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Thomas 1996

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The growth of the southern sea
otter population has been steady, but
slow in comparison to Alaskan subspecies,
and range expansion in California
has faltered. Slower growth is occurring
in California despite birth rates
comparable to those in Alaska, so biologists
have reasoned that mortality is
hindering the growth of the California
population (Riedman and Estes 1990;
see Estes et al., this issue). In order to
investigate this issue, research efforts
have been directed toward identifying
the causes of death in southern sea
otters.
Several major causes of mortality
in the southern population were recognized
in the past and are currently being
addressed. These include protections
from overharvesting and accidental entanglements
in fishing gear, as well as
oil spill prevention and contingencies.
Still to date, the problem of slow population
growth and expansion persists.
The California Department of Fish
and Game has studied sea otter mortality
since 1968. A salvage network,
maintained through the cooperation of
State and Federal agencies and scientific
institutions, verified beach-cast carcasses
and examined them to estimate
the causes of death. By 1989 nearly
1700 dead sea otters had been documented
(see Table 1; Ames et al. 1983,
unpublished data; Riedman and Estes
1990). Substantial mortality from net
drownings was identified and the prevalence
of trauma from predators, shooting, fighting and mating activities were
documented. Pup abandonment and a
variety of miscellaneous conditions and
diseases were recorded. Since 1992,
laboratory diagnostic efforts at the National
Wildlife Health Center (NWHC),
Madison, Wisconsin, supplemented the
stranding network's activities in California,
so that knowledge about the
causes of mortality has been further
refined. It is these recent perspectives
on the causes of mortality in the southern
seaotter that are outlined here, along
with consideration of their implications
for sea otters and the Pacific marine
ecosystem.

Causes of mortality

Since 1992 approximately 50 southern
sea otter carcasses per year were
examined at the NWHC as part of a 5
year intensive necropsy study. Carcasses
were selected for the NWHC
study on the basis of good postmortem
condition from the approximately 110
to 160 carcasses found per year in California.
At the NWHC, microscopic
examination supplemented gross examination
of the carcasses and a variety of
laboratory techniques in bacteriology,
virology, parasitology, and toxicology
were conducted to arrive at a diagnosis.
By this means a greater proportion of
the animals with inapparent causes of
death were diagnosed. Only a prelirninary
analysis of the 1992-95 data has
been done, but some interesting patterns
are emerging from the 195 cases studied (and additional
samples have been collected through 1996).
The proportionate
causes of mortality identified at the NWHC bore
similarities to past data
but also had interesting
differences. Sea otter mottallties from 1968-1989 (n=1,680), fungal, or bacterial dis- taken from Ames 1983 and Riedman and Estes 1990.
eases caused the deaths
of 38.5% of the sea otters
examined at the NWHC. Twenty percent
died from traumatic injuries. Another
10% were emaciated at death and
no specific cause for their debility could
be identified. Miscellaneous conditions,
such as neoplasia, or gastrointestinal or
urinary obstructions, accounted for
13% of the mortality. In 18.5% of the
animals no cause of death could be
ascertained.
Traumatic causes, emaciation and
a variety of miscellaneous conditions
were similar to those described in sea
otters in the past. Ames summarized the
causes and distribution of traumatic injuries
in sea otters examined from 1968
to 1989 (as presented in Riedman and
Estes 1990). The most frequently identified
cause of trauma in the past was
shark attack (Ames andMorejohn 1980);
the shark-bitten sea otters were collected
throughout the range but the largest
proportion were found north of Point
Sur. In the recent study shark attack
was also the most frequently diagnosed
source of trauma (7% of all mortality,
n=14), and more than 70% of the sharkbitten
sea otters were found north of
Point Sur. In the past, gunshot injuries
were documented predominately south
of Cambria. Ames speculated that the
frequency of shark attacks in the northern
extent of the range and gunshot
mortalities in the south may have an
impact on range expansion (as presented
in Riedman and Estes 1990). Gunshot
was diagnosed in 4% (n=8) of the sea
otters in the recent study but these cases
were equally distributed between the
range south of Cambria and north of
Point Sur.

