NOTE TO READER: The text below was developed by the Cook Inlet Beluga Whale Recovery Team and is a detailed description of an analysis of necropsies of 34 CI belugas conducted by Burek-Huntington et al. (2013) from 1998–2009. In Section II.D.3 of this document, we provided information on causes of death in necropsied CI belugas sufficient to justify recovery criteria and actions, including new information for necropsies of four CI belugas conducted from 2010– 2013 (for those four belugas, trauma was determined to be the cause of death; for additional details, see Huntington-Burek et al. 2015). Additional information about the necropsy results from 1998–2009 follows.
From 1998 to 2009, only 34 carcasses out of 136 observed dead stranded belugas (Table H1) were subjected to some degree of post-mortem examination or necropsy. These carcasses were concentrated close to Anchorage and along the road system (Figure H1). In the 34 CI beluga carcasses examined between 1998 to 2009, the cause of death was not identified in a third of the cases examined, primarily because the vast majority were in an advanced state of decomposition (Burek-Huntington et al. 2013). Categories of identified causes of death in CI belugas are discussed below.
Cause of death
CI beluga (1998 to 2009, n = 34) a
St. Lawrence Estuary beluga (1983 to 2012, n = 222) b
North American oceanaria beluga (1974 to 2000, n = 45)c
|o Combined bacterial / parasitic||6||0||0|
|o Not determined||0||0||4|
|Post live stranding||30||–||Not applicable|
Notes: Infectious disease causes are further broken down into different types of pathogens when possible. Parasitic diseases include those due to protozoa and to metazoan parasites. When a specific pathogen could not be isolated but the lesions were consistent with an infectious etiology, the cause of death was categorized as “Infectious disease-Not determined.” Miscellaneous causes of death included conditions with vague causation or conditions that did not fit well in the other categories including anaphylaxis and drowning in captive belugas, dystocia (abnormal labor or birth) in wild belugas, and fishing gear entanglement.
Perinatal mortalities included deaths of four fetuses and one neonatal beluga calf in Cook Inlet (Burek-Huntington et al. 2013). All four fetuses were in an advanced state of decomposition and a clear cause for the abortion or stranding was not found. It is noteworthy that all four fetuses were recovered in 2008, which may suggest a common cause, but the sample size and insufficient common findings from postmortem exams and testing makes it impossible to support such a conclusion. Neonatal mortalities and dystocia (complications during birth) have also been observed in aquariums and in animals from the SLE (Table H2). In the wild, carcasses of young animals would be harder to find due to their small size and tendency to sink, so perinatal mortalities are undoubtedly underreported. Olesiuk et al. (1990) inferred that mortality during the first few months of life of killer whales in British Columbia could be as high as 37–50%. Hammill (2007) reported a fairly low rate of neonatal mortalities in SLE belugas during the time period covered by the report; however, in 2010 to 2012 there has been a notable increase in perinatal morality for SLE beluga adult females and calves (P. Béland, St. Lawrence National Institute of Ecotoxicology, unpub. data).
Cause of death (n)
Cause of death (%)
Source: Burek-Huntington et al. 2013.
Nineteen of the 34 examined stranded CI belugas had at least one disease and 11 had two or more diseases considered contributory to death, including bacterial, viral, and parasitic diseases (Table H3). However, diseases are easily missed in decomposed carcasses, which describes most of those examined from Cook Inlet. Therefore, the reported contribution of disease to overall mortality rates represents a minimum (Burek-Huntington et al. 2013). A greater proportion of deaths due to infectious diseases was seen in SLE, 32% (S. Lair pers. comm. to C. Goertz), and in oceanaria, 51% (L. Dunn, pers. comm. to C. Goertz), where carcasses are more reliably accessed in a timely manner.
