Permit No774 Inventory Updates (65pgs)

. ....-.
ea World
ofTeas
July 3, 1991
Dr. Nancy Foster
Director, Office of Protected Resources
and Habitat Programs
National Marine Fisheries Service
1335 East-West Highway, Room 8268
Silver Spring, Maryland 20910
Dec.!:" Dr. Foster:
Please find enclosed a gross necropsy and histopathology report for
a female killer whale of approximately 14 to 16 years, identified
as SWF-Oo-7803. The animal died suddenly and without warning near
dawn on May 14, 1991.
For security reasons, killer whales at Sea World of Texas are
attended twenty four hours a day. The three whales (one male, two
females) maintained at Sea World of Texas had spent an uneventful
night together. The officer on duty observed a sudden
turbulence of water around one of the whales. The other two whales
remained quiet and undisturbed in a distant part of the pool. The
officer proceeded immediately to the site of the disturbance and
observed evidence of some bleeding from the mouth of the whale
involved. The officer immediately informed the park dispatcher of
an animal emergency. curatorial personnel were promptly
by the dispatcher and arrived at the killer whale pool within ten
minutes of the emergency report. The government was notified of
the death, and a necropsy was performed.
The immediate conclusion drawn from the gross necropsy report is
that the animal died as a result of skull fractures and blood loss.
Further review of the post mortem findings identifies an intestinal
tumor of neural origin which is of a type known to be capable of
producing excruciating pain. We believe the killer whale
experienced a sudden and significant amount of while resting,
causing a panicked and uncontrolled response. As a result, she
collided with the pool wall causing multiple skull fractures which
induced rapid loss of blood and cerebral contusions leading to a
swift death.
A brief history of the animal is necessary for an understanding of
the circumstances surrounding her death.
Sea World of Texas
10500 Sea World Drive
San Anton10. TX 78251
'512. 523-3000
BuS<'tl EntertainnwrH
1 r , r ... r, f 11 ) r 1
Nanc; Foster
?age T; .
The animal was collected in 1978 at approximately two years of age
and was in apparent good health until October 1990. In the
seventh month of her first pregnancy (17 month gestation), she
exhibited acute signs of abdominal pain, fever, inappetence, and
lethargy.
A team of staff and consulting veterinarians diagnosed her
condition as impending spontaneous miscarriage. The animal was
placed on appropriate medication and twenty-four hour care and
observation.
The animal was considered in serious condition until after the
November 6, 1990 expulsion of a 33
11
decomposing fetus. The
placenta was passed two days later, and her medical condition began
to improve substantially. By January 2nd the clinical picture was
within a normal range for this animal. The only remaining
condition of note was a variable appetite from pre-miscarriage
levels. During the weeks before death, her clinical and behavioral
state was considered within normal parameters. As previously
noted, death was unexpected and sudden on May 14, 1991.
We would like to re-emphasize that this animal was in apparent good
health pri6r to the onset of the illness preceding the miscarriage.
After a recovery period, she returned to a clinically and
behaviorally normal condition. We had no reason to suspect the
presence of any illness. In any case{ the technology necessary to
detect and treat cancer of this type in killer whales does not
exist.
Sincerely,
/)
v fJ1. rf) v. {/, 1'1
Les Dalton, DVM
Staff Veterinarian
GROSS NECROPSY REPORT
Facility: Sea World of Texas Prosector: Craw<ley, Young, Hines, Anderson
I
Genus/Species: Orcinus orca ID #: SWF-Oo-7803
Age: Approximately 15 yrs. - -sex: Fema:te
Date of Death: 5L14L91 0609 hrs. Date of Necropsy: 5L14L91 0900 hrs.
EXTERNAL MORPHOMETRieS: (metric only)
WEIGHT: 2077.27 kg
TOTAL LENGTH: 508 em GIRTH AT AXILLA: 289.6 em
GIRTH AT ANUS: 226.1 c ~ L U Y ~ WIDTH: 134.6 em
GIRTH AT UMBILICUS: 312.4 em DORSAL FIN HEIGHT: 67.31 em
HISTORY:
This animal had been in apparent good health from the time of her
arrival at Sea World until October 23, 1990 when she presented with
acute lethargy and inappetence. She appeared to have abdominal
pain and was immediately started on medication. Due to the
leukogram and the progesterone levels monitored since conception
in March of 1990, a tentative diagnosis of impending spontaneous
abortion was made. The animal aborted a 33 inch, 16 lb. partially
autolyzed fetus on November 6, 1990. The entire placenta was
passed on November 8, 1990. After the miscarriage, she began to
return to normal as reflected by appetite, behavior, chemistries,;
and hemogram. Medications were discontinued on November 20, 1990.
Intensive monitoring continued after medication was stopped until
February 6, 1991 when she was returned to a routine monitoring
schedule which included daily veterinary observations and monthly
physical examinations. She had returned to normal with the
exception of her appetite which remained variable. During the
weeks prior to her death, her behavior and clinical picture were
excellent and appetite appeared to be stabilizing. Death occurred
without warning at 6:09 a.m. on May 14, 1991.
GENERAL EXTERNAL APPEARANCE: (oral cavity, external nares, skin, eyes)
There is a 4 em ovoid superficial abrasion over the mandibular
symphysis. There is a degloving wound over the area of the
mandibular symphysis. Multiple lacerations of the gingivae are
present. The dentition of the left mandibular arcade is dQsrupted.
Two teeth are missing from the anterior aspect of the lower arcade.
No recent rake marks are present on the skin.
Pl-.GE 2 Sj..,'J:'-Oo-7803
SUBDERMAL CONDITION: (blubber, muscles, lymph;nodes)
The blubber thickness is approximately 7-8 em which is normal.
There is a contusion around the left orbit.

CRANIAL EXAM: (ears, melon, pterygoid sinus)
The mandibular symphysis is separated. There is a slab fracture
of the anterior dorsal aspect of the mandible which includes the
first two teeth on the left and right side. There is a compound
comminuted fracture of the mid-left horizontal ramus. There is an
oblique, hairline fracture of the right horizontal ramus. There
are hairline fractures of the right frontal, parietal, and
occipital bones. There is a simple fracture extending to the right
temporal bone.
CENTRAL NERVOUS SYSTEM: (brain, pituitary, spinal cord)
The dura mater is lacerated over the right cerebral hemisphere.
There is a 5 em subdural ecchymotic hemorrhage over the right mid
dorsal cerebrum. There is a localized area of superficial
hemorrhage over the left cerebral hemisphere.
THORACIC CAVITY: (pleura)
There is evidence of extensive hemorrhage in the mediastinum.
No source for the apparent mediastinal hemorrhage can be
identified. Suffusion hemorrhage is present along the serosal
surface of the thoracic esophagus.
UPPER RESPIRATORY SYSTEM: (nasal sacs, nares, larynx)
Appears normal grossly.
LOWER RESPIRATORY SYSTEM: (trachea, bronchi, lungs, lynph nodes)
The left lung lobe contains two bullous air-filled structures.
There is a 9 em diameter mass with a 2 ern diameter caseous center.
There is froth present in the major bronchi.
CARDIOVASCULAR SYSTEM: (heart, aorta
1
major vessels)
ABDOMINAL CAVITY: (lymph nodes)
All organs appear dry and appear to contain very little blood. All
lymph nodes appeared very prominent and exuded a fluid on
cut surface.
ID F
DIGESTIVE SYSTEM: (esophagus, stomach, intestihe, cecum, rectum,
lymph nodes)
The jejunum contains thick brownish-red )..iquid. The mucosa is
friable. There are serosal petechiae and ecchymoses involving the
distal small intestine. There is a solid white 6 em by 3 em mass
in the distal small intestine that extends from the mucosal surface
to the serosal surface. No gastrointestinal ulcers are present.
LIVER: (biliary system)
The gross appearance of the liver is normal.
PANCREAS:
SPLEEN:
The spleen is small with fibrous tags on the capsule.
significant gross lesions.
REPRODUCTIVE SYSTEM: (testicles, ovaries)
There are no
The right ovary contains several developing follicles and one
atrophic corpus luteum. There is a large round 1-1.5 em corpus
luteum noticeable on the surface of the left ovary. The remainder
of the ovary appears to be composed of luteal tissue. There is a
2 em cyst in the left mesovarium. The cyst is firm and fluid
filled. Three small, fibrous plaques are present on the serosa of '
the left uterine horn. These appear to be scars, not active
lesions. The reproductive tract appears essentially normal.
URINARY SYSTEM: (kidneys, ureter, bladder, urethra)
ADRENAL GLANDS:
SKELETAL SYSTEM:
Appears normal grossly. See cranial exam.
PARASITE SUMMARY:
No parasites found.
SPECIAL TESTS:
Histopathology
Microbiology
:0=
Magnetic resonance imaging (brain)
GROSS SUMMARY:
1. intestinal mass
2. pulmonary mass
3. multiple fractures of the skull and mandible
4. laceration of the cerebral dura mater
5. subdural cerebral hemorrhage
6. mediastinal hemorrhage
HISTOPATHOLOGY SUMMARY:
1. intestinal neurofibroma j ganglioneuromatosis
2. meningeal hemorrhage, multifocal of varying severity
3. granulomatous pneumonia, single focus, mycotic-inactive
4. hepatitis, multifocal, minimal-insignificant
MICROBIOLOGY SUMMARY:
No significant findings.
RESONANCE IMAGING
No significant lesions.
CONCLUSIONS:
The animal had an intestinal neoplasm of neural orlgln which is of 2
type known to be capable of producing excruciating pain. During agonal
throes, the whale collided with the side of the pool, which induced
nultiple fractures of the skull and cerebral contusions. These lesions
resulted in severe hemorrhage, loss of consciousness, and death.
Date:
Signed/=-
... _
_c i
.- I
/
Department of Laboratory Animal Resources
June 20, 1991
Accession number: 91T5-87
Animal number: 116 377 532
Submitted by: Dr. Dalton
The lini\ ,,j Tt:-:a-..
Health Science (enter at' ::;,;Hl :\ntonio
Floyd !Jr 1\t
San Antonio, Texas
\5'12) 567-6166
A. intestine - mucosa autolytic, increased cellularity involving
the myenteric plexus. There is marked spindle cell
proliferation around the myenteric ganglia and along nerves
into the inner circular smooth muscle layers and outer
longitudinal smooth muscle layers. After traversing the
muscle layers the spindle cells form a dense layer between the
inner circular muscle layer and the submucosa. Likewise a
dense layer of spindle cells is formed between_ the outer
longitudinal muscle layer and the serosa. Mitotic figures are
not found in this population of spindle cells. The spindle
cells have a single oval nucleus with wavy cytoplasmic
processes extending from each end. The cells are arranged
with parallel cytoplasmic processes which stain for
with a trichrome stain.
B. intestine - similar to A but with more pronounced involvehlent
of the submucosal and subserosa! areas. There are also
globoid masses arising from the ganglion area between the
muscle layers. There are ganglion cells which appear to be
trapped in these masses. The masses are composed of loosely
arranged spindle cells forming whorls and interdigitating
bundles. These cells have long wavy cytoplashlic processes
that stain less intensely for collagen than the de thctt
extend outward along nerves from these masses. Hy impression
is that this lesion represents a neurofibroma and is cohlposed
of fibroblasts and Schwann cells. I cannot determine if the
ganglion cells are part of the neoplastic process or are
entrapped within the neoplastic tissue. If the ganglion cells
are part of the neoplastic process the diagnosis 1s
ganglioneurofibroma.
C. intestine - same as B
D. intestine - edge of A
,-
,.
Accession
Animal number: 116 377 532 Page 2 c f =
E. submandibular l]'1!1ph node - fatty infiltratio1l, hemosiderir-,
accumulation in medullary
F. submandibular lymph node - same as E
G. mesenteric lymph node - no lesion
H. mesenteric lymph node - no lesion
I. mesenteric lymph node - minimal medullary fibrosis
J. lung - H&E, focal granulomatous pneumonia with caseous exudate
containing numerous hyphal structures with the typical
morphology of Asoergillus Q. The lesion has a thick capsule
of fibrous connective tissue, lymphocytes, plasma cells, and
foreign body giant cells. There is chronic obstructive
pulmonary disease in the lung tissue surrounding the mycotic
lesion. The adjacent bronchioles and alveoli are dilated and
contain a mucoid secretion.
J.
K.
K.
L.
L.
M.
N.
0.
lung GMS - same as J H&E
lung H&E - section of lung adjacent to mycotic granuloma with
chronic obstructive pulmonary disease as described in J.
lung GMS - negative fungal elements
lung H&E - same as J
lung GMS - same as J
lung - no lesion
lung - same as K
lung focus of subacute to chronic bronchopneumonia
by exudation of mixed population of leukocytes
and organizing fibrin into bronchioles and 3lv2oli.
P. lung - no lesion
Q. small intestine - autolytic mucosa, no lesion
small intestine - prominent Brunners glands, infiltrates of
plasma cells and lymphocytes at the interfc.ce of Brunners
glands and the superficial mucosa.
R. small intestine - autolytic mucosa, no lesior;
small intestine - autolytic mucosa, no lesion
::l-=-=-8/
l }(; 377 "J32
s. SBall intestine - autolytic mucosa,
f!_Q
lesion
large intestine - autolytic mucosa, subserosa!
T. small intestine - autolytic mucosa, no lesion
small intestine - autolytic mucosa, no lesion
U. small intestine - autolytic mucosa, no lesion
glandular stomach - no lesion
" glandular stoBach - no lesion
non glandular stomach - no lesion
W. small intestine - autolytic mucosa, no lesion
X. ovary (left) - large corpus luteum, no lesion
Page _:. of .,
hemorrhage
Y. ovary (right) - corpus albicans and few primordial follicles
in stroma - no lesion
Z. hepatic lymph node - mild edema and mild erythrophagocytosis
AA. pancreas
lesion
mild interstitial edema, slight autolysis, no
BB. adrenal gland - no lesion
CC. kidney - early autolysis, no lesion
DD. spleen - no lesion
sublumbar lymph node - no lesion
EE. kidney - no lesion
adrenal - no lesion
FF. heart - no lesion
spleen - no lesion
GG. heart - no lesion
heart - no lesion
HH. - no lesion
heart - no lesion
II. heart - no lesion
heart - no lesion
JJ. heart - no lesion
- no lesion
Accession number:
;._':limal number:
91T5-87
116 377 532
KK. skeletal muscle - no lesion
thyroid gland - no lesion
LL. skeletal muscle - no lesion
MM. liver - minimal hepatocytic vacuolization, expansion of space
of Disse, occasional focal accumulation of mononuclear
leucocytes.
NN. pelvic lymph node - slight edema
1. anterior cervical spinal cord - minimal hemorrhage in grey
matter around central canal, minimal spongy change in
matter which is indistinguishable from early autolysis.
2. cerebellar cortex- no lesion
3. cerebellum, choroid plexus, medulla -hemorrhage in meninges
4. vermis of cerebellum- congested meningeal vessels with focal
meningeal hemorrhage
5. posterior colliculus - no lesion
6. left cerebrum - extensive meningeal hemorrhage
7. thalamus -no lesion
8. roof of 3rd ventricle - hemorrhage, mainly perivascular, in
white matter
9. cerebral cortex - no lesion
10. left cerebral cortex - extensive meningeal hemorrhage over
surface and extending down sulci, perivascular hemorrhagc.in
underlying white matter of gyrus.
ll. left cerebral cortex (acoustic area) - no lesion
12. right cerebrum- no lesion
l3. right cerebral
hemorrhage
(occipital) minimal meningeal
hcccssion number: 91TS-87
Animal number: 116 377 532 Page 5 of 5
Diagnoses:
--
1. intestinal neurofibroma
2. granulomatous pneumonia, focal, mycotic
3. meningeal hemorrhage, multifocal of varying severity
4. hepatitis, multifocal, minimal
Ronald R. D.V.M., Ph.D.
Veterinary Pathologist
RRC:tc
Ref: RRC1/91T5-87.SW
8r<1r: l--.r-

