-We present prevalence of Bartonella spp. for multiple cohorts of wild and captive cetaceans. One hundred and six cetaceans including 86 bottlenose dolphins (71 free-ranging, 14 captive in a facility with a dolphin experiencing debility of unknown origin, 1 stranded), 11 striped dolphins, 4 harbor porpoises, 3 Risso's dolphins, 1 dwarf sperm whale and 1 pygmy sperm whale (all stranded) were sampled. Whole blood (n = 95 live animals) and tissues (n = 15 freshly dead animals) were screened by PCR (n = 106 animals), PCR of enrichment cultures (n = 50 animals), and subcultures (n = 50 animals). Bartonella spp. were detected from 17 cetaceans, including 12 by direct extraction PCR of blood or tissues, 6 by PCR of

Aflatoxin B1 (AFB1) is a mycotoxin which causes toxicity through oxidative damage. Selenium (Se), an antioxidative agent, can antagonize some toxicity induced by oxidative stress. The aim of this work was to investigate the toxicity of AFB1 and the protective effects of Se on duckling liver in vivo. The study consisted of three groups: AFB1, AFB1Tx, and a control group. AFB1 group was administered aflatoxin intragastrically (0.1 mg/kg body weight). AFB1Tx group was administered AFB1 intragastrically (0.1 mg/kg body weight) plus sodium selenite (1 mg/kg body weight). The control group was given the same volume of dimethyl sulfoxide (DMSO) via intragastric intubation. All three groups received daily administrations for 28 days. Blood samples were obtained on the 14th, 21st, and 28th days of post-administration, and the serum alanine aminotransferase (ALT) and aspartate transaminase (AST) were evaluated. A high level of serum ALT and AST was observed in AFB1 group. The activity of ALT and AST was significantly lower in Se treatment group than those in AFB1 group. Liver samples were collected on the 14th, 21st, and 28th days of post-administration, and concentrations of Bcl-2, Bax, caspase-3, and p53 were measured. Increased expression level of Bax, caspase-3, and p53 and decreased Bcl-2 expression level and Bcl-2/Bax ratio were observed in AFB1 group. Se diminished hepatic dysfunction, or damage and modulated the expression of apoptotic related proteins, in a time-dependent manner. In conclusion, concurrent treatment with Se reduced the AFB1-induced hepatic dysfunction and apoptosis.

The potential for stranded dolphins to serve as a tool for monitoring free-ranging populations would be enhanced if their stocks of origin were known. We used stable isotopes of carbon, nitrogen, and sulfur from skin to assign stranded bottlenose dolphins Tursiops truncatus to different habitats, as a proxy for stocks (demographically independent populations), following the Deepwater Horizon oil spill. Model results from biopsy samples collected from dolphins from known habitats (n = 205) resulted in an 80.5% probability of correct assignment. These results were applied to data from stranded dolphins (n = 217), resulting in predicted assignment probabilities of 0.473, 0.172, and 0.355 to Estuarine, Barrier Island (BI), and Coastal stocks, respectively. Differences were found west and east of the Mississippi River, with more Coastal dolphins stranding in western Louisiana and more Estuarine dolphins stranding in Mississippi. Within the Estuarine East Stock, 2 groups were identified, one predominantly associated with Mississippi and Alabama estuaries and another with western Florida. δ 15 N values were higher in stranded samples for both Estuarine and BI stocks, potentially indicating nutritional stress. High probabilities of correct assignment of the biopsy samples indicate predictable variation in stable isotopes and fidelity to habitat. The power of δ 34 S to discriminate habitats relative to salinity was essential. Stable isotopes may provide guidance regarding where additional testing is warranted to confirm demographic independence and aid in determining the source habitat of stranded dolphins, thus increasing the value of biological data collected from stranded individuals.

The potential role of morbillivirus was evaluated in the deaths of >1100 bottlenose dolphins Tursiops truncatus and other small cetaceans that stranded from February 2010 through July 2014, during the northern Gulf of Mexico (GoM) unusual mortality event (UME). Morbillivirus analysis was carried out on 142 live or freshly dead cetaceans and results were combined with samples from 102 live, free-ranging bottlenose dolphins sampled during capture-release health assessments conducted from 2011 to 2014. Polymerase chain reaction (PCR) testing for morbillivirus showed that 9.9% (14/142) of the stranded cetaceans and 1% (1/83) of the free-ranging live dolphins were positive for dolphin morbilliviral (DMV) RNA. In contrast, previous DMV dolphin die-offs had DMV detectable by PCR in 61 to 97% of animals tested. Histologic findings consistent with morbillivirus infection, including lymphoid depletion, bronchointerstitial pneumonia, syncytial cell formation, or meningoencephalitis, were found in 6.6% (9/136) of the cetaceans that underwent histologic examinations. Serological analysis using a virus neutralization assay found that 29% (5/17) of live stranded and 23% (23/102) of live free-ranging bottlenose dolphins had titers of 64 or greater for cetacean morbillivirus, indicating prior but not necessarily recent exposure to morbillivirus. Current findings suggest that DMV infection, although present in the northern GoM, was sporadic and occurred at low levels and therefore was not the primary cause of the northern GoM UME. Confirmation of DMV infections and existing DMV titers demonstrate continued exposure to morbillivirus among northern GoM cetaceans since the first detection of this virus in the early 1990s.

Serum sucrose concentrations in samples collected during routine health evaluations of captive dolphins can be reliably measured by use of LC-MS-MS. Correlating serum sucrose concentrations with endoscopic observations of the gastric mucosa of dolphins will validate this approach for use in screening for the prevalence and severity of gastric ulcers and determining the efficacy of treatment regimens.