Bacteria: Bacterial infections implicated as the cause of death in examined CI belugas included a systemic infection, pneumonia, and lung abscess (Burek-Huntington et al. 2013). Culture of specific bacteria was not possible because of advanced decomposition, but organisms were seen on microscopic examination of tissues. Bacterial infection was the major cause of mortality in captive belugas (L. Dunn, pers. comm. to C. Goertz). Pathogenic bacteria isolated from captive beluga include Nocardia spp. (MacNeil et al. 1978), Erysipelothrix (Calle et al. 1993), Vibrio parahaemolyticus (Higgins 2000), Edwardsiella (Higgins 2000), and Mycobacterium (Bowenkamp et al. 2001). Several bacteria (Edwarsiella tarda, Aeromonas hydrophila, Vibrio cholera, Vibrio fluvialis, Kingella kingae, Morganella morganii, Pleisiomonas shigelloides, Shewanella putrefaciens, and Nocardia spp.) that affected SLE beluga are generally found in water with high loads of organic pollutants (L. Dunn, pers. comm.to C. Goertz; Martineau et al. 1988; De Guise et al. 1995a; Martineau 2003). The high bacterial load of the SLE likely contributes to these bacterial infections (St. Lawrence Centre 1996). Bacteria identified in the deaths of SLE belugas were typically opportunistic, normally found in the environment and/or healthy hosts, but usually only causing disease when the host’s immunological defenses were compromised. Any factor that results in a compromised immune system may render SLE belugas, and presumably other belugas, more susceptible to opportunistic bacteria.
Viruses: The only virus identified in CI belugas was the herpes virus, which was the cause of death in one case (Burek-Huntington et al. 2013). Herpes viral dermatitis was an incidental finding in other CI belugas examined post-mortem, and herpes-like marks have been observed in photographs of live CI belugas (T. McGuire, LGL, pers. comm.). This type of herpes infection is typically localized, usually not significant to the overall health of the animal, and eventually becomes latent leaving a distinctive scar. However, latent infections can be reactivated by such factors as stress and immune-suppression and can further compromise the individual (Kennedy et al. 1992). Serological testing for antibodies to viral diseases of concern is only possible with blood from a live or very freshly dead animal, which does not include any of the carcasses in the CI beluga mortality study; in addition, serological testing has not been done on samples from live-captured CI belugas, so it is unknown what other viruses may be active in this population. Viruses have been implicated in the death of three captive belugas including one with herpes virus-like particles identified by transmission electron microscopy (L. Dunn, pers. comm. to C. Goertz). A few SLE animals had microscopic lesions of non-suppurative encephalitis, most consistent with a viral etiology; however, a subsequent test could not identify a specific virus, and the clinical significance of these lesions was not always clear, even if this inflammation of the brain was believed to have been the cause of the stranding in the most severe cases (S. Lair, pers. comm. to C. Goertz).
Parasites: Significant parasitic infestations were noted in the lungs and kidneys of many necropsied CI belugas, sometimes in both sets of organs in the same individual. Thirteen animals (38%) had varying degrees of lungworm infection from incidental infection to association with bronchopneumonia. The species of pulmonary nematodes or roundworms in CI belugas has not been identified; species known to affect belugas include Pharurus pallasii, Stenurus artomarinus, Halocercus monoceris, and Stenurus minor (Measures 2001). In some beluga populations, infection with pulmonary nematodes was found in otherwise healthy robust animals, possibly suggesting a commensal relationship (Woshner et al. 2001). However, in SLE belugas, lungworms were listed as a significant factor in stranding mortalities (Martineau et al. 2003), and pneumonia, usually of parasitic origin, was one of the most common causes of death (De Guise et al. 1995b).
Single kidneys from 19 of 26 CI belugas contained a nematode identified as Crassicauda giliakiana, which has been only rarely observed in other beluga populations (Martineau et al. 1988, De Guise et al. 1995a, Vlasman and Campbell 2003, Burek-Huntington et al. 2013). While extensive damage and tissue replacement has been noted in some kidneys from CI belugas, it is unclear whether this change results in functional damage since up to 75% of a kidney can be damaged in other species before causing renal failure. However, heavy burdens could compromise young animals or individuals stressed by other conditions. The life cycle of C. giliakiana is not well understood. If an intermediate host is involved, the relatively high prevalence of kidney nematodes in CI belugas likely reflects a variation in their diet as compared to other beluga populations.
