Diseases of Marine Mammals

April 8, 2002

Robert B. Moeller, Jr. D.V.M.

California Animal Health and Food Safety Laboratory System

University of California

Tulare, California 93274

rbmoeller@ucdavis.edu

559-688-7543

The author of this lecture wishes to thank Drs. Migaki, Sweeney, Keyes, Walker, Montali, Magee,

Albert, Stroud, McNeil, Hammond, Barr, Gage, Wilson, Britt, Domingo, Haines, Garner, Gulland, Wada,

Lapointe, Dunn, Pollock and Martineau for supplying photographs of the various diseases of marine

mammals to the Registry of Veterinary Pathology.

 Viral Diseases

1. Pox Virus

A. Dolphin Pox
Dolphin pox is also known as "tattoo." Clinically, this disease is characterized by prominent
well-delineated lines of hyperpigmentation of the epidermis with various design patterns. These design
patterns have been described as targets, circles, and pinhole lesions. The lesions are usually smooth and
flat, but may be raised. They are primarily located on the dorsal body, flippers, dorsal fins, and fluke.
Although this virus does not appear to cause serious illness in cetaceans, the development of these lesions
usually coincides with periods of poor health and stress.
Histologically, the lesion consists of ballooning (hydropic) degeneration of the deep layers of the
stratum intermedium. Irregularly shaped or round variably size intracytoplasmic inclusions are present in
the cells undergoing ballooning degeneration. The stratum externum may become thickened. Minimal
inflammation is observed; this maybe the reason for persistence of the lesion. The cause of the
hyperpigmentation is unknown, but there are various theories on this process. One theory is that
stimulation of the dermal melanocytes by the viral infection causes hyperpigmentation of the dermis and
epidermis. Another theory postulates that damage to the stratum externum and intermedium leads to
filling in of these defects with debris and bacteria which then causes the discoloration of the epidermis.
This is an unusual pox lesion since it is not a proliferative lesion. The virus persists for long periods
of time in the epidermis and slowly spreads on the affected animal. Affected animals appear to not
develop antibodies to the virus; however, once antibodies develop to the pox virus, the lesion regresses
with the affected skin becoming raised and bleached. The effected skin then undergoes necrosis and
sloughing. Scraping the lesion has been known to cause regression. If lesions are biopsied, the pox
lesion may regress in a zonal pattern around the biopsy site.

B. Seal Pox
Seal pox is a parapoxvirus that is known to affect numerous species of pinnipeds. An orthopox has
also been isolated from a grey seal, (Halichoerus grypus). The disease is most prevalent in California sea
lions, South American sea lions and harbor seals. Cutaneous spread of this disease is mostly by head and
neck rubbing, a common social behavior of sea lions and other pinniped. This viral disease is rarely fatal,
but can cause a high morbidity. Infected animals may demonstrate clinical disease for up to 15 weeks.
Seal pox is a proliferative lesion characterized by the formation of numerous 2 to 3 cm cutaneous
nodules. These nodules eventually ulcerate and are slow to heal. Areas of alopecia develop over the
healed areas. The lesions are most numerous over the head and neck but can occur anywhere on the
body.
Microscopically, the lesion is characterized by ballooning degeneration of the stratum spinosum
with pustule formation. Affected cells have one or two eosinophilic intracytoplasmic inclusions 2 to 15u
in diameter. The affected epidermis ia acanthotic with orthokeratotic and parakeratotic hyperkeratosis.
Inflammation can be prominent, especially during regression of the lesion.
The histologic features of pox virus in South American sea lions is unique with a downward
proliferation of the epidermis with ulceration and pustule formation. In affected epithelial cells, only one
large eosinophilic or basophilic intracytoplasmic inclusion body is observed. These inclusions are usually
surrounded by a thin halo and the nucleus is compressed. These lesions can occasionally resemble the
human disease molluscum contagiosum.

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2. San Miguel Sea Lion Virus
San Miguel sea lion virus (SMSV) is caused by a calicivirus. This calicivirus is believed to be the
viral agent responsible for vesicular exanthema of swine. Most viral strains of San Miguel sea lion virus
are antigenically related to vesicular exanthema of swine. The disease occurs in sea lions and seals. It is
characterized by the formation of vesicles on the flippers. These vesicles usually rupture and form
prominent slow healing ulcers. This virus has also been implicated in causing ulcerative lesions on the
lips, nose, chin, and gums. Microscopically, the lesion consists of spongiosis of the stratum spinosum,
which later progresses to subcorneal vesicle formation. Intracytoplasmic or intranuclear inclusions are
not present.
Several serotypes of San Miguel sea lion virus have been isolated from aborting sea lions and
aborted fetuses. These serotypes of San Miguel sea lion virus are indistinguishable from serotypes of
vesicular exanthema virus that cause abortions in swine. The relationship of San Miguel sea lion virus
infection and abortions in affected marine mammals is suspected but not proven. The virus has been
isolated from the opal-eye fish (Girella nigricans) which is believed to function as a reservoir for the
spread of this disease. This fish is known to develop an active infection with viral replication in the
spleen. The fish remains infected for about 31 days. Clinical disease has not been observed in infected
fish.
A similar calicivirus has been isolated from Atlantic bottlenosed dolphins. These animals are
presented with vesicular skin lesions that are eroded and leave shallow ulcers. It was felt that this virus is
infective for both sea lions and dolphins.
It is interesting to note that there are over 34 serotypes of marine caliciviruses isolated. The
relationship of these viruses to vesicular disease in marine mammals as well as terrestrial mammals is
subject to much speculation and will require further investigation.

3. Sea Lion Hepatitis Virus

Sea lion hepatitis virus is caused by an adenovirus. This virus is not highly virulent. Only a few
animals demonstrate clinical disease, however, serological surveys demonstrate that large numbers of
animals are exposed to the virus. Sea lions, seriously affected by this agent, usually die acutely with little
clinical evidence of infection. At necropsy these animals are usually presented with icterus, splenomegaly,
mesenteric lymphadenopathy, and discoloration of the liver. Microscopically, the liver lesion consists of
random areas of coagulative and lytic necrosis of hepatocytes. In many cases, the necrosis is most severe
in the centrolobular region of hepatic lobules. Large pale eosinophilic to dark basophilic intranuclear
inclusions are present in hepatocytes and occasionally in Kupffer cells. The inflammatory response is
usually minimal, with a few macrophages, lymphocytes, and neutrophils at the periphery of the necrotic
lesion.

4. Influenza Virus
The influenza virus observed in seals has been identified as an influenza A virus (Type
A/Seal/MA/1/80, Type A/Seal/MA/133/82, Type A/Seal/MA/3807/91, Type A/Seal/MA/3810/91, Type
A/seal/M/3911/92) and influenza B virus (Type B/seal/netherlands/1). Most influenza A viruses have
been identified as an H3 influenza viruses. This subtype of virus is most frequently detected in birds, pigs,
horses, and humans. It is felt that the viruses infecting seals are most closely related to H3 avian
influenza viruses. Some feel that seals, like swine, may play a role in genetic reassortment of these
influenza viruses, thus causing a potential for interspecies transmission. It should also be noted that
several influenza A viruses have been also identified in sick long-finned pilot whales. It is unclear as to
the seriousness of these viruses in cetaceans.
These viruses have been associated with high mortality in harbor seals. This virus causes serious
respiratory distress in affected seals. Affected animals are usually presented weak and have serious

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respiratory difficulties. A white mucinous to bloody discharge is observed in the trachea and bronchi.
Pulmonary, mediastinal, and subcutaneous emphysema is commonly observed. Microscopically, there is a
severe interstitial and hemorrhagic bronchopneumonia with hemorrhage in alveoli and prominent necrosis
of bronchioles and bronchi. Mycoplasma (Mycoplasma phocidae) and other bacteria have been isolated
from affected animals. It is felt that there is a synergic effect between the virus and bacterial agents since
seals experimentally challenged with only the virus develop a mild respiratory disease.
In one outbreak (A/seal/mass/1/80, an H7N7 virus), personnel working with sick seals developed a
severe conjunctivitis which lasted 3 to 4 days. Virus was cultured from affectected individuals. A type B
influenza found in the Netherlands is similar to the human type B influenza that circulated in humans in
1995 and 1996. Seals after 1995 had a 2% incidence of this virus and may have the potential of infecting
people.

5. Phocine morbillivirus (Phocine distemper virus, PDV-1, PDV-2)

Several disease outbreaks that killed thousands of seals in Northern Europe and Lake Biakal in
Siberia have been attributed to a morbillivirus. The morbillivirus affecting harbor seals (Phoca vitulina)
and grey seals (Halichoerus grypus) in Northern Europe and North America is caused by the
morbillivirus, phocine distemper virus-1 (PDV-1). This virus is similar to, yet antigenically distinct, from
canine distemper virus. Differences in DNA sequencing between PDV-1 and canine distemper are of such
great magnitude that they need to be considered separate species. Serologic studies have demonstrated
that harbor seals (Phoca groelandica), hooded seals (Cystophora cristata) and ringed seals (Phoca
hispida) have an immune response by viral neutralization to PDV-1. The morbillivirus, phocid distemper
virus-2 (PDV-2), isolated from Siberian seals (Phoca siberica) in Lake Baikal is closely related to a field
strain of canine distemper virus found in Germany. Seals can also be suseptible to canine distemper virus.
A mass die off of Caspian seals (Phoca caspica) in the Caspian Sea (Spring 2000) has been attributed to a
canine distemper virus. Canine distemper virus has also been implicated in the die off of crab-eating seals
(Lobodon carcinophagus) in Anartica (in 1955).. A morbillivirus isolated form sick Mediterranean monk
seals (Monachus monachus) most closely resembles those morbilliviruses identified in cetaceans. Atlantic
walruses have had neutralizing antibodies to phocine distember virus but have not had clinical disease.
Clinically, affected seals are very weak and have severe respiratory distress. A mucopurulent to
serous oculonasal discharge is often observed. Many animals developed subcutaneous emphysema
primarily around the neck and thorax. On necropsy, these animals have edematous lungs with sharply
demarcated areas of red consolidation. Emphysema involving the interlobular septa and pleura of the
caudal lung lobes is present. Many animals developed emphysema of the mediastinum, neck, fascia, and
subcutis. Congestion and a thick mucopurulent exudate is observed in the upper respiratory tract.
Pulmonary lymph nodes are edematous. Hydropericardium, hydrothorax, and hepatic congestion are
common. Histologically, the lung lesion consists of a bronchointerstitial pneumonia with syncytial cells
and type II pneumocyte proliferation. Eosinophilic intracytoplasmic inclusions are present in bronchial
epithelium and syncytial cells. The brain has a nonsuppurative (lymphocytic) encephalitis characterized
by necrosis of neurons (primarily in the cerebral cortex), nonsuppurative perivascular cuffs, and gliosis.
Many affected neurons contain intranuclear and intracytoplasmic inclusions. Demyelination of the
subependymal white matter is also observed. Prominent depletion and necrosis of lymphocytes in
lymphoid tissues is present. Some seals develop a necrotizing nonsuppurative myocarditis. Like canine
distemper, intranuclear and intracytoplasmic inclusions are observed in the gastric mucosa and
transitional epithelium of the urinary bladder and renal pelvis.