Zoolo-;;'cal Ope!!on'
September 5, 1991
Or. Nancy Foster
1335 East-Hest Highway. Room 8268
Silver Spring. MD 20910
Dear Or. Foster:
This responds to your request for additional information pertaining to
the death of a killer whale at our San Antonio facility. He would
also like to comment briefly on a letter to the Service from the
Marine Mammal Commission.
First, we have submitted with this letter the following documents
which you have specified:
o Narrative description of observations by the Sea Horld
security officer who observed the animals in question;
o laboratory reports relating to the neurofibroma,
including John H. Pletcher, OVH, MPH and Robert B. Moeller,
DVM, Armed Forces Institute of Pathology, Washington, D.C.,
and R. Craig Platenberg, HD, (MRI Report);
o Communications from additional medical experts: Sam H.
Ridgway, DVM, PhD; Clifford J. Hixson, VHO; Hayne R.
Patterson, PhD; D. L. Chumley, HD; and Steven Schenker, HD
o A copy of the APHIS report.
Seaworld. Inc.
Orlando. FL 32821-8097
(407) 363-2155
FAX (407) 345-5397
Busch En_tertainmerl!
Corporcttlon
I
.. : ; .- r - ..' .- - : y
Throughout our 1nvestigation, we have been thorough, utilizing
veterinarians and other individuals in the medical field. It is the
combined judgment of these experts. both inside and outside of Sea
Horld, that led us to our opinions and conclusions regarding the cause
of the animal's death. Again. the experts have relied upon include
the following:
Leslie H. Dalton. DVM
Staff Veterinarian
Sea Horld of Texas
San Antonio, TX 78251
Ronald OVH
University of Texas Health Science Center
San Antonio. TX 78284
Gary Anderson. DVM
Veterinarian
Lackland Air Force Base
San Antonio. TX 78236
John H. Pletcher. DVM, MPH
Robert B. Moeller. DVM
(in consultation with the Neuropathology Department)
Armed Forces of Pathology
Washington. DC 20306
Sam H. Ridgway, DVM, PhD
Naval Ocean Systems Center
San Diego. CA 92152
Or. James McBain
Sr. Staff Veterinarian
Sea Horld of California
San Diego, CA 92109-9980
He have considered all of the points raised by the Marine Hammal
Commission. Our deliberations are reflective of a professional,
competent and detailed inquiry and stand by our opinions and
conclusions.
Regarding the Commission's comments about the animals thoracic ccvity,
the fact that no source for the apparent mediastinal hemorrhage was
identified distinctly indicated the lack of involvement of any lcrge
blood vessels. The amount of blood involved was sufficient to produce
the suffusion hemorrhage as described in our report. My
correspondence on July 11, 1991, that the "likely cause of this
hemorrhage was trauma to mediastinal tissue caused by the sudden'
deceleration of the relatively large cetacean heart" is a good faith
attempt, by a number of professionals, to describe what appears to
have been the most likely scenario to have resulted in the lesion
noted.
The bleeding that produced this lesion was ofcapillary origin and not
the result of esophageal laceration, laceration of any other type, or
trauma from outside the thorax. lf any other cause for the hemorrhage
would have seemed likely, our reports would have indicated this. In
any event, we can state with confidence that no foreign object was
present at the necropsy. As we have stated before, we have no
indication of aggressive behavior that would have caused a collision
with a pool wall.
As previously stated, the other whales were inspected after the death
of their companion: Nothing unusual was detected during the
examination requiring furter observation or treatment; consequently
there is no documentation of the examination. Also, contrary to the
information recently received by the Marine Mammal Commission, there
is no survei1lance video of the death.
Finally, we did not state or imply that the neurofibroma was
malignant. Details about the tumor are contained in the necropsy
report.
This concludes our report on the death of the killer whale identified
as SWF-Oo-7803. Two copies of the marine mammal collection/inventory
report are attached.

Brad Andrews
Vice President
Zoological Operations
Attachments
,_
Q. 91-lll
N/A
14 MAY 91 0609
,M; of PAG!
2 2
, t'IP& or
;TAf>It.l1/).. P01 COO HUMAN
* .
. At appccx!Htely 0609hra on l.f MAY 91, Ottioet 1] vt.a on My &t ShaiN
Wh!l on My P' 1] Qne of tht tw hmalt !tiller 11hal., thrUhih; in tM vat.r.
[ .. 1 J valkin; tovd the back -.rea of the r19ht pool notice4 tM
Hh&le eocne up <IUt of the vater at the ge.tt that dividta tM rJ.iht and left ;ioola CJ&tc
( ... 11 ot>secvtd blocd llixe<S vith vat.-. At thia tiN the FlmUe14hol
vent urdtr VAttr up, noa. \l), epit r.c:a blooa. [ .. 1] not1!14t<2
the Diape.tchu ( ,.., AM E ] of Code tr4'ANIMAL Hll'.ANS lNVCt V!D. MUle [* jJ
vq talkin9 the t"' way radio, tM l4C&l. orJt cf tM
noat pointing up, an4 apit up cnot:e the Whale vu throahing in all d\lrlnr;
tht ineidQnt. ['-l] vtnt to tM TrA!Mra buildiDJ and the tlphQn
c! the incident. At appr:odmately 06l0hra ot!icer [ J..] arrim at SMAMU STADIU1, lj
( d..] beSM looking toe t.he Whe.l. w ooW.d not tine! due to th vater i
tM pool being ve&y clM'j The other Male nd l'err.tl Whales vere tM
front of tht pool vocy cal.JQ en .w:toe inju.r.d Fesr.sle va.
undeOtater &Urfaced. At A.ppt:oxim&ttly 061Sht' a.crivea e.t
S&MU Sl'ADIU1. (- .1] &dviee\1 l'OO.Ct of P* l] , [ .:lJ , loo)(ing
toe: the l'tltlalt Wh6le. vu e.})lt to the injutied FCICT41Cil Wnal in th
o! the pool at thia time the ha4 cleared up ae. vith fluh
lighta. (*1] lORe& 1t ht vould llake turthoe llr.cgency notif1cat1ooa.
FC({C replied &eked to contact ISlF.alDINt ct A!fll'IAL SCitNC.t
wtGDKAL, DUOc.tt .. P\lrthQC notit'ic.tione vtre tM t.alephoM.
(Security details------------- ---------------------------------.)
[REDACTED FOR SECURITY REASONS]