Other parasites found in CI belugas includes nematodes in the gastrointestinal tract (Anisakis or Contracaecum sp.) and in blubber (a Crassicauda sp.) as well as protozoa in muscle (Sarcosystis sp.), but were considered incidental and did not contribute to death (Burek- Huntington et al. 2013). One instance of a trematode infection, most likely a Campulid, was noted in a liver. Endoparasites found in other beluga populations include: gastrointestinal nematodes (Contracaecum spp., Anisakis simplex sometimes in association with ulcers, Leucastella arctica) (Klinkhart 1966; Department of Fisheries and Oceans [DFO] and World Wildlife Fund 1995); trematodes or flukes (Hadwenius seymouri); and protozoa (Toxoplasma and Sarcocysitis spp.) (Kenyon and Kenyon 1977, Wazura et al. 1986, De Guise et al. 1993, Martineau et al. 1994, Mikaelian et al. 2000, Measures 2001, Woshner 2001, Houde et al. 2003). Trichinella spiralis, a nematode found in muscle, was reported from one beluga from the Arctic coast of Alaska (Brandly and Rausch 1950). Many of these parasites are transmitted primarily through the ingestion of infected prey and often do not affect the host’s general health. Parasitic disease in captive animals is rarely seen due to the use of anthelminthics (i.e., drugs that expel parasitic worms from the body) and the practice of feeding restaurant-quality, frozen fish, which disrupts parasitic life cycles.
Type of disease
Cause of death
|Combined bacterial / parasitic infections||2|
|Nematode – kidney||14||5|
|Nematode – blubber||9|
|Nematode – lung||11||2|
|Nematode – stomach||5|
|Trematode – liver||1|
Source: Burek-Huntington et al. 2013.
Fungi: Fungal organisms, including candida and Aspergillus fumigatus, have been implicated in the deaths of some captive animals but may be related to the use of antibiotics, which, in addition to suppressing pathogenic bacteria, can also suppress normal flora that helps protect against fungal diseases. Additionally, captive facilities put belugas in closer proximity to environmental sources of fungal organisms, which are not normally found in open waters. However, fungal and other infectious organisms can be liberated during major earth-moving operations and may travel airborne some distance (Bowenkamp et al. 2001). There have been no reports of fungus-related death in Cook Inlet or SLE animals.
Harmful Algal Blooms (HABs): HABs have the potential of producing toxins that can kill marine mammals or make them more susceptible to death due to other causes, such as predation or boat strikes. Additionally, algal blooms are expected to increase with the warmer ocean conditions anticipated for Alaska in the coming years. As part of Food and Drug Administration requirements, the ADEC tests all commercial shellfish for Paralytic Shellfish Poisoning (caused by harmful algae) as part of their Marine Biotoxin Program. However, commercial shellfish harvesting in Cook Inlet is limited to the area between Polly Creek and Crescent River in upper Cook Inlet and to Kachemak Bay in lower Cook Inlet, leaving large areas unmonitored. Furthermore, ADEC does not routinely test for other harmful algal toxins. The Kachemak Bay Research Reserve participates in NOAA’s Phytoplankton Monitoring Network, though participation is relatively new and has been sporadic. A high-mortality event of SLE belugas was caused by an algal bloom in 2008 (Lair et al. 2009).
Findings of disease in other marine mammals in Cook Inlet: There is limited evidence of disease transfers among marine mammal species. However, because beluga and other species may be exposed to the same disease source via prey or the environment, understanding conditions that affect other marine mammals in Cook Inlet could provide insight into pathogens that might also affect belugas. Stranded harbor seals (n = 59) found in Cook Inlet during 1997 to 2011 were screened for a variety of diseases (Goertz, in prep). Most seals were young of the year and found by serology to be negative for evidence of exposure to the following diseases: avian influenza, canine distemper virus, dolphin morbillivirus, porpoise morbillivirus, Leptospira canicola, L. grippotyphosa, L. pomona, Neospora, Sarcocystis, and Toxoplasma. One animal tested positive for antibodies against Brucella spp. and another was positive for phocine distemper virus. A few animals tested positive for antibodies to seal herpesvirus-1, L. Bratislava, L. hardjo, and L. icterohemorrhagiae. All titers were stable or declining, suggesting waning maternally derived antibodies, except one animal had an increasing titer for seal herpesvirus-1. Fecal pathogen screenings yielded low levels of pathogenic and opportunistic bacteria, though none of concern for seal health. Causes of mortality and morbidity of Northern sea otters in Cook Inlet have also been intensely investigated, in part because of an unusual mortality event in lower Cook Inlet involving a streptococcal infection associated with heart damage, encephalitis, and sepsis. The source of the highly pathogenic bacteria and the conditions that may predispose sea otters to infection were not determined (Counihan-Edgar et al. 2012).