6. Morbillivirus in Cetaceans
A morbillivirus causing similar lesions to those observed in the phocine morbillivirus has also been
observed in cetaceans. This viral infection was first identified in harbor porpoises (Phocoena phocoena)
from the Irish Sea during the 1988 European phocine morbillivirus outbreak. This virus has killed

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numerous striped dolphins (Stenella coeruleoalba) along the Spanish Mediterranean coast, has been
identified in outbreaks affecting bottlenosed dolphins along the Eastern Atlantic and Gulf Coast of the
United States and has been identified in sick common dolphins (Delphinus delphis ponticus) on the
northern shores of the Black Sea. Pilot whales (Globicephala sp.) are also infected with this or a similar
morbillivirus. Morbilliviral infection has also been noted in the lymph nodes of a stranded fin whale
(Balaenoptera physalus). (Syncytial cells in the lymph node which stain positive for morbillivirus and
electron microscopy identification of viral nucleocapsid material compatible with morbillivirus.) The
viruses affecting harbor porpoises and striped dolphins are closely related, but antigenically distinct.
These viruses are antigenically distinct from phocine morbillivirus and other mammalian morbilliviruses.
However, the cetacean morbilliviruses appear to be related to the ruminant morbillivirus peste-des-petits
ruminants. Serologic evidence of morbillivirus infection has been identified in numerous odontocete
cetaceans in the western Atlantic and may have a potential impact on these species. Affected cetaceans
develop similar pulmonary and central nervous system lesions that are observed in affected seals.
Grossly, these animals develop a severe pneumonia with multiple foci of atelectasis and consolidation.
Lung associated lymph nodes are often enlarged and edematous. Histologically, there is a
bronchointerstitial pneumonia characterized by necrosis of bronchial and bronchiolar epithelium with a
prominent mucopurulent exudate. Acidophilic intracytoplasmic inclusions are observed frequently
(occasionally intranuclear inclusions are also observed). Type II pneumocyte hyperplasia and prominent
mononuclear inflammation is observed in alveoli. Syncytia are observed in both the alveoli and
bronchiolar epithelium. A non-suppurative meningoencephalitis is observed in most affected animals.
This involves primarily the cerebral grey matter with occasional eosinophilic intranuclear inclusions
present. Necrosis of the bile duct epithelium and transitional epithelium of the urinary bladder with
occasional eosinophilic intracytoplasmic inclusions is also observed. The lymph nodes have prominent
lymphoid depletion with scattered multinucleated syncytial cells present throughout the lymph node.
Multinucleated syncytial cells and inflammation have been observed in the mammary gland. All affected
areas demonstrate intense immunohistochemical staining for morbillivirus. Many affected dolphins also
have serious secondary systemic infections of toxoplasmosis, aspergillosis and other fungi.
It is interesting to note that the Florida manatee (Trichechus manatus latirostris) has seroconverted
by virus neutralization to dolphin morbillivirus. To date no clinical disease has been reported in these
animals.

7. Seal Herpesvirus
Several herpesviruses have been isolated from harbor seals and a California sea lion. Two distinct
types have been isolated from affected animals, these have been identified as phocid herpesvirus type 1
and type 2 (PHV-1and PHV-2). PHV-1 is characterized as a member of the alpha-herpesvirus subfamily
and closely related to canid and felid herpesvirus. PHV-2 has been classified as a gamma-herpesvirus.
Numerous pinniped species have antibodies to PHV-1 and PHV-2 (Ringed seals, spotted seals, harbor
seals, bearded seals, ribbon seals, Steller sea lions, Northern fur seals and walrus). Most animals with
seroconversion to these viruses do not demonstrate clinical disease.
PHV-1 affects mostly young harbor seals. This virus has been shown to cause a serious systemic
infection. Affected animals demonstrated an acute pneumonia, necrotizing hepatitis and necrotizing
adrenalitis. Occasionally, a non-suppurative encephalitis is observed with rare neuronal necrosis. The
pneumonia is characterized as a diffuse interstitial pneumonia with multifocal fibrinous exudation and
emphysema. Within the liver and adrenal gland, there is multifocal necrosis of the hepatic and
adrenocortical parenchyma with a minimal mononuclear cell infiltrate. Acidophilic intranuclear inclusion
bodies are observed in the areas of necrosis. Electron microscopy demonstrates unenveloped hexagonal
viral particles 90 to 100 nm with a central dense core and cytoplasmic enveloped particles 150-160 nm in
diameter. The nature of this virus and its potential to cause disease in wild and captive populations of
seals is still unknown. This virus has been inoculated in young seals with only minimal upper respiratory

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signs (nasal discharge). Phocine herpesvirus, like most mammalian herpesviruses, is most often fatal in
the young and seriously stressed animal. Most sick animals also have concurrent bacterial or protozoal
infections that may mask the herpes viral infection. Like most herpesviruses, this herpesvirus probably
expresses itself in times of stress, as either subclinical oral or genital lesions.
The phocine herpesvirus-2 was isolated from a California sea lion with a severe bacterial
pneumonia, free ranging harbor seals and from seals with abortions during the early epizootic of
morbillivirus infection in Northern Europe. The importance of this virus in the pathogenesis of this
pneumonia is unknown. (A non-oncogenic retrovirus was also isolated from the skin of this affected sea
lion). This virus is highly cell associated and causes little or no disease in pinnipeds.
A gamma herpesvirus has been identified in a metastatic carcinoma of the lower genital tract from
California sea lions. This virus is associated with the neoplastic cells. The association of the virus and
the development of neoplasia of the vagina and cervix is unknown.

8. Herpesvirus in Beluga Whales (Delphinapterus leucas)

A herpesvirus has been observed to cause a focal dermatitis in beluga whales. These epidermal
lesions consisted of random variably sized multiple discrete raised pale grey areas which eventually
ulcerate and are slow to heal. Histologically the epithelial lesion involved the superficial epidermis with
the epithelial cells undergoing intercellular edema, necrosis and microvesicle formation. The infected
epithelial cells contained prominent eosinophilic intranuclear inclusion bodies.

9. Herpesvirus of Sea Otters (Enhydra lutris)

A herpesvirus has been implicated in causing extensive oral lesions in sea otters. Clinically these
lesions consist of variably sized irregular white plaques and/or deep often bilaterally symmetrical ulcers.
These lesions are commonly found mostly on the gingiva and under the tongue. In severely affected
animals, the ulcers tend to coalesce to cover extensive areas of the buccal, labial, gingival and glossal
mucosa. Infected animals rarely show a reluctance to eat, even with extensive oral lesions.
Histologically, the lesions reveal extensive chronic ulcers with associated mixed bacterial colonies and
separate foci of epithelial necrosis and intracellular edema. Numerous eosinophilic intranuclear inclusion
bodies are observed in the degenerating and necrotic cells.

10. Herpesvirus of Bottlenosed dolphins

A disseminated herpes viral infection was identified in an immature female bottlenosed dolphin. On
necropsy, the animal had an enlarged thymus, pericardial hemorrhage and hydrothorax. Histologically
there was a necrotizing interstitial pneumonia, lymphocytic myocarditis, splenic and lymphoid necrosis,
and a necrotizing adrenalitis. Intranuclear inclusions are observed in numerous cells of the thymus,
spleen, adrenal gland, heart, lungs, and glomeruli. Sequencing of DNA products indicates this virus is an
alpha herpesvirus.

11. Hepatitis B-Like Infection in Dolphins

A hepatitis B-like infection has been identified in a Pacific white-sided dolphin (Lagenorhynchus
obliquidens). This animal developed cyclic periods of inactivity, anorexia, and icterus. Blood values
demonstrated a leukocytosis with neutrophilia, lymphopenia, and eosinopenia. Biochemical values
showed markedly elevated alanine transaminase (ALT), aspartate transaminase (AST), gamma
glutamyltransferase (GGT), lactic acid dehydrogenase, total bilirubin, direct bilirubin and indirect
bilirubin. These findings suggested a chronic active hepatitis. Supportive measures were instituted and
the dolphin eventually recovered. Serum from the animal was found to be positive for antihepatitis B
virus core (anti-HBc) activity, hepatitis B virus DNA (HBV-DNA) and hepatitis B surface antibodies
(Anti-HBs). Other cetaceans and humans who had contact with this animal were examined for hepatitis
B antigens. One killer whale was positive while all other cetaceans and humans were negative.

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12. Papillomas in cetaceans
Papillomas have been reported on the skin, penis,genital slit, vagina, tongue, pharynx, and first
gastric compartment of cetaceans. Although a papillomavirus has not always been implicated as the cause
of these lesions, they should be suspected. In the beluga whale , the gastric papillomas identified in the
first gastric compartment are white (like the surrounding normal mucosa), well defined, exophytic masses
with a central wart like core composed of small filamentous papillae. Histologically, the papilloma
develop into an exophytic cup shaped mass with marked epithelial proliferation supported by a thin
fibrovascular proliferation forming numerous arborizing projections from the submucosa. The
proliferating epithelium consists of a flattened basal cell layer 3 to 15 cells thick with a mature epithelium
overlying the basal cells. Scattered amongst the hyperplastic epithelium, individual and small groups of
epithelial cells undergo hydropic degeneration (cells become swollen and globular with a pale granular
cytoplasm). Ultrastructurally, the cells undergoing hydropic degeneration with aggregates of small 40
nm hexagonal viral particles observed in the cytoplasm. These viral particles are consistent with
papillomavirus. It is unclear if any of these papillomas cause physical problems with the affected animals.
Papillomas on the penis are usually raised plaques on the mucosal surface. Like man, papillomavirus may
infected the cervical mucosa and might cause neoplasia from this region.

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 Bacterial Diseases

Bacterial diseases are the leading cause of death in marine mammals. These organisms are usually
observed as opportunistic invaders in conjunction with parasitic, viral or traumatic injuries. The
inhibition of bacteria in the marine mammal's environment is one of the most important factors in
maintaining marine mammal health in captivity.
One must remember that these animals are mammals and therefore are affected by the same bacteria
as their terrestrial counterparts. This discussion will focus only on bacteria that have gained notoriety as
pathogens in the marine mammal.

1. Erysipelothrix rhusiopathiae
Erysipelothrix rhusiopathiae is a small pleomorphic gram positive rod. This bacteria causes two
distinct forms of disease in dolphins: a dermatological disease and a septicemic disease. The
dermatological disease is characterized by dermal infarction that results in sloughing of the epidermis.
Occasionally micro-infarcts result in the characteristic rhomboid areas of cutaneous necrosis. If
untreated, these animals will usually die. The septicemic disease is usually peracute, with the animal
found moribund or dead. At necropsy, affected animals may demonstrate multifocal areas of necrosis and
inflammation involving numerous organs. Culturing the agent (a small pleomorphic gram positive bacilli)
from affected tissues and blood (lymph nodes, kidney, liver, heart, blood) is the only way of identifying
this organism as the agent responsible for the septicemia. A killed bacterin is available for vaccination.
This vaccine has produced excellent results in controlling the disease, however, the vaccine is known to
cause anaphylactic reactions in some cetaceans. It is important to remember that Erysipelas is commonly
found in fish; ingestion may be the route of infection in cetaceans.

2. Pseudomonas Infection
Various species of Pseudomonas (gram negative bacilli) have been incriminated in causing bacterial
disease in both pinnipeds and cetaceans. It is felt that this organism is an opportunistic pathogen which
colonizes wounds and can lead to septicemia. Pseudomonas aeruginosa has caused bronchopneumonia
and multiple large cutaneous ulcers in Atlantic bottlenosed dolphins. The bacteria are known to progress
deep into the cutaneous tissue, causing serious damage to the animal. Many times pseudomonas
septicemia causes a characteristic proliferation of gram negative bacilli into the wall of affected blood
vessels. If affected animals develop a septicemia, cutaneous lesions similar to those observed with
erysipelas may develop. Thus, culturing the lesions is the only method of determining which organism is
responsible for the animals illness.
Pseudomonas pseudomallei is a pathogen found in Southeast Asia. The organism is a water
contaminant and is thought to gain entrance into the animal through cutaneous wounds. A septicemia
soon follows which may result in death. Animals often die peracutely with no clinical signs. Grossly and
histologically, lesions are characterized by multifocal areas of necrosis and inflammation involving many
organs (lungs, liver, spleen, kidneys, and lymph nodes). This agent is infectious to man and may be
transmitted via cuts or abrasions as well as by aerosol transmission.