Infectious disease

The high frequency of infectious
diseases (38.5%, n=75) was unexpected.
Many of these diseases were reported
but uncommon in the past. Peritonitis
induced by acanthocephalan parasites
(see below) was the diagnosis for 14%
(n=27) of the sea otters examined at the
NWHC, comprising the single most frequent cause of death, as well as the most
frequent infectious disease. Most (67%,
n=18) cases of acanthocephalan peritonitis
occurred in pups or juvenile sea
otters. Peritonitis occurs when larval
acanthocephalan parasites that reside in
the intestine aberrantly migrate through
the intestinal wall allowing bacteria to
infect the abdominal cavity. Additionally,
in many of these cases, thousands
of acanthocephalans were embedded in
the intestinal wall, and there was profuse
bloody enteritis. The parasite causing
this condition, Polymorphus spp.,
belongs to one of two genera of acanthocephalans
found in southern sea otters
(there is a current taxonomic dispute
on the Polymorphus species identification).
The other, Corynosoma
enhydri, was found frequently but
caused no detectable deleterious effects.
Acanthocephalans are transmitted to sea
otters through invertebrate intermediate
hosts. The spectrum of invertebrate
hosts of Polymorphus spp. is unknown.
Polymorphus spp. were reported in small
numbers (2-206 per otter) in 10% of the
southern sea otters examined by
Hennessy and Morejohn (1977). Both
the prevalence and intensity of
Polymolphus spp. infections appear substantially
greater in recent years.
Protozoal encephalitis was the
cause of death in 8.5% (n=17) of the sea
otters examined at the NWHC. This is
the first report of this organism or disease
in sea otters. Most (88%, n=15) of
the affected otters were adults or subadults.
Otters with encephalitis had no
gross evidence of the condition but,
microscopically, inflammation in the brain was associated with intermediate
stages of protozoal parasites. The characterization
of this disease syndrome
was confounded by the fact that the
protozoan (Toxoplasma gondii) was isolated
from the brains of sea otters with
and without encephalitis. Immunohistochemical
tests indicated that a second
protozoan was present in some of the
cases, suggesting that two agents may
be involved. In each year of the recent
study, encephalitis cases were restricted
to the spring and summer. The means of
transmission of these agents to sea otters
is unknown. The typical infectious
stage, the oocyst, of T. gondii is shed in
the feces of a species-specific definitive
host, the cat. Intermediate stages of
several protozoan agents are found in
animal tissues and may also be directly
infectious if ingested. The intermediate
stage of T. gondii is found in a wide
variety of vertebrates including humans
world wide, but serious illness from
the infection is sporadic. Illness is
more common in the very young, aged,
or as a complication of impaired immune
function.
Eight cases of coccidioidomycosis
(4% of all mortality), a systemic infection
caused by the fungus, Coccidioides
immitis, were diagnosed from 1992-95
(Thomas et al. 1996). Only one case
had been reported previously, in 1976
(Cornell et al. 1979); this may be an
emerging problem. The affected sea
otters were adult or subadult. All 8 sea
otters, and the prior case in 1976, were
found at the southern end of the range at
San Luis Obispo County. The disease,
also known as San Joaquin Valley fever,
is endemic in certain arid regions of
the Southwest U.S., notably the Central
Valley of California. This fungus grows
in soil to form arthrospores that produce
disease when inhaled by susceptible
individuals. Coccidioidomycosis most
often manifests itself in the respiratory
tract, but many organs, including the
brain, may be affected. A wide variety
of species, including humans, are susceptible
to coccidioidomycosis. The
results of exposure vary, depending on
both species and individual factors, from
no ill effects to death. In all sea otter
cases the infection was widely disseminated
to affect multiple organs.
The deaths of 12% (n=23) of the
otters were attributed to various bacterial
infections. The affected sea otters
were all adult or subadult. Bacterial
infections were manifested primarily as
pneumonia, heart valve infection, abscess
or septicemia. The origins of
infection were likely to be inhalation or
traumatic injuries, but were inapparent
in most cases. Bacterial infections occurred
as individual cases with no apparent
links among them, so direct transmission
between sea otters was unlikely.
The most frequently isolated bacteria
were different strains and species of
Streptococcus, but the agents varied
widely and mixed infections in the same
individual were common.
 
