFICANCE: The observed amoebocyte responses indicate that sea fan corals use cellular defenses to combat fungal infection and temperature stress. The ability to mount an inflammatory response may be a contributing factor that allowed the survival of even infected sea fan corals during a stressful climate event

Reactance and Public Health Messages: The Unintended Dangers of Anti-tobacco PSAs

This study examined smokers’ reactions to antismoking messages that emphasized either the harms of secondhand smoke or vulnerability to smoking addiction and framed the need for smoking cessation using either gain or loss message frames. One hundred fifty-four college smokers participated in a study that used a 2 x 2 factorial design crossing message type (secondhand smoke appeals, smoking addiction appeals) and message frame (gain, loss) with the addition of a control group. The primary outcomes assessed were participants’ intentions to quit smoking and psychological reactance. Secondhand smoke appeals paired with a loss-framed smoking cessation message yielded greater reactance and lower intentions to quit compared to smoking addiction PSAs paired with a gain-framed smoking cessation message. Overall, loss framed smoking cessation messages elicited greater message reactance compared to gain framed smoking cessation messages

Induced defenses in response to an invading crab predator: An explanation of historical and geographic phenotypic change

The expression of defensive morphologies in prey often is correlated with predator abundance or diversity over a range of temporal and spatial scales. These patterns are assumed to reflect natural selection via differential predation on genetically determined, fixed phenotypes. Phenotypic variation, however, also can reflect within-generation developmental responses to environmental cues (phenotypic plasticity). For example, water-borne effluents from predators can induce the production of defensive morphologies in many prey taxa. This phenomenon, however, has been examined only on narrow scales. Here, we demonstrate adaptive phenotypic plasticity in prey from geographically separated populations that were reared in the presence of an introduced predator. Marine snails exposed to predatory crab effluent in the field increased shell thickness rapidly compared with controls. Induced changes were comparable to (i) historical transitions in thickness previously attributed to selection by the invading predator and (ii) present-day clinal variation predicted from water temperature differences. Thus, predator-induced phenotypic plasticity may explain broad-scale geographic and temporal phenotypic variation. If inducible defenses are heritable, then selection on the reaction norm may influence coevolution between predator and prey. Trade-offs may explain why inducible rather than constitutive defenses have evolved in several gastropod species

Impacts of aspergillosis on sea fan coral demography: modeling a moving target

Little is known about how epizootics in natural populations affect vital rates and population structure, or about the process of recovery after an outbreak subsides. We investigated the effects of aspergillosis, an infectious disease caused by the fungal pathogen Aspergillus sydowii, on the demography of a gorgonian coral, Gorgonia ventalina. Caribbean sea fans were affected by a seven-year epizootic, marked by an initial period in 1994 of high infection prevalence, high mortality rates, and almost complete reproductive failure of infected fans. Post epizootic, in 2005, host populations were relatively healthy, with low disease prevalence. Using longitudinal data from populations on coral reefs in the Florida Keys (USA) and the Yucatán Peninsula (Mexico), we documented changes in the epidemiology of sea fan aspergillosis over the course of the epizootic. We developed an "integral projection model" that scales disease impacts from individual to population levels using direct estimates of vital rates. Within-colony lesion growth rate and host mortality were higher during the peak of the epizootic. Effects on individuals and populations changed substantially post-epizootic; recruitment increased, mortality of infected adults decreased, and the size dependence of infection was reduced. Elasticity analysis indicated that population growth is more sensitive to changes in the growth and survival of established colonies than to recruitment, due to slow colony growth and the longevity and fecundity of large adults. Disease prevalence in our monitored populations decreased from ∼50% in 1997 to <10% by 2003 and <1% in 2007 and was accompanied by very high mortality during the early stages of the epizootic. The population model suggested that host evolution (due to selection for higher disease resistance through differential mortality) could proceed quickly enough to explain the observed changes in prevalence and in the size independence of infection risk. Our model indicates that the time required for population recovery following an outbreak is largely determined by the percentage of healthy tissue lost from the population. However, recovery following an especially severe outbreak (i.e., 80% or more tissue loss) is much faster if the affected population receives an external supply of recruits from unaffected areas

Disease epidemic and a marine heat wave are associated with the continental-scale collapse of a pivotal predator (Pycnopodia helianthoides)

Multihost infectious disease outbreaks have endangered wildlife, causing extinction of frogs and endemic birds, and widespread declines of bats, corals, and abalone. Since 2013, a sea star wasting disease has affected > 20 sea star species from Mexico to Alaska. The common, predatory sunflower star (Pycnopodia helianthoides), shown to be highly susceptible to sea star wasting disease, has been extirpated across most of its range. Diver surveys conducted in shallow nearshore waters (n = 10,956; 2006-2017) from California to Alaska and deep offshore (55 to 1280 m) trawl surveys from California to Washington (n = 8968; 2004-2016) reveal 80 to 100% declines across a similar to 3000-km range. Furthermore, timing of peak declines in nearshore waters coincided with anomalously warm sea surface temperatures. The rapid, widespread decline of this pivotal subtidal predator threatens its persistence and may have large ecosystem-level consequences

Growth anomalies on the coral genera Acropora and Porites are strongly associated with host density and human population size across the Indo-Pacific

Growth anomalies (GAs) are common, tumor-like diseases that can cause significant morbidity and decreased fecundity in the major Indo-Pacific reef-building coral genera, Acropora and Porites. GAs are unusually tractable for testing hypotheses about drivers of coral disease because of their pan-Pacific distributions, relatively high occurrence, and unambiguous ease of identification. We modeled multiple disease-environment associations that may underlie the prevalence of Acropora growth anomalies (AGA) (n = 304 surveys) and Porites growth anomalies (PGA) (n = 602 surveys) from across the Indo-Pacific. Nine predictor variables were modeled, including coral host abundance, human population size, and sea surface temperature and ultra-violet radiation anomalies. Prevalence of both AGAs and PGAs were strongly host density-dependent. PGAs additionally showed strong positive associations with human population size. Although this association has been widely posited, this is one of the first broad-scale studies unambiguously linking a coral disease with human population size. These results emphasize that individual coral diseases can show relatively distinct patterns of association with environmental predictors, even in similar diseases (growth anomalies) found on different host genera (Acropora vs. Porites). As human densities and environmental degradation increase globally, the prevalence of coral diseases like PGAs could increase accordingly, halted only perhaps by declines in host density below thresholds required for disease establishment