Risk Factors for an Outbreak of Leptospirosis in California Sea Lions (Zalophus californianus) Stranded in California in 2004
IAAAM Archive
Stephanie Norman1; Ronald DiGiacomo1; Frances M.D. Gulland2; Scott Meschke3; Gina Ylitalo4
1Department of Epidemiology, School of Public Health and Community Medicine, University of Washington, Seattle, WA, USA; 2The Marine Mammal Center, Marin Headlands, Sausalito, CA, USA; 3Department of Environmental Health and Occupational Medicine, School of Public Health and Community Medicine, University of Washington, Seattle, WA, USA; 4Northwest Fisheries Science Center, NOAA Fisheries, Seattle, WA, USA


Leptospirosis, caused by the spirochaete bacterium Leptospira, is recognized as an emerging zoonotic infectious disease that affects many species of mammals, including humans. Infection results in disease manifestations that range from mild subclinical infection to a severe syndrome of multiple organ infection with high morbidity and mortality.1 Outbreaks of leptospirosis have been reported in California sea lions (Zalophus californianus) since 1970.2 Although the transmission cycle between terrestrial animals and sea lions is unknown, outbreaks in California sea lions have been correlated with increased incidence of leptospirosis in domestic dogs in the vinicity.3 Leptospirosis in sea lions has been observed to be cyclical, with significantly higher prevalence occurring every 3-4 years.4 Such a peak occurred in 2004, when an unusually large number of sea lions with leptospirosis stranded in northern and central California. The goal of the present study was to identify demographic and environmental risk factors for leptospirosis in California sea lions that stranded in 2004, using a Geographic Information System (GIS), to help reveal potential sources of infection.

Cases were defined as animals having one or more of the following: a California sea lion that stranded alive or dead in California in 2004, with either a serum MAT titer of >1:200 to one or more Leptospira serovars, clinical signs (i.e., severe depression, and either one or more of the following: excessive thirst, anorexia, and tucked-up posture5), abnormal serum chemistry (blood urea nitrogen >100 mg/dl, mean phosphorus levels greater than calcium, and creatinine >1.0 mg/dl), gross necropsy findings indicative of leptospirosis (i.e., marked swelling of the kidneys, loss of differentiation between the renule medullae and cortices, pale tan colored cortices and/or swollen, friable livers and severe gastric ulceration)4, histopathologic lesions consistent with leptospirosis, culture or PCR resulting in detection of leptospires. Controls were defined as: a California sea lion stranded alive or dead in 2004 in California with a <1:200 titer for any Leptospira serovar and negative for any other diagnostic or clinical findings as described for cases.

Potential risk factors for leptospirosis were determined using a GIS: age class, sex, stranding location (county) and season, county subdivision human population density (surrogate for exposure to rats), county cattle density (cattle population divided by county farmland area), 1971-2000 mean annual rainfall, 2004 mean annual rainfall, proximity to any freshwater body, and proximity to a dog park (surrogate for exposure to dogs).

A total of 462 individual California sea lions stranded (multiple strandings of individual animals and fetuses were excluded) in 2004, of which 315 were positive for leptospirosis and 147 were negative. A significantly greater proportion of cases were male (79%), juveniles (86%) or subadults (57%) (p<0.001) compared to controls. Cases were located significantly closer to freshwater sources and dog parks, in areas of less mean monthly precipitation by watershed (1 month prior to the stranding), in counties of higher cattle and human population density, and stranded more often in the summer and autumn months, than controls (p<0.001).


The authors thank The Marine Mammal Center staff and volunteers for their help, and Mark Lowry from NOAA/Southwest Fisheries Science Center, for use of his 2004 sea lion census data.


1.  Levett PN. 2001. Leptospirosis. Clin Microbiol Rev 14: 296-326.

2.  Vedros NA, Smith AW, Schonewald J, Migaki G, Hubbard RC. 1971. Leptospirosis epizootic among California sea lions. Science 172: 1250-51.

3.  Ward MP, Glickman LT, Guptill LF. 2002. Prevalence of and risk factors for leptospirosis among dogs in the United States and Canada: 677 cases (1970-1998). J Am Vet Med Assoc 220: 53-8.

4.  Gulland FMD, Koski K, Lowenstine LJ, Colagross A, Morgan L, Spraker T. 1996. Leptospirosis in California sea lions (Zalophus californianus) stranded along the central California coast, 1981-1994. J Wild Dis 32: 572-80.

5.  Dierauf LA, Vandenbroek DJ, Roletto J, Koski M, Amaya L, Gage LJ. 1985. An epizootic of Dieptospirosis in California sea lions. J Am Vet Med Assoc 187: 1145-48.

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Stephanie A. Norman

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