Or. Les Dalton
Sea World of Texas
San Antonio, TX 78251
L
) .. :-- ' . : ' :_ : r . : :. -,.'. . . .. r'
}---
i
1
ANIMAL, CETACEAN WHALE
A-000-91 T
SU"GtCAUAUTOPSY PATH ACC(SSI()fj "S
DATE:
_j
CONSULTATION REPORT ON CONTRIBUTOR MATERIAL
CPU-V
jMP /RBM/mab
19 June 1991
t-.FIP Olt-GNOSIS: 116377532 l. Intestine: Ganglioneuromatosis, killer whale, cetacean.
2. Lung: Granuloma, caseonecrotic, focally extensive, severe, with
fungal nyphae consistenr with Aspergillus sp. and adjacent granulomatous
inflammation.
3. Brain, meninges: Hemorrhage, multifocal, mild.
4. Liver: Hepatitis, acute, minimal.
Corm1ent: This case was revie;.,ed by the Departments of Veterinary Pathology,
Neuropathology and Gastrointestinal Pat11ology. The cause of t-he abnor.nal behavior of
this prior to death coula not be identified histologically. The intestinal
gangiioneuroonatosis .-:as characterized by pro;nir.ent bundles of spindle cells
infiltrating into the tunica .nuscularis_ ana ser-osa. Scattered a.r;Jongst these spinale
cells were indiviaual ganglion cells. The spindle cells were S-100 positive. The
focal granuloma in the lungs contained numerous fungal hyphi which are consistent wiJh
Aspergillus sp. Although Aspergillus infections can be serious in whales, this lesion
was focal and well encapsulated. lne hemorrh2ge in the CNS may have resulted from tne
trauGa of colliding with the pool
Animals affected with intestinal ganglioneuromatosis have demonstrated clinical signs
of constipation and tenesmus. In man, this neoplasm has been associated with a type
of familial multiple endocrine neoplasia, which includes pheochromocytoma and
medullary thyroid carcinoma, and von RecKlingilausen's disease (neurofibromatosis).
Individuals affected are usually asymptomatic but can show symptoms of constipation,
cramps and/vr abdominal distension. such sisns in a wnale would Cduse erratic
swirnni11g ana a collision is unknown. Thank you for submitting this irrter.cstir1g case
to the Registry of Veterinary Pathology.
?J1-t f!;;ifct_'Z
ROBERT B. MOELLER, DVM
LTC, VC, USA
Department of Veterinary Pathology
M. PLETCHER, DVM, MPH
Colonel, VC, USA
Chairman, Department of Veterinary Pathology
SOBJ: -oRO. HRI
TO: Les Dalton DVM
TECHNIQUE:
Multiple spin echo and echo sequences were done on a
GE 1.5 Tessla SIGNA system. Tl weighted sagittal, axial and coronal
views were undertaken with TR/TE of 600-650/20 msecs. T2 weighted axial
views were done with TR/TE of 3,000/30,80 msecs. SPGR images with a flip
angle of SO degrees, TRITE 37/9 and GRE images with a flip angle of 45 degrees
and TR/TEof 27/12 were also obtained.
FINDINGS:
A solitary punctate area of increased signal on T2 images
is noted in the right thalamus. This observation in humans corresponds
to a dilated Vlrchow-Robin space or possibly to a focal area of ischemia
or gliosis which is usually seen in hypertensive individuals. The
significance of this finding in the Orca species is unknown. No mass,
mass effect, significant signal abnormality nor an=tomic
l.!ere detected.
IMPRESSION:
No significant anatomic abnor8ality. No MRI evidence for ir.fection,
neoplasia nor hemorrhage.
Thank you for this most interesting opportunity to assist you ir. your
evaluation of this amazing If I may be of please
feel free to contact me.
Sincerely,
?, ")
R. Craig Platenberg,
',.J -./
I
Department of Medicine
Divitoion of Ga6troentcrology 2lnd Nutrition
August 23. 1991
Dr. Les Dalton
Veterinarian
SEA WORLD
Sz.n Antoaio, Texas
The o( TCY...a!S
Health Science Center at San Antonio
7703 Floyd Curl Drive
San Antonio, Ttxas 78284-787:)
(512) 567--4880
FAX No. 523-3299
This is a follow up on y<Jur telepht'):le czll coucernlng the death of whale <!t So::a \Vo.-lcl.
- -
As I understand lr, on aurops;' a 6 x 3 em sp<mniug 1/3 of tle circumferenc:! of the small intestine,
was found. This rumor imad::j the muscularis and the serosa. this was G
neuroendocrine tumor.
The question i_s whether such a tumor c:.n Cluse p2in wbici1, in turn, result in excitement of the
animal and secondary injury. Obviously I have no experience with whales (although my colleagues feel
that I am a of a docwr-). However, extrapolating from huwan p?.rtial from
the tumor could cause distension of Ul!! bowel and L'l'Js pain. This would be the must Iikdy cllusc of any
pain present in such a Concei\'2hly, of pain receptors in a strctc:.cd bowel wall
could be another mechanism of pain. Small bowel tumors in patients often are silem and tlifticult to-
detect unless they bleed or cause ohstrucl!on wid1 Tnus, wbik I can!lot s2.y that the "hale hcd pi!in,
this could have been t.."'-1c problem.
Good wishes.
Sincerely,
Steven Schenker, M.D.
Professor of Medicine and Pharmacology
Chief, Diviaion of
and Nutrition
StAff Phy3ician, Audic L. Murphy
Memorial Veteraru' Hospital
SS!am.
cc: John P. Howe, M.D., President
September 3, 1991
To: Dr Les Dalton
SeaWorld of Texas
RE: Pain Associated With small Bowel Tumors
It is the reeling or Dr Wayne Patterson and myself that a
small bowel tumor of neural origin could, in some cases, cause
pain, especially if the tumor impaired function resulting in
strangulation.
;fpu K/ Z<?t_)
L Clifforfi/ Hixson, VMD
-Diploma't:, American College of Veterinary Pathologists

)eputy Director
1
Clinical Research
Hall USAF Medical Center
;
'1 -./I ..-./ _.i

' I
. '- ,- -
of Son Anronio,
Lcs D.titon
1

World of Texas
D.aa:- D-:-. Dalton:
D L Churnley. M.D
J Tnornas Swan. M.D.
R:Jtrick A tv1osters. MD
! writing to verify my with you. Based upon my
training and experience and the it i$ my optnton
ne;.;:-ogenic tumors which the 5:Ja11 ':lowel can produce not only
SP.d intussusception also psin. Furthermore, this pain can be
transient and cblicky in natcre or be very severe upon the
location and si'ze of the neurcgcnic tumor. Tnese symptor.a; can
from
ar.y neurogenic tumor as or
D. L. Churn 1 e y
1
DLC:et
To: Dr. Les Dalton
Veterinarian
Sea World of Texas
San Antonio ,1 TX
Tel. 512
Fax: 512 523 3299
Fron: Dr. Sam Ri.dgway
NOSC
Code 5107
San Diego, CA 92152
Fax: 619 553 1355
Tel: 619 553 1374
Dear Les,
August 29, 1991
Please my apclcgy for so long to get you
in writing the killer whale brain we
examined in the company of Dr. a r.eurologist from
wilford Hall Medical Center, last May. You identified the brain
to me as from a female of 508 em, 2077 kg and l< to 16 of
age having.been in Icelandic wcters at a age in 1978.
The animal. had been at Sea Kcrld facilities since time. The
brain was fixed !n formalin and en the fix weighed
6299 g. As you recall, the brain in slices
about 1 em and examined slice thoroughly. The pathologist
took several specimens for examination. My
examination of the fixed brain revealed no gross abnormalities,
cs I mentioned at the cf 2nC in our
telephone
Ke have your (IC#SW?-Oo-7803).
Th intestinal is the report2d from a whale.
Certainly it is worthy of careful as to the .
cause of death. Over fifty tumors have been reported,
forn wild animals or stranded cetaceans, never this
ex=ct kind. Possibly pair. from the together with the
rwpture of focal les:ons could resulted
in violent, likely involuntary, activ:ty at death. The lack of
gross damage to the brain suggests the rner.ir.seal
acutely terminal or
.
Sam H. Ridg,;ay
OMD NO. EX.P 31 _; ".
ISNI
1SP1
ASN1
ANREPt
Ll' I
f'r,
NMF!I l1Nl. Y
,'ll ll' (iN 1 MIU.. liOLO[fl t
Ml\111 I I (lN/1 NVLN I IJIIY IILPilftl
Mortalitv_
TYPE OF
S0.aWorld, Inc.
DrH OF H!::POflT 1
9/5/91

f>C1CtJTIFIC _O_r:_cinUS CtrCa
I --------:..-------------- ------ .. - ----
COMMON NAMa _____ Killer Whale
---------------------------
IS I
; ,_, \t l<il ME I I E: I
, 1 tl f 1 F 1 CAT I ON I X I
EST 1 I DrHE I 1
B 1 fl TH I IIUTH011 I TAKEN OR I Hh{C I
YEAR IDOCUMENTIACCU!f1EDITYPEI
LOCATION OF TAKE
PLACE NrtM AND
LAT I TUDC::-L.ONG I TUDE
COLLECTOR
Oil SOURCE
I
cunR 1
STAT I
DEATH OR DISPOA!TION
DATE XPLANAf lOt<

' . I I I I I I. I I I
,.Jf -Oo-7803 rl I #240 110/26/7;8 LMI Iceland I Sea World I 0 I 5/14/91
____________ ,_, ______ , ________ , ________
l 1 1 1 1 Trauma; Intestinal
1 1 1 1 1 1
1 1 1
neurofibroma/
___________ ,_, ______ , ________ , ________ , ____ , __________________________
1 1 1 1 1 1 1 1 1
ganglioneuroJllatosis
I I
____________ ,_, ______ 1 ________ , ________ , ____ , __________________________ , ______________ 1-----1--------------------------
I I I I I I I 1 I
I I I I I I I I I
_____________ ,_, ______ , ________ , __ , ______ , ____ , __________________________
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September 5, 1991
Or. Nancy Foster

