Abstract

From December 2010 thru December 2012, 23 manatees presented with signs attributed to cold stress syndrome (CSS) to Tampa's Lowry Park Zoo (TLPZ). The distribution of skin lesions suggested a vascular disturbance and led to the exploration of thromboembolic disease (TE) as a major contributor to the pathology of CSS. Fourteen of these animals had coagulation profiles including D-dimers analyzed with 24 hours of admission. All 14 animals with CSS signs had what were consider elevate D-dimers (> 250 ng/ml; mean 914 ng/ml range 258–2879). Thirteen of the 14 animals had D-dimers drop to low levels or zero at the time of the release with one fatality among this group of 14. This individual animal had the highest levels of the entire group. D-dimer is a specific degradation fragment of cross-linked fibrin utilized in the diagnosis of systemic thrombosis, pulmonary thromboembolism (PTE), and disseminated intravascular coagulation (DIC). The vasculature anatomy of the manatee has been described and differs from many other mammals in that the division of vessels resembles the arrangement of a broom or brush rather than that of a tree with branching limbs. This division is associated with a significant decrease in size of the vessel as it courses distally. This sharp change in diameter of vessels may make manatees more likely to develop TE that other species. Recent gross pathology and histopathology of CSS in manatees have demonstrated pulmonary emboli and thrombi in the small pulmonary arteries.

With clinical findings, clinical pathology, pathological evidence, and a case series all suggesting TE disease in manatees with CSS; the question arises: what is the source? In the case of CSS, a primary coagulopathy should be considered as the main differential, specifically cold agglutinin disease. Cold agglutinin disease results when antibodies react at cold temperatures with proteins on the surface membrane of red blood cells. IgM autoantibodies can be agglutinating or nonagglutinating. The clinical findings of microcapillary stasis with subsequent manifestations including acrocyanosis and necrosis of the nose, tips of the ears and tail, digits, scrotum, and prepuce in various species strongly parallel the clinical findings of manatees with CSS.

Aside from the potential for TE to have a role in CSS, TE may need to be explored in other aspects of manatee health. Thrombosis may be seen in colic syndromes, poisonings, sepsis, surgical complications, DIC, and with primary coagulopathies. At TLPZ, elevated D-dimers can be seen with other inflammatory conditions but their presence is unpredictable and not consistent. Trauma expected to produce an obvious inflammatory state can often reveal low to zero d-dimers. Sepsis is another confounder in interpreting d-dimers as they may be elevated. These findings should not be thought of as erroneous but suggest that there is some thrombotic events occurring with the sepsis. Chronic recurring lesions in animals with smoldering infections could potentially be at risk for developing more avascular lesions and prolonging any existing condition.

Acknowledgements

I would like to thank Drs. Trevor Gerlach, Lizzy Arnett, and Nicholas Maldonado for clinical support and contributions to this work, the Veterinary and Florida Mammals Department at Lowry Park Zoo, and Dr. Martine deWit and the staff at the Marine Mammal Pathobiology Laboratory in St. Petersburg, Florida.

* Presenting author