Significance of disease

The implications of the recent
necropsy results appear complex. Past
mortality surveys suggested that the influences
of "natural" (that is, not directly
human-inflicted) mortality might
be significant (Ames et al. 1983). The
preliminary data presented here corroborate
that mortality from natural
causes, specifically infectious diseases,
is occurring at a high rate. Disease
mortality is not only frequent but some
diseases appear to be on the rise while
others are newly reported. Several of
the diseases are predominately affecting
prime age, breeding adults. Taken
in total, the findings regarding infectious
disease mortality appear to bear
some disturbing implications for sea
otters. The immediate questions are
whether this frequency is truly unusual
and whether it is remediable. In comparison to endangered terrestrial
top-level predators, these results
are unusual, and, at the moment,
there is no comparable data available
for other, more vigorous sea otter populations.
The NWHC is carrying out
similar mortality studies on gray wolves
(Canis lupus) in the Great Lakes Region
and for the red wolf (Canis rufus)
reintroduction program. In these terrestrial
species the greatest proportion of
mortality (55% for gray wolves and
42% for red wolves) is accidentally or
intentionally human-inflicted by shooting,
trapping, poisoning, or vehicle
trauma. Infectious diseases cause a
relatively minor proportion of the mortality
in these species, at a rate of 9% in
gray wolves and 8% in red wolves.
The question of whether the sea
otter's disease mortality has a remedy is
not readily answered in our current state
of knowledge. Missing details about
the transmission cycles of the more frequently
encountered diseases may provide
the keys to effective control measures.
Before focusing on the transmission
cycles of individual diseases, it
may be useful to consider the underlying
significance of a high rate of infectious
disease from a broad perspective.
In order to exhibit a high frequency and
variety of infectious disease mortality,
are southern sea otters highly vulnerable
to many diseases or are they undergoing
high rates of exposure?
A state of general susceptibility is
suggested by the variety of infections
encountered in sea otters. Unusual vulnerability
is also suggested by the fact
that otter deaths are repeatedly attributed
to diseases that are expected to
cause only sporadic mortality in other
species. Generalized vulnerability to
infections implies that immune function
is ineffective. Although assessing
and understanding the exact mechanisms
of immune function impairment is complicated,
in general, immunologic defects
may be congenital or have a genetic
basis, or arise from certain viral
infections, environmental toxins, or malnutrition.
The factors that affect the rates of
infectious disease exposure in sea otters
differ among the different diseases encountered.
The potential sources of the
disease agents and means of exposure
differ, as do the reasons why an apparent
increase or emergence might be
taking place. Exposure rates may be
linked to population density for certain
diseases but density-independent for
others. Identification of the key factors
that affect exposure and the significance
of each disease in relationship to
population dynamics will be important
distinctions to make if we are to
arrive at effective mortality-reduction
strategies.
Polymorphus spp.
Over the last 5 years the prevalence
and intensity of Polymorphus spp. infections
in otters and the frequency of
extraintestinal migration of
acanthocephala has increased. In order
to understand this increase in deleterious
Polymorphus spp. infections in sea
otters, we need to examine the predatorprey
dynamics of the definitive host
species (sea birds) and probable intermediate
hosts (crabs). It is this predator-
prey relationship that the
Polymorphus spp. depend upon for
completion of the life cycle. Preliminary
data suggest that Emerita analoga
and Blepharipoda sp. of crab are two
intermediate hosts for this acanthocephalan,
however there may be more invertebrate
species involved. Birds such as
gulls, scoters and sea ducks prey upon
infected crabs and harbor the egg-producing
adult Polymorphus spp. The
eggs are deposited with feces into the
environment. Sea otters can become
infected with the Polymorphus spp., by
eating the infected crabs, however, the
sea otter is a dead-end host and no eggproducing
acanthocephalans have
been found. Abiotic or biotic factors
that influence the population densities
and predator-prey interactions of
the bird, invertebrate hosts, or sea
otters could affect the risk of infection
in sea otters.
There are three broad facets to examine
to determine why increases may
be occurring in otters.
( I ) Factors impacting birdpopulations.
A larger infected bird population
(as higher prevalence and/or higher
acanthocephalan burdens) could be due
to factors that caused an increase in
certain sea bird populations, or factors
inducing bird aggregations (for example,
beach utilization by humans, distribution
and management of landfills, aggregation
of crab species or other food
items).
(2) Factors influencing intermediate
hostpopulations. A larger infected
intermediate host community (as increased
prevalence and/or larval acanthocephalan
burdens) could be related
to an increase in infected birds that
contaminate the beaches with feces and
acanthocephalan eggs. Add to this the
complicating fact that some
acanthocephala species alter their intermediate
host's behavior, thereby increasing
the risk of predation so that birds
prey disproportionately on infected
crabs. Certain conditions such as a rise
in water temperature and phytoplankton
proliferation can favor the survival
of crab offspring, thereby providing a
larger intermediate host community for
potential infection.
(3) Factors affecting the sea otter
population. A food habit change by
some sea otters could increase their
predation on infected crustaceans. This
prey selection might occur if more optimal