1335 East-Hest Highway, Room 8268
Silver Spring, Maryland 20910
Dear Or. Foster:
This letter contains the gross necropsy and histopathology of the
Kiner Hhale identified as SHC Oo7602, which died August 6th at Sea
Horld of Florida.
This adult female Killer Hhale (Orcinus orca Oo7602) exhibited a
depressed appetite on 8/5/91. Prior to this time, she was clinically
healthy, except for a tooth infection for which treatment was
initiated on 7/21/91 and which was clinically normal at the time of
the necropsy. In the afternoon of 8/5/91, she was also reluctant to
interact with her trainers and unwilling to present her fluke for.
blood collection. She was alert and active at this time and her
respiratory rate was nor.mal. However, early in the morning of 8/6/91,
her condition began to deteriorate rapidly. Hhen her respiratory rate
increased and she began to show erratic behavior. the medical team was
called and emergency treatment was given after she was guided
into and held to the side of the medical pool. The animal did not
respond to treatment and died within five hours of the onset of the
increased respiratory rate.
The gross necropsy was performed immediately following her death. The
necropsy team consisted of Michael T. Halsh, DVM, Sea Horld of
Florida; Terry H. Campbell, OVH; PhD, Sea Horld of Florida; Loren 0.
Kintner, DVM, PhD, Florida Dept. of Agriculture and Consumer Services,
Division of Animal Industry/Kissimmee Diagnostic Laboratory; and Scott
0. Hright, PhD, Marine Mammal Research Institute, Florida Department
of J. Kelly, DVM, a veterinary medical
officer for the Animal and Plant Inspection Service of the United
States Department of Agriculture was an independent observer during
the necropsy. The gross necropsy, histopathology and bacteriology
indicated that the animal died of a severe, necrotizing, hemorrhagic
bacterial pneumonia that resulted in a fatal overwhelming septicemia
and pulmonary anoxia.
Sincerely,
f?(_._--_._._/; /( Jl
Hi chae l L Ha 1 sh, 0V).4
Sea Horld of Florida
/ '/ [;/;/.
-I Zty Li( ;_ i
Terry H. Campbell, OVH, PhD
Sea Horld of Florida
Sec World of Florida. Inc. 7007 Sea '>:orld Onve Orlando. FL 32821 (407) 351-3600
I ' ' :
I "' ... ' I
VEitR I Nr1H I
DR. TERRY SEAWURLD
7007 SEA WOHLD DH. < ANH1AL Ct,HE/LAB)
ORLANDO FL
SPECIES/TYPE MAMMAL I SEA*
NUhBER OF 1
SPECIMENS - DEAD ANIMAL.
'
-. -- \_'
. - , ... ,
..._:."; ...... ,.._.
ACCESSION tl <il-016110
DATE REC'D 08/06/91
OWNER
SEA ANIMAL CARE LAB.
7007 SEA DRIVE
ORLANDO FL 32821
AGE 16 YEARS

f-EMALE
TESTS REQUESTED AND HISTORY ON FILE. COPY AVAILABLE UPON REQUEST.
REPORTS- 03/07 TELEPHONE
FINr1L 08/0S/91
CASE COORDINATOR DR. L. D.
RESULTS OF EXAMINATION:
:+:!\.I LLE::R WHr1LE
NECRO?SY
THE NE.C:-:Cii>'=;y W(iS DONE THE rWFd<ING Or (;uC:L!:::n WITH THE WHt;LE ON
HER LEFT SIDE. SHE P:DEUUr,TELY NOURISiiED AND FHEE OF BRUISES t;t;[.

THE ANTERIOVENTRAL OF EACH LUNG WAS CONGESTED WHICH
INCREASED ITS AND GAVE IT A DARK RED CULOR. EACH LUNG HAD A
CM SPHERICAL AREA OF HEMORRHAGE AND PARTIAL LIQUIFICATION THESE
TWO FOCI WERE JUST UNDER l"HE PLEURA IN THE DORSAL-LATERAL PORTION OF
THE CO:DH,C F'OIHION OF THL LUNG. THE SPI-li:.P..ES BULGED 6 TO CM ?i80l.'E
THE SUFHGUNDING COlHOUF . THE LESIUi-1 NO DOOR AND
CEf'T?,[:L'J INlU f",DF:E t-!CR.fI{,L LLIUG THI::. BR.UNCI:JAL TREE W(;;:: FF:I::t OF
EXUDATE UR FOftEIGN MATERIAL. THE PULMONARY VESSELS WERE AND
FREE OF E.f-iL::OLI. THE Si<IRT LYI"Wfl NODES (Gi-{ES TO THE I..'ENTR(lL
.?URFAL'E lJF THE LUNG) WERE 5 BY 10 BY 10 CM. OR HH1URJUIP,GE
WAS IN 1-': or- L.Yr:;-: UUDES.
THE PERIU1HDIAL StiC 1/2 LITER OF CLEAR FLUID. BOTH VEN-
TRICLES OF THE: HEART STOPPE.C IN DIASTALE. THE. HEART
WERE NORMAL. SEVERAL 1/2 CM SACCULATIUNS UFF THE PANCREATIC DUlT
f[\.1 1 10 2 f'ttt COi'lCF:EI 5 CM SJZL
L YfWH .ru r:1E TilE Pr .. ucnr:r2 cutHAINED UP TL.: 3 OR
. r:M IN lHcSE Hr-,D NECROTIC AND
TO BE I![ALED {;RANULUrlAS DUE TO PRE'JIUUS PAHASITISM UP.
\
o:: [;J irl::.-:.: ._... ._,-:::_.
WI:TH 1HlN LAYUZ ,<.:::.d::i. UiJ[ Uf\ i!Ui:::: l/2 cr, ULCERS Wl:i(E:.
IN IHL f-;Ucoc_;(', OF THL FOI\E-STD!,{:,CH. lHE f'lUCOSr: IN Tt-ll (IF
TI-lE ESOPIIAl.iUS IIPoD A SLIGHlL Y
THtn !,.JERE J. T\...1 3 C1"1 IN DHoiiETEH t=dW 1/:.:' rii'1 DEEP. ,6cLL OF
CHANGES lN HIE DIGESTIVE H\ACT ?oPPEAHEO TO BE
HfE. CCJNTttiNE:D (.', 12 MUNTHS FElUS TJ-H,T i-'f'PEARED lQ 1-JAVF 2EEN
t1LIVE UNTIL HIE DAt-1 DIEDh rHE RIGHT ADRENAL LJAS DIFFUSELY BLACK WIHi
HEMORRHAGE. l"HE LEFT ADRENAL HAD A RED CORTEX AND A NON-REMARKABLE
MEDULLA. THE UTHER .ORGANS WERE NOT REMARKABLE. TISSUES WERE SAVED
FOR A VARIETY OF LABORATORY TESTS.
Lh D. KINTI'ltR.
Og/08/91 HISTUPATHULOGY
SIGNIFICANT LESI8N5 WERE TO THE SYSTEri. LUNG
TISSUE IN THE HEMORRHAGIC, SYMI"lETRICr.;L,. BULGING t\REAS l:JAS
TOl;!iLLY NECROTIC. TISSUE AOf'\PHOLOGY w,.:-,s SO DESTROYED, NO ALVEOLI,
BRONCHIOLES UR THE ITSELF COULD BE RECOGNIZED. LUNG
TISSUE PERIPHERAL TO THE AREA WAS ALSO NECROTIC, BUT
ALVEOLAR WALLS REMAINED INTACT. ALVEULI WERE STUFFED WITH BLOOD.
NU NUCLEAlE::D CELLS hUfZE LUNG W?iS CON;::oLIDfHED vHTH
PNEUMONIA. BRONCHIOLES AND ALVEOLI WERE FILLED
CELLS AND LEUKpCYTES. BRONCHIOLAR AND ALVEOLAR
WERE UNDERGOING NECROSIS. SUME UF THE MUSCULAR VESSELS CUN-
1 ;U NED TI-IF.:OfiB I. THC: TRfiCHEA Wr::::: L. I NED WITH CUE! 0 I CELLS. C I L u,
LOST. THE SU8(1UCOSA SLlGiHL Y THICKENED WITH ANL
EXCESSIVE NUMBlRS OF LYMPHOCYTES. SOME OF THE LYMPH NODES, PR08A8LY
FR.Of-1 THE 1:: iURACIC AREA,. HAD GF.EATL Y SWULLEN SINUSOIDS DUE TO EDEi'1A,.
AND LEUKOCYTES.
SLIDE 8 AMONG OTHER THINGS CONTAINS THE AMNIOTIC snc, CHORIOALLANTOIS
MID THE CYSTIC TISSUE FOUND Ot\ THE FLOOH OF THE LAHYNX. THE LATTER
L.:AS TISSUE: TI:.,:.T C:UNHtiNED CRYPTS LINED Will-I J
PSEUDCCOLUMNAR EPITHELIUM. IT WAS PROBABLY NORMAL TISSUE.
ADRCNALS MASSIVE, SUFFUSION HEhORRHAGE, ESPECIALLY
CC2TEX. THE CORTICAL CELLS THE RIGHT ADRENAL l"ENDEO TO BE
BY MANY Of l"HESE CELLS PYKNOl.IC NUCLEI.
SOME UF THE LATTER MAY HAVE BEEN POSTMORTEM AUTOLYSIS, AS THE
TEl UNDERGOES I D P OSTMUI\TH'l
IHE FI8ROUS NODULES THE t"IESEtHERIC L YMPi-: NODES CONTrilNEG BROWU
OPERCULATED EGGS. WERE PROBABLY FLUKE EGGS.
IHE fHNHIAL EROSIONS,. HEi"'lUP.F.HAL:ES {;NO CONlS; IO;.; IN THE f'lUCOSr,
l.i THE Gt.=
UG til: t..E WEHE IN THE ; ;C:tdi.T, LEEU, K I Y, A,
E LU[! E: E.R., I....'U.:, riLJ;;.;CLE, r- n-:c:;:._::._;,s TI-IYRCtl C.
L. D. KINTNEh
NATIONAl. V!:TF.RINARY SER'JICES U..ECRf..TORES
50010
DATE RECEIVED: 08/09/91
SUBMITTED BY:
SEA \lORLD
7007 SEA \lORLD DRIVE
ORLANDO, FL 32821
PATHOBIOLCGY REPORT
PURPOSE: GENERAL DIAGNOSTIC
COLLECTED BY: DR. CAMPBELL
SPECIES: UNKNOWN
ACCESSION: 91-39319
REFERRAL:
OWNER:
SEA \lORLD OF FLORIDA
ORLANDO ,FL
LOCATION OF ANL"'iALS:
ORANGE COUNTY, FL
DATE COLLECTED: 08/06/91
SAMPLE ID: i.IST ON FILE

