Abstract
Dolphin and whale strandings provide a unique opportunity for gaining insight into the increasingly threatened health and conservation status of these iconic sea creatures. Indeed, all cetaceans are included in the International Union for the Conservation of Nature’s “red list” that periodically updates the extinction risk faced by each species. For this reason, all stranded cetaceans should undergo in-depth postmortem and ancillary investigations taking into special account the degree of autolysis of beached specimens. 10
Within such context, there are a number of spontaneously occurring cetacean diseases that morphologically resemble their human counterparts. This is especially true for central nervous system (CNS) disorders like Alzheimer’s disease (AD) and subacute sclerosing panencephalitis (SSPE). Despite being the most common form of dementia worldwide, AD cannot yet rely on animal models to faithfully recapitulate the entire spectrum of its key brain neuropathological features, namely, amyloid-β (Aβ) extra-neuronal plaques and hyperphosphorylated tau protein neurofibrillary tangles. 15 It is noteworthy that AD-like lesions were reported some years ago in the brain tissue from striped dolphins (Stenella coeruleoalba) and bottlenose dolphins (Tursiops truncatus) found stranded along the Spanish coastline. 11 Furthermore, AD-related immunohistopathologic changes have been recently described in stranded beaked whales (Ziphiidae), with these findings having been linked to cerebral hypoxia. 17 Most recently, AD-like neuropathology has been also reported in 3 oceanic odontocete species, namely, bottlenose dolphin, white-beaked dolphin (Lagenorhynchus albirostris), and long-finned pilot whale (Globicephala melas). 21
Beta-methylamino-
Another human CNS disease with which cetaceans share neuropathological similarities is SSPE. While SSPE is a rare neurological sequela found in a small subset of measles virus (MeV)–infected patients, striped dolphins infected by dolphin morbillivirus (DMV), which is a cetacean morbillivirus (CeMV) strain responsible for several mass die-offs of cetaceans from the Western Mediterranean, the Eastern Atlantic USA coast, and elsewhere in the last 35 years, 12 may develop a peculiar, “brain-only” form of infection. 8 SSPE-like lesions were detected in 25% of striped dolphins washed ashore along the Mediterranean Spanish coast after the 2006–2007 DMV epidemic, 20 with CeMV being regarded as a major pathogen responsible for cetacean stranding and death, alongside Herpesvirus, Brucella ceti, and Toxoplasma gondii, 3 additional neurotropic agents of concern to cetacean health and conservation.1,5,6,9,19
Despite the identification of neuronal and glial populations infected by DMV in striped dolphins carrying SSPE-like pathological changes, 14 the cell receptor(s) allowing viral persistence and spread throughout the brain is/are still unknown, with this knowledge gap being also present in the understanding of SSPE-affected people. 22 Conversely, MeV phosphoprotein (P), matrix (M), and fusion (F) gene mutations may promote viral spread in infected human brains, with subsequent SSPE development.2,18,22,23 Nevertheless, as we are dealing also in this case with descriptive findings, a much deeper genetic, biomolecular, and phenotypical definition of striped dolphin SSPE-like alterations is required before concluding they mirror (or not) their human “analogues.”
Cetacean diseases, with special emphasis on CNS disorders, may be also relevant from a “One Health” perspective, thus acting as putative “mirrors” for their human “counterparts,” and this should be adequately brought to the attention of marine mammal pathologists and, more in general, of the scientific biomedical community. Indeed, shedding light on the herein described encephalopathies may represent an intriguing opportunity from the comparative pathology viewpoint. This could also pave the way for an increased interest of the pathologists’ community in these and other neurological conditions that naturally affect dolphins and whales. Within such a framework, the potential impact of AD-like and SSPE-like pathologies and, more in general, of CNS disorders on cetacean health and conservation should be carefully assessed by means of in-depth postmortem and laboratory investigations on each stranded specimen. To this aim and in view of their extraordinary research potential, cetacean CNS disorders could also benefit from ad hoc investigation protocols allowing to characterize the differential expression of relevant host genes driving disease susceptibility/resistance. 23
Footnotes
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, authorship, and/or publication of this article.
