Leptospirosis Age-Class Specific Pathology in California Sea Lions (Zalophus californianus) During the 2018 Epidemic
IAAAM 2019
Pádraig J. Duignan1*; Emily R. Whitmer1; Barbie Halaska1; Isabella Cebreros1; Weston Hustace1; Dayna Goldsmith2; Frances M.D. Gulland1; Shawn P. Johnson1; Carlos Rios1; Cara L. Field1
1The Marine Mammal Center, Sausalito, CA, USA; 2California Animal Health & Food Safety Laboratory, Tulare, CA, USA


Leptospirosis, associated with Leptospira interrogans serovar Pomona, is an endemic infection in free-ranging California sea lions (Zalophus californianus; CSL) that causes periodic epidemics of acute disease.1 Epidemics resulting in high rates of morbidity and mortality, particularly among juvenile males, have been documented by The Marine Mammal Center (TMMC) since the early 1980s, with nephritis as the most common necropsy finding.2,3 Beginning June 2018, there was a marked increase in CSL admissions at TMMC with clinical signs of renal insufficiency and failure (see Whitmer et al. this conference). Based on standard age-class criteria for this species, all four age classes were affected with the greatest prevalence of infection observed respectively among juveniles, followed by sub-adults, yearlings and then adults. The epidemic curve for juveniles peaked in August while that for sub-adults peaked in October. Too few yearlings and adults were admitted to define disease characteristics in these age classes, so an age-class specific pathology comparison was based on two age classes: (1) combined yearlings and juveniles and (2) combined sub-adults and adults. Class 1 had significantly (X2 8.225, p=0.0041) higher survival post-admission than Class 2. At necropsy, lesions ranged in severity from nephritis with malnutrition and dehydration to an advanced uremic syndrome that included nephritis, buccal ulceration, hemorrhagic gastric ulceration, diffuse pulmonary edema, epidermal ulceration and occasionally, cerebral edema. For Class 1, approximately equal numbers of animals had these two pathologic presentations. However, for Class 2, significantly more animals presented with the advanced uremic syndrome (X2 5.451, p=0.0196). Whether this reflects a less competent immune response in younger animals with a fatal outcome earlier in the course of infection, or failure of older animals to strand and show clinical signs of illness until disease is more advanced, requires further investigation.


The authors thank the staff and volunteers of The Marine Mammal Center for their dedicated patient care and assistance with necropsy and sample processing.

* Presenting author

Literature Cited

1.  Lloyd-Smith JO, Greig DJ, Hietala S, Ghneim GS, Palmer L, St. Leger J, Grenfell BT, Gulland FMD. 2007. Cyclical changes in seroprevalence of leptospirosis in California sea lions: endemic and epidemic disease in one host species? BMC Infect Dis. 7: 125.

2.  Dierauf LA, Vandenbroek DJ, Roletto J, Koski M, Amaya L, Gage LF. 1987. An epizootic of leptospirosis in California sea lions. J Am Vet Med Assoc. 187:1145–1148.

3.  Gulland FMD, Koski M, Lowenstine LJ, Colagrass A, Morgan L, Spraker T. 1996. Leptospirosis in California sea lions (Zalophus californianus) stranded along the central California coast, 1981–1994. J Wildl Dis. 32(4):572–580.


Speaker Information
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Pádraig Duignan
Department of Veterinary Sciences
The Marine Mammal Center, Fort Cronkhite
Sausalito, CA, USA

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