Histopathology Results 91-39319/91RASOS:
Formalinized tissue specimens from a female killer whale and its fetus were
received. Tissues were routinely processed for histopathologic examination.
Sections of lung, liver, kidney, spleen, lymph nodes, heart,
esophagus, stomach, intestine, adrenal, tonsil, trachea, pancreas, large
artery, oral mucosa, peripheral nerve, uterus, placenta, and fetal tissues are
examined. Sections of lung reveal a severe, necrohemorrhagic pneumonia
characterized by diffuse hemorrhage in airways, marked necrosis of pulmonary
parenchyma, and large numbers of gram-negative bacilli colonizing the necrotic
interstitium. At the demarcation between the pneumonic and more normal lung
there are moderate numbers of neutrophils and degenerating leukocytes. Many
leukocytes contain large numbers of phagocytized gram-negative bacilli.
Kidney sections reveal mild to moderate focal thickening of glomerular
capillary tuft and tubular basement membranes. In one section of connective
tissue, a large encapsulated accumulation of mixed leukocytes surrounds an
oval structure morphologically typical of a trematode. Fetal liver sections
contain moderate extramedullary erythropoiesis. No other significant lesions
are noted.
Morphologic diagnosis: Pneumonia, acute, diffuse, necrotemorrhagic,
with associated gram-negative bacilli
Glomerulonephropathy, chronic, multifocal,
membranous, mild
Abscess, with associated trematode
Comments: The pulmonary lesions are suggestive of a severe, acute, bacterial
pneumonia. The mild renal lesions and the parasitic lesion are considered
incidental to the cause of death. No evidence of disease was noted the
fetal tissues.
s
General and

luoJuqic;JJ r'.1.tllolog) l
KP11t G. Usl.Jorn, J)VM
Hi c:; t bpa t I to 1 ogy
!
H: 91SWMX.OBA I
Submitted by: World,
Received: 00-12-91
Date Reported: 08-29-91
1 IJ
SpP.cie5:
Se'<: female
Common
8n;1ed
House
OI"'Ca
killer whale
Age: adult, 15-16
Oo7602
I
1. pleura, inflam:natior, nF>utrophilic
as!iociatPd with
2. lung,
i
. I
3. lymph node, not otlt-rwi'o-P' '!>pgocified (t.JOS),
in'flammatJon, nii'utrophilic
bacteori.l, I
I
wjth
4. vejn NOS.
neutroph:iljc jnfillrate
with node, in-flammation,
5. trachea,
neutrophi lie ir, f i 1 t <t\t
;
m1lM
I
I
trach{?a,

7. uterus,
Jymphtlc'Ytic
rnild inflamm ... tury ir"lflltr-AtP,
c:md Of-tl1i l1c
8. meser1ter ic nodule ar.d
tr t-flldtodf""
7. fundic stomach. uiJmuLU'=>o,
l'iith dr?<JCner.'\tion, c&uc;e
unde termi nc:-o I
I
I
(sliue nutnber in -,
I
The follOl-.Jinq li"::Ssues wr->r(' Px<lmine fTdtrr:>sr:npir:nlly And -found
t(J essentiallv ronriT'rl1: ttJlon (l'l), ;:.nd
( E ) , l c en t B ( B ) , 1 y m p h r. o :-j e N 0 S { B ) , fp roc ,- P. .3 s ( D ) , L1 l u tJ tJ e r
1
( F ) ,
lymph node NOS (Fl. F), nervi'? .;<nd
(Fl, thyroid (G), kidney (Gl, hf" rt (H), lvmph node NOS (H)
!
,.
On 91 SM X _ 0011
I
2
Lesions arH.ltor nol,:\ul4' f.ind1ng!:. 'lr-E' in the
1ollowing t
mucosa uu_: Two ons of here consist
of a thick layer of stratified epithel.ium over-
dE?nsGJly collaQP.nOU'L sug estiveo of muco&a. The
sub"' pit IH:d i .:.d mucosc.1, i mmed i at"' l y. i:ldj .ace11 t to the epithelium
contoins lymphoplamctti<. popultioo,
(A): The is edematous and contains
hemottt.age. al 'Surface hds some post
mortem epithelJal loss ba terial One
mi3r1 . ulti"l'ccal mild
neutrophilic itd lammatiDn .;;and pale 1 i.e. .-naterial.
Submucos Hr this drea is mil ly edematous, with
hemorrhage. lhere is minimal mild diffuse super-ficial
submucusal infi trate.
OK: trachei:l, hemorrhage, mild
neutrophilic i filtrate
Dx: trachea, serosa, emorrhage
uterug? (A): a thi k of in
three l<!yers. Tire- mucosa e.-pit 1elium consists of simple
cuboidal to columnar 1tpithel1um on th'"' luminal iind in
densely occa.ional ly ching
1
CJl&nds that
through depth of probably uterus.
A mild mixed infiltrate of lymp c;nd is
presl?nt in thP sulmucbsa.
Ox:
.itlf.llttate, lym'-'tocytic and
ild mixed inflammatory

1 ymph nod eo, _!NOS LUU_: This 1 ymph node
is heavily infiltrated by On sidP, sinusPs,
soinus and tis small to very
large numbers oi Many wjth largeo
of do not hav
Ox r 1 ym;Jh rrodP, not nthPrwi eo spec i 1 Jed (NOS), severe
inflE<mmllt.Lon. nP.ulrophilic i 1iltratP, associated with
tJactPri.:., rods.
!OnJ>!..LJJU: Mo!OOt lymphoid iol 1 ic.l e
(secondary) Largp nt.m
present in the udjac
withuut QS!OOCi.!!ted neulrophllo;;.
to those in thti> pre-viousl
p r e s P n t h P r "' r ., ,- E? a c t i v e
-er!:. o'f
nt tn ton1;.i lar but
bacteria
desc r i bf'rl 1 ymph """hade.
_l_ym!Jh nod,..'-LNOU\.J: Three o-f lymph nc("1e ..,,... .. proent
here, wjth ."'!; c11?scrjbE>d 1'or- R. Jn one
large th1n Wd]}pd blood to the node
toa!:. ll modcr.-.te neutrophil 1nf.:iltrrlte w1ih1n 1tc:
D)<t vpiro IJOS. w.itt ly11plo ruc.l<>. Jni!c;mm."tir;n,
I
Un7l>02. '71SMX.OOA
.,
lung ..J_g_t Therp 1c, '5PV ... re- cot'gule\ivP nP.-rroe>is il"l two
lur.y with thP J"lrPf'>Pnr& of bronchiolar t:art.ilayt-- thl::'
ffOAtur"' mAJ.P." thPm idnti1iAb]_,. ..... lung.
large numbf'r-:. of rods rp in tSreoe!>,
with one sect]on .:dso !Jact _ria in caloniPs.
D)( : 1 ung c. tCIIJu l .t. t j vfi> nt:>c: r
ThP t ion t-d lung hP.ro very c;pverE' hemorrhage.
IntE>rstit.:i"l it- l<Hgp]y replaced by of
rad"5. 1-Jo l'llvt.cder brnnc.l1idl epith!O>lium is

