Molecular Identification of a Novel Gamma Herpesvirus in Hawaiian Monk Seals (Monachus schauinslandi)
IAAAM Archive
Tracey Goldstein1; Frances M.D. Gulland2; Robert C. Braun3; George A. Antonelis3; Leslie M. Dalton4; Teri Rowles5; Jonna A.K. Mazet6; Brian M. Aldridge7; Jeffrey L. Stott7
1The Marine Mammal Center, Golden Gate Recreation Area, Sausalito, CA, USA and UC Davis School of Veterinary Medicine, Wildlife Health Center and Department of Pathology, Microbiology and Immunology, Davis, CA, USA; 2The Marine Mammal Center, Golden Gate Recreation Area, Sausalito, CA, USA; 3NMFS Honolulu Laboratory, Honolulu, HI, USA; 4SeaWorld of Texas, San Antonio, TX, USA; 5NMFS Office of Protected Resources, Silver Springs, MD, USA; 6UC Davis School of Veterinary Medicine, Wildlife Health Center, Davis, CA, USA; 7UC Davis School of Veterinary Medicine, Department of Pathology, Microbiology and Immunology, Davis, CA, USA


The Hawaiian monk seal (Monachus schauinslandi) was listed as an endangered species in 1976. The population declined 60 percent from 1958 to 1992 and has remained relatively stable since 1993 at a population of about 1300 seals.1 Known reasons for monk seal mortality and the lack of population growth over the last two decades include entanglement in marine debris, male aggression, shark predation, human disturbance, and malnutrition. Epidemiological surveys since 1998 have not demonstrated disease to be a significant impediment to population recovery. Studies have implicated traumatic injuries and infectious diseases, such as parasitism and bacterial infection, as contributors to individual animal deaths.2 While limited data are available relative to the role of viral diseases in compromising monk seal health, the possible association of a morbillivirus infection with a mass mortality event in Mediterranean monk seals (Monachus monachus) in 1997 demonstrates the potential impact a viral infection might have on an endangered population of animals.3,4

Serological evidence for the existence of a herpesvirus infection in Hawaiian monk seals has recently been detected utilizing an enzyme linked immunosorbent assay (ELISA) (Goldstein, unpublished data). This observation was made during studies into the natural history of infections caused by a pathogenic isolate of phocine herpesvirus-1 (PhHV-1), which causes extensive morbidity and mortality in stressed neonatal Pacific harbor seals (Phoca vitulina). While the Hawaiian monk seal sera were positive for anti-herpesviral antibodies by ELISA, the sera were unable to neutralize the PhHV-1 isolate. This implied that the herpesvirus infecting the Hawaiian monk seal was not identical to PhHV-1.

The overall goal of this study was to identify and characterize this putative monk seal herpesvirus in nasal swab samples collected from wild and captive Hawaiian monk seals. Previously published degenerate primers that amplify a sequence of a conserved region of the herpesviral DNA polymerase gene were used to initially identify the novel herpesviral sequence.5 All samples were then analyzed with a monk seal herpes specific primer pair. The PCR analysis resulted in the identification of a previously unknown gamma herpesviral molecular isolate in 20.2 percent (20/99) of the animals that was similar to viruses such as ateline herpesvirus-3 and porcine lymphotropic virus. These types of herpesviruses are generally associated with respiratory disease and leukocytosis and tend to be predominantly lymphotropic. This newly identified herpesvirus in monk seals has not yet been associated with disease. Since herpesviruses are known to reactivate during periods of stress, the animals that tested positive may be indirect evidence of a population under stress, or they may be a natural part of the cycle of infection. A further understanding of the natural history of this infection in monk seals, and the ability to detect it, may be useful in managing this endangered population in the future.


This work was supported from grants from the Marine Mammal Health and Stranding Program, Office of Protected Resources, National Marine Fisheries Service, The Marine Mammal Center and the UC Davis Wildlife Health Center. The authors wish to thank the many dedicated researchers from the Marine Mammal Research Program, Honolulu Laboratory, National Marine Fisheries Service for their technical support and help with collection of field samples, and the U.S. Fish and Wildlife Service and the State of Hawaii Department of Land Natural Resources for their logistical support. We would also like to thank Jerry Saliki for providing phocine herpesvirus-1 and 2 isolates from Atlantic harbor seals and Don King for providing an otarine herpesvirus-1 isolate from a California sea lion for comparative purposes. Samples were collected under the authority of Marine Mammal Protection Act permit number 848-1135.


1.  Carretta JV, J Barlow, KA Forney, MM Muto, J Baker. 2001. U.S. Pacific Marine Mammal Stock Assessments: 2001. NOAA-TM-NMFS-SWFSC-317, Pp. 280.

2.  Banish LD, WG Gilmartin. 1992. Pathological findings in the Hawaiian monk seal. Journal of Wildlife Diseases 28(3): 428-434.

3.  Harwood J. 1998. What killed the monk seals? Nature 393(6680): 17-18.

4.  Osterhaus A, M van de Bildt, L Vedder, B Martina, H Niesters, J Vos, H van Egmond, D Liem, R Baumann, E Androukaki, S Kotomatas, C Komnenou, B Abou Sidi, AB Jiddou, ME Barham. 1998. Monk seal mortality: virus or toxin. Vaccine 16(9-10): 979-981.

5.  VanDevanter DR, P Warrener, L Bennett, ER Schultz, S Coulter, RL Garber, TM Rose. 1996. Detection and analysis of diverse herpesviral species by consensus primer PCR. Journal of Clinical Microbiology 34: 666-1671.

Speaker Information
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Tracey Goldstein
The Marine Mammal Center, Marin Headlands
Sausalito, CA, USA

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