Evaluation of cardiac lesions and risk factors associated with myocarditis and dilated cardiomyopathy in southern sea otters (Enhydra lutris nereis)

Kreuder, Christine; Miller, Melissa A.; Lowenstine, Linda J.; Conrad, Patricia A.; Carpenter, Tim E.; Jessup, David A.; Mazet, Jonna A. K.

doi:10.2460/ajvr.2005.66.289

Cited by 69 publications

(57 citation statements)

References 66 publications

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“…1). These study sites were selected based on previous work showing high otter mortality or exposure to T. gondii and S. neurona in these regions (Miller et al, 2002a;Kreuder et al, 2003;Kreuder et al, 2005;. All fresh carcasses recovered in good postmortem condition (postmortem interval ,72 hr) from the two study sites between January 1998 and December 2004, and that received a full necropsy by pathologists, were considered for inclusion in the study.…”

Section: Sea Otter Case Selectionmentioning

confidence: 99%

“…Protozoal mortality cases were selected if T. gondii or S. neurona encephalitis were identified as the primary or contributing cause of death according to the following case definition. A histopathologic diagnosis of ''protozoal encephalitis'' (PE) was defined when moderate to severe inflammation of brain tissue was observed in association with proliferating protozoa (Kreuder et al, 2003). Toxoplasma gondii mortality cases were defined based on presence of multifocal, lymphoplasmacytic protozoal encephalitis on histopathology, combined with T. gondii isolation in cell culture from brain or positive staining on immunohistochemistry (IHC; Miller et al, 2002b).…”

Section: Sea Otter Case Selectionmentioning

confidence: 99%

“…Infections with the two protozoan parasites Toxoplasma gondii and Sarcocystis neurona, are leading causes of deaths in sea otters. These pathogens can cause severe encephalitis and infections with T. gondii or S. neurona collectively listed as primary causes of death of 23% of beach-cast otter carcasses examined between 1998 and 2001 (Kreuder et al, 2003). In addition to causing mortality in sea otters, T. gondii is a zoonotic pathogen that infects up to one third of the human population (Hill and Dubey, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Temporal Association Between Land-Based Runoff Events and California Sea Otter (Enhydra Lutris Nereis) Protozoal Mortalities

Shapiro¹,

Miller²,

Mazet³

2012

Journal of Wildlife Diseases

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ABSTRACT:Toxoplasma gondii and Sarcocystis neurona have caused significant morbidity and mortality in threatened Southern sea otters (Enhydra lutris nereis) along the central California coast. Because only terrestrial animals are known to serve as definitive hosts for T. gondii and S. neurona, infections in otters suggest a land to sea flow of these protozoan pathogens. To better characterize the role of overland runoff in delivery of terrestrially derived fecal pathogens to the near shore, we assessed the temporal association between indicators of runoff and the timing of sea otter deaths due to T. gondii and S. neurona. Sea otter stranding records 1998-2004, from Monterey and Estero bays were reviewed and cases identified for which T. gondii or S. neurona were determined to be a primary or contributing cause of death. Precipitation and stream flow data from both study sites were used as indicators of land-based runoff. Logistic regression was applied to determine if a temporal association could be detected between protozoal mortalities and runoff indicators that occur in the 2 mo preceding mortality events. A significant association was found between S. neurona otter deaths at Estero Bay and increased stream flow that occurred 30-60 days prior to mortality events. At this site, the cause of otter mortality following increased river flows was 12 times more likely to be S. neurona infection compared with nonprotozoal causes of death. There were no significant associations between the timing of T. gondii otter deaths and indicators of overland runoff. Our results indicate that the association between overland runoff and otter mortalities is affected by geography as well as parasite type, and highlight the complex mechanisms that influence transmission of terrestrially derived pathogens to marine wildlife. Policy and management practices that aim to mitigate discharges of contaminated overland runoff can aid conservation efforts by reducing pathogen pollution of coastal waters, which impacts the health of threatened marine wildlife and humans.

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Section: Sea Otter Case Selectionmentioning

confidence: 99%

Section: Sea Otter Case Selectionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Temporal Association Between Land-Based Runoff Events and California Sea Otter (Enhydra Lutris Nereis) Protozoal Mortalities

Shapiro¹,

Miller²,

Mazet³

2012

Journal of Wildlife Diseases

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“…Inflammatory cells were also observed in both the atrial and ventricular myocardium. 26 In contrast, however, DOM toxicity studies conducted on an exposed Californian sea lion population showed myocardial degeneration limited to the ventricles. 28 The link between DOM exposure and the reported cardiomyopathies has not as yet been characterized, and it remains to be determined whether the damage is the consequence of a direct (ie, cardiotoxic) or indirect [ie, central nervous system (CNS)/autonomic discharge] interaction.…”

mentioning

confidence: 97%

“…26,27 Cardiac lesions within a Californian sea otter population have been described to include myocardial pallor and multifocal myocardial necrosis associated with myocardial hemorrhage. Inflammatory cells were also observed in both the atrial and ventricular myocardium.…”

mentioning

confidence: 99%

Ischemic Cardiomyopathy Following Seizure Induction by Domoic Acid

Vranyac-Tramoundanas

Harrison

Sawant

et al. 2011

The American Journal of Pathology

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Exposure to the excitotoxin domoic acid (DOM) has been shown to produce cardiac lesions in both clinical and animal studies. We have previously shown that DOM failed to directly affect cardiomyocyte viability and energetics, but the development of this cardiomyopathy has remained unexplained. The present study compared effects of high-level seizure induction obtained by intraperitoneal (2 mg/kg) or intrahippocampal (100 pmol) bolus administration of DOM on development of cardiac pathologies in a rat model. Assessment of cardiac pressure derivatives and coronary flow rates revealed a significant time-dependent decrease in combined left ventricular (LV) systolic and diastolic function at 1, 3, 7, and 14 days after intraperitoneal administration and at 7 and 14 days after intrahippocampal DOM administration. LV dysfunction was matched by a similar time-dependent decrease in mitochondrial respiratory control, associated with increased proton leakage, and in mitochondrial enzyme activities. Microscopic examination of the LV midplane revealed evidence of progressive multifocal ischemic damage within the subendocardial, septal, and papillary regions. Lesions ranged from reversible early damage (vacuolization) to hypercontracture and inflammatory necrosis progressing to fibrotic scarring. Plasma proinflammatory IL-1␣, IL-1␤, and TNF-␣ cytokine levels were also increased from 3 days after seizure induction. The observed cardiomyopathies did not differ between intraperitoneal and intrahippocampal groups, providing strong evidence that cardiac damage after DOM exposure is a consequence of a seizure-evoked autonomic response.

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The Molecular and Integrative Basis to Domoic Acid Toxicity

Ramsdell¹

2007

Phycotoxins: Chemistry and Biochemistry

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Evaluation of cardiac lesions and risk factors associated with myocarditis and dilated cardiomyopathy in southern sea otters (Enhydra lutris nereis)

Cited by 69 publications

References 66 publications

Temporal Association Between Land-Based Runoff Events and California Sea Otter (Enhydra Lutris Nereis) Protozoal Mortalities

Temporal Association Between Land-Based Runoff Events and California Sea Otter (Enhydra Lutris Nereis) Protozoal Mortalities

Ischemic Cardiomyopathy Following Seizure Induction by Domoic Acid

The Molecular and Integrative Basis to Domoic Acid Toxicity

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