D:><: 1tg. hPmur r h.:ye I
I
I
_1Ql: Nu c:Ht- recpqn.ized (NLR). Lymphoid
pupulelir:m wJlh _110 1nllicle'!i.
I
abscess (D)_: lhl.S is a "'PI! le_sion a thick
-fibrouw. c:c.p-.ulP. Thlt LUll Blfl':> 1-i rr)x"'d 1nflammatory
thi-it includes lyrnrhnryt b' cells;
mild numbprc; o--f Hrt" associ-.ted with
Ll't-rnatndP. At one l?dqg lS
popul.-.tjon o-f lymphor.ytli<'os, tile- uf .- lymph node.
Thi5 probably c-orr.,c;pond$ the lymph
nodQ nodules At
D)(I nddu)P. .:\nd lymph node. associted
wjth J
. .
I
inf J i::!lllthr..tiqn l!. in this node.
ico. ml!-'dullctry !:!>it1US! erythrocytosis. Lymphoid
population is mj}d. cortical f!ullicles .,,-"' They
non reartive and havp hyaljnJili<'d follicular
I
Mutll::'riltP upli<'rficial mucoo;:.al
jc; prpo;ont in thP t.wn '::.tu(lldCt"t bQCtions present
SupE>r11c1al mucosal th""l ium i!!. nost l due to
No is
fundic; llrf-' submucoc;;a, t the
conjtain a mode-rately large
lyrnphop]agmacytjc population. Vffry onell numb&>rs of
within infiltrte.
Within l111:" ly&rs:. o-f rr.ut060i d1-f'fu5E'
Ppithelial char by
will int
Thit; rroL,rllJly to th10>
recognizf!'d at necrop!>y, though lu'::> not .:1n ulcer, OlS
tn the iun.
D><: -fundit. '::.tCHIIdt.:l. c:;ubfnucosa,
in-filtratE>, w1th mucoc.l'l, ep1lh-l.1al
d '""y p n t r ,, I 1 '-- 11 1 , ( ,:. i__ 1 c, p u r. d c t c r m t r. P d
Oo7t>07, 91;MX.oon
4
liver__ill: t:entrllobular conge-stion ic;
i!dl"'enel (G): ThPn?
Js
jur,ction congE>stion.
nodG>t-a
I
I
corticomedullary
lung (l,J)I Tlese stlcticns prl!st'nt a varioC\bl!!' app>Arance.
Those in slide I a rto]alivvly nor mal, but r.:ont<"in !>Cflttered
foci oi erythrocyte ed iwed at with bacteria
as desctibttd, i tJistal'airways and alvPoli.
In othgr i!:'> pulmonary edema.
Gram St.3in tt"vl?.:ds thP bac.ter-ial, pupulation5 to consist at
Gram flfCQativ- c!ind G:am positivejrods, well as smaiJer-
numbers of Gram po'3itjve c.uLci. 1ln 1 ttf"' ar-e
sevare 1 y ;.1 t e>c ted, wi tit severe acute
pleural inflammc-diorl, oi li\rgE' numbe>rs of
neut.-ophil!'-.
D><: lung, !>evere neutrorhilic
iniillrdte, wtth
Dx: lung, heoron,-rhdyf:'
I
I
i
Cau .. "' of death in th1s is, probably shock associated
with The o1 from her cal-f
helps to suppOt-t lhjs suggesting a terminal
oeG?pticl!'mia. this, .it is to what the
initiating problwm in this no lesions suggesting
d primary viral etiology are thib not rule out
possibility that a may hYQ providgd the insult, with
the bacterial pulmu11ary in'iection then
1
coming in tills a secondary,
but major problem.
,
Sea World of Florida
Sea World of Florida Dr. Terry Campbell. Dr.
Walsh. Dr. Kintner, Or. Scott Wriaht
Orcinus orca
ID NVMBER: Oo7602 AGB: 15-16 years Sl!X: .f
DATE 07 DBATX: S/6/91 OATS OF NBCROPST; 8/6/91
Only) See sheet
WEIGR'l': 2445 Kg TOTAL L.EllGTii:
549 em
J+STORY
This adult female killer whale ex.'libited no medical problems since he::::-
arrival at Sea World cf Florida on 2/18/91 until 7/21/91 when she was treated
for an tooth. The animal remained clinically until 8/5/91
vhen she refused to eat after her first meal. Although she remained
and alert, she would not respond to her trainers
1
request tor contact. At
J:OO a.m.: twenty-four hour watch, her respiratory rate began to
increase. The veterinary and curatorial staffs were noti!ied immediately
and arrived to assess her condition. Cl'inically the animal's condition
deteriorated rapidly and she appearec to be incoherent to her
and exhi=iting gastric retching. She was coaxed into the medical peel
where she "Was given therapy for shock including
antibiotics, K, and oxygen. Minutes prior to death she exhalec
blood-tinged fluid from her blow. In spite of therapy, she cied at. 7: 15
a.m., apparently of respiratory failure.
2 I.O. NO. 007602_
GBNERAL E%TEBHAL AP?BARANCE: (oral cavity, external nares, skin, eyes)
The necropsy was performed with the animal in le!t recumbency. There
were no external indicators of trauma. The eyes and external nare were
claar. The oral cavity appeared normal. No swelling was !ound around the
lower third right tooth which had previously been infected.
SVBDEgKAL CQNPITION; (blubber, muscles, lymph nodes)
The ani=al was in good condition and had an adequate amount of blUbber. No
muscle pathology was detected and superficial lymph nodes appeared normal.
No significant gross lesions were found. The pterygoid sinus area clean
and free of parasites.
CENTRAL NERvous SYSTEM: (brain, pituitary, spinal cord)
The brain was removed in one piece for magnetic resonance imaging, gross
pathologic, and histologic evaluation. There were no significant gross
lesions.
TBORACIC CAVITY: (pleu::-a}
There were occasional patchy roci of ecchymoses and petechia on the parietal
pleura and diaphragm. Diffuse ecchymoses was also found on the dorsal costal
pleura ventral to the rete area. Approximately 300 cc or serosanguinous
fluid was found in the right hemithorax.
UPPER SYSTEM: (nasal sacs, nares, lQrynx)
No significant gross lesions were found in the nasal sacs, nares, and larynx.
?age 3 r.o.
LOWER RESPIRATORY SY&TXM: (trachea, bronchi, lungs, nodes)
The trachea contained a small amount ot blood tinged fluid. There were no
gross tracheal or bronchial lesions. The anterioventral one-third of each
lung was congested with the increased density giving it a dark red color.
Each lung had a 15 to 20 em elevated spherical area on the dorsal border one-
third of the way from the anterior leading edge. The spheres bulged 6 to 10
em above the surrounding lung contour. These lesions blended imperceptibly
into the more normal lung tissue. Hemorrhage and pattial liquefaction
necrosis when viewed on the cut surface. The lesions had no odor. The
major pulmonary appeared normal and free o! emboli. Approximately
50 percent of the lung tissue was hemorrhagic. There were several l""'21lllll
pigmented, subpleural tracts leading to the pulmonary skirt lymph nodes found
in both lungs. These tracts, possible lymph channels, were located on the
eentral portion of the lung and appeared to contain diluted blood. _ Both
skirt lymph nodes (those attacked by the ventral lung surface) were edematous
vith semi-clear fluid. Congestion and hemorrhage were present in a portion
of these lymph nodes.
SYSTEM; (heart, aorta, major vessels)
Pericardia! petechia and ecchymoses were seen in isolated areas. The heart
contained well formed current jelly clots and both ventricles stopped in
diastole. The heart and vessels were normal. There was approximately 500
ml of amber colored pericardial fluid that contained particulate material.
ABDOMINAL Cl.Y'ITlJ ( 1 ymph nodes)
The abdominal cavity contained a small amount of clear fluid. There was a
generalized enlargement of the lymph nodes. Several 5 em sized lymph nodes
(mesenteric) near the pancreas contained up to 3 or 4 fibrous spheres 8
in diameter. These spheres had necrotic centers and appeared to be healed
granulomas due to previous parasitism or infection.
PIGESTIVJ SYSTEM: (esophagus, stomach
1
intestine, cecum, rectum
1
lymph nodes}
The first compartment of the stomach contained a small amount of sand and
sm3ll round stones. Twrc G. 5 em healed mucosal ulcers "'ere found in the
junction between the first and second compartment of the stomach. A portior.
of the second stomach had everted into the first compartment.
Occasional ecchymotic lesions were found on the serosal surface of the
intestine beginning at the mesenteric junction and rotating bilaterally over
the intestine. The mucosa normal. One small ecchymotic lesion four.d
in the mucosa colon.
The liver was normal in size and shape. No significant gross lesions were
found.
?age 4
PMCREAS:
The pancreas was of normal size shape. It had a uni!ormly gray sur!ace.
The visceral surface contained a few petechial lesions. Several 0.5 em sized
sacculations ott the pancreatic duct contained a !ew l to 2 mm concretions.
SPLlUDI:
The spleen appeared normal except for a single 1.5 em diameter outgrowth.
UPRQPUCTin SISTJM; (testicles, ovaries)
The uterus contained a 12-month male !etus that appeared to have been .alive
until the dam died. A large corpus luteum was found on the left ovary.
Vl!INAEY SYSTEM: (kidneys, ureter, bladder, urethra)
Kidneys were of normal size and shape.
found in the urinary tract.
ADRENAL GLAlfi)S:
No signiricant gross lesions were
The right adrenal gland wa3 difrusely discolored !rom hemorrhage. The left
adrenal gland had a red cortex and a non-remarkable medulla.
SDLITAL SYSTEM:
No significant gross lesions.
PmBI'l'E S{OO(ARY:
No parasites were found.
SPECIAL TESTS;
Tissues submitted for histopathology,
anaerobic bacterial cultures, mycotic
toxicology.
cytology
cultures,
of fluids, aerobic
virus
and
and
?age 5 I.D. liO. Oo/6Q2
GROSS SUMMARY:
Bilateral pulmonary lesions characterized by hemorrhage, congestion, and
liquefaction necrosis- severe
Pulmonary pleura and pericardia! petechial and ecchymotic hemorrhage,
moderate
Generalized lymphadenopathy
Hemorrhaqe of the right adrenal- severe
110 lb. male fetus
TJHTATIVB DIAGNQ6IS:
- Acute hemorrhagic pneumonia, diffuse, severe, probably infectious in ori9in
- Septicemia
CQNCLUSIONl (after histology & clinical pathology review)
The cause of death in this animal was a severe, necrotizing, hemorrhagic,
bacterial pneumonia that resulted in a tatal overwhelming septicemia and
pulmonary anoxia.
Although a variety of bacteria were isolated by culture and seen en
histology, the primary pathogen was aeruginosa. The hemorrhage
!rom the blow prior to death resulted from the hemorrhagic lung lesions
andjor terminal disseminated intravascular coagulation [OICj as determined
by a positive fibrin split products test. The generalized lymphadenopathy,
petechia, and ecchymoses found on 9ross necropsy were associated with the
septicemia and DIC. The histologic chan9es seen in the liver and
associated with anoxia caused by the cardiovascular collapse just prior to
death. Several nodules along the gastrointestinal tract contained trematode
eggs indicating a previous infection with trematode parasites. The fluid
found in the thoracic cavity and pericardial !luict resulted from the
infections process. The corpus luteum was a corpus luteum of pregnancy.
The agonal, erratic observed in many dying cetaceans which often
results in additional trauma did not occur in this case because the animal
was restrained by personnel in the medical pool which did not allow !or
swiliil!ling room.
Page E I D NO . Q_o 7 6 0 2
has been recovered from numerous cetaceans which have
not shown any evidence of clinical illness and it is in
many areas including the gastroin.testinal tract of mammals. The same
organism in the lung was also found in the intestinal tract. The toxins that
can be produced by fseudomonas aeruginosa include hemolysin, !ibrinolysin,
elastase coagulase, endotoxin, enterotoxin and exotoxin. Some of the$e may
contribute to its pathogenicity. The rapid decline of this animal was due
to the overvhelming loss of functional lung tissue resulting !rom the
bacterial pneumonia and DIC.
DA'l'B : ___ ?-_: /_?_A_Y..;.../ __ _
DATE: _______ ____ _
I . /
SIGNED: J:r ;J_
Michael T. Walsh, DVM
7007 Sea world Drive
Orlando, FL 32821
1
' --
.- I / .' I
SIGNED: 2--t h
1
, '--;;:'i, r<?-.fJ.
Terry w Jcampbell, bVM, Pi?D
orlando, FL 32821
DEPARTMENT
OF COMPARATIVE AND
EXPERIMENTAL PATHOLOGY
Mr. Art Jeffers
Office of Protected Resources
United States Department of Commerce
National Oceanic and Atmospheric Administration
1335 East West Highway
Silver Spring, MD 20910
Mr. Jeffers:
College of \'eierinary \k.::-:1ne
PO Box 100145
Gaines,ille, florida 0-01 !S
(904) 392-1221
(904) 392-5426 FAX
September 24, 1991
Thank you for taking the time to talk to me today. As I mentioned in our phone
conversation, Dr. Ruth Francis-Floyd provided copies of the necropsy reports and
letters associated with the deaths of the two killer whales at the Sea World
Facilities located in Texas and Florida to me. I independently reviewed these
documents and believe that the deaths of these two animals were not related. The
facts are presented clearly and honestly. I cannot detect any evidence to
suggest that information has been knowingly omitted.
The cause of death in the whale located in Florida seems clear cut, as gross
necropsy findings, along with histopathological observations and culture results
support the diagnosis of acute, severe, necrotizing pneumonia due to Pseudomonas
a well recognized pathogen. Although several predisposing conditions may
allow this organism to grow, it is often not possible to identify these
circumstances by the time an becomes clinically ill.
The cause of death of the whale at the Texas facility is less straightforward.
The observations of the security guard and the lesions found at necropsy support
the diagnosis of trauma as the immediate cause of death. I don
1
t believe,
however, the reason for this animal's violent behavior prior to death can be
determined with certainty. As in this case, ganglioneuromas have primarily occur
in younger animals. Some of the clinical signs associated with intestinal
ganglioneuromas described in animals include straining, constipation, or gaseous
dilat,:ition of the intestines. While I know of no case in which violent behavior
occurred because of the presence of a ganglioneuroma, I would not absolutely rule
out this possibility. Though I would personally prefer to say that the cause of
the apparently self-induced trauma could not be determined at necropsy, relating
these findings is a reasonable interpretation.
Thank you for permitting me to review this information.
LR: jgm
Sincerely,
Lois Roth, D.V.M., Ph.D.
Diplomate, A.C.V.P.
,
J. Hillis Miller Health Science Center lnstitu:e of Food and Agricultural Sciences
', .''. '-'
HAM M 0 N D C 0 N SULTAN T S, IN C.
ANIMAL SPECIALISTS
123 N. STECKEL OR.
SANTA PAULA, CA. 93060
TEL: (805) 5259544 Fax# (805) 6438490
Ms. Ann Terbush, Chief, Permit Division
U.S. Department of Commerce, OPR, NMFS, NOAA
Permit Division, -SSMCI, Room 7324
1335 East-West Highway
Silver Spring, MD 20910
September 24, 1991
Dear Ms. Terbush:
I have reviewed the material you sent to me concerning the death of a Killer
Whale at Sea World of Florida and a second animal's death at Sea World of San
Antonio, Texas. I have also had Informal talks with some of the Sea anlmai
husbandry and veterinarian staff.
There appears to be three areas of review concerning the deaths of these two
Killer Whales:
a. Is the death of Killer Whale SWC 007602 due to an infective process?
b. Is the death of Killer Whale SWC 007803 due to trauma, and If so, was It self
Induced?
c. Are there any animal husbandry or veterinarian policies or procedures that
merit changing?
Review of Necropsy reports of Killer Whale SWC Q0-7602 (animal died August 6,
1991 at Sea World of Rorlda).
1. The necropsy was conducted In the presence of several competent
professionals. The tissue samples were sent to publicly funded facilities
that are well known for their unbiased work. '
2. The description of the gross pathology, histopathology and bacteriology
confirm that the Killer Whale SWC 00-7602 died from bacterial pneumonia that
was the result of a terminal overwhelming septicemia and pulmonary anoxia.
fJPr

