Causes of death and pathogen prevalence in bottlenose dolphins Tursiops truncatus stranded in Alabama, USA, between 2015 and 2020, following the Deepwater Horizon oil spill.

Between 2010 and 2014, an unusual mortality event (UME) involving bottlenose dolphins Tursiops truncatus occurred in the northern Gulf of Mexico, associated with the Deepwater Horizon oil spill (DWHOS). Cause of death (COD) patterns in bottlenose dolphins since then have not been analyzed, and baseline prevalence data for Brucella ceti and cetacean morbillivirus, 2 pathogens previously reported in this region, are lacking. We analyzed records from bottlenose dolphins stranded in Alabama from 2015 to 2020 with necropsy and histological findings to determine COD (n = 108). This period included another UME in 2019 associated with prolonged freshwater exposure. A subset of individuals that stranded during this period were selected for molecular testing for Brucella spp. and Morbillivirus spp. Causes of death for all age classes were grouped into 6 categories, including (1) human interaction, (2) infectious disease, (3) noninfectious disease (prolonged freshwater exposure and degenerative), (4) trauma, (5) multifactorial, and (6) unknown. Two additional categories unique to perinates included fetal distress and in utero pneumonia. Human interaction was the most common primary COD (19.4%) followed closely by infectious disease (17.6%) and noninfectious disease (freshwater exposure; 13.9%). Brucella was detected in 18.4% of the 98 animals tested, but morbillivirus was not detected in any of the 66 animals tested. Brucella was detected in some moderately to severely decomposed carcasses, indicating that it may be beneficial to test a broad condition range of stranded animals. This study provides valuable information on COD in bottlenose dolphins in Alabama following the DWHOS and is the first to examine baseline prevalence of 2 common pathogens in stranded animals from this region.

Attenuated live infectious bronchitis virus QX vaccine disseminates slowly to target organs distant from the site of inoculation.

Infectious bronchitis (IB) is a highly contagious respiratory disease of poultry, caused by the avian coronavirus infectious bronchitis virus (IBV). Currently, one of the most relevant genotypes circulating worldwide is IBV-QX (GI-19), for which vaccines have been developed by passaging virulent QX strains in embryonated chicken eggs. Here we explored the attenuated phenotype of a commercially available QX live vaccine, IB Primo QX, in specific pathogens free broilers. At hatch, birds were inoculated with QX vaccine or its virulent progenitor IBV-D388, and postmortem swabs and tissues were collected each day up to eight days post infection to assess viral replication and morphological changes. In the trachea, viral RNA replication and protein expression were comparable in both groups. Both viruses induced morphologically comparable lesions in the trachea, albeit with a short delay in the vaccinated birds. In contrast, in the kidney, QX vaccine viral RNA was nearly absent, which coincided with the lack of any morphological changes in this organ. This was in contrast to high viral RNA titers and abundant lesions in the kidney after IBV D388 infection. Furthermore, QX vaccine showed reduced ability to reach and replicate in conjunctivae and intestines including cloaca, resulting in significantly lower titers and delayed protein expression, respectively. Nephropathogenic IBVs might reach the kidney also via an ascending route from the cloaca, based on our observation that viral RNA was detected in the cloaca one day before detection in the kidney. In the kidney distal tubular segments, collecting ducts and ureter were positive for viral antigen. Taken together, the attenuated phenotype of QX vaccine seems to rely on slower dissemination and lower replication in target tissues other than the site of inoculation.