Bartonella species detection in captive, stranded and free-ranging cetaceans

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 enrichment cultures, and 4 by subculture isolation. Bartonella spp. were more commonly detected from the captive (6/14, 43%) than from free-ranging (2/71, 2.8%) bottlenose dolphins, and were commonly detected from the stranded animals (9/21, 43%; 3/11 striped dolphins, 3/4 harbor porpoises, 2/3 Risso's dolphins, 1/1 pygmy sperm whale, 0/1 dwarf sperm whale, 0/1 bottlenose dolphin). Sequencing identified a Bartonella spp. most similar to B. henselae San Antonio 2 in eight cases (4 bottlenose dolphins, 2 striped dolphins, 2 harbor porpoises), B. henselae Houston 1 in three cases (2 Risso's dolphins, 1 harbor porpoise), and untyped in six cases (4 bottlenose dolphins, 1 striped dolphin, 1 pygmy sperm whale). Although disease causation has not been established, Bartonella species were detected more commonly from cetaceans that were overtly debilitated or were cohabiting in captivity with a debilitated animal than from free-ranging animals. The detection of Bartonella spp. from cetaceans may be of pathophysiological concern

Relationship between plasma iron concentration and gastric pH in captive adult bottlenose dolphins (Tursiops truncatus)

OBJECTIVE: To determine the correlation between plasma iron concentrations and gastric pH in a population of captive Atlantic bottlenose dolphins (Tursiops truncatus). ANIMALS: 6 adult female dolphins that ranged from 16 to 30 years of age. PROCEDURES: Blood and gastric samples were collected from each dolphin to allow measurement of plasma iron concentrations and gastric pH, respectively. Samples were collected each month for 12 months. RESULTS: Within each dolphin, plasma iron concentrations and gastric pH did not differ significantly over time. There was a strong negative correlation (r = -0.85) between plasma iron concentration and gastric pH, which suggested that dolphins with a lower gastric pH had a higher plasma iron concentration. CONCLUSIONS AND CLINICAL RELEVANCE: Analysis of results reported here suggested that gastric pH may play an important role in iron absorption in dolphins

Hematoxylin and eosin (HE) stained section of liver from a juvenile dolphin that stranded fresh dead in Barataria Bay in July 2012.

<p>There is severe centrilobular hepatocellular vacuolation, necrosis, and loss with lobular collapse (arrow). Star indicates a portal triad. Arrow head indicates unaffected liver parenchyma for comparison. Bar = 500μm.</p

Prevalence comparisons of lesions detected using histologic examination for fresh dead, stranded common bottlenose dolphins (<i>Tursiops truncatus</i>) among 1) UME cases from Louisiana, Mississippi, and Alabama, 2) Barataria Bay, Louisiana UME subset, 3) all reference dolphins, and 4) slide-reviewed and standardly scored reference dolphin subset.

<p>Denominators varied based upon information available, tissues collected from, and tests conducted on individual UME and reference dolphins.</p><p>¹Barataria Bay, Louisiana UME dolphin subset values different (<i>P</i> < 0.05) than standardly scored reference dolphins.</p><p>²UME dolphin values different (<i>P</i> < 0.05) than full reference group.</p><p>³Represents encephalitis, meningitis, or meningoencephalitis.</p><p>C:M = adrenal corticomedullary ratio. CNS = central nervous system.</p><p>Prevalence comparisons of lesions detected using histologic examination for fresh dead, stranded common bottlenose dolphins (<i>Tursiops truncatus</i>) among 1) UME cases from Louisiana, Mississippi, and Alabama, 2) Barataria Bay, Louisiana UME subset, 3) all reference dolphins, and 4) slide-reviewed and standardly scored reference dolphin subset.</p

Prevalence comparisons of lung lesions detected using histologic examination for fresh dead, stranded common bottlenose dolphins (<i>Tursiops truncatus</i>) among UME dolphins from 1) Louisiana, Mississippi, and Alabama, 2) slide-reviewed and standardly scored reference dolphin subset, 3) Barataria Bay, Louisiana UME dolphin subset, 4) and all reference dolphins.

<p>Denominators varied based upon information available, tissues collected from, and tests conducted on individual UME and reference dolphins.</p><p>¹Barataria Bay, Louisiana UME dolphin subset values different (<i>P</i> < 0.05) than standardly scored references;</p><p>²All reference dolphin values different (<i>P</i> < 0.05) than all UME dolphins</p><p>Prevalence comparisons of lung lesions detected using histologic examination for fresh dead, stranded common bottlenose dolphins (<i>Tursiops truncatus</i>) among UME dolphins from 1) Louisiana, Mississippi, and Alabama, 2) slide-reviewed and standardly scored reference dolphin subset, 3) Barataria Bay, Louisiana UME dolphin subset, 4) and all reference dolphins.</p

Total number, stranding dates, and locations of 152 freshly dead stranded non-perinatal (greater than or equal to 115 cm in total body length) common bottlenose dolphins (<i>Tursiops truncatus</i>) from the ongoing northern Gulf of Mexico cetacean Unusual Mortality Event (UME) and reference groups.