3. Edwardsiella
Edwardsiella species are gram negative bacilli that are common inhabitants of water. These bacteria
are noted to cause bacterial septicemia in fish. This organism can be a pathogen in both pinnipeds and
cetaceans. Affected animals present with a serious necrotizing enterocolitis and/or septicemia. Animals
with septicemia can develop a severe embolic interstitial or bronchointerstitial pneumonia, a necrotizing
hepatitis and a necrotizing splenitis. Animals with an intestinal lesion develop a necrotizing and
hemorrhagic enteritis/colitis similar to that found in salmonella infections. Isolation of Edwardsiella from
the lungs and liver are usually suggestive of a septicemia. Animals that develop this disease are usually
debilitated or stressed and probably get these organisms from ingestion of contaminated fish.
4. Salmonella
Salmonella are gram negative, non-lactose fermenting bacilli. Salmonella infections have been
observed in both cetaceans and pinnipeds. Salmonella typhimurium, S. enteritidis and S. newport are
the most prevalent salmonella that cause disease. Other Salmonella species have been isolated from
marine mammals without apparent disease. These bacteria are of particular concern for animals housed in
rehabilitation centers. Thus, recently stranded animals should be quarantined and monitored for
salmonella prior to placing with other animals. Salmonella infections usually occur in animals that are
debilitated and/or stressed. Animals present with a hemorrhagic diarrhea and/or septicemia. Animals
with the hemorrhagic diarrhea usually have a necrotizing enterocolitis. Culturing the feces is
recommended for isolation of the organism. Animals that develop a septicemia can die acutely with no
clinical signs. On necropsy, the animal may have a bronchopneumonia and/or a diffuse embolic interstitial
pneumonia. A necrotizing hepatitis and splenitis are common; meningoencephalitis may occur. Isolation
of the organism from the lungs and liver are usually consistent with a septicemia.

5. Leptospirosis
Leptospirosis, primarily caused by Leptospira pomona is known to cause abortions and renal
disease in California sea lions and Northern fur seals. L. grippotyphosa, L. icterohemorrhagiae, and L.
bratislava have been identified serologically, however, this may be due to antigen cross reactivity of L
pomona with these leptospira. This disease is believed to be endemic in rookeries in California and is
most prevalent in the autumn affecting predominately subadult and young adult males. Animals are
usually depressed, anoretic, pyrexic, and reluctant to move due to posterior limb paresis. Other lesions
include icterus, oral ulcerations and excessive thirst. Clinically most animals have a leukocytosis and
elevated creatinine, phosphorus and BUN levels, which indicate renal disease. Grossly, the kidneys are
swollen. On cut surfaces the renal cortex and medulla are pale with loss of differentiation. Hemorrhage at
the corticomedullary junction and subcapsular region is commonly observed in the kidney. In some
animals the liver is swollen and friable. Histologically, a lymphoplasmacytic interstitial nephritis with
tubular necrosis is present with the spirochete present in the renal tubular epithelium and free in the
lumina. In newborn and aborted fetuses, the disease is characterized by subcutaneous hemorrhage and
hemorrhage into the anterior chamber of the eye (The disease Red Eye). This disease may have
zoonotic significance since affected sea lions have demonstrated that they may shed the bacteria in the
urine for up to 154 days. In the live animal, rising titers or titers above 1:3200 are considered to be
infected with leptospirosis.

6. Dermatophilus congolensis
Dermatophilus congolensis is a disfiguring cutaneous disease affecting pinnipeds (South American
sea lion). This disease is characterized by a scruffy pustular or exudative dermatitis involving the entire
body. These lesions are elevated above the skin, forming very prominent scabs. Mortality is low, but
morbidity is high.
Histologic examination of the epidermis demonstrates the characteristic multiple layers of
coagulative necrosis of the epidermis with a peripheral line of degenerating neutrophils separating each
necrotic layer. Numerous gram positive cocci that form the characteristic parallel rows are observed in
the necrotic debris.

7. Mycobacteriosis
Several species of Mycobacteria have been isolated from seals (M. tuberculosis complex (M.
bovis), M. fortuitum, M. chelonei), a California sea lion (M. smegmatis), and several manatee (M.
chelonei and M. marinum). These infections have been presented as either nonhealing chronic cutaneous
lesions, generalized infections with caseonecrotic granulomas in various organs and lymph nodes or
pulmonary infections with granulomas present. Numerous acid-fast bacteria are observed in the
cutaneous lesions. Microorganisms may be more difficult to find in granulomas caused by M.
tuberculosis complex (M. bovis). It should be noted that the bacteria of the Mycobacterium tuberculosis
complex isolated from seals are very closely related to Mycobacterium bovis but do demonstrate some
genetic and biochemical differences. Since several of these species of Mycobacteria are found in the soil
and water, persistent nonhealing cutaneous lesions should be cultured for Mycobacterium. All these
organisms have a zoonotic potential, care should be taken when treating and handling these wounds.

8. Staphylococcus sp.
Staphylococcus aureus has been implicated as one of the cause of pneumonia in dolphins
maintained in captivity. Staphylococcus has also been isolated from a septicemia which lead to an
embolic nephritis and cerebral abscesses as well as cutaneous lesions. This organism has also been
identified in subcutaneous abscess and umbilical abscess of pinnipeds. S. aureus is a part of the normal
flora of the blow hole of many normal dolphins. However, some investigators feel that if it is present in
the upper respiratory tract, it should be considered a potential pathogen. Staphylococcus delphini has
been isolated from a purulent dermatitis in dolphins. In seals, staphylococcus has been identified in
animals with cutaneous abscesses or pneumonia.

9. Clostridial disease
Clostridium perfringens has been reported to cause enterotoxemia in young pinnipeds, gas
producing myositis in dolphins and cutaneous abscesses in fur seals. The necrotizing myositis observed in
dolphins and the subcutaneous abscesses in pinnipeds has been attributed to injection site contamination.
Since Clostridium perfringens and other clostridial organisms are normal inhabitants of the gut and
common in dead animals, it is best to do impression smears from the lesion (gut or muscle) on clean glass
slides for bacterial evaluation.

10. Klebsiella
Klebsiella (Gram negative bacilli) has seen associated with pneumonia, encephalitis and ocular
infections in marine mammals. As usual, bacterial cultures are necessary to differentiate this organism
from other bacterial infections.

11. Nocardia
Nocardia asteroides has been isolated from numerous cetaceans. This organism has been
associated with necrotizing and pyogranulomatous lymphadenitis, pleuritis, encephalitis and mastitis.
The organism is a thin filamentous gram positive organism which can be acid fast.

12. Brucella
Brucella has been identified in several species of cetaceans (Atlantic white-sided dolphins,
Lagenorhynchus acutus; striped dolphins, Stenella caeruleoalba; Common dolphins, Delphinus delphis;
harbor poipoises, Phocaena phocoena; minke whale; and bottlenosed dolphin, Tursiops truncatus),
pinnipeds (hooded seal, Cystophora cristata; grey seal, Halichoerus grypus; Pacific harbor seals, Phoca
vitulina richardsi; and ringed seals) and a European otter (Lutra lutra). These organisms have been
cultured from the placenta and aborted fetus of a bottlenosed dolphin (Tursiops truncatus) and from
lesions in the subcutis (sub-blubber abscesses), lymph nodes, liver, spleen, epididymis, bones and lungs
from other affected animals. The placenta developed a necrotizing placentitis with gram negative
coccobacilli within the trophoblast. Lesions in lymph nodes, liver and lungs are characterized by a
multifocal granulomatous inflammation. Biotyping of the bacteria indicates that these bacteria are closely
related to Brucella abortus or Brucella melitensis. However, it is felt that these may represent a new
species of brucella with several different biovars. Some have suggested that the brucella organism
identified in the bottlenosed dolphin be called Brucella delphini. Others have suggested that there is much
polymorphism at the omp-2 locus of these brucella isolates resulting in the characterization of these
Brucella into two separate species, Brucella pinnipediae and Brucella cetaceae. It is currently unclear as
to what impact this organism has on marine mammals. However, antibodies to Brucella species are widely
distributed among many different marine mammals in the north Atlantic. Brucella organisms have been
identifies in Parafilaroides sp.of lungworms. Brucella organisms have been observed in the uterus and
intestines of this lungworm. The importance of this lungworm in the transmission of brucella to animals
is unknown. These parasites may represent an important transport host for the dissemination of this
bacteria in the wild.

13. Streptococcus
Streptococcus spp. have been isolated from seals with pneumonia and septicemia and cetaceans
with septicemia, metritis, pneumonia and skin lesions. These are primarily beta-hemolytic streptococcal
species (Gram positive diplococci). Most are normal inhabitants of the skin and upper respiratory tract.
A beta-hemolytic streptococcus, Streptococcus phocae, was isolated from many of the seals that died of
pneumonia during the phocine morbillivirus outbreak in the North Atlantic. Most animals present
themselves clinically with dyspnea, coughing and a nasal discharge. Pathological examination
demonstrated a severe pneumonia with areas of consolidation of the lungs, purulent exudate in the
bronchi and bronchioles, interlobular edema and emphysema. Rarely do streptococcal organisms cause a
primary infection. These organisms usually are associated with viral infections. Streptococcus viridans
has been associated with umbilical and skin abscesses, pneumonia, and occasionally septicemias in
pinnipeds.

14. Coxiella burnetii

Coxiella burnetii has been identified in the placenta of an aborted Pacific harbor seal (Phoca vitulina
richardsi). This full term fetus was born alive (but euthanized) from a seal that had an encephalitis caused
by Sarcocystis neurona-like protozoan. The placental trophoblasts were distended with large spherical
aggregates of dense basophilic granular material. The cytoplasmic aggregates stained pink on Gram stain
and pale pink with a Gimenez stain for rickettsia. There was marked necrosis and drop off of
trophoblasts and abundant eosinophilic cellular debris on the chorioallantoic membrane just adjacent to
the placental labyrinth. Multifocal hemorrhage was noted in the chorioallantoic connective tissue, but no
inflammation as noted. Organisms stained positive for Coxiella burnetii using anti-Coxiella burnetii
antibody. No fetal lesions were observed. It is unknown how common placental infections with C.
burnetii are in seals. The source of the infection is unknown, but like most teresteral mammals, infection
may occur with or without abortions. Handlers of placental tissues and/or newborn pups should take
precautions because of the potential zoonotic concerns that are known to exist with this organism.

15. Listeria inanovii

Listeria inanovii has been isolated from skin and umbilical abscesses, keratitis, meningitis,
osteomyelitis, pneumonia and septicemias in California sea lions and elephant seals.
 Mycotic Diseases

Numerous mycotic diseases have been reported in pinnipeds and cetaceans. Most have been single
reportable cases; only several fungal organisms have been associated with outbreaks of disease.
Since fungal organisms are usually opportunistic or secondary invaders; these organisms pose a serious
health risk to the animal that is immunocompromised. Animals that are malnourished, have preexisting
viral or bacterial diseases, have undergone prolonged drug (antibiotic) therapy, or immunosuppressed due
to stress are predisposed to get these infections.

1. Candidiasis
Candida albicans is the most common species of Candida to cause clinical disease in stressed
pinnipeds and cetaceans. Infected animals usually develop cutaneous and/or intestinal infections with
lesions occurring primarily at mucocutaneous junctions, blowhole and vagina. Disseminated candidiasis
has been reported in the killer whale and other cetaceans. It is felt that most marine mammals can be
infected by Candida. Infections are usually observed in animals that are severely stressed and/or under
prolonged antibiotic therapy. These lesions appear as white or yellow creamy plaques. In internal organs,
prominent focal areas of necrosis are visible. Histologically large colonies of septate hyphae,
pseudohyphae (3 to 7 microns wide) and blastospores (3 to 5 microns diameter) are observed in the
necrotic lesions. The finding of Candida in the esophagus or vagina is very common and may be
identified histologically as an incidental finding. However, when the organism invades healthy tissue, the
fungus is considered pathogenic.