prey items were unavailable or they
may be taken by inexperienced or incapacitated
sea otters that seek easier prey
such as Emerita and Blepharipoda.
A combination of two or more of
the above factors may be interacting to
cause an increase in the parasitism of
the sea otter. Given the complexity of
the ecology influencing the predatorprey
dynamics, several species of invertebrates
and vertebrates need to be
considered in order to identify the factors
influencing the sea otter's
Polymorphus spp. infections.
Eradicating Polymolphus spp. from
the normal bird and invertebrate hosts
would be impossible. However, a reversal
of the sea otter's current mortality
trend from Polymorphus spp. is feasible
if we could reduce the prevalence of this
parasite. Effective management strategies
may be to disperse the responsible
bird species or increase the availability
of alternate uninfected prey species to
sea otters. However, before such management
strategies can be developed
basic questions must be answered, including which crab species act as intermediate
hosts, which beaches have
highly infected intermediate or definitive
host communities, and what factors
correlate with the distribution of infected
sea otters.
Toxoplasma gondii
The source of Toxoplasma gondii
exposure to sea otters is most likely
oocysts from cat feces. [1] Transmission
by preying on infected intermediate
hosts is unlikely because only warmblooded
animals have been reported as
intermediate hosts, and the sea otter is
reported only rarely to eat birds.
Sea
otters could ingest oocysts in water contaminated
with cat feces through runoff
from beach soils, or possibly by
eating filter feeding invertebrates that
are transporting oocysts in their alimentary
tracts. If oocysts are entering the
water via sewage effluent, the contamination
of the marine ecosystem could be
much greater than just that from beach
or adjacent shoreline run-off. This
would be an important source to identify
and is potentially manageable. To
investigate the connection between sewage
disposal and otter exposure, the
survivability of oocysts through local
sewage treatment systems and the viability
of oocysts in sea water should be
evaluated. Temporal studies could determine
whether peaks in contamination
correlate with seasonal patterns of
disease. Laboratory studies could be
designed to investigate whether crabs
and other crustaceans could act as
phoretic agents in the transmission of T.
gondii to sea otters. Vertical transmission
of T. gondii from mother to offspring
can cause abortion in sheep,
goats, and humans. Toxoplasmosis in
the very young sea otter may be underrepresented
in post mortem sampling
because carcasses of fetuses or neonates
are less likely to be found
(Riedman and Estes 1990).
Toxoplasmosis, may be more than
the other diseases, raises concern about
the sea otter's general ability to resist
disease. Infection with T. gondii does
not always cause disease in the host.
Disease and death more often occurs in
animals that are vulnerable due to age,
irnrnuno-compromise, or in species (e.g.,
Australian marsupials or arboreal New
World monkeys) that evolved isolated
from felids or their feces. Subadult and
adult sea otters, not just the young or
aged, had protozoal encephalitis, so age
does not appear to be an important factor. 
[2] Sea otter immune competence has
not been well studied, so its status to
date is unknown.
Regarding the species
experience with T. gondii, there is little
information. Most reports of T. gondii
infection of marine mammals are from
captive animals. However, reports of
this protozoan causing disease in the
wild northern fur seal (Callorhinus
ursinus) (Holshuh et al. 1985), the West
Indian manatee (Trichechus manatus)
(Buergelt and Bonde 1983) and five
species of dolphin (Di Guardo et al.
1995) indicate that other wild marine
mammals are also exposed to T. gondii.
Regardless of whether resistance to toxoplasmosis
is an individual or species
phenomenon, we can evaluate the sea
otter's degree of susceptibility by evaluating
the frequency of exposure. Such
studies would help discern if most otters
are exposed to T. gondii and resist
disease or if the few that are exposed
break with disease.
Coccidioides immitis
The occurrence of infections by the
soil-associated fungus, Coccidioides
immitis, in the marine environment is
puzzling. The means of transmission to
sea otters presumably is similar to that
in other species, specifically by
inhalation of airborne arthrospores.
Recurrent dry winds from the east may
disperse the spores from the soil in
endemic sites around the city of San
Luis Obispo or in the San Joaquin Valley.
Coccidioidal spores survive and may
even grow in salt water, so the
accumulation of spores in the marine
environment has also been postulated
(Dzawachiszwili et al. 1964). The
apparent increase in prevalence of
coccidioidomycosis in sea otters since
1992 may be due to the application of
more sensitive diagnostic methods, but
it coincides with a marked increase in
human cases in 1991 to 1993. The
human outbreak was tentatively
attributed to unusual weather and
environmental conditions rather than
human-related factors, so occurrence in
sea otters may lend support to that
hypothesis. Prospects for control of this
disease in sea otters are not promising, but
knowledge about coccidioidomycosis
prevalence has predictive value that may
particularly apply to the population in
the southern extent of range.
Many of the infectious diseases of
concern in southern sea otters are not
species specific; they may affect other
marine mammals, sea birds and human
beings. Some of the epizootiologic factors
that potentially play a role in promoting
disease emergence or frequency
in otters also may have broad effects in
the marine environment. The successful
recovery of the southern sea otter
population is of immediate concern, but
obstacles to their recovery could have
wider implications for the marine ecosystem. 
[3] The sea otter could be a sensitive
indicator of the health of the Pacific
near-shore marine ecosystem.

