Abstract

Hawaiian monk seals (Monachus schauinslandi) are among the most endangered pinnipeds in the world. These animals are distributed throughout the leeward sides of the northwestern Hawaiian Islands and occasionally frequent the main islands. Over the course of the last 5 decades, there has been a dramatic decline in overall population census, which has been attributed in large part to shark predation, human disturbances, biotoxins (ciguatera intoxication), net entanglement, and pollution. To establish baseline information on the health status of monk seals on Laysan Island, a preliminary field investigation was undertaken in May 1978. The examined animals included 10 live yearling and juvenile seals, as well as a single adult animal that were captured and sampled for clinical chemistry, hematology, serology (calicivirus and Leptospira spp), attempted virus isolation (on Vero and PK-15 cell lines), rectal Salmonella culture, and fecal parasitology. Tissues from an additional 13 dead animals were obtained for microscopic assessment and representative tissues were harvested for dioxin and ciguatoxin analysis. Three live animals were emaciated. There were select individuals with abnormal hematology and clinical chemistry results. Bacterial culture of rectal swabs yielded Edwardsiella tarda from 7-8 animals and Salmonella sieburg from a single individual. No viruses or Leptospira spp were recovered and 1 seal had serum neutralizing antibodies to calicivirus (1:40 for VESV I55). Multiple, mixed cestode and nematode parasites were identified within the feces and gastrointestinal tracts of posted animals, including Corynosoma rauschi, Contracaecum turgidum, Diphyllobothrium caeroni, D elegans, and D hians. Pathologic findings included generalized emaciation with occasional serous atrophy in all 13 individuals, pulmonary hemorrhage and congestion (8/15 examined animals), putative lymphoid depletion, ulcerative gastritis with intralesional nematodes, and eosinophilic enteritis due to cestodes. In this case series, individual animals were positive for ciguatoxin and maitotoxin and there was detectable dioxan in sampled livers.

In a follow up review of diagnostic findings of 42 animals (neonates to adults) examined between 1981 to 1985, primary disease processes included emaciation, parasitism, trauma, infections (localized inflammation to generalized septicemia), a few cases of acquired and congenital cardiovascular disease, pneumonia, and sporadic ectopic (dystrophic) calcification, ophthalmologic disease, and gall stones. Ancillary diagnostic testing was not documented in the report. To further resolve pathologic entities and assess possible emergence of novel disease processes which may have contributed to monk seal morbidity and mortality, an overview of 90 additional cases (consisting of 84 necropsies and 6 biopsies) recorded between 1989 and 2004 was initiated.

Through public education and trained field staff, National Marine Fisheries Service has increased surveillance and attendance of dead and moribund monk seals. Field post mortem examinations are generally conducted on-site and after pertinent location and historical information have been documented, morphometric data are recorded and representative tissues for histopathology are harvested. Duplicate formalin fixed tissues are forwarded to a veterinary diagnostic laboratory (Colorado State University) and an independent reference laboratory (the Armed Forces Institute of Pathology) for histopathology and there was good concordance between pathologic findings in examined case reports between the respective facilities.

Evaluation of diagnostic findings between 1992 and 2004 revealed comparable pathologic findings to previous observations, including emaciation, parasitism, trauma (including shark attack, mobbing, post partum crush injury and a single incident of rope entanglement), ophthalmic lesions, congenital anomalies, dental wear, and (pleuro)pneumonia (Table 1). Prime differences with this review and previous case reports included detection of liver parasites (hepatozoonosis), myocellular sarcocystosis, presumptive herpesvirus infections, lymphoid depletion (predominantly in neonates and juveniles), thyroid colloid depletion, and individual cases of hepatocellular carcinoma, congenital pancreatic hypoplasia, and steatitis (yellow fat disease) in the 2005 cohort. Moreover, of the more significant pathologic findings of 1992, congenital cardiovascular lesions (patent ductus arteriosus, anomalous moderator band with a ventricular septal defect, and patent foramen ovale), and more incidental diagnoses of gall stones and ectopic calcification were not detected in those animals examined between 1989 and 2004. In the latter group, cardiovascular lesions were limited to aortic myxomatous degeneration and aortic, large mesenteric artery fibromuscular intimal proliferations, and varying degrees of myocarditis in select individuals. Post mortem findings of aborted fetuses, which were not included in the 2 previous case series, included emaciation, lymphoid depletion, and congenital anomalies.

Based on the gross and histopathology, the proximate cause of death for those animals examined between 1989 and 2004 are presented in table 2. Despite established necropsy protocols and sample check lists, post mortem decomposition, unavailability of ancillary diagnostics, and deficiencies in gross observations (or incomplete reports) hampered microscopic assessment of harvested case material. With future strandings, efforts to digitally record the external features and any internal lesions, as well as more thorough documentation of post mortem findings should be undertaken. In addition, with the advent molecular diagnostics, representative tissues should be routinely collected, frozen, and screened for pathogens of concern (such as Brucella spp, Toxoplasma gondii, canine distemper virus, Leptospira spp). Post mortem heart blood may be harvested in fresh dead animals and samples forwarded for serology, attempted immunoglobulin quantification (to assess passive immunization in neonates), heavy metal (including liver mercury and selenium), vitamin A and E determination, biotoxin screening, attempted virus isolation, and routine bacteriology. Emaciation was a primary or secondary contributor to morbidity in multiple animals. In fetuses and neonates, this phenomenon is likely related to in utero malnutrition and follow up evaluation of the nutritional status and caloric requirements of pregnant dams may be warranted. Due to the declining population status of monk seals, each stranded animal represents a unique opportunity to further the resolve the natural history and health status of individual animals with potential implications to susceptible populations.

Table 1. Comparison of diagnostic findings between 42 animals evaluated between 1981 and 1985 and 90 monk seals assessed between 1989 and 2004.

To facilitate comparison of histologic findings between the two cohorts, the categories and format from the previous case series has been retained and expanded to include additional and more recent pathologic findings.

Table 2. Categorical ranking of proximate cause of death in monk seals examined between 1989 and 2004.