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Bacterial Diseases of Marine Mammals


Nocardiosis (see Nocardiosis) is commonly reported in debilitated marine mammals. It has been diagnosed in bottlenose dolphins, beluga whales, pilot whales (Globicephala spp), harbor porpoises, killer whales (Orcinus orca), false killer whales (Pseudorca crassidens), spinner dolphins (Stenella longirostris), and leopard seals (Hydrurga leptonyx). Infections due to Actinomyces spp also have been diagnosed in bottlenose dolphins.

Serologic evidence of brucellosis in marine mammals was first reported in 1994. Since then, a wide range of pinniped and cetacean species have been shown to have antibodies to Brucella spp. Several marine Brucella species have been cultured, and genetic analyses show these to be different from known terrestrial Brucella spp. The names Brucella ceti and B pinnipedialis are now accepted for isolates from cetaceans and seals, respectively. Strains from dolphins, porpoises, and pinnipeds appear to be distinct from each other, but strains from one type of animal do not seem to vary much from the Atlantic to the Pacific ocean. Diagnosis remains controversial with challenges in both culture techniques and serologic methods. Little is known about the pathophysiology of brucellosis in marine mammals. Infections have been reported to cause orchitis, abortions, and meningoencephalitis. When present, brucellae often appear to be secondary or opportunistic pathogens. Clinical experience with the disease is not extensive and no therapy or control methods are established. Zoonotic potential has not yet been determined, although human infection has been reported.

Severe myositis due to infections with Clostridium spp has been diagnosed in captive killer whales, pilot whales, bottlenose dolphins, California sea lions, and manatees. All marine mammals are probably susceptible. The disease is characterized by acute swelling, muscle necrosis, and accumulations of gas in affected tissues, accompanied by a severe leukocytosis. Untreated, it can be fatal. Diagnosis is based on detection of gram-positive bacilli in aspirates of the lesions and is confirmed by anaerobic culture and identification of the organism. Treatment includes systemic and local antibiotics, surgical drainage of abscessed areas, and flushing with hydrogen peroxide. Commercially available inactivated clostridial bacterins are used routinely in some facilities, although efficacy in marine mammals has not been studied. Botulism has been reported in captive California sea lions during an endemic outbreak of the disease in waterfowl. Affected animals stopped eating and appeared unable to swallow several days before dying.

The chief cause of death in captive marine mammals (other than polar bears) is believed to be pneumonia. Most cases of marine mammal pneumonia have significant bacterial involvement, and most organisms cultured from terrestrial species have been identified in marine mammals. Pneumonia often can be considered the result of mismanagement. Marine mammals require good air quality, including high rates of air exchange at the water surface in indoor facilities. Tempered air or acclimation to cold temperatures is also important to prevent lung disease, even in polar species. Animals acclimated to cold temperatures are usually quite hardy; however, sudden transition from warm environments to cold air, even with warmer water, can precipitate fulminating pneumonias, particularly in nutritionally or otherwise compromised animals. Clinical signs include lethargy, anorexia, severe halitosis, dyspnea, pyrexia, and marked leukocytosis. The disease can progress rapidly. Diagnosis is usually based on clinical signs and confirmed by response to therapy. Treatment consists of correction of environmental factors and intensive antibiotic and supportive therapy. The initial antibiotic is usually broad-spectrum, commonly cephalexin (40 mg/kg, tid-qid); adjustments are based on cultures and sensitivities from blowhole or tracheal samples.

Erysipelas can be a serious infectious disease of captive cetaceans and pinnipeds. The organism, Erysipelothrix rhusiopathiae, which causes erysipelas in pigs and other domestic species, is a common contaminant of fish. A septicemic form of the disease in marine mammals can be peracute or acute; affected animals die suddenly either with no prodromal signs or with sudden depression, inappetence, or fever. A cutaneous form that causes typical rhomboidal skin lesions is a more chronic form of the disease. Animals with this form usually recover with timely antibiotic treatment.

Necropsy of peracute cases generally fails to reveal grossly discernible lesions other than widespread petechiation. Diagnosis is based on culture of the organism from the blood, spleen, or body cavities. Arthritis has been found in animals that have died with the chronic form.

Treatment of the peracute and acute forms has rarely been attempted because the absence of prodromal signs obscures the diagnosis. Animals with the dermatologic form usually recover with administration of penicillins, tetracyclines, or chloramphenicol and supportive treatment.

Control seems primarily related to the provision of high-quality fish that is properly stored and handled. Vaccination is controversial, and vaccine breaks can occur. Vials of killed erysipelas bacterin should be cultured for surviving organisms before use in marine mammals. Modified live bacterins should be avoided for the initial vaccination. Fatal anaphylaxis can occur on revaccination. For this reason, some vaccination programs have been reduced to one-time administration even though antibody titers fall below the presumed effective level.

