Marine Mammal Center

Since 2020, H5Nx highly pathogenic avian influenza viruses (HPAIVs) have caused widespread disruptions not only to global agriculture and trade but also to the health of free-ranging wildlife. Pinnipeds have experienced greater mortality from H5Nx HPAIV than any other mammalian taxa. Emergent virus strains, persisting over long time periods and vast geographic distances, have repeatedly triggered large-scale mortality events in pinniped populations. Of particular concern is the spread of H5Nx HPAIV to the Southern Hemisphere—including the emergence of a marine mammal-adapted clade in South America and detections in the sub-Antarctic and Antarctic—and to other remote ecosystems such as the Hawaiian Islands. These developments elevate concern for the world’s endangered, isolated, and endemic pinnipeds. While managing HPAIV in any animal population is a formidable task, working with free-ranging marine mammals poses unique challenges. In this review and perspective piece, we attempt to synthesize complexities at this intersection. We describe lessons learned from HPAIV investigations in marine wildlife, highlight gaps in knowledge and capacity, and discuss the incorporation of outbreak risk assessment and countermeasures into pinniped conservation. Finally, we propose ways that pinnipeds—and marine wildlife broadly—could be better integrated into existing systems for HPAIV intelligence, control, and prevention.

Domoic acid-producing algal blooms are increasing in size, frequency, and duration along the eastern Pacific coastline resulting in regular and repeated exposure of marine mammals to the toxin. Because of their prolonged gestation, large numbers of marine mammals are now encountering this excitotoxin in utero, with potential long-term developmental effects. Evidence of developmental neurotoxic effects is accumulating in California sea lions particularly, which serve as an accessible sentinel species for studying the effects of domoic acid exposure in mammals. In biomedical settings, rodent models have revealed some developmental aspects of early domoic acid exposure, including a tendency for gross neurobehavioral changes to emerge after puberty. However, rodents are altricial and have a truncated developmental course. In contrast, marine mammals are precocial and mature slowly. Further, neurobehavioral responses to domoic acid have notable differences between those in adult rodents exposed in vivariums and in free-ranging wildlife. Primate models address some of these gaps, but are limited by practical constraints. There is a clear need to establish an ecologically valid model of brain development and clinical progression of developmental domoic acid exposure in long-lived and precocial mammals. Here we present California sea lions born in wildlife rehabilitation facilities to mothers with documented domoic acid toxicosis as a promising and accessible disease model, and we provide a framework for future research. Hundreds of adult sea lions in rehabilitation centers have already taken part in veterinary assessments and experimental assays of brain and behavior, demonstrating the plausibility of careful and scalable science with these animals. We discuss preliminary work with a juvenile sea lion enrolled in a longitudinal study with repeated clinical, behavioral, and neurobiological assessment, and advocate for cohort-based studies of maternally exposed sea lions.

Background/Objectives: Human-driven environmental change can promote cancer development in wild species, yet the pathophysiology of wildlife cancers remain largely unexplored. Urogenital carcinoma (UGC) in the California sea lion (CSL) (Zalophus californianus) is one of the most common cancer types documented in any wild mammal. The pathogenesis of UGC in CSLs is known to be multifactorial, with links to environmental contaminant exposure and infection by Otarine Herpesvirus-1 (OtHV-1); however, the genomic features of these cancers have not been thoroughly explored. Understanding UGC pathogenesis in the CSL has important implications for the health of humans and other species that share environment and diet. Methods: We leveraged the evolutionary conservation between the domestic dog and CSL genomes to perform cross-species whole-exome sequencing (WES) of CSL UGC tumors and matched normal tissue pairs. We also used PCR and Sanger sequencing to investigate the prevalence of DNA from OtHV-1. Results: Bioinformatic analyses identified shared somatic variants and DNA copy number aberrations in UGC tumor samples, including recurrent exonic single-nucleotide variants in CD274/PD-L1, and recurrent copy number gains in CD274/PD-L1, TNFRSF14, CD200, CDK4, and PLCG2. In an extended cohort of 70 CSLs (tumor, matched normals, and controls), a recurrent C > T single-nucleotide variant in exon 4 of CD274/PD-L1 was identified in 54 of 68 (79.4%) CSLs with diagnosed UGC. OtHV-1 DNA was detected in 67 of 70 individuals (95.8%). Conclusions: These results demonstrate that cross-species exome capture provides a means to identify genomic alterations that may play a role in the molecular pathogenesis of UGC in the CSL and adds to the body of evidence for an association between OtHV-1 and UGC in this species.

A unique clinical syndrome characterized by polyphasic rhabdomyositis associated with Sarcocystis neurona has been reported in both free-ranging and managed care California sea lions (CSLs; Zalophus californianus). The pathogenesis of this disease is poorly understood. Specific S. neurona genotypes have been associated with more severe sarcocystosis and mortality in other marine mammals; however, S. neurona genotypes infecting CSLs with rhabdomyositis have not yet been investigated. The objective of this study was to characterize genotypes of S. neurona from CSLs with rhabdomyositis and to compare these with genotypes described in other marine and terrestrial hosts. Archived skeletal muscle samples from 25 affected free-ranging CSLs were screened for S. neurona DNA using polymerase chain reaction (PCR) targeting a multi-copy locus (ITS1), followed by genotype characterization using a PCR-based multilocus sequence typing approach targeting six polymorphic loci. Among these 25 CSLs, 15 different S. neurona genotypes were identified. Of these, six have been previously identified in southern sea otters (Enhydra lutris nereis) and/or other hosts, but the remaining nine have not been reported in any host to date. This study, although limited in sample size, demonstrates a wide diversity of S. neurona genotypes infecting free-ranging CSLs affected with rhabdomyositis, some shared with other hosts in the region, but many others that appear to be unique to sea lions.

BACKGROUND:Historically, dermatological disease is a common cause for rescue of northern elephant seals (NES) in California, yet its aetiology and pathogenesis remain poorly understood. OBJECTIVES:To provide the first formal histological and ultrastructural description of two hair shaft lesions in NES: crescentic hair shaft defects (CHSD) and fungal (piedra)-like lesions (PLL). ANIMALS:Forty-one animals from The Marine Mammal Center and 10 animals from San Nicolas Island were examined, 38 with skin lesions and 13 without. MATERIALS AND METHODS:Age, sex, comorbidities, cause-of-death, gross skin lesions and evidence of northern elephant seal skin disease (NESSD) were recorded. Histologically, we examined each case for CHSD, PLL, suppurative luminal folliculitis (SLF), furunculosis, bacteria and fungal elements within CHSD, and fungal elements within follicular lesions. Grocott-Gomori methenamine silver, Gram and Fontana-Masson's stains were performed on 17, 11 and 8 cases, respectively. RESULTS:NESSD, CHSD, PLL, SLF and furunculosis were noted in 10 of 38 (26%), 23 of 38 (61%), 23 of 38 (61%), 20 of 38 (53%) and 6 of 38 (16%) animals with skin lesions, respectively. Within CHSD lesions, bacteria were identified in 13 animals and fungi in seven. CHSD and PLL frequently co-occurred, limited to NES over 7.5 months old and often associated with SLF, and were observed exclusively in animals with dermatological disease and present in most cases of NESSD, suggesting a pathological association. Panfungal PCR from 10 animals identified several fungi, including Cladosporium spp., a reported cause of white piedra in humans. CONCLUSIONS AND CLINICAL RELEVANCE:Although the aetiology of CHSD remains unclear, we suggest that fungal and/or bacterial colonisation of the hair shaft may contribute.