2. Loboa loboi
Lobomycosis is a fungal disease that affects the skin of the Atlantic bottlenosed dolphin and man.
Grossly, these lesions are located anywhere on the animal's body (head, fin and flukes are the most
common sites) and are white, multiple and nodular. These lesions have a cobble stone appearance on the
skin. Histologically, there is a superficial granulomatous dermatitis involving the papillary dermis. This
granulomatous dermatitis is composed almost entirely of macrophages and multinucleated giant cells
containing numerous round yeast forms (5-10 microns in diameter) connected to each other and forming
long chains. Some yeast forms contain a 1 to 2 micron central body. Larger yeast forms may have a rough
and spiny surface. The epidermis over these areas of inflammation is acanthotic with downward growth
of the rete pegs. Clinically the animals are not seriously affected by the growth of the organisms;
however, if these become large, the animal may become debilitated and die (usually due to secondary
bacterial infections). Treatment has not proven successful, however, removal of the affected area has
shown positive results.

3. Fusarium
Outbreaks of Fusarium-induced dermatitis has been observed in a group of captive California sea
lions, grey seals, harbor seals, Atlantic white sided dolphins and a pygmy sperm whale. The lesions
consisted of papules and nodules on the face, trunk, flippers and the caudal portions of the body.
Histologically, there is hyperplasia of the follicular and epidermal epithelium with associated chronic
active inflammation and numerous fungal hyphae (Septate branching hyphae, 2 to 5 microns in width with
parallel sides). In marine mammals, Fusarium spp. are most likely opportunistic invaders of the skin.
Animals that are immunocompromised due to stress or illness may be most susceptible. Damage to the
integument due to excessive chlorination of the water and high fluctuating pool temperatures may also
play an important role in this disease. Treatment of the animals with ketoconazole caused the dermatitis
to resolve in 3 to 4 weeks.

4. Aspergillus and Zygomycetes Infections:

Aspergillus and Zygomycetes infections cause serious disease in individual animals. As with
infection with Candida, the affected animals are usually stressed and/or under prolonged antibiotic
therapy. Infection can involve focal areas, usually the esophagus or lungs; however, systemic spread of
the fungus is common. Lesions involving the esophagus and trachea usually appear as ulcers with yellow
to cream colored plaques over the affected area. Systemic spread leads to necrosis of multiple tissues
with liver and kidney commonly involved. Diagnosis is by observing the characteristic hypha
(Aspergillus: long branched septated hyphae, 3 to 4 microns wide with parallel walls. Zygomycetes:
long non-septate non-parallel walled hyphae with irregular branching).

5. Dermatophytosis: Microsporum and Trichophyton spp.

Cutaneous infections with Microsporum canis and Trichophyton spp. have been reported in both
cetaceans and pinnipeds. Microsporum canis has been isolated from harbor seals and Trichophyton spp.
in Northern fur seals (Callorhinus ursinus), Steller sea lions (Eumetopias jubatus) and bottlenosed
dolphins (Turciops truncatus) and Malassezia from a California sea lion, grey seal, and harbor seal.
Infections in the seals are characterized by round depilated areas, 2 to 3 cm in diameter on the face and
back. These depilated areas spread over the entire body. Histologically there is epidermal hyperplasia
with hyperkeratosis, parakeratosis, necrosis and microvesiculation and microabscess formation.
Numerous neutrophils are present in the affected epidermis. Numerous branched septated hyphae 2 to 7
microns in diameter are observed in the parakeratotic and necrotic regions consistent with Microsporum
and Trichophyton infections. Water quality issues appear to be the primary cause of these infections.

6. Coccidioides immitis
Coccidioides immitis has been identified as an endemic disease in the California sea lion (Zalophus
californianus) and an isolated case in the California sea otter (Enhydra lutris) and bottlenosed dolphin
(Tursiops truncatus gilli). This organism appears to be endemic in animals that inhabit the southern and
central part of their range from Baja California, Mexico in the south to Monterey County, California in
the north. Coccidioides immitis is an infectious agent to numerous animal species and is a serious health
risk to man (Valley Fever) when living in endemic areas. Endemic areas are Arizona, Southern and
Central California, Mexico, New Mexico, Nevada, Utah and Texas. This organism probably infects sea
lions, like most animals, as a mild respiratory disease. Recovery usually occurs after a short illness. Some
animals develop a serious disseminated disease. Sick animals usually beach and are presented ill. Gross
necropsy findings are focal to disseminated granulomas involving the lungs, liver, pancreas, numerous
lymph nodes (retropharengeal, submandibular, mesenteric, and tracheobronchial lymph nodes) and
occasionally a purulent pleuritis and peritonitis. Histologically the affected organs develop
pyogranulomatous inflammation with variable numbers of multinucleated giant cells and large round
double contoured wall spherules, 10-70 micron in diameter. Filling the spherules are numerous small 2-5
micron endospores. Animals are most likely infected by the inhalation of spores. Coccidioides immitis is
also known to survive in sea water for several weeks. It is unknown if sea water could be a means of
infecting animals.
 Protozoal Diseases

1. Sarcocystis sp.
Sarcocystis species have been reported in numerous pinnipeds and cetaceans and the sea otter.
These species of sarcocystis are S. balaenopteralis in a whale (Balaenoptera borealis), S. neurona in a sea
otter and harbor seal, and several unnamed species of Sarcocystis in a sperm whale (Physeter catodon),
Northern fur seal (Callorhinus ursinus), striped dolphin (Stenella caeruleoalba) and ringed seals (Phoca
hispida). These protozoal organisms appear to be incidental findings in these animals. Little is known
about their life cycle. A necrotizing hepatitis characterized by multifocal areas of necrosis has been
observed in a captive sea lion. This organism appears to be similar to Sarcocystis canis. It is not known
whether this organism is normally found in this animal. In a captive sea otter, encephalomyelitis (most
severe in the cauda equina region) has been observed caused by Sarcocystis neurona-like organisms. The
source of the infection was not known. In another sea otter both Sarcocystis neurona and Toxoplasma
gondii were isolated from lesions in the brain.

2. Toxoplasma gondii
Toxoplasma gondii has been observed in several species of marine mammals including: the
California sea lion, Northern fur seal, harbor seal, manatee, Atlantic bottlenosed dolphin (Tursiops
truncatus), and Spinner dolphin. These animals have demonstrated a disseminated infection with necrosis
of numerous organs containing toxoplasma tachyzoites. It is felt that these animals probably were
immunocompromised leading to infection. Transplacental transmission is unknown but probably can
occur. Sera tested for toxoplasma antibodies have demonstrated that in one study 27% of the beluga
whales, 22% of the Southern sea otters, and 7.6 % of the harbor seals examines had antibodies to
Toxoplasma gondii. These results indicate that Toxoplasma gondii exposure can be a common
occurrence in these wild marine mammals.

3. Ciliated Protozoa of Dolphins

A ciliated protozoa (Kyaroikes cetarius, possible) has been identified in necrotic cutaneous lesions
in Atlantic bottlenosed dolphins, spotted dolphins (Stenella attenuata), common dolphins, pygmy sperm
whales, Frazers dolphins, and killer whales. These lesions are usually a pyogranulomatous dermatitis and
cellulitis with large ciliate protozoa scattered amongst the necrotic debris. These ciliated protozoa are
large (up to 60 to 100 microns in diameter with a large 20 micron nucleus). These organisms have also
been associated with pneumonia and lymphadenitis. These protozoa may be opportunistic invaders since
these protozoa are commonly found in and around the blowhole of dolphins (50% of wild dolphins)
without any inflammation or disease .

4. Giardiasis
Giardia sp. oocyst have been identified in fecal samples from ringed seals (Phoca hispida), harp
seals (Phoca groenlandica), grey seals (Halichoerus grypus), and harbor seals in the arctic, subarctic and
eastern regions of Canada. Infected animals have not demonstrated illness. The zoonotic potential of
infected seals to act as reservors for human infection is unknown. To date, feces from beluga whales and
northern bottlenosed whales (Hyperoodon ampullatus) were negative for Giardia sp. cysts.
 External Parasites

1. Lice
Lice are a common finding on pinnipeds. Only anopluran (sucking) lice have been found on these
animals. Antarctophthirius microchir is a common louse noted on sea lion pups. These insects cause
alopecia in infected animals. These organisms are believed to be the intermediate host for the filarid
nematodes of pinnipeds; however, this has not been proven. An arbovirus (Alphavirus) has been isolated
from the elephant seal louse, Lepidophthirus macrorhini, which implies that these lice can transmit viral
infections from one animal to the other.
Cetaceans are also known to harbor lice. Several species of lice have been isolated from the skin of
these animals. Clinical disease has not been associated with these organisms.

2. Mites
Demodex zalophi has been observed in California sea lions. These animals develop alopecia and
thickening of the skin over the genitalia, flippers and ventral body. The mites live in hair follicles and are
diagnosed by skin scrapings.
Sea otters have also been observed to have demodex mites. These mites are observed in hair
follicles around the face. No serious dermatologic conditions have been observed in these animals.
Demodex mites only cause a mild follicular ectasia and minimal associated folliculitis.

3. Barnacles
Barnacles are common on certain cetaceans. These can be either sessile or pedunculated. They do
not cause damage to the skin of affected animals.
 Internal Parasites of Pinnipeds

Respiratory System

(1) Lung mites:

Lung mites are common parasites of the nasal passages, trachea, bronchi, and bronchioles. Both
seals and sea lions are affected. The most common mites observed are Orthohalarachne diminuata and
Orthohalarachne attenuata. O. diminuata inhabits the airways of the lung, and O. attenuata are found in
the nasopharynx. The nasal mite, Halarachne miroungae has been observed in sea otters. Grossly these
mites are seen as small white specks on the mucosa of the respiratory tract (O. attenuata, .5 to 5 mm; O.
diminuata, .6 to .8 mm). Clinically, these mites do not cause any serious problems, however, they might
cause copious amounts of mucus in the upper respiratory tract and nose, nasal discharge, dyspnea, and
coughing.

(2) Lungworms

(a) Parafilaroides decorus is the most common lungworm of young (1- to 2-year-old)
California sea lions. The intermediate host for this metastrongylid is the opal eye fish (Girella nigricans).
After ingestion of the fish and release of the larvae into the gastrointestinal tract, the larvae migrate to the
lungs (alveoli), where maturation occurs. Females release larvae in the alveoli; larvae then migrate up the
respiratory airways, are swallowed, and are then discharged with the feces. Histologically, uncomplicated
infections result in goblet cell hyperplasia of the bronchiolar epithelium in which mucoid obstruction is
observed. A suppurative or granulomatous bronchopneumonia is observed if a secondary bacterial
infection occurs. Grossly, these lungs have a patchy, or mottled, appearance of red and grey hepatization.
Other Parafilaroides species have been noted in the lungs of other species of pinnipeds. Parafilaroides
lungworms have been identified with brucella bacteria present in their uterus and gut. These lungworms
may cause brucellosis infection in pinnipeds.

(b) Otostrongylus circumlitus is another large Metastrongylid nematode that inhabits the
primary and secondary bronchi of harbor seals and northern elephant seals. This parasite causes
prominent bronchiectasis. Bronchiectatic abscesses containing these parasites are occasionally observed.
Histologically, the bronchi and bronchioles have marked goblet cell hyperplasia of the peribronchiolar
glands; mucus plugs fill the dilated bronchioles. As with most lungworms, a verminous pneumonia may
develop as a result of secondary bacterial infection.