<p>Standardly scored subset references had both histopathology reports and archived tissues available for evaluation.</p><p>Total number, stranding dates, and locations of 152 freshly dead stranded non-perinatal (greater than or equal to 115 cm in total body length) common bottlenose dolphins (<i>Tursiops truncatus</i>) from the ongoing northern Gulf of Mexico cetacean Unusual Mortality Event (UME) and reference groups.</p

Hematoxalin and eosin (HE) stained section of lung from an adult female common bottlenose dolphin (<i>Tursiops truncatus</i>) that stranded in Barataria Bay, Louisiana in December 2011 with primary bacterial pneumonia.

<p>Airspaces and septae are obscured by accumulations of neutrophils and fibrous connective tissue that surround large bacterial colonies (arrows). Bar = 500 μm.</p

Adrenal Gland and Lung Lesions in Gulf of Mexico Common Bottlenose Dolphins (<i>Tursiops truncatus</i>) Found Dead following the <i>Deepwater Horizon</i> Oil Spill

<div><p>A northern Gulf of Mexico (GoM) cetacean unusual mortality event (UME) involving primarily bottlenose dolphins (<i>Tursiops truncatus</i>) in Louisiana, Mississippi, and Alabama began in February 2010 and continued into 2014. Overlapping in time and space with this UME was the <i>Deepwater Horizon</i> (DWH) oil spill, which was proposed as a contributing cause of adrenal disease, lung disease, and poor health in live dolphins examined during 2011 in Barataria Bay, Louisiana. To assess potential contributing factors and causes of deaths for stranded UME dolphins from June 2010 through December 2012, lung and adrenal gland tissues were histologically evaluated from 46 fresh dead non-perinatal carcasses that stranded in Louisiana (including 22 from Barataria Bay), Mississippi, and Alabama. UME dolphins were tested for evidence of biotoxicosis, morbillivirus infection, and brucellosis. Results were compared to up to 106 fresh dead stranded dolphins from outside the UME area or prior to the DWH spill. UME dolphins were more likely to have primary bacterial pneumonia (22% compared to 2% in non-UME dolphins, <i>P</i> = .003) and thin adrenal cortices (33% compared to 7% in non-UME dolphins, <i>P</i> = .003). In 70% of UME dolphins with primary bacterial pneumonia, the condition either caused or contributed significantly to death. Brucellosis and morbillivirus infections were detected in 7% and 11% of UME dolphins, respectively, and biotoxin levels were low or below the detection limit, indicating that these were not primary causes of the current UME. The rare, life-threatening, and chronic adrenal gland and lung diseases identified in stranded UME dolphins are consistent with exposure to petroleum compounds as seen in other mammals. Exposure of dolphins to elevated petroleum compounds present in coastal GoM waters during and after the DWH oil spill is proposed as a cause of adrenal and lung disease and as a contributor to increased dolphin deaths.</p></div

Prevalence comparisons of causes of death for fresh dead, stranded common bottlenose dolphins (<i>Tursiops truncatus</i>) among 1) unusual mortality event cases from Louisiana, Mississippi, and Alabama, 2) slide-reviewed and standardly scored reference dolphin subset, 3) Barataria Bay, Louisiana UME dolphin subset, and 4) all reference dolphins.

<p>Denominators varied based upon information available, tissues collected from, and tests conducted on individual UME and reference dolphins.</p><p>*Values different (<i>P</i> < 0.05) than reference dolphins.</p><p>Prevalence comparisons of causes of death for fresh dead, stranded common bottlenose dolphins (<i>Tursiops truncatus</i>) among 1) unusual mortality event cases from Louisiana, Mississippi, and Alabama, 2) slide-reviewed and standardly scored reference dolphin subset, 3) Barataria Bay, Louisiana UME dolphin subset, and 4) all reference dolphins.</p

Prevalence of key histologic lesions among fresh dead, stranded common bottlenose dolphins (<i>Tursiops truncatus</i>) by year in Louisiana, Mississippi & Alabama: June 2010 to December 2012.

<p>The gray line represents the percentage of lesion prevalence among standardly scored reference dolphins. All years had prevalence of lesions greater than the reference group (<i>P</i> > 0.05).</p