Conclusions and recommendations

The following series of recommendations
are proposed as means to assess
the impact and implications that have
arisen from investigations into sea otter
mortality.
(1) Complete the 5 year intensive
necropsy study. The 5 year database
under development at the NWHC will
be completed at the end of 1996. The
recent health and mortality data have
undergone only preliminary evaluation.
Further analyses for age, gender, and
temporal and geographic differences are
necessary to distinguish significant patterns
and compare with previous data.
(2) Analyze the population data.
Further examination of recent necropsy
data by integration with other mortality
and demographic data may provide valuable
insight into the significance of disease
and the role of mortality in population
recovery. The relationship between
the various infectious disease conditions
and population dynamics needs to
be explored. Identification of mortality
factors with the greatest potential for
limiting population growth should guide
research priorities.
(3) Identify key factors in the disease
cycles. The key to reducing mortality in the southern sea otter may be
found by identifying critical points at
which important disease transmission
cycles can be interrupted by knowledge-
based management strategies. The
greatest gaps involve the transmission
of acanthocephalan peritonitis and protozoal
encephalitis. Elucidation of disease
cycles may also provide a measure
of the role of human intervention or
human responsibility in the emergence
of sea otter disease.
(4) Develop comparative data.
Comparison with similar data from a
more vigorous sea otter population
would provide another means to assess
the significance of mortality and various
mortality factors to the southern sea
otter population. The best comparison
would include both the causes and rates
of mortality.
(5) Continue mortality monitoring.
Continuation of a mortality monitoring
system is the basis for identifying
trends, investigating, and interpreting
the patterns in sea otter mortality. The
activities of the sea otter stranding network
are critical to that end.
(6) Evaluate the rates of disease
exposure. By comparing the rates of
disease exposure to the rates of disease
mortality we can evaluate the general
vulnerability of the southern sea otter to
infectious disease.
(7) Assess immunefunction. Evaluation
of the adequacy of the wild southern
sea otter's immune function is a
means to investigate whether generalized
vulnerability to infectious disease
exists.
(8) Assess environmental contaminant
exposure. Otter tissue analyses for
organochlorine compounds and heavy
metals were discontinued in 1980. No
serious threats to sea otter health were
revealed in these early analyses. Evaluation
of recent environmental contaminant
burdens in sea otters in correlation
with mortality factors is a means to
assess the current role of toxic contaminants in sea otter disease vulnerability,
debility, or neoplasia.
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