Abstract

From May through July 2003, 20 yearling California sea lions (Zalophus californianus--CSLs) stranded along the northern California coast, were admitted to The Marine Mammal Center (TMMC), and died within 1 to 28 days (mean 5.8 days) due to acute proximal duodenal perforation. 60% were female, 40% were male, and all were emaciated (mean length 100 cm, mean body weight 16.5 kg). Duodenal perforation also was found in 88 (5.0%) of 1773 CSLs that died at TMMC between 1992-1999. All died within 0 to 46 days (mean 4.2 days), 58% were female, 42% were male, 79.5% were yearlings, and 31% presented between May and July 1998, during the El Niño Southern Oscillation Event. Case review in 1999 suggested an association with infection with Contracaecum ogmorhini (C. corderoi).

For the 2003 cohort, necropsy was performed at TMMC, during which stomach and/or peritoneal samples were submitted for aerobic culture (n=3), gastroduodenal parasites were submitted for identification (n=3), and representative tissues from 15 animals were immersed in 10% neutral buffered formalin and submitted for histological review to University of California, Davis. Fixed tissues were processed routinely into 5 µm, hematoxylin and eosin stained sections, and gastrointestinal sections were stained with Steiner's, Giemsa, and/or Brown and Brenn stains for spiral and other bacteria. Additionally, the entire gastrointestinal tracts from two CSLs without gross gastrointestinal lesions were submitted to detail gross and microscopic anatomy to facilitate accurate localization of histological sections. Systematic review of the 2003 cohort revealed that each CSL had chronic gastroenteritis focused on the pylorus and duodenum and peracute to acute perforating ulceration within 2 cm of the pyloric-duodenal junction. In the proximal gastrointestinal tract, the presence of mixed bacteria (n=10), spiral bacteria (n=6), Anisakidae nematodes (Pseudoterranova decipiens n=2, Contraceaecum ogmorhini n=1, unidentified n=3), Cryptosporidium sp. (n=1), and sharp foreign bodies (n=1) was inconsistent, and there was no predisposing extra-gastrointestinal disease or neoplasia.

Pyloric-duodenal ulcers and perforations result from an imbalance between mucosal defense mechanisms and aggressive factors, like increased gastric secretions or infection. Potential etiologies in human and non-human animals include specific Helicobacter infections, nonsteroidal anti-inflammatory drugs, parasitism, foreign body, regional ischemia from physiologic stressors like sepsis, chronic hepatic or renal disease, exogenous substances that alter gastroduodenal function, gastrin-secreting neoplasms, and idiopathic. In humans, idiopathic ulcers are recognized increasingly, more associated with complications, more refractory to therapy, and probably reflective of the interplay of genetic predisposition, rapid gastric emptying, acid hypersecretion, defective defense mechanisms, and psychological stress. In CSLs, this review suggests that perforating ulcerative gastroduodenitis in yearlings is a syndrome that does not have a common etiology in gastrointestinal parasitism, mixed or spiral bacteria, foreign bodies, apparent extra-gastrointestinal disease, or cancer. Instead, it may involve factors similar to those described for idiopathic ulcers in humans. Results from this study, including an increased understanding of gastrointestinal anatomy, more consistent sampling technique, more systematic identification of gastrointestinal findings, and increased recognition of this syndrome, may help elucidate the underlying pathophysiology of perforating ulcerative gastroduodenitis in CSLs in the future.

Acknowledgements

The authors thank Daniel Fletcher, Nancy Kock, and Murray Dailey for their previous work on this subject, Kathleen M. Colegrove for helpful review, and the support staff at TMMC and UCD Pathology Service for tissue collection and histotechnique.