I!V;r I . 'f
Rev1ew of Necropsy reports of Killer Whale SWC oo-7803 (animal died May 14, 1991
at Sea Wor1d of San Antonio, Texas.
1. The etiology of the death of this animal Is from trauma and the resulting
Injuries It suffered. The source of the trauma had to be sustanled from
a violent Impact. If the two accompanying whales had been Involved In
traumatizing this whale, all animals connected with the encounter would have
had some degree of injury. Physical examination of the two surviving whales
did not show any signs of trauma. The whale 00-7803 had none of the classic
"rakeM markings caused from teeth raking across the skin.
The descriptions given in the necropsy report and the night watchman are all
In keeping with self Induced trauma.
2. The assumption has to be made that whale SWC 00-7803 died from trauma It
received when the animal struck its body against the wall(s) of the pool
resulting In It own death. The difficulty remains as to how to account for the
animal's behavior resulting in striking Its body against the pool wall.
The necropsy and histopathology reports confirmed the presence of a small
tumor. There are medical reports that this cell type (see various pathology
reports In this brief), has In some species, produced sever pain. If the tumor
was malignant or not is academic at this point since there was only one tumor
found. The question remains If this tumor could crate sufficient pain to cause
. the animal to traumatize Itself resulting In its own death.
I find that the most probable working hypothesis Is that the presence of the
tumor could have caused a functional colic condition as well as producing a .,
primary source of pain. I experienced "colic" behavior in a killer whale
In Hong Kong. This animal would have sustained substantial bodily harm to
Itself had we not drained the pool and restrained the whale. A functional
obstruction Is one In which there Is no torsion or physical blockage of the
Intestinal tract A section of intestines lacks motility and/or is In muscle
spasm resulting in gas formation within the Intestinal tract. This symptom
alone Is sufficient to cause excruciating pain similar to that seen In horses
with colic.
Based upon the information given and having experienced treating a Killer
Whale with colic, I feel the correct diagnosis has been made of death due
to skull fractures and blood loss. The whale had experienced excruciating
pain In part or as the sole result of a tumor of neural origin. A resulting
"colic like" condition developed causing the whale striking its head
and body against the pool wall. '
2
Review of Animal Husbandary Procedures and Pracitices at Sea World:
Sea World has had a marine breeding program for several years. Their
dolphin breeding program has produced some 35 calves. In fact, Sea World
has not had to capture any dolphins for their performance or feeding pools
since the late 1970's. This Is by far the best breeding program of any facility
world wide.
Sea World has undertaken to breed Killer Whales and has had 7 successful
births. Six of the calves are still alive. The one calf that died had a
congenital heart disease and died of natural causes. Considering that 45%
of all Killer Whale calves In the wild die within the first 18 months of life, the
longevity of the calves at Sea World is exceptional.
When any killer Whale becomes ill or requires any unusual medical treatment,
the veterinarian attending the whaie immediately faxes all pertinent
Information to all other veterinarians at the various parks 1n the Sea World
complex. This affords the other veterinarians a chance to participate
from the Immediate onset of the problem to its conclusion. In addition, there
are weekly telephone conference calls between all veterinarians at all
locations.
Each veterinarian responsible for marine mammals, visually checks his
animals twice dally and meets with the trainers and lay staff at least once
a day. Routine physical and blood and blow hole samples are taken at that
time.
The success of the dolphin breeding program provides a strong indication of
how successful the animal husbandry program is at the various Sea World
locations.
I find no reason for Sea World Inc. to change any of Its procedures or policies
regarding the husbandry of Killer Whale or Dolphin programs.
Sincerely yours,/- J
1\/
Hammond
D.V.I\'Y . .
I
.3
University of Florida
Institute of Food and Agricultural Sciences
School of Forest Resources and Conservation
UNIVERSITY OF FL0"t0A
DEPARTMENT OF FISHERIES AND AQUACULTURE
Telephone: 904/392-9617
September 27, 1991
Mr. Art Jeffers
Office of Protected Resources
United States Department of Commerce
National Oceanic and Atmospheric Administration
1335 East West: Highway
Silver Springs, MD 20910
Dear Mr. Jeffers,
7922 N.W. 7151 Street
Gainesville, Florida 32606-0300
At your request, I have reviewed the necropsy reports and
related correspondence for killer whales #SWF-Oo-7803 and #SWC-Oo-
7602 which died in Sea World parks earlier this year. With your
permission, I forwarded this information to Dr. Lois Roth, a board
certified veterinary pathologist, for independent review. Dr. Roth
will forward her findings under separate cover.
Following careful review of all documents, it is my opinion
that there is no association between the two deaths. Each mortality
represented an isolated incident, and, in my opinion, neither event
could have been anticipated or prevented. It is an unfortunate
coincidence that these mortalities occurred within a few months of
each other, but I see no linkage between them. From this point on
I shall discuss the two mortalities separately.
The first incident involved a mature female killer whale
(#SWF-Oo-7803) which died suddenly, and traumatically, on May 14,
1991 near 6:00 am. The event occurred at Sea World of Texas. The
incident was observed, and reported immediately, by security staff.
Animal care personnel arrived within 10-15 minutes. Necropsy of
this animal was initiated within three hours of death. Prosectors
included an independent veterinary pathologist and an independent
veterinarian.
There seems little doubt that the immediate cause of death in
this animal was head trauma caused by collision with the concrete
pool wall. The principle concern, therefore, seems to be hat
caused the whale to behave in such a violent, and ultimately fatal,
manner.
,
The security report seems to adequately rule out interaction
with other whales which might have resulted in fatal injury to
whale SWF-Oo-7803. The security report states, "the other nale
and female whales were ... very calm, and floating on the surface"
T'e of Fooc and Agncultural Sciences is an Equal Employm;1 Opportumty- Atf.,mahve Actton Employer aumomed lo provide educatoonai
S'f'w'tces only 10 mc:v1duals and mst1tut10rs that 1unct.on wtlhout regard to race. cotor. sex. c.gt. handtca; or ':'rtgtn.
:cc ,- c . '. .,., '"' 1-'-'': FCONOf.ICS STP.TE OF FLOFli')t. IFt_C FLC" -:;t.
during the incident. If one or both of these animals had been
involved in the incident they most likely would have been swirring
around the pool at a rapid rate of speed, possibly chasing the
animal which died. This was not observed. Lack of involvement by
the other whales seems to be further substantiated by the lack of
"recent rake marks" on the dead animal, and lack of trauma or rake
marks on the surviving whales.
The question remains as to what would cause this animal to
thrash violently enough to incur multiple skull fractures and fatal
injury. Sea World has hypothesized that acute abdominal pain,
caused by a tumor (neurofibroma/ganglioneuroma) in the distal small
intestine, resulted in the behavior observed. This assessment seems.
plausible. Cetaceans are particularly prone to abdominal discomfort
from bowel distention because of the restricted space within the
peritoneal cavity (Sweeney, 1990). Distended loops of bowel were
not reported on the gross necropsy report for this animal, however
prosectors did observe thick brownish-red liquid in the jejunum,
anterior to the tumor. In addition, the animal's history of erratic
appetite is consistent with intestinal disease (Sweeney, 1990). The
animal's appetite had been irregular for at least 6 months prior to
death, and this behavior had been attributed to convalescence from
an apparently unrelated medical problem which was successfully
treated in the fall of 1990.
It is worth mentioning that there is precedent for self-
inflicted injury in captive killer whales. In the early 1970s a
male killer whale housed in Miami hit an observation window with
enough force to break the window, causing loss of a significant
volume of water, and slicing off the end of his nose. The attending
veterinarian for that incident was Dr. Jesse White. I have listed
Dr. White's present address and phone number at the end of this'
letter should you wish to contact him with specific questions about
that event.
A final point concerns speculation about an "unidentified
foreign body" contributing to hemorrhage in the mediastinum of the
dead whale. Ingestion of foreign body certainly has a place on the
differential diagnosis for a captive cetacean which died suddenly,
however, in this case the facts seem to effectively rule out this
possibility. In my own mind, the severity of the trauma which was
observed seems sufficient to cause substantial soft tissue injury
which could include hemorrhage in the mediastinum. The esophagus
and major blood vessels in an animal of this size are sufficiently
large that a laceration or other abnormality should be apparent
during gross necropsy. In addition, ingestion of foreign body is
generally considered a preventable disease (Sweeney, 1990).
Prevention is achieved through close surveillance of pools housing
marine mammals, particularly those where public v ~ w i n g is
permitted. Sea World had taken this precaution as evidenced by
assignment of security personnel to the killer whale pool around-
the-clock.
The death of whale # SWC-Oo-7602 at Sea World in Orlando
occurred near 7:00 am on August 6, 1991, less than 24 hours after
the whale first showed behavioral signs of illness. The animal was
necropsied the same day. Prosectors included two staff
veterinarians, and two independent pathologists. Tissues collected
during the gross necropsy were submitted to three separate
veterinary pathology laboratories. The final diagnosis was the same
from each of these independent laboratories. The whale died of an
acute necrotizing pneumonia of bacterial origin. The pathogen
Pseudomonas aeruginosa was isolated from the respiratory tract of
the dead whale as well as from the 12 month fetus which died in
utero. Fatal consequences of this acute bacterial infection
included septicemia, probable endotoxemia, and terminal
disseminated intravascular coagulation (DIC) . Given the grave
nature of these sequelae it is difficult to imagine how the outcome
for this animal might have been changed.
The rapid onset of illness and mortality reported in this
animal is consistent with other Pseudomonas infections reported in
captive cetaceans (Liong et al., 1985). Bacterial pneumonia is the
most common cause of mortality in captive dolphins (Sweeney, 1986)
and it is not uncommon for behavioral signs of disease to be masked
until the disease process is quite advanced (Sweeney, 1990).
In summary, the loss of Sea World killer whales #SWF-Oo-7803
and #SWC-Oo-7602 is a tragic loss, but it is my opinion that the
deaths of these animals could not have been anticipated or
prevented. Independent pathologists and other specialists have
contributed to the knowledge base for each animal. Information has
been presented in a forthright and honest manner by Sea World
staff.
Thank-you for the opportunity to review these materials. If I
can be of fuither assistance to you please do not hesitate to
contact me.
Sincerely,
~ ~ C V v Lv'1- (r- \v\. \d
Ruth Francis-Floyd, DVM, MS
Assistant Professor
Aquatic Animal Medicine
I
Literature Cited:
Sweeney, J. C. 1990. Marine Mammal Behavioral Diagnostics. In:
Handbook of Marine Mammal Medicine: Health, Disease, and
Rehabilitation, L.A. Dierauf (ED). CRC Press, Boca Raton, FL. pp
53-72.
Liong, E.; Hammond, D.o.; Vedros, N.A. 1985. Pseudomonas
pseudomallei infection in a dolphin (Tursiops gilli): a case study.
Aquatic Mammals 11:20.
Sweeney, J.C. 1986. Infectious Diseases (marine mammal section).
In: Zoo and Wild Animal Medicine, Second Edition, M. Fowler (ED).
W.B. Saunders Co., Philadelphia PA. pp 778.
Additional Resource:
(Re: self-inflicted trauma in captive killer whales)
Dr. Jesse White
12025 N. Elkcam Blvd.
Dunnellon FL 32630
(904) 489-8142
SEA WORLD
FACILITY: Sea World of Florida PROSECTOR: T.W. Campbell and M.T. Walsh
Tursiops truncatus
ID NUMBER: MH-82-221-Tt AGE: est. 25 yrs SEX: female
DATE OF DEATH: 1/16/91 DATE OF NECROPSY: 1/16/91
MORPHOMETRICS: (metric only)
WEIGHT: 175 Kg
TOTAL LENGTH: 242 em GIRTH AT AXILLA: 125 em
GIRTH AT ANUS: 84 em FLUKE WIDTH: 72 em
GIRTH AT UMBILICUS: 135 em DORSAL FIN HEIGHT: 26 em
HISTORY:
days prior to her death, this animal had a history of anorexia, but ap-
peared otherwise normal. She was examined on the day before her death and
was determined to be suffering from renal failure, based upon her blood
chemistries [elevated BUN, Creat. and Phos] and urinalysis [hematuria,
proteinuria, marked number of renal epithelial cell, and cellular
Her leukogram showed a leukopenia with a marked left shift and toxic
neutrophils. Treatment for primary renal failure was initiated, but she
died the next day while administering therapy. A necropsy was performed im-
Dediately following her death.
,
l
PAGE 2 12 NO. MH-82-221-Tt
(oral cavity, external nares, skin, eyes)
The oral cavity contained many small round hyperemic lesions primarily in
the area of the palate. These lesions were not present the day before. No
other significant gross lesions were observed.
SUBDERMAL CONDITION: (blubber, muscles, lymph nodes)
NSGL [No Significant Gross Lesions)
NSGL
NSGL
NSGL
NSGL
LOWER RESPIRATORY SYSTEM: (trachea, bronchi, lungs, lymph nodes)
NSGL
CARDIOVASCULAR SYSTEM: (heart, aorta, major vessels)
NSGL
2
PAGE 3
HH - S2-.221-Tt
CAVITY: (lymph nodes)
NSGL
DIGESTIVE SYSTEM:(esophagus,stomach, intestine, cecum, rectum, lymph nodes)
NSGL, the gastric and intestinal mucosa appeared healthy.
LIVER: (biliary system}
NSGL
PANCREAS:
NSGL
SPLEEN:
NSGL
REPRODUCTIVE SYSTEM: (testicles, ovaries}
NSGL, three corpus albicans were noted on the left ovary and one on the
right ovary.
The kidneys appeared slightly enlarged and contained numerous small gray to
green stones throughout the parenchyma. The .urinary bladder was full of
urine and appeared thickened, but contained no calculi.
ADRENAL GLANDS:
NSGL
SKELETAL SYSTEM:
NSGL (saved for anatomical study)
SUMMARY
No parasites were found.
SPECIAL TESTS
Necropsy tissues were collected in 10% NBF for routine histology. The renal
stones were submitted for stone analysis. Tissues were also collected for
heavy metal and pesticide analysis as a routine procedure., Microbial cul-
tures were taken from the lung, intestines, liver, and kidney.
3
::i:D NO.
GROSS SUYJV..RY
Bilateral nephrosis with renal calculi.
TENTATIVE DIAGNOSIS:
Death was due to renal failure. The cause of the renal disease and renal
stone formation will depend upon information collected from the histology
and stone analysis.
Stone analysis : subcrystalline ammonium acid urate, with protien matrices.
CONCLUSIONS: (after histology & clinical pathology review)
Histologic findings suggested the cause of death was related to cardiovas-
cular collapse resulting in multifocal renal tubular necrosis and
congestion. The cardiac lesions indicated myocardial fibrosis involving the
Purkinje fibers which may have resulted in a conduction block to a portior.
of the myocardium resulting in cardiac failure. Cardiac disorders such cs
this are common in geriatric animals.
DATE: 4/23/91
Terry W. Campbell, DVM, PhD
SV.. WORLD
FACILITYz Sea World of California PROSECTOR: T. H. Reidarson< D.V.M.
GENUS/SPBCIES: ________
ID NUMBER: SWC-Cc-8327/ SW 91032 AGE: ____ SEX: ___
DATB OF DATE OF NECROPSYs ___
.Erl'ERNAL MORPHOME'l'RICS: (metric only)
WEIGHT: __
BLUBBER TBICKNESS: _______
TOTAL LENGTH: ____
GIRTH 'I.T AXILLA: 81 em

