Leptospirosis in Northern Elephant Seals (Mirounga angustirostris) Stranded Along the California Coast: Clinical and Pathologic Features
IAAAM Archive
Kathleen M. Colegrove1; Linda J. Lowenstine2; Frances M.D. Gulland3
1Veterinary Medical Teaching Hospital, Anatomic Pathology Service, University of California at Davis, Davis, CA, USA; 2School of Veterinary Medicine, Department of Pathology, Microbiology and Immunology, University of California at Davis, Davis, CA, USA; 3The Marine Mammal Center, Marin Headlands, Sausalito, CA, USA


Leptospirosis is a bacterial disease that affects humans and a wide variety of domestic and wild animal species. Among marine mammal species leptospirosis has been reported in California sea lions (Zalophus californianus), northern fur seals (Callorhinus ursinus), and Pacific harbor seals (Phoca vitulina richardsii).1,2 Because several northern elephant seals (Mirounga angustirostris) have shown high titers to Leptospira interrogans serovars grippotyphosa and bratislava, we hypothesized that this species is also susceptible, and we sought pathological confirmation of infection.3

Medical records of stranded elephant seals housed at The Marine Mammal Center, Sausalito, CA were evaluated for evidence of leptospirosis. Suspects included six elephant seals, four females and two males that stranded between April 4, 1995 and July 12, 1995, that had renal disease of unknown etiology. Estimated age at stranding ranged from three months to three years and the time in rehabilitation ranged from two to 100 days. Clinical signs prior to death or euthanasia included weight loss, anorexia, and moderate to severe lethargy. Significant clinical pathology abnormalities included: elevated blood urea nitrogen and serum creatinine, sodium, phosphorus, and calcium.

Gross necropsies were performed on all six seals within three hours post mortem, and significant findings included swollen kidneys with pale cortices and loss of renicular and corticomedullary differentiation. Histologically, all six seals had tubulointerstitial nephritis, with varying degrees of renal tubular degeneration, necrosis, and regeneration. Moderate to large numbers of lymphocytes were present in the cortical interstitium. Multiple tubules were dilated, lined by flattened epithelial cells, and contained protein casts, sloughed epithelial cells, and small numbers of neutrophils.

Warthin-Starry silver stains and immunohistochemistry against Leptospira sp. antigen were performed on paraffin embedded sections of kidney to identify spirochete organisms. On Warthin-Starry stained sections, spirochetes were identified within the lumen of renal tubules in four of the six seals; however, staining of necrotic debris often made identification of organisms difficult. By immunohistochemical staining, we identified variable numbers of spirochete organisms within the lumen of renal tubules in all six seals. Positive staining within numerous tubule epithelial cells and intertubular inflammatory cells (likely macrophages) was also present. Chronicity of infection, antibiotic treatment, and clumping of organisms within the tubules likely influenced the number of positive staining spirochetes identified.

The source of the Leptospira sp. infection in this group of elephant seals is unknown at this time. Five of the six infected seals developed renal disease during rehabilitation, suggesting that exposure may have occurred at the center. California sea lions, harbor seals, local free ranging terrestrial wildlife, or other elephant seals are all possible sources of exposure. One infected seal died within two days of stranding and had no known contact with other captive seals. There is a 4- to 10-day interval between exposure and leptospiral bacteremia, indicating that this seal was likely infected prior to arriving at the center, and providing evidence that leptospirosis occurs in free ranging elephant seals.4 A retrospective serologic study is currently underway to determine which Leptospira interrogens serovar these seals were exposed to, and possible exposure sources.


1.  Colagross-Schouten AM, JAK Mazet, FMD Gulland, MA Miller, S Hietala. 2002. Diagnosis and seroprevalence of leptospirosis in California sea lions from coastal California. Journal of Wildlife Diseases 38(1):7-17.

2.  Gulland FMD, M Koski, LJ Lowenstine, A Colagross, L Morgan, T Spraker. 1996. Leptospirosis in California sea lions (Zalophus californianus) stranded along the central California coast, 1981-1994. Journal of Wildlife Diseases 32(4):572-580.

3.  Stamper MA, FMD Gulland, T Spraker. 1998. Leptospirosis in rehabilitated Pacific harbor seals from California. Journal of Wildlife Diseases 34(2):407-410.

4.  Stevens E, TP Lipscomb, FMD Gulland. 1999. An additional case of leptospirosis in a harbor seal. Journal of Wildlife Diseases 35(1):150.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Kathleen M. Colegrove

MAIN : Infectious Diseases : Leptospirosis in Elephant Seals
Powered By VIN