RESUMO
Testudines are a highly threatened group facing an array of stressors, including alteration of their sensory environment. Underwater noise pollution has the potential to induce hearing loss and disrupt detection of biologically important acoustic cues and signals. To examine the conditions that induce temporary threshold shifts (TTS) in hearing in the freshwater Eastern painted turtle (Chrysemys picta picta), three individuals were exposed to band limited continuous white noise (50-1000 Hz) of varying durations and amplitudes (sound exposure levels ranged from 151 to 171 dB re 1 µPa2 s). Control and post-exposure auditory thresholds were measured and compared at 400 and 600 Hz using auditory evoked potential methods. TTS occurred in all individuals at both test frequencies, with shifts of 6.1-41.4 dB. While the numbers of TTS occurrences were equal between frequencies, greater shifts were observed at 600 Hz, a frequency of higher auditory sensitivity, compared to 400 Hz. The onset of TTS occurred at 154 dB re 1 µPa2 s for 600 Hz, compared to 158 dB re 1 µPa2 s at 400 Hz. The 400-Hz onset and patterns of TTS growth and recovery were similar to those observed in previously studied Trachemys scripta elegans, suggesting TTS may be comparable across Emydidae species.
Assuntos
Estimulação Acústica , Limiar Auditivo , Tartarugas , Animais , Tartarugas/fisiologia , Fatores de Tempo , Ruído/efeitos adversos , Potenciais Evocados Auditivos/fisiologia , Perda Auditiva Provocada por Ruído/fisiopatologia , Perda Auditiva Provocada por Ruído/etiologia , Masculino , Feminino , Audição/fisiologiaRESUMO
Noise pollution in aquatic environments can cause hearing loss in noise-exposed animals. We investigated whether exposure to continuous underwater white noise (50-1000 Hz) affects the auditory sensitivity of an aquatic turtle Trachemys scripta elegans (red-eared slider) across 16 noise conditions of differing durations and amplitudes. Sound exposure levels (SELs) ranged between 155 and 193 dB re 1 µPa2 s, and auditory sensitivity was measured at 400 Hz using auditory evoked potential methods. Comparing control and post-exposure thresholds revealed temporary threshold shifts (TTS) in all three individuals, with at least two of the three turtles experiencing TTS at all but the two lowest SELs tested, and shifts up to 40 dB. There were significant positive relationships between shift magnitude and exposure duration, amplitude, and SEL. The mean predicted TTS onset was 160 dB re 1 µPa2 s. There was individual variation in susceptibility to TTS, threshold shift magnitude, and recovery rate, which was non-monotonic and occurred on time scales ranging from < 1 h to > 2 days post-exposure. Recovery rates were generally greater after higher magnitude shifts. Sound levels inducing hearing loss were comparatively low, suggesting aquatic turtles may be more sensitive to underwater noise than previously considered.
Assuntos
Surdez , Perda Auditiva Provocada por Ruído , Tartarugas , Animais , Perda Auditiva Provocada por Ruído/etiologia , Ruído/efeitos adversos , Potenciais Evocados Auditivos , Limiar Auditivo/fisiologia , Fadiga AuditivaRESUMO
There are approximately 3,000 southern sea otters (Enhydra lutris nereis) in the nearshore environment along the California coast, US, and the species is classified as Threatened under the Endangered Species Act. We tested sera from 661 necropsied southern sea otters sampled from 1997 to 2015 to determine overall exposure to influenza A viruses (IAVs) and to identify subtype-specific antibody responses. Using an enzyme-linked immunosorbent assay (ELISA), antibodies to IAV nucleoproteins were detected in 160 (24.2%) otters, with seropositive animals found in every year except 2008. When the ELISA-positive samples were tested by virus microneutralization, antibody responses were detected to avian-origin hemagglutinin subtypes H1, H3, H4, H5, H6, H7, H9, and H11. Strong antibody responses to pandemic H1N1 (pdmH1N1) were also detected, indicating that epizootic transmission of pdmH1N1 occurred among the southern sea otter population after the emergence of this human-origin virus in 2009. We conclude that southern sea otters are susceptible to infection with avian and human-origin IAV and that exposure to a wide array of subtypes likely occurs during a given otter's 10- to 15-yr life span. Important unanswered questions include what effect, if any, IAV infection has on sea otter health, and how these animals become infected in their nearshore environment.