Abstract

The adrenal gland is functionally one of the most important organs in the stress response of marine mammals, and, in phocids, it is also an integral component of the osmoregulatory system, as well as having immunomodulatory effects. In Pacific harbor seals (Phoca vitulina richardsii), a herpesvirus has been observed in adrenals of animals dying during rehabilitation. The virus is associated with severe adrenal necrosis, and seals die with severe glucose and electrolyte imbalances. Although the epidemiology of this disease is unclear, it is likely that stress plays an important role in its pathogenesis, either by enhancing activation of latent virus in the adrenal, or by increasing susceptibility to horizontal transmission. This study aims to evaluate changes in adrenal function in Pacific harbor seals during rehabilitation and during herpesvirus infection through determination of circulating cortisol and aldosterone levels, monitoring responses to adrenocorticotrophic hormone (ACTH) administration, and monitoring fecal cortisol levels.

ACTH stimulation tests were performed on 14 recently weaned harbor seals at 2-week intervals for up to 8 weeks during rehabilitation, and on five wild seals that were caught manually in nets and held for 2 hours for testing, then released. Circulating cortisol and aldosterone levels were also measured in control animals that received intramuscular saline rather than ACTH.

Fecal samples were collected from the same animals, and fecal cortisol levels determined by radioimmunoassay. Fecal cortisol levels were approximately 3 fold higher than plasma cortisols, and correlated significantly with baseline plasma cortisol in all animals tested.

Baseline plasma cortisol levels did not differ significantly between wild and rehabilitated seals (means 78.7 and 93.1 ng/dl) while baseline aldosterones did (727 and 272 pg/ml respectively). Both wild and rehabilitated seals showed an increase in plasma cortisol 90 minutes post ACTH injection, but only rehabilitated seals showed an increase in plasma aldosterone level. Baseline cortisol and aldosterone levels, and size of responses (fold and absolute), decreased during rehabilitation in animals that survived to be released. In contrast, in seals that died with adrenal necrosis during rehabilitation, both baseline and response levels of hormones increased through rehabilitation until the seals died.

These results suggest herpesvirus infection causes significant changes in adrenal function in rehabilitated harbor seals, causing chronic release of both cortisol and aldosterone. These changes could explain clinical signs observed in herpesvirus infected seals, and may have other important physiological effects.