Corneal opacity is frequent in captive pinnipeds kept in either freshwater or saltwater; it is also seen in captive cetaceans but is rare in wild animals. It can be due to various environmental problems. Transient cases can be caused by simply moving an animal to freshwater from saltwater, or vice versa. Lack of shade and excessive bright light have been implicated. Poor water conditions (eg, high bacterial loads or overuse of oxidative disinfectants in the water) also have been associated with the disease. Nutritional deficiencies have been suggested as causes, but response to supplementation with vitamin C or A has not been dramatic. The condition is usually self-limiting if the underlying insult to the cornea is removed early enough in the pathogenesis.
These occur frequently in captive pinnipeds and cetaceans. They can be the result of direct trauma or the sequelae of unresolved or untreated cases of corneal edema. Diagnosis is by observation of epithelial defects on corneas stained with fluorescein. In trained animals, small lesions can be treated topically. In untrained animals, subconjunctival injections of antibiotics and steroid are required. Extensive lesions benefit from protection by suturing the eyelids. Deep ulcers or lacerations in danger of eroding Descemet's membrane should be stabilized with a thin methylacrylate patch. As in corneal edema, successful resolution and prevention of recurrence depend on removal of the underlying cause.
Many captive marine mammals develop the habit of swallowing objects dropped into their pools. In cetaceans, the opening to the second compartment of the stomach is small, and foreign objects remain in the first compartment. In pinnipeds, the small pylorus prevents passage of most foreign bodies. Frequently, no clinical signs are evident. On occasion, anorexia, regurgitation, or lethargy may be seen. Diagnosis is often made by observing the animal swallow an object. Smaller animals can be radiographed; in small cetaceans, the esophagus can be palpated to establish the presence of foreign bodies. Animals occasionally regurgitate foreign bodies; however, assisted removal is usually indicated. Removal is usually best performed by gastroscopy, which is also used as a method of diagnostic confirmation. All efforts should be made to prevent ingestion of foreign bodies. Training animals to retrieve for reward as a displacement to swallowing foreign objects is thought to be beneficial.
GI ulcers are a significant problem in captive marine mammals. Ulcers of the first compartment of the cetacean stomach are a common necropsy finding and pose less severe clinical problems than do ulcers of the pyloric region or proximal duodenum. Gastric ulcers in pinnipeds frequently progress to perforation, which results in peritonitis and subsequent death. Gastric ulcers also occur in sirenians. Although ulcers in cetaceans perforate less frequently than in pinnipeds, they should be treated as a serious problem. Various etiologies, including parasitic damage and increased histamine content of spoiled fish, have been suggested, but the disease must be considered primarily an environmental or stress-related condition. Dramatic environmental changes, including changes of personnel or companion animals, can precipitate serious GI ulceration in cetaceans or pinnipeds.
Clinical signs include lethargy, partial anorexia, abdominal splinting, pallor, and occasionally regurgitation. Animals with bleeding ulcers show anemia and possibly leukocytosis. Diagnosis generally is based on identification of mammalian RBC in gastric washes; confirmation is by endoscopic visualization of the lesions. Palliative treatment of nonperforating ulcers consists of administration of cimetidine (4.5 mg/kg, bid) and alumina-gel-based antacids with or without simethicone, along with frequent small meals. The underlying cause must be identified and corrected for successful resolution. Management of perforating ulcers with resulting peritonitis includes intensive broad-spectrum antibiotic and fluid therapy. As in humans, stress-induced GI ulcers are more likely to develop in marine mammals that have previously had an ulcer.
Traumatic lesions (eg, cuts, wounds from gunshots or propeller blades) are common in marine mammals. Propeller injuries are a major problem in manatees, which commonly enter heavily navigated recreational waters in Florida. Traumatic wounds should be cleaned, debrided, and generally allowed to heal as open wounds unless body cavities are breached. Antibiotics should be administered during convalescence to prevent gross infection. Maintenance of good water quality and a high plane of nutrition is beneficial to the healing process. Large wounds frequently heal uneventfully.
Exposure of marine mammals to spills of petroleum hydrocarbons is a major concern. Sea otters are particularly susceptible to such exposure because of their natural grooming habits and their lack of an insulating blubber layer. Hepatotoxicity, renal toxicity, GI damage, and loss of homeothermic ability are important effects of exposure to petroleum hydrocarbons; however, the most devastating effects are due to direct pulmonary damage from inhalation of volatile hydrocarbons.
Experimental evidence suggests cetaceans and pinnipeds will avoid petroleum spills if possible (unlike sea otters) and are relatively resistant to toxicities from direct skin contact. Ingestion of large quantities of oil by these species is unlikely and although baleen fouling occurs in mysticete whales, it usually resolves within 24–36 hr. Pinnipeds and cetaceans are susceptible to severe pulmonary damage due to inhalation of volatile hydrocarbons as are other mammals, including humans. Efforts to reduce human exposure to hydrocarbons when dealing with oil-contaminated animals must be a top priority. Treatment of exposed animals includes removal of oil from both the skin (using mild detergents, eg, 2% New Dawn) and the GI system (activated carbon gavage), along with physiologic supportive therapy. It is critical to recognize that capture, transport, and holding stresses appear to lower the threshold of hydrocarbon toxicity in these animals.
Last full review/revision April 2012 by Michael K. Stoskopf, DVM, PhD, DACZM