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Tattoo skin disease (TSD) is a poxviral dermatopathy diagnosed in cetaceans. We review the literature on TSD aetiology, clinical characteristics, pathology and epidemiology and evaluate immune responses against the virus. In addition, necropsy reports for fifty-five harbour porpoises (Phocoena phocoena), twenty-two Delphinidae and four Kogiidae stranded in northern California in 2018-2021 were checked for diagnostic tattoo lesions. TSD occurs in the Mediterranean, North and Barents Seas, as well as in the Atlantic, eastern Pacific and Indian Oceans in at least 21 cetacean species, with varying prevalence. Two cetacean poxvirus (CePV) clades are recognised: CePV-1 in odontocetes and CePV-2 in mysticetes. CePV-1 isolates were recovered from six Delphinidae and one Phocoenidae in the Americas, Europe and Hong Kong. Strains from Delphinidae are closely related. Among Phocoenidae, poxviruses were sampled only in harbour porpoises around the British Isles. CePV-2 isolates were obtained from southern right whales (Eubalaena australis) and a bowhead whale (Balaena mysticetus). In healthy animals, an immune response develops over time, with young calves protected by maternal immunity. Salinity and sea surface temperature do not seem to influence TSD prevalence in free-ranging cetaceans. High concentrations of immunotoxic halogenated organochlorines may cause a more severe clinical disease. Substitution and loss of genes involved in anti-viral immunity may favour CePV entry, replication and persistence in the epidermis. Off California, Delphinidae were less often (26.3%) affected by TSD than harbour porpoises (43.6%). Male porpoises were significantly more prone (58.1%) to show clinical disease than females (25%). Among males, TSD affected a high proportion of juveniles and subadults. TSD was not detected in the Kogiidae.

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Clinical and epidemiological features of tattoo skin disease (TSD) are reported for 257 common bottlenose dolphins held in 31 facilities in the Northern Hemisphere. Photographs and biological data of 146 females and 111 males were analyzed. Dolphins were classified into three age classes: 0-3 years, 4-8 years, and older than 9 years. From 2012 to 2014, 20.6% of the 257 dolphins showed clinical TSD. The youngest dolphins with tattoo lesions were 14 and 15 months old. TSD persisted from 4 to 65 months in 30 dolphins. Prevalence varied between facilities from 5.6% to 60%, possibly reflecting variation in environmental factors. Unlike in free-ranging Delphinidae, TSD prevalence was significantly higher in males (31.5%) than in females (12.3%). Infection was age-dependent only in females. Prevalence of very large tattoos was also higher in males (28.6%) than in females (11.1%). These data suggest that male T. truncatus are more vulnerable to TSD than females, possibly because of differences in immune response and susceptibility to captivity-related stress.

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We review the molecular and epidemiological characteristics of cetacean morbillivirus (CeMV) and the diagnosis and pathogenesis of associated disease, with six different strains detected in cetaceans worldwide. CeMV has caused epidemics with high mortality in odontocetes in Europe, the USA and Australia. It represents a distinct species within the Morbillivirus genus. Although most CeMV strains are phylogenetically closely related, recent data indicate that morbilliviruses recovered from Indo-Pacific bottlenose dolphins (Tursiops aduncus), from Western Australia, and a Guiana dolphin (Sotalia guianensis), from Brazil, are divergent. The signaling lymphocyte activation molecule (SLAM) cell receptor for CeMV has been characterized in cetaceans. It shares higher amino acid identity with the ruminant SLAM than with the receptors of carnivores or humans, reflecting the evolutionary history of these mammalian taxa. In Delphinidae, three amino acid substitutions may result in a higher affinity for the virus. Infection is diagnosed by histology, immunohistochemistry, virus isolation, RT-PCR, and serology. Classical CeMV-associated lesions include bronchointerstitial pneumonia, encephalitis, syncytia, and lymphoid depletion associated with immunosuppression. Cetaceans that survive the acute disease may develop fatal secondary infections and chronic encephalitis. Endemically infected, gregarious odontocetes probably serve as reservoirs and vectors. Transmission likely occurs through the inhalation of aerosolized virus but mother to fetus transmission was also reported.

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We reviewed prominent emerging infectious diseases of cetaceans, examined their potential to impact populations, re-assessed zoonotic risk and evaluated the role of environmental stressors. Cetacean morbilliviruses and papillomaviruses as well as Brucella spp. and Toxoplasma gondii are thought to interfere with population abundance by inducing high mortalities, lowering reproductive success or by synergistically increasing the virulence of other diseases. Severe cases of lobomycosis and lobomycosis-like disease (LLD) may contribute to the death of some dolphins. The zoonotic hazard of marine mammal brucellosis and toxoplasmosis may have been underestimated, attributable to frequent misdiagnoses and underreporting, particularly in developing countries and remote areas where carcass handling without protective gear and human consumption of fresh cetacean products are commonplace. Environmental factors seem to play a role in the emergence and pathogenicity of morbillivirus epidemics, lobomycosis/LLD, toxoplasmosis, poxvirus-associated tattoo skin disease and, in harbour porpoises, infectious diseases of multifactorial aetiology. Inshore and estuarine cetaceans incur higher risks than pelagic cetaceans due to habitats often severely altered by anthropogenic factors such as chemical and biological contamination, direct and indirect fisheries interactions, traumatic injuries from vessel collisions and climate change.

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