Trauma was the cause of death in three (9%) of the cases that formed the basis of the mortality review in Cook Inlet (Burek-Huntington et al. 2013); two cases involved killer whale interactions, and one was blunt trauma from an unknown source. Two lactating females were found dead with rake marks consistent with killer whale attacks, following an observed interaction between killer whales and a large group of belugas on 23–26 of September 2000 (Vos et al. 2005). Only one of these lactating females was necropsied and included in the mortality review. Another adult female found in 2007 had extensive blunt trauma, and the final trauma case was coded based on tissues collected in September 2008 from the site of a witnessed killer whale attack on a beluga. Net entanglements or propeller injuries were not confirmed in nonspecific trauma cases, which may have been due to the poor carcass conditions. Photo- identification studies have documented several live CI belugas with scars consistent with propeller injuries and rake marks (LGL 2009). Shelden et al. (2003) estimated killer whales kill an average of one beluga/year, although this could be an underestimate. Additional information about killer whale interactions is included in Sections II.D.1.and III.A.9. Of the 6% of SLE deaths attributed to trauma, the majority were due to boat strike (S. Lair, pers. comm. to C. Goertz). One beluga from an aquarium was euthanized due to complications associated with a mandibular infection secondary to a traumatic injury (L. Dunn, pers. comm. to C. Goertz).
Six belugas from Cook Inlet included in the mortality review were in poor body condition; namely, they were so thin that poor nutrition was considered either the cause of, or a contributing factor to, death (Burek-Huntington et al. 2013). One of the contributory cases involved a fetus with no measurable blubber layer, implying poor nutritional status of the mother. Causes of poor nutrition could be due to lack of appropriate prey, inability to obtain prey due to debilitation from secondary injury or infection, or a disease process itself. Most of these animals were young; only one was a mature whale. This category was not used in assigning cause of death in the SLE data that were provided; however, primary starvation is being considered as a cause of death in some cases currently assigned to the “other” category (S. Lair, pers. comm. to C. Goertz).
Cardiomyopathy, or heart damage, was noted but not considered a cause of, or contribution to, death in three older CI belugas and may have been age related. Ruptured vessels have been diagnosed in a captive animal with an aortic rupture (Bowenkamp et al. 2001) and in three SLE adult males with pulmonary trunk aneurysms (Martineau et al. 1986). Central nervous system abnormalities, namely encephalomalacia (softening of the brain) and encephalopathy (brain degeneration) of unknown cause, have been diagnosed in captive animals (L. Dunn, pers. comm. to C. Goertz). Due to the difficulties involved in opening a beluga skull in the field, it is rare that the brain of CI beluga is examined.
Ice entrapment: While reported in other cetaceans and other populations of belugas (Armstrong 1985, Heide-Jørgensen et al. 2002), there have not been reports of ice entrapment of CI belugas nor of mortalities that may have been due to such an event. Given the environmental conditions during the winter and decreased human presence in the Inlet, such an event may go unnoticed.
Cancer: Cancer is a major cause of mortality in SLE beluga (15%) and may relate to their heavy contaminant loads (Martineau et al. 2002). Cancers have also been observed in captive belugas (Ridgway et al. 2002) and accounted for 5% of the deaths in oceanaria (L. Dunn, pers. comm. to C. Goertz). There have been no reports of cancer in CI belugas.