2) Digestive tract

(a) Stomach worms

Contracaecum and Anisakis are the most common nematode stomach worms of both
pinnipeds and cetaceans. These parasites cause ulceration of the gastric mucosa and submucosa during
migration. Occasionally Anisakine parasites may induce nodules in the gastric mucosa and submucosa.
On histologic examination, parasites are found in the ulcerated regions. In cetaceans (odontocete), these
parasites are located in the first and third chamber of the stomach. These parasites are usually incidental
findings; however, they have been noted to cause hemorrhage and melena in both pinnipeds and
porpoises. The life cycle is not fully understood; it is felt that a crustacean is the first intermediate host
and a fish (many different species) is the second intermediate host. (The Pacific herring is the second
intermediate host for Anisakis spp.)

(b) Hookworms (Uncinaria lucasi and Uncinaria hamiltoni)

 Hookworms are common in sea lions and the Northern fur seal. Uncinaria lucasi is the
most pathologic hookworm for Northern fur seal pups. Young fur seals and sea lions become infected
during ingestion of the mother's milk. The parasites become adults within several weeks and cause severe
hemorrhage into the intestines, which results in anemia. Surviving Northern fur seal pups usually shed
the parasites after three months. California sea lion pups tend to maintain infections longer with adult
worms present until 6 ot 8 month. Surviving animals later become reinfected with the third-stage larvae
by larval penetration of the skin or by ingestion of the larvae. These larvae migrate to the blubber of the
ventral abdomen or mammary glands, where they remain dormant until they are shed in the females milk.
Shedding in the milk occurs only during a short time post partum . In both sea lions and northern fur
seals this transmammary shedding is usually less than 24 hours postpartum. Larva tend to be present in
the sand on beached during only the fall and winter months.

(C) Liver Flukes

Zalophotrema hepaticum is the liver fluke of sea lions. This fluke causes little damage and
is found in the common bile duct, intrahepatic bile duct, and gallbladder. Occasionally these flukes will
cause cystic cavitation in the hepatic parenchyma.
In sea otters, (also bearded seals) the gallbladder fluke, Orthosplanchnus fraterculus, causes
cystic hyperplasia of the gallbladder mucosa. It also is believed to be responsible for causing a chronic
fibrosing cholecystitis which is sometimes characterized by nodular thickening of the periductal and
gallbladder connective tissue. This parasite does not appear to adversely affect the host.
These flukes are very small, 1-3mm in length. The eggs are the characteristic yellow color of fluke eggs
and triangular in appearance.

(d) Acanthocephalids
Acanthocephalids are common intestinal parasites in pinnipeds and sea otters. These
parasites are primarily of the genus Corynosoma. Acanthocephalids are observed usually as incidental
findings in the colon and small intestine (ileum and jejunum). These parasites bury their heads deep into
the mucosa and submucosa. In pinnipeds they rarely cause problems. However, in sea otters they are
known to burrow through the intestinal wall and cause a life threatening peritonitis. Three other species
of Acanthocephalids also occasionally infect sea otters, Falsifilicollis altmani, F. kenti, and F. major.

3. Cardiovascular system

Heartworms
Heartworm disease in pinnipeds is caused by both Dirofilaria immitis and Dipetalonema
spirocauda. D. spirocauda is the most common heartworm found in most feral pinnipeds (primarily
harbor seals). The life cycle is unknown, but the louse is suspected to be the intermediate host. These
parasites are observed in the right ventricle and pulmonary arteries. Severe infection causes dilatation of
the right ventricle and myocardial hypertrophy. Microscopically, the pulmonary arteries and arterioles
have prominent intimal proliferation. Secondary chronic passive congestion may be observed in severely
affected animals.
Dirofilaria immitis is occasionally observed in captive pinnipeds. These parasites live in the same
location and cause the same problems as D. spirocauda. The identification of microfilaria is helpful in
separating D. immitis from D. spirocauda. The microfilaria of D. immitis are usually larger (300 x 5
microns) than D. spirocauda (225 x 4 microns). However, microfilaria from D. spirocauda cannot be
differentiated morphologically from the common nonpathogenic subcutaneous filariid Dipetalonema
odendhali.
Dipetalonema odendhali is often found in the subcutaneous tissue, in the intermuscular fascia,
beneath the parietal peritoneum, free in the abdominal and thoracic cavities, and in the pericardial sac.
4. Musculoskeletal system

Trichonella nativa
Trichinella in marine mammals is primarily an arctic disease. It is commonly found in polar bears
but is increasingly identified in walruses, bearded seals, and ringed seals. It has also been identified in a
beluga whale. Cannibalism in the arctic environment is believed to play an important part in maintaining
the cycle. However the ingestion of fish or birds that have fed on infected carcasses could also be a
means of spreading these parasites. Trichinella nativa has been identified in these animals. This parasite is
cold tolerant and is infectious to man. Clinical disease in marine mammals is unknown.
 Internal Parasites of Cetaceans

(1) Respiratory tract

(a) Nasitrema sp.

Nasitrema flukes are common flukes located in the head sinuses of many porpoises,
dolphins, and toothed whales. These flukes range in size from 9 to 12 mm (Nasitrema stenosomum) to 28
to 35 mm (Nasitrema gondo). This parasite is normally found in the submucosal glands of these sinuses.
Occasionally this fluke is observed in the middle ear. This parasite rarely causes problems; however, these
flukes will occasionally migrate to the brain and cause serious central nervous system damage. Lesions
caused by this fluke usually contain numerous small yellow triangulated fluke eggs (60 to 80 microns on
the long axis with a single operculum). Numerous strandings have been associated with parasitic
migration of this parasite into the brain. The life cycle is unknown.

(b) Hunterotrema caballeroi

This is a rather large fluke (up to 25 cm long) observed in the Amazon River dolphin. This
parasite causes a mild to moderate mucoid exudate in the bronchi of these animals. However, it has been
incriminated in bronchial obstruction, bronchiectasis, and atelectasis.

(c) Stenurus sp.

This is another common nematode (metastrongyle) located in the pulmonary parenchyma of
the harbor porpoise and dall porpoise. These parasites usually cause subpleural nodules, which are filled
with the parasites. This parasite has been known to migrate and fill the tympanic bullae. These parasites
have been incriminated in dolphin strandings when the parasites have been observed in the tympanic
bullae.

(d) Halocercus sp.

The nematode Halocercus is a lungworm (Metastrongyle) that affects dolphins and
porpoises. These parasites inhabit the small bronchi and bronchioles. Heavily infected animals may
develop a neutrophilic and eosinophilic bronchopneumonia. These parasites form granulomas within the
bronchioles, which become encapsulated and calcify. The bronchopneumonia is often accompanied by
hypertrophy of the smooth muscles of the terminal bronchioles. The life cycle of this lungworm is
unknown, but believed to be direct. Infections of young dolphins with these parasites also suggests
transplacental transmission of the parasite.

(e) Crassicauda sp.

These nematodes are commonly found in the pterygoid air sinus and are associated with
erosions of the pterygoid bone. Migration of this organism to the brain or tympanic bulla can lead to
CNS lesions and strandings of affected animals. Crassicauda sp. have been found in the mammary gland,
air sinuses, blubber and muscle.

2. Digestive Tract

(a) Braunina cordiformis

This fluke is usually observed in the second chamber of the stomach of Atlantic bottlenosed
dolphins. It causes minimal damage and irritation to the gastric mucosa. The fluke, when attached to the
gastric mucosa, has a characteristic urn shaped appearance (5 mm x 5mm) in the lumen of the stomach.

(b) Pholeter gastrophilus

Pholeter gastrophilus is another fluke observed in the second chamber of the stomach of
dolphins. This parasite buries deep in the submucosa, forming prominent small black cavitary nodules
that can be identified on palpation. The mucosa usually remains intact over these parasitic nodules. The
nodules have abundant fibrous connective tissue surrounding the parasite with a variable granulomatous
and eosinophilic inflammatory reaction. These flukes have prominent cuticular spines on the tegument
and yellow, single operculated eggs.

(c) Cyclorchis campula (Also Campula pilliata & C. oblonga)

This is a trematode that primarily inhabits the bile and pancreatic ducts of cetaceans. This
parasite causes extensive irritation of the ducts, with hyperplasia of the ductal epithelium and fibroplasia
developing around the ducts. This chronic irritation may progress to a chronic fibrosing hepatitis and
pancreatitis. Numerous parasites are found in the large dilated pancreatic ducts; the smaller ducts are
usually sclerotic. The fluke has numerous prominent tegumental spines. This parasite, like Nasatrema,
have characteristic small yellow triangular eggs.
 Miscellaneous Diseases

1. Freshwater and Cetaceans

Cetaceans that are not maintained in ocean sea water (3.4% salt) can develop skin and corneal
lesions. These lesions usually develop in animals that have been maintained for a week or longer in water
containing less than 1% salt. These lesions are characterized by areas of ulceration and necrosis of the
epidermis and corneal opacity. Histologically, the lesion is characterized by ballooning degeneration of
the stratum externum (parakeratotic layer). Later the entire thickness of the epidermis becomes necrotic
and/or ulcerated. If these animals are placed back into normal sea water, recovery usually occurs.

2. Pinniped Hyponatremia
This is a problem observed primarily in seals. This disorder is characterized by a decline (either
sudden or gradual) in blood sodium levels and is observed primarily in animals held in fresh water. It is
brought on by various stresses or disease (i.e., Vitamin E deficiency). Clinically, affected animals
demonstrate one or more of the following signs: lethargy, ataxia, head and body shaking, convulsions,
and sudden death. Diagnosis is confirmed by finding blood sodium levels between 120 and 147 mEq/L
(normal, 150 to 160 mEq/L). Salt administration is the treatment of choice in affected animals.

3. Thiamine Deficiency
Thiamine deficiency has been observed in both pinnipeds and cetaceans. This deficiency is
associated with the ingestion of thiaminase-containing fish (herring, smelt, capelin). Clinically, these
animals develop anorexia, irregular breathing, and unresponsiveness to touch, noise, and light stimulation.
Untreated animals develop central nervous system signs (tremors and spasms, capable of leading to
death). It does not appear that any consistent histologic lesions are associated with thiamine deficiency in
these animals. It has been reported that affected sea lions had a dilated left ventricle and myelin sheath
degeneration of the peripheral and vagus nerves. Treatment and prevention are by the use of thiamine
supplements in the diet.

4. Vitamin E Deficiency
Vitamin E deficiency develops in marine mammals that are fed improperly stored fish that are high
in unsaturated fatty acids. This deficiency is felt to cause both muscle degeneration and steatitis. Seals
are the marine mammal most commonly affected. Affected animals are usually anorectic, reluctant to
move, and have an arched posture. Histologically, the muscles are undergoing degeneration and necrosis.
Steatitis has been observed in California sea lions and Amazon River dolphins. These animals developed
a fatal condition characterized by weakness and generalized subcutaneous nodules of fat necrosis.
Vitamin E supplements aid in the prevention of the disease and should be established on the basis of fat
content of the fish, storage, and method of preparation and feeding. Since the viscera of fish contain
more vitamin E than the flesh, it is preferable to feed whole fish instead of eviscerated fish. It is
important to remember that pinnipeds suffering from vitamin E deficiency are more likely to develop
hyponatremia. Treatment of choice for seals with hyponatremia is vitamin E supplementation and the
addition of salt to the diet.