GIRTH AT ANUS: __
FLUKE WIDTH: __________
GIRTH AT UMBILICUS: _____ DORSAL FIN HEIGHT: _______
HISTORYa This animal was collected on 11/24/83. She has successfully given
birth to two calves. She was in her last trimester of pregnancy with
drop in serum progesterone. On 5/6/91 ahe became lethargic and anorexic,
swimming occasionally with the other animals. A blood sample was taken as
well as cultures of the blowhole, anus and vagina. The blood demonstrated
leukocytosis with mature left shift. Chemistries demonstrated mild
dehydration and moderate liver emyme elevation. Based on lab work, we
ascertained that she had a fairly severe infection, and we immediately
instituted antibiotic therapy. She died approximately two hours after he;
second treatment.
Code, in parentheses, for samples takent
C culture7 V - virology, M metals7
P = pesticides, E = electron microscope samples
------------------------------------------------------------------------
EXTERNAL APPEARANCE: (oral cavity, externQl nares, skin, eyes)
There is an abrasion over the right eye. The animal's is very good.
SUBDERMAL CONDITIONs (blubber, muscles, lymph nodes)
The blubber layer is 2 em thick over the lateral thorax.
CRANIAL EXAM: (ears, melon, pterygoid sinus}
No gross leeions.
CENTRAL NERVOUS SYSTEMt (brain, pituitary, spinal cord)
Normal. The brain i 725 gm.
I
PAGE 2 I.D. NO. SWC-Cc-8327/ SW 91032
No gross lesions.
UPPER RESPIRATORY SYSTEMs (nasal sacs, nares, larynx)
No gross lesions.
LOWER RESPIRATORY SYSTEMs (trachea, bronchi. lungs, lymph nodes)
There are multiple 1-3 em firm nodules throughout all the lung lobes. The
pultnonary lymph nodes are enlarged and have adhesions to the parietal
pleura. Many nodules contain yellow 3-5 mm crystaline structures within
the capsule. Many bronchi contain light green mucopurulent material.
CARDIOVASCULAR SYSTEMs {heart, aorta, major vessels)
No gross lesions.
.No gross lesions.
DIGESTrvE SYSTEM: (esophagus, stomach, intestine, rectum, cecum,
lymph nodes}
There is partially digested fish in the first and second chambers of the
stomach. Several fibrin strands are evident on the surface of the small
intestine and liver.
LIVERs (biliary system)
No gross lesions.
PANCRRASa
No gross lesions.
SPLEEN:
No gross lesions.
REPRODUCTrvE SYSTEMs (testicles, ovaries)
There is a late term fetus with a patch of sloughed epithelium from the
left lower lip. The placenta is completely detached from the uterus
purulent material contained within the space... The amniotic fluid is very
dG.rk.
URINARY SYSTEMs (kidneys, ureter, bladder, urethra)
The urine is dark brown.
GLANDS 1
Normal.
SKELETAL SYSTEM:
Normal.
I
?AGE 3 r.D. No. swc-cc-8327/ sw 91032
SPECIAL TESTS: Histopathology of pulmonary lymph nodes, bronchi, heart,
kidney, liver and spleen. Culture of heart blood, pulmonary scare, kidney
and bronchi, as well as fluids from the pleural space, urine amnionic sac
and placenta.
Old pneumonia scars. GROSS SUMMARY: 1)
2)
4)
5)
Purulent endometritis and placentitis with fetal death.
Focal purulent pneumonia.
Mild fibrinous peritonitis.
TENTATIVE DIAGNOSIS& Bronchopneumonia, and placentitis.
Early fetal death due to from endometritis, placentitis and broncho-
which ultimately lead to death of the mother.
DATE : __ ,_-_t__'1_1 ___ _
,
SEA WORLD
Facility: Sea World of Texas Prosector: Dr. Dalton
Genus/Species: Zalophus californianus ID t: swc-zc-8746
Age: Pre Act sex: Female
Date of Death: 7/26/91 Date of Necropsy: 7/26/91
EXTERNAL MORPHOMETRICS: (metric only)
WEIGHT: 118.2 kg
HISTORY:
This animal was in good health until February of 1991, when she presented
with sporadic inappetence. A clinical workup, to include radiographs and
ultrasound, revealed right side heart failure and ascites indicative of
peritonitis. The prognosis at that time was grave. The animal
appeared to have recovered by the end of April. Death was sudden on 7/26/91.
A 4 mm wart type mass in the skin caudal and slightly medial to the right
eye.
Blubber was brownish yellow.
No lesions noted.
Not examined.
THORACIC CAVITX: {pleura)
No lesions noted.
No lesions noted.
PAGE 2 ID NO. SWC-Zc-8746
LQWER RESP!&ATQRY SYSTEM: (trachea, bronchi, lungs, lymph nodes)
Lungs appeared congested and were a deep purplish-red.
Lymph nodes were enlarged.
The right A-V valve was thickened and nodular. The right ventricular wall
appeared thin.
The abdominal cavity was filled with a green, putrid liquid containing 2-5
mm white clumps. The omentum was brick red with multiple adhesions.
DIGESTIVE SYSTEM: (esophagus, stomach, intestine, cecum, rectum, lymph
nodes)
Multiple areas of petechial and ecchymotic hemorrhage were observed
throughout the GI tract. A 5 em mass (walled off, ruptured abscess) was
found approximately midway through the small bowel. A 3 mm hole allowed
intestinal contents to escape into the abdomen.
No lesions noted.
PANCREAS:
No lesions noted.
SPLEEN:
No lesions noted.
The serosal surface was inflamed. The right uterine horn contained a 6 mm
X 20 mm cyst, 5 em from the ovary.
The serosal surface of both kidneys and the bladder were inflamed.
ADRENAL GLANDS:
,
The serosal surