Brucella Sp. Infected Bottlenose Dolphin (Tursiops truncatus) Cases in Two Populations: Serologic and Clinical Evaluations
IAAAM Archive
Jenny Meegan1; Cynthia R. Smith2; Stephanie K. Wong2; Eric D. Jensen2; William G. Van Bon2 Tracy Romano1; Inga Sidor1; J. Lawrence Dunn1
1Mystic Aquarium and Institute for Exploration, Mystic, CT, USA; 2U.S. Navy Marine Mammal Program, Space and Naval Warfare Systems Center, San Diego, CA, USA


Demonstration of serologic conversion, with a significant rise in antibody titer, using a species-specific assay is an important tool in the diagnosis of many infectious diseases. Serial testing of infected or exposed animals is also beneficial in evaluating the effects of treatment, assessing the duration of an animal's immunity to a microbe, and identifying animals with possible ongoing infections.11

Many serologic studies have been conducted to assess the prevalence of marine-origin Brucella exposure in free-ranging marine mammal populations. These surveys demonstrate seroprevalence in multiple cetacean and pinniped species ranging from 3-34% and 2-49% respectively.3,4,9,10,12,13,14,16,17,19

Despite the global distribution of Brucella, knowledge of its impact on marine mammal populations remains incomplete.

The present report describes the use of long-term serologic testing, paired with clinical evaluations, for monitoring six bottlenose dolphins (Tursiops truncatus) from two populations with culture confirmed Brucella sp. infections. A previously described dolphin-specific indirect enzyme-linked immunosorbent assay (iELISA) was utilized to retrospectively screen serially collected serum samples from each animal for the presence and magnitude of antibody titers against marine-origin Brucella.5,8 Clinical observations associated with these cases were reviewed.

Three adult females developed reproductive disease resulting in abortion, and did not mount a significant serologic response against Brucella until shortly after abortion.7 Post-abortion antibody levels in two of these females declined over time and each had subsequent live births. Assuming exposure to Brucella occurred prior to abortion, these observations are consistent with the ability of Brucella to evade the host's immune response until proliferation of the organism in an active infection, and also suggest clearance or latency after abortion.1,15,18

Three other dolphins had chronic disease processes including a male and a female with vertebral osteomyelitis, and one female with a pulmonary granuloma found incidentally at necropsy.2,7 Serologic data from these dolphins demonstrate differences in the immunologic response that appear to be based on the nature and site of the Brucella infection. Those animals developing lesions involving the musculoskeletal and pulmonary systems developed persistently high titers, likely due to chronic antigenic stimulation.

Our previous research has revealed a high seroprevalence (up to 66%) in healthy wild bottlenose dolphin populations.6 Other animals within one of the current study populations also demonstrate positive titers against Brucella and have shown no clinical evidence of brucellosis. In the current study, as seen in terrestrial species, our findings suggest that significant increases in titer may be detected in marine mammals during active Brucella infections. Further, animals with chronically active lesions associated with Brucella may maintain high titers. While a seronegative result does not definitively indicate absence of a previous infection or latent disease, conversely, a seropositive result does not distinguish between active infections and sustained immunity to a cleared infection. This study stresses the importance of longitudinal serologic monitoring in dolphins when diagnosing, treating, and monitoring for Brucella sp. infections.


The Brucella Project is funded by NOAA Oceans and Human Health Initiative Grant No. NA04OAR4600209, and previously received support from NOAA Fisheries Prescott Grant Award No. NA03NMF4390408. We acknowledge Risa L. Daniels and Kevin P. Carlin for their time and effort spent on this project. The authors also thank Dr. Cara Field, Jolene Carlson, and James Kniffen for all their laboratory and diagnostic assistance. We also acknowledge the assistance of Drs. Sylvain De Guise and Salvatore Frasca from the University of Connecticut.


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Jenny Meegan

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