5. Capture Myopathy
Exertional rhabdomyolysis has been noted in captive marine mammals during capture, restraint, and
transportation. These animals develop skeletal muscle degeneration and necrosis. It is felt that low or
deficient levels of vitamin E may play an important role in the development of this condition.
6. Scombroid Poisoning
Scombroid poisoning is a condition in man and marine mammals associated with the ingestion of
poorly preserved scombroid fish (tuna and mackerel). Clinically, affected animals develop nonspecific
signs (inappetence, debilitation, irritable behavior, gastric ulcers, and pulmonary edema), which disappear
on change of diet. Animals that have ingested this poorly preserved fish usually recover. One should
always use caution when feeding scombroid fish. Ensure that these fish have been stored frozen for less
than four months.

7. Microphthalmia and Freshwater Dolphins

Many species of freshwater dolphin (particularly the Ganges River dolphin) have microphthalmia
and apparent blindness. This is a normal finding in these animals. Histologically, these eyes have a
minimal slit-like opening between the eyelids and a microphthalmic eyeball. The eye is nonfunctional and
has a thick cornea, iris, ciliary body, retina, and optic nerve.

8. Disaccharide Intolerance in Pinnipeds

Pinnipeds have no tolerance for dietary disaccharides, including both lactose and sucrose. If
abandoned pups are fed formula high in sugars, diarrhea develops; as the intolerance progresses, a
dermatitis develops and death follows. It appears that pinniped milk does not contain lactose or any
other carbohydrate. These animals lack enzymes in the intestine to properly degrade these sugars.
Formulas composed of fish or marine products containing a high fat content and only simple sugars
should be used when feeding abandoned pups.

9. Cutaneous Gout
The Amazon dolphin (Inia geoffrensis) has higher serum uric acid levels than other cetaceans (10
mg/dl, which is approximately 10 times higher than that reported for other cetaceans). One Amazon
dolphin developed near the base of the flippers an ulcerative dermatitis that was characterized by a
granulomatous inflammatory reaction associated with numerous urate crystals in the tissue. The animal
was treated with allopurinol over a six-month period. The treatment decreased the animal's serum uric
acid concentration and healed the lesions.

10. Heat Prostration

Since cetaceans have a thick layer of blubber surrounding their body, dissipation of heat can be a
serious problem in stranded animals. Stranded animals need to be kept shaded, cool and moist at all
times. Ideally they should be kept out of the sun to prevent sunburn. Once an animal is stranded and left
out of water in the sun, its body temperature greatly increases causing serious problems for the animal.
Animals that die of heat prostration usually demonstrate diffuse edema and congestion of the lungs.

11. Sunburn in Cetaceans

Cetaceans need to have their skin protected from the direct affects of the sun. Animals that are
either out of the water due to stranding or for physical examination need to be monitored to protect them
from the sun. Sun screens (zinc oxide) can be useful in protecting these animals. Animals that are
sunburned have ballooning degeneration of the epidermis which, in severe cases, can ultimately lead to
necrosis of the epidermis.

12. Sea Otter Hemorrhagic Gastroenteritis

The cause of sea otter hemorrhagic gastroenteritis is unknown. This disease is usually observed in
severely stressed or debilitated animals. Affected animals develop a severe bloody diarrhea and are
usually depressed and anoretic. Most affected animals usually die.
 At necropsy the only lesion observed is blood in the entire intestinal tract extending from the
duodenum to the rectum. Histologically, there is little damage to the intestinal mucosa: prominent
pooling of blood in the mucosa and submucosa is often observed. Isolation of bacteria from the lesion
have failed to identify a specific bacterial agent. The pathogenesis of this lesion is unclear. It is felt that
the gastrointestinal tract may act as a shock organ with pooling of blood into the intestinal mucosa and
diapedesis of blood into the intestinal lumen.

13. Nephrolithiasis in Pinnipeds

The finding of kidney stones in seals is a common finding. These stones appear to be incidental
findings in many seals and are considered of little pathologic significance.

14. Trauma
Trauma due to shark bites, whale bites, or man-made actions such as shooting or boat strikes can
be observed in all marine mammals. Shark bites are often characterized by parallel rake or bite marks on
the body. Dolphin attacks on harbor porpoises and young (usually male) bottlenosed dolphins are
observed. It is felt that such attacks by male bottlenosed dolphins is common.

15. Cardiomyopathy in Pygmy and Dwarf Sperm Whales

A cardiomyopathy involving the right ventricle has been observed in pygmy (Kogia breviceps) and
dwarf (Kogia simus) sperm whales. This lesion has been observed primarily in adult animals. Grossly,
the right ventricle is enlarged and flabby. Histologically there is moderate to focally extensive myocardial
fibrosis involving the right ventricle and ventricular septa. Myofiber degeneration characterized by
hyaline change and loss of striations is frequently associated with the fibrosis. Occasionally remaining
myofibers demonstrate crisscrossing or whirling patterns, and myofiber hypertrophy with enlarged nuclei
and nucleoli and sarcoplasmic lipofuscinosis. No changes were observed in the coronary arteries,
endocardium, pericardium or aorta. Most livers have centrolobular hepatocellular loss and/or necrosis
suggestive of right side heart failure. The cause of this lesion is unknown.

16. Vaginal calculi in Dolphins

Vaginal calculi have been observed in the common, Pacific white-sided and spotted dolphins. These
calculi become very large, exhibit concentric crystallized layers and contain calcium phosphate
compounds. These calculi are found associated with the cervix, pseudocervix, and vagina. Most calculi
contain fetal bones which suggests that parts of the fetal skeleton become entrapped in this location and
crystallize.

17. Northern Elephant Seal Skin Disease (NESSD)

Northern elephant seal skin disease (NESSD) is a skin condition of unknown etiology involving
young seals less than 2 years of age. The skin lesions are characterized by variably sized areas of alopecia
and hyperpigmentation with variably sized areas of epidermal ulceration and necrosis. Microscopically
the lesions are characterized by an ulcerative dermatitis with marked hyperkeratosis of the epidermis and
follicular epithelium, acanthosis and sebaceous gland metaplasia and atrophy. Some follicular dilatation
with prominent amounts of keratin within the dilated follicle has also been observed. Secondary
suppurative inflammation due to bacterial infections are common. Diseased seals have depressed
thyroxine, triodothyroxine, retinol, serum iron, albumen, calcium and cholesterol levels. Alanine
aminotransferase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transpeptidase,
BUN, and uric acid were elevated. Diseased seals are usually smaller in size (15% smaller) than non-
affected animals. Affected animals have elevated serum polychlorinated biphenyl (PCB) and p,p
dichloro-diphenyl-dichloroethane (p.pDDE; a metabolite of DDT) levels. Lesions observed in affected
animals are similar to those observed in PCB toxicosis.
 Necropsy Procedures on Marine Mammals

The necropsy is important in the determination of the cause of death of any marine mammal.
Performing the necropsy in an organized manner so that all organs are examined and lesions annotated on
the necropsy form will greatly assist in rendering a diagnosis. Not only should the necropsy proceed in an
organized fashion but also the person performing the necropsy should be aware of the proper organs to
collect and sample to take for microbiology, toxicology and pathology so that the cause of death can be
properly determined. When performing a necropsy, it is recommend that the respiratory system be
evaluated first, the cardiovascular system next, followed by the digestive system, urogenital system, and
central nervous system. If the animal has undergone serious central nervous system problems, it would
be wise to evaluate the brain first since this organ can decompose quite rapidly.
Since these animals have a large layer of body fat to retain body heat and usually die in the water,
marine mammals can decompose rapidly which can complicate the post mortem examination. It is best to
necropsy morbid animals first to obtain adequate bacterial and viral cultures and tissue samples for
histopathology so that the clinician and pathologist have the best chance to identify the cause of death.
Fresh and formalin-fixed tissues should be saved for further examination. If the animal cannot be sent to
the diagnostic laboratory and must be necropsied at the site, fresh tissue samples should be obtained
(usually lung, liver , kidney, spleen, and tied off sections of intestines), placed in individual containers, and
submitted to the laboratory on wet ice (not with dry ice!!) for culturing. Never send formalin fixed
tissue with fresh tissue unless it is double bagged and sealed to prevent formalin vapors from sterilizing
the fresh tissues. If frozen samples from all organs are required, samples should be individually package
and labeled in its own bag before freezing. It is important that formalin-fixed tissues be no thicker than
1cm to insure rapid penetration of the formalin. Also, it is important that lesions as well as normal tissue
be trimmed and sent to the pathologist for examination.

Abortion cases:

In abortion cases, the examination of both fetal and placental tissues gives the pathologist a better
chance of identifying the cause of the abortion. One should culture the placenta, particularly in areas of
placental and uterine attachments and allantoic surfaces. Fetal cultures should be taken from the stomach
(aspiration of fetal fluid from the stomach into a syringe) and lungs. If a bacterial septicemia is suspected
in the animal, the liver should also be cultured. Aerobic bacterial cultures should be performed with
blood agar, MacConkey agar, and chocolate blood agar. Campylobacter culture media would be an
additional culture media to use. Impression smears from fetal kidney should be made for evaluation of
kidney tissue for Leptospira-like organisms on FA examination. Fetal fluids (peritoneal or thoracic fluids)
should be obtained and frozen for future serological evaluation. Lung, liver, kidney, spleen, and portions
of the brain should be frozen and saved for later use if needed. Liver, kidney, and fat should be saved for
toxicology. At a minimum, the following tissues should be submitted for histological examination: brain
(cerebrum, mid brain, and cerebellum at a minimum), trachea, lung, tonsil, heart, liver, kidney, adrenal
glands, spleen, thymus, lymph node, thyroid, skeletal muscle, tongue and/or oral mucosa, esophagus,
stomach (different chambers if present), intestine (multiple sections), and placenta.

Respiratory cases:

For animals with respiratory disease, the lungs should be cultured from at least two different
areas. In addition to the lungs, the liver and large intestine (distal region of the intestine) should also be
cultured. Aerobic cultures from the lungs and liver should be done on blood agar, MacConkey agar, and
chocolate blood agar. Mycoplasma cultures could be attempted to determine if Mycoplasma are present.
Samples of the large intestine should be cultured, particularly for Salmonella using Salmonella enhancing
media. Frozen tissue samples saved for additional workup should consist of: pneumonic lung, liver,
kidney, spleen, and brain. The following tissues should be submitted for histological examination: brain
(cerebrum, mid brain, and cerebellum at a minimum), trachea, lung (pneumonic and normal sections),
tonsil, heart, liver, kidney, adrenal glands, spleen, thymus, lymph node, skeletal muscle, tongue and/or
oral mucosa, esophagus, stomach (different chambers if present), and intestine (multiple sections). If one
is concerned that the respiratory distress is due to a toxic event, lung, liver and kidney should be saved
for toxicological evaluation. Fecal material should be taken for parasite evaluation.

Diarrhea Cases:

In cases where diarrhea is a concern, bacterial cultures of the lung, liver, ileum region, and large
intestine region should be obtained for aerobic cultures. Feces from the large bowel portion should be
cultured (If the gall bladder is present, a sample containing large intestine content and some bile should
also be cultured) for Salmonella on Salmonella enhancing media. If the mesenteric lymph nodes are
enlarged, these should also be cultured aerobically. Tissues saved and frozen for further culturing should
be: lung, liver, kidney, spleen, brain, sections of small intestine (placed in individual bags), and sections of
large intestine (placed in individual bags). Tissues submitted for histopathology should include: brain,
trachea, tonsil, lung, heart, liver, kidney, adrenal glands, thymus, spleen, mesenteric lymph nodes, tongue,
and oral mucosa (if ulcers are present), esophagus (if ulcers are present), at least one sample from each
chamber of the stomach, small intestine (duodenum, sections of jejunum, and ileum) and one to two
sections of large intestine. In animals that lack distinctive small and large intestine sections, sections from
different regions of the intestine would be appropriate. If a Clostridial enteritis is suspected samples must
be from a fresh or immediately dead animal in order to culture since Clostridial organisms are a common
post mortem bacterial growth.
Neurological Cases:

In animals with neurological signs, it is important that the brain be examined first. Aerobic
bacterial cultures of the brain stem, cerebrum, and thalamic regions are appropriate. In addition, lung and
liver samples should have aerobic cultures. The large intestine region should have Salmonella cultures
completed.
Because the brain is fairly large and complex in most of our marine mammals, and multiple people
require brain tissue for various ongoing studies, a section of thalamus, hippocampus, cerebrum, medulla,
cerebellum, mid-brain, and obex region should be submitted for histopathology to insure that CNS lesions
are not overlooked. Additional tissues from the other organs of the animal should also be submitted for
histologic examination. Dont forget to examine the middle ear for lesions since this can cause
neurological signs too.