If cetaceans are to be revaccinated, sensitivity tests should be performed by injecting a small amount of bacterin submucosally on the lower surface of the tongue. Hypersensitive animals develop swelling and redness at the injection site within 30 min. Because the vaccine is extremely irritating, no more than 3–5 mL should be used at any one site, even in nonsensitive mammals. A long needle (≥ 2 in. [5 cm]) should be used to assure that the vaccine is deposited in the muscle and not between muscle and blubber, or a sterile abscess can result. Bacterin should be administered in the dorsal musculature anterior and lateral to the dorsal fin. Administration posterior to the dorsal fin can result in a severe tissue reaction, immobilizing the animal for several days. To maintain high antibody titers, a booster after 6 mo and annual revaccination are required.

This has been diagnosed in otarid pinnipeds and bears. In seals, the disease is characterized by depression, reluctance to move, polydipsia, and pyrexia. It may also cause abortions and neonatal deaths in California sea lions and Northern fur seals. Lesions include a severe, diffuse, interstitial nephritis, with renal tubules packed with spirochetes. The gallbladder may contain inspissated black bile, but hepatitis may not be apparent grossly. Hyperplasia of Kupffer's cells, erythrophagocytosis, and hemosiderosis are seen histologically. Gastroenteritis can be a feature. Antibodies to various Leptospira serovars (L Canicola, L Icte-rohaemorrhagiae, L Autumnalis, and L Pomona) have been identified in affected animals by fluorescent antibody techniques. Treatment in pinnipeds is similar to that in dogs (see Leptospirosis in Dogs). Control in captive animals requires serologic examination of new animals during quarantine. Captive animals can be vaccinated in endemic areas. Leptospirosis is zoonotic, and appropriate precautions should be taken.

Streptothricosis, a subcutaneous bacterial infection with Dermatophilus congolensis, has been reported in pinnipeds and polar bears. It must be distinguished from sealpox. Simultaneous infections of streptothricosis and pox have been recorded in sea lions. Cutaneous streptothricosis usually manifests as sharply delineated nodules distributed over the entire body and usually progresses to death. Diagnosis is based on demonstration of the organism in biopsies or culture. Treatment with prolonged high dosages of systemic antibiotics can be successful.

Sporothrix schenckii, the cause of a subcutaneous mycosis, has been reported in Pacific white-sided dolphins (Laegenorhynchus obliquidens).

Marine mammals are susceptible to various mycobacteria. Unconfirmed mycobacteriosis has been reported in a stranded, wild bottlenose dolphin in the Mediterranean, and evidence points to mycobacterial disease being possibly endemic in free-ranging otarids off the coast of Australia. Originally thought to be caused by Mycobacterium bovis, subsequent molecular assessment places the isolates from free-ranging southern hemisphere pinnipeds in a unique cluster now assigned its own species in the M tuberculosis complex. Subantarctic fur seals (Arctocephalus tropicalis) are thought to be the common link in the spread of the disease to other pinniped species because they cohabit with the other known affected species, Australian sea lions (Neophoca cinerea) and New Zealand fur seals (Arctocephalus forsteri). Otherwise, mycobacteriosis has been a disease of captivity. Pinnipeds, cetaceans, and sirenians have developed disease due to M bovis, M smegmatis, M chitae, M fortuitum, M chelonae, and M marinum. Cutaneous and systemic forms are seen. There are strong indications that immunosuppression may be involved in the development of infections by the atypical mycobacteria.

Intradermal testing with high concentrations of bovine or avian purified protein derivative tuberculin can be used to screen exposed animals; however, anergy occurs and the usefulness is controversial. In pinnipeds, injections in the webbing of the rear flippers should be read at 48 and 72 hr. ELISA screening has identified antibodies in seals but requires further evaluation before it can be considered a screening test. Diagnosis is made by culture and identification of the organism from lesion biopsies, tracheal washes, or feces. Mycobacteriosis in marine mammals is an emerging disease and is possibly of public health significance. (See also Tuberculosis and other Mycobacterial Infections.)

Marine mammals are probably susceptible to the entire range of pathogenic bacteria. Pasteurella multocida has caused several outbreaks of hemorrhagic enteritis with depression and abdominal distress leading to acute death in dolphins and pinnipeds. It has also been reported to cause pneumonia in pinnipeds. In dolphins, Mannheimia haemolytica has been incriminated in hemorrhagic tracheitis that responded to chloram-phenicol therapy.

Plesiomonas shigelloides has been responsible for gastroenteritis in harbor seals. Burkholderia pseudomallei has caused serious fatal outbreaks of disease in various marine mammals in captivity in the Far East. Salmonella spp have caused fatal gastroenteritis in manatees and beluga whales. Staphylococcal septicemia has caused the death of a dolphin with osteomyelitis of the spine (pyogenic spondylitis). Another case of intradiskal osteomyelitis, due to Staphylococcus aureus, was treated successfully with a prolonged course of cefazolin sodium and cephalexin. S aureus also has been incriminated in a fatal pneumonia in a killer whale. Vibrio spp infect slow-healing wounds of cetaceans managed in open sea pens.

Last full review/revision April 2012 by Michael K. Stoskopf, DVM, PhD, DACZM

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