Unknown Deaths:

Animals, presented dead with no clinical history or signs, should have aerobic bacterial cultures of
the lung and liver. Contents from the large intestine regions should be submitted for Salmonella cultures.
All organs should be removed and examined with appropriate samples submitted for histopathology. If
the animal was lactating, examination of the mammary glands for mastitis and the culturing of infected
glands would be appropriate. Feces should be submitted for parasitological examination. Urine, stomach
content, large and small intestinal content, and sections of liver, kidney, and fat should be saved and
frozen for toxicological examination.

Toxicology Cases:

Toxicological cases are often difficult and can be extremely expensive and unrewarding. In order
to come up with a correct diagnosis, one must identify possible toxic substances that could be affecting
the animal. The shot-gun approach (just asking for toxicology) is of little help since there are thousands
of toxic compounds that could cause a toxicological event. Without some direction as to what the cause
may be (i.e. organophosphates, heavy metals, etc.) toxicological results are worthless. Bacterial cultures
of the lung and liver and Salmonella cultures of the intestines should still be completed since peracute
bacterial infection can often lead to deaths that are suspicious of a poisoning. If organophosphates are
believed to be the cause of the lesions, blood from a live animal looking for cholinesterase levels is
appropriate. If the animal is dead, brain tissue submitted for cholinesterase levels may enable you to
identify this as a toxicological event. In organochlorine toxicity, one should be sure that liver and fat are
submitted for examination. Liver and kidney samples are best when a heavy metal is suspected as the
toxicological agent responsible for the injury.
In unknown toxic events, it is best to obtain stomach content (usually first chamber), mid-
intestinal content (ileum) and lower intestinal content (large intestine) for examination. Liver, kidney, and
fat as well as lung tissues placed in individual containers and frozen may also be helpful in obtaining a
diagnosis.
In summary, it is important to remember that the necropsy of fresh animals are more likely to
render a diagnosis than animals that have undergone marked decomposition. Bacterial cultures should be
obtained quickly after death and placed on the appropriate media so that organisms to do not die.
Bacterial samples, if taken at the site of a field necropsy, should be rushed to the laboratory for culturing.
If this cannot be done, important tissues that are to be cultured should be removed from the animal,
placed in individual, clean plastic bags, set on ice or freezer packs and kept cool until they can be
transported to the laboratory for culturing. Samples that are submitted for bacteriology or virology
sampling should never be submitted with dry ice. Dry ice can form carbonic acid in the tissues causing
sterilization of the tissues; therefore, these samples should only be submitted with freezer packs.
Toxicology samples should be frozen as soon as possible and submitted frozen.

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 Bacterial Diseases

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22) Gutter A.E.: Generalized mycobacteriosis in a California sea lion (Zalophus californianus). J. Zoo.
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25) Johnson S.P.: Antimicrobial susceptibility of bacteria isolated from pinnipeds stranded in Central
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28) Keyes M.C.: Pathology of the Northern fur sea., JAVMA. 147: 1090, 1965.
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32) Medway W.: Respiratory problem in captive small cetaceans. JAVMA. 163:571-573, 1973.
33) Miller WG.: Brucella induced abortions and infections in bottlenose dolphins (Tursiops truncatus).
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34) Montali R.J.: Mycobacterium tuberculosis in zoo and wildlife species. Rev Sci Tech Off Int
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35) Morales, P.: Systemic Mycobacterium marinum infection in an Amazon manatee. JAVMA.
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37) Pier A.C. Cetacean Nocardiosis. J Wildl disease 6: 112-118, 1970.
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39) Rand C.S. Nodular suppurative cutaneous cellulitis in a Galapagos sea lion. Journal of wildlife
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40) Ross H.M.: Brucella species infection in sea mammals. Vet Record. 134 (14): 359, 1994.
41) Ross H.M.: Brucella species infection in North Sea seal and cetacean populations. Vet Record.138
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42) Siebold H.R.: Erysipelothrix septicemia in the porpoise. JAVMA. June 1, 537-539, 1956.
43) Simpson C.F.: Cutaneous lesions in a porpoise with erysipelas. JAVMA. 133: 558, 1958.
44) Smith A.W.: A preliminary report on potentially pathogenic microbiological agents recently
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45) Smith A.W.: Naturally occurring Leptospirosis in Northern Fur Seals. J. Wild. Dis. 13: 144, 1977.
46) Smith A.W.: Leptospira pomona, and reproductive failure in California sea lions. JAVMA. 165:
996, 1974.
47) Stroud R.K. Salmonella meningoencephalitis in a Northern fur seal (Callorhinus ursinus). Journal
of wildlife Diseases 16: 15-18., 1980.
48) Sweeney J.C. Survey of Diseases in free-living California sea lions. Journal of Wildlife Disease 10:
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49) Sweeny J.C.: Common diseases of pinnipeds. JAVMA. 165: 805, 1974.
50) Sweeney J.C.: Common disease of small cetaceans. JAVMA. 167:533-540, 1975.
51) Stadlander C.T.: Characterization of cytopathogenicity of aquarium seal mycoplasmas and seal
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52) Streitfeld M.M.: Staphylococcus aureaus infections of captive dolphins (Tursiops truncatus and
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53) Stoskopf M.K.: Tuberculosis in pinnipeds. Proc. Anim. Meet An. Assoc. Zoo Vet. P. 393, 1987.
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56) Tryland M.: Evidence of Brucella infection in marine mammals in the North Atlantic ocean.Vet
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57) Varaldo, P.E.: Staphylococcus aureus NOV., a Coagulase positive species Isolated from dolphins.
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59) Wells S.K.: Cutaneous mycobacteriosis in a harbor seal: Attempted treatment with hyperbaric
oxygen. J. Zoo and Wild. Med. 21(1): 73, 1990.
60) Woods, R.: Tuberculosis in a wild Australian fur seal (Arctocephalus pusillus dorifesus) from
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61) Van Pelt R.W.: Staphylococcal infection and toxoplasmosis in a young harbor seal. J. Wildl. Dis.
9: 258, 1973.

Mycotic Diseases

1) Caldwell D.: Lobomycosis as a disease of Atlantic bottle-nosed dolphins. Amer J Trop Med Hyg,
24: 105, 1975.
2) Cornell L.H. Coccidioidomycosis in a California sea otter (Enhydra lutris). J. Wild. Dis 15:373-
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3) Carrol J.M. Pulmonary aspergillosis of the bottlenosed dolphin (Tursiops truncatus). Veterinary
Clinical Pathology 2:139-140, 1968.
4) Dilbone R.P.: Mycosis in a manatee. JAVMA 147: 1095, 1965.
5) Dunn J.L.: Candidiasis in captive pinnipeds. JAVMA. 185; 1328, 1984.
6) Dunn J.L.: Candidiasis in captive cetacean. JAVMA. 181; 1316-1321, 1982.
7) Fauquier D.A. Coccidioidomycosis in free-living California sea lions (Zalophus californianus) in
central California. J. Wild. Dis. 32(4): 707-710, 1996.
8) Farnsworth R.J. Dermatomycosis in a harbor seal causes by Mycosporum canis. Journal of Zoo
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harbor seals. JAVMA. 208 (5) 727-729, 1996.
10) Medway W.: Some bacterial and mycotic diseases of marine mammals. JAVMA. 177; 831, 1980.
11) Migaki, G.: Lobo's disease in an Atlantic bottle-nosed dolphin. JAVMA. 159; 578, 1971.
12) Migaki G.: Pulmonary cryptococcoses in an Atlantic bottlenosed dolphin (Tursiops truncatus). Lab
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13) Migaki G.: Sporotrichosis in a Pacific white-sided dolphin (Lagenorhynchus obliguidens). AJVR.
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14) Montali R.J.: Cyclic dermatitis associated with Fusarium sp. infection in pinnipeds. JAVMA. 179:
1198, 1981.
15) Nakeeb S. Chronic cutaneous Candidiasis in bottle-nosed dolphins. JAVMA. 171:961-966, 1977.
16) Pollock C.G.: Fungal dermatitis in captive pinnipeds. Journal of zoo and Wildlife Medicine 31:374-
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17) Reed R.E.: Coccidioidomycosis in a California sea lion (Zalophus californianus). J Wild Dis.
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18) Reidarson T. H. Coccidioidomycoisis in a bottlenosed dolphin. J Wildlife Dis. 34(3)629-631.
19) Sweeney J.C.: Common diseases of pinnipeds. JAVMA. 165: 805, 1974.
20) Sweeney J.C.: Systemic mycosis in marine mammals. JAVMA. 169:946-948, 1976.
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22) Williamson W.M.: North American blastomycosis in a Northern sea lion. JAVMA. Nov. 15, 1959:
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23) Wilson T.M.: Histoplasmosis in a harp seal. JAVMA. 165: 815-817, 1974.
 Protozoal Diseases

1) Akao, S.: A new species of Sarcocystis parasitic in the whale (Balaenoptera borealis). J. Protozool.
7:290-294, 1970.
2) Bishop L.: Parasites related to lesions in a bearded seal. .J Wildl. Dis. 15: 285, 1979.
3) Brown R.J.: Sarcocystis in the Northern fur seal. J. Wildl. Dis. 10: 53, 1974.
4) Cole R.A.: Biological and molecular charactrerization of Toxoplasma gondii strains obtained from
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5) Dailey, M.D.: Parasites and associated pathology observed in cetaceans stranded along the Oregon
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6) Hadwen S.: Cyst forming protozoa in reindeer and caribou and a Sarcosporidean parasite of the seal
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7) Buergelt C.D.: Toxoplasmic meningoencephalitis in a West Indian manatee. JAVMA. 183: 1294,
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8) Holshuh H.J.: Toxoplasmosis in a feral Northern fur seal. JAVMA. 187: 1229, 1987.
9) Howard E.B.: Pathology of Marine Mammal Disease. CRC press, Boca Raton, Fl., 1993.
10) Inskeep W.: Toxoplasmosis in Atlantic bottlenosed dolphins (Tursiops truncatus). J Wild Disease.
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16) Migaki G.: Sarcosporidiosis in a ringed seal. JAVMA. 177: 917, 1986.
17) Migaki G.: Toxoplasma in a California Sea Lion. AJVR. 38: 135, 1977.
18) Mikaelian I.J.: Toxoplasmosis in beluga whales (Delphinapterus leucas) from the St. Lawrewnce
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19) Munday B.L.: Sarcocystis and related organisms in Australian wildlife. J Wild Dis. 14: 417, 1978.
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21) Rosonke BJ.: Encephalomyelitis associated with a Sarcocystis neurona-like organism in a sea otter,
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22) Schulman FY.: Dermatitis with invasive ciliated protozoa in dolphins that died during the 1987-1988
Atlantic bottlenose dolphin morbilliviral epizootic. Vet Path 36:171-174,1999.
23) Van Pelt R.W.: Staphylococcal infection and toxoplasmosis in a young harbor seal. J Wild Dis.
9:258, 1973.

Parasites
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2) Bishop L.: Parasite-related lesions in a bearded seal, Erignathus barbatus. J Wild Dis. 15:285, 1979.
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165: 804, 1974.
4) Conlogue G.J.: Pediculosis and severe heartworm infection in a harbor seal. Vet Med. 75:1184-
1187, 1980.
5) Conlogue G.J.: Parasites of the Dalls porpoise (Phocoenoides dalli). J. Wildl Dis. 21:160-166,
1985.
6) Dailey M.: Parasites and associated pathology observed in cetaceans stranded along the Oregon
Coast. J Wild Dis. 14: 503, 1978.
7) Dailey M.: Evidence of prenatal infection in the Bottlenosed dolphin (Tursiops truncatus) with the
lungworm Halocercus lagenorhynchi. J Wildl Dis. 27:164-165, 1995.
8) Dailey M.D.: Parasitism as a factor in single strandings of Southern California cetaceans. J
Parasitology. 64; 593, 1978.
9) Dailey M.D.: Disease of Mammalia: Cetacea. In Disease of Marine Mammals. Vol IV, Part 2. O.
Kinne (ed.) Biologische Anstaff Helgoland, Hamburg, Germany. 1985, p805-847.
10) Dunn J.L.: Dipetalonema spirocauda Infection in the Atlantic harbor seals (Phoca vitulina concolor).
J Wild Dis. 12: 531, 1976.
11) Eley T.J.: Dipetalonema spirocauda In Alaskan marine mammals. J Wild Dis. 17: 65, 1981.
12) Forbes L.B.: The occurrence and ecology of Trichonella in marine mammals. Vet Parasitology
93:321-334, 2000.
13) Forrester D.J.: Heartworms in captive California sea lions. JAVMA. 163: 568, 1973.
14) Fowler M.E.: Zoo and Wild Animal Medicine. W.B. Saunders Company, Philadelphia, PA, 1986.
15) Garner M.M.: Evidence of Brucella infection in Parafilaroides lungworms in a Pacific harbor seal
(Phoca vitulina richardsi). J. Vet. Diagn. Invest. 9:298-303,1997.
16) Howard E.B.: Pathobiology of Marine Mammal Diseases, CRC Press Boca Raton, Florida, 1983.
17) Johnston D.G.: Parasitism in some marine mammals. JAVMA. 155:1064, 1969.
18) Keyes M.C.: Pathology of the Northern fur seal. JAVMA. 147: 1090, 1965.
19) Kim K.C.: Population, microhabit preference and affect of infestation of two species of
rthohalarachne in the Northern fur seal. J Wild Dis. 16:45,1980.
20) Koie M. The life cycle of Contracaecum osculatum senso stricto in view of experimental infections.
Parasitology Res. 81(6):481-489,1995.
21) Lewis R.J.: Brain lesions in a Pacific white-sided dolphin (Lagenorhynchus obliquidens). Wild Dis.
24(3): 77, 1988.
22) Lyons E.: Uncinariasis in Northern fur seals and California sea lion pups from California. J.
Wild.Dis. 33(4): 848-852, 1997
23) Lyons E.T.: Comparative biology of Uncinaria spp. In the California sea lion (Zalophus,
californianus) and the Northern fur seal (Callorhinus ursinus) in California. Journal of Parasitology
86: 1348-1352, 2000.
24) Medway W.: Dirofilaria immitis infection in a harbor seal. JAVMA. 167: 549, 1975.
25) Migaki G.: Hepatic trematodiasis in a Ganges River dolphin. JAVMA. 175: 926, 1979.
26) Migaki G.: Some histopathological lesions caused by helminths of marine mammals. J Wild Dis. 7:
281, 1971.
27) Morales G.A.: Verminous pneumonia in California sea lions. Vet Path. 7: 89, 1970.
28) Morimitsu T.: Mass stranding of Odontoceti caused by parasitogenic eight cranial neuropathy. J
Wild Dis. 23: 586, 1987.
29) Moser M.: The lungworm Halocercus spp. In cetaceans from California. J. Wildl, Dis. 29(3):507-
508, 1993.
30) Olsen S.W.: Life cycle of Uncinaria lucasi stiles, 1901 (Nematoda: Ancylostomatidae) of fur seals,
Callorhinus ursinus, on the Pribilof Islands, Alaska. J Parasitology. 51:689, 1965.
31) O'Shea T.J.: Nasitrema associated encephalitis in striped dolphin (Stenella caeruleoalba) stranded in
the Gulf of Mexico. J. Wild Dis. 27(4):706-709, 1991.
32) Parker G.A.: Cerebral trematodiasis in a dolphin. Mil Med. 142:861, 1977.
33) Perry M.L.: A New species of Dipetalonema from the California sea lion and a report of icrofilaria
from a Stellar sea lion (Nematoda: Filarioides). J Parasito. 53:1076, 1967.
34) Ridgeway S.H.: Cerebral and cerebellar involvement of trematode parasites in dolphins and their
possible role in strandings. J. Wild Dis. 8:33-43, 1972.
35) Rausch R.: Studies on the helminth fauna of Alaska. XIII. Diseases in the sea otter, with special
reference to helminth parasites. Ecology. 34: 584-604, 1953.
36) Schryver H.F.: The stomach fluke Brauninia cordiformis in the Atlantic bottlenosed dolphin.
JAVMA. 151: 884-886, 1967.
37) Stroud R.K.: Parasites and associated pathology observed in pinnipeds stranded along the Oregon
coast. J Wild Dis. 14: 292, 1978.
38) Sweeny J.C.: Common diseases of pinnipeds. JAVMA. 165: 805, 1974.
39) Wazura K.W.: Helminths of the beluga whale (Delphinapterus leucas) from the Mackenzie river
delta, Northwest Territories. J Wild Dis. 22: 440-442.
40) Wild P.W.: A report on the sea otter, Enhydra lutris, in California Department of Fish and Game.
Marine Resources Technical Report No. 20, 1974.
41) Woodard J.C.: Some parasitic disease of dolphins. Path Vet 6: 257, 1969.
42) Young P.G.: Larval nematodes from fish of the subfamily Anasakinae. J Comp Path. 79: 301, 1969.

Miscellaneous Disease
1) Alexander J.W.: Vertebral osteomyelitis and suspected disko-spondylitis in an Atlantic bottlenosed
dolphin (Tursiops truncatus). J Wild Disease 25: 118-121, 1989.
2) Baker J.R.: Pollution associated uterine lesions in grey seals from the Liverpool Bay area of the Irish
Sea. Vet Record. 125: 330, 1989.
3) Barnett J.E.F.: Conditions in grey seals (Halichoerus grypus) presented for rehabilitation. Vet Record
147, 98-104, 2000.
4) Beckmen K.B.: Clinical and pathological characterization of Northern elephant seal skin disease. J.
Wild. Dis. 33(3): 438-449, 1997.
5) Bossart G.D.: Invasive gingival squamous cell carcinoma in a California sea lion (Zalophus
californianus). J Zoo and Wild Med. 21: 92-94, 1990
6) Bossart G.D.: Cardiomyopathy in stranded pygmy and dwarf sperm whales. JAVMA. 187: 11,
1137-1140, 1985.
7) Citino S.B.: Nutritional myopathy in a captive California sea lion. JAVMA. 187: 1234, 1985.
8) De Guise S.: Tumors in St. Lawrence beluga whales (Delphinapterus leucas). Vet. Path. 31:444-
449, 1994.
9) De Guise S.: Non-neoplastic lesions in beluga whales and other marine mammals from the St.
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10) De Guise S.: Intestinal adenocarcinoma in two Beluga whales (Delphinapterus leucas). Can Vet J.
36(9): 563-565, 1995.
11) De Guise S.: Pathology and toxicology of Beluga whales from the St. Lawrence estuary, Quebec,
Canada. Past, present and future. Sci. Total Environ. 154(2-3): 201-215, 1994.
12) De Guise S.: True hermaphroditism in a St. Lawrence Beluga whale (Delphinapterus leucas). J.
Wildl. Dis. 32(3): 548-551, 1996.
13) Fowler M.E.: Zoo and Wild Animal Medicine. W.B. Saunders Company, Philadelphia, PA, 1986.
14) Frasca S.: Acute gastric dilatation with volvulus in a Northern fur seal (Callorhinus ursinus). J.
Wildl. Dis. 32(3): 548-551, 1996.
15) Garman R.H.: Cutaneous gout in an Amazon dolphin. JAVMA. 1983: 1292, 1983.
16) Geraci J.R.: Dietary disorders in marine mammals synthesis and new finding. JAVMA. 179: 1183,
1981.
17) Geraci J.R.: Experimental thiamine deficiency in captive harp seals. Can J Zool. 50: 179, 1972.
18) Geraci J.R.: Hyponatremia and the need for dietary salt supplementation in captive pinnipeds.
JAVMA. 161: 618, 1972.
19) Geraci J.R.: Thiamine deficiency in seals and recommendations for its prevention. JAVMA. 165:
801-803, 1974.
20) Geraci J.R.: Tumors in cetaceans: Analysis and new findings. Can J Fish Aquat Sci. 44: 1289-1300,
1987.
21) Gulland F.M.: Metastatic carcinoma of probable transitional cell orgin in 66 free living California sea
lions, 1979-1994. J. Wildl. Dis. 32(2): 250-258, 1996.
22) Gulland F.M.: Baseline coagulation assay values for Northern Elephant seals (Mirounga
angustirostris) and disseminated intravascular coagulation in this species. J. Wildl. Dis.
32(3):536-540, 1996.
23) Heidel J.R.: Intestinal volvulus in a Bowhead whale, Balaena mysticetus. J. Wildl. Dis. 30(1): 126-
128, 1994.
24) Hirst L.W.: Pathologic findings in the anterior segment of the pinniped eye. JAVMA. 183: 1226-
1231, 1983.
25) Howard E.B.: Pathobiology of Marine Mammal Diseases, CRC Press, Boca Raton, Florida, 1983.
26) Martineau D.: Pathology of stranded Beluga whales (Delphinapterus leucas) from the St. Lawrence
Estuary, Quebec, Canada. J Comp Path. 98: 287-311, 1988.
27) Martineau D.: Transitional cell carcinoma of the urinary bladder in a Beluga whale (Delphinapterus
leucas). Can Vet J. 26: 297-302, 1985.
28) Martineau D.: Pathology and toxicology of beluga whales from the St. Lawrence estuary, Quebec,
Canada, Past, present and future. Science of the Total Environment. 154: 201-215, 1994.
29) Migaki G.: Renal adenoma in an Atlantic bottlenosed dolphin. AJVR. 39: 1920-1921, 1978.
30) Miller G.J.: Ecotoxicology of petroleum hydrocarbons in the Marine environment. J Applied Tox.
2: 88-97, 1982.
31) Morimitsu T. Histopathology of eighth crainal nerve of mass stranding dolphins at Gato Island.
Japan. J Wildl Dis. 28(4): 656-658, 1992.
32) Shlosberg A.: Lead toxicosis in a captive bottlenosed dolphin (Tursiops truncatus) consequent to
ingestion of air gun pellets. J. Wild. Dis. 33(1):135-139, 1997.
33) Stoskopf M.K.: Ocular anterior segment disease in Northern fur seals. JAVMA. 187: 1141-1145,
1985.
34) Stroud R.K.: Nephrolithiasis in a harbor seal. JAVMA. 175: 924-925, 1979.
35) Stroud R.K. Lymphosarcoma in a harbor seal. (Phoca vitulina richardii). J Wildlife Diseases
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36) White J.R.: Thiamine deficiency in an Atlantic bottle-nosed dolphin on a diet of raw fish. JAVMA.
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37) Woodhouse C.D.: Observations of vaginal calculi in dolphins. J. Wildl. Dis. 27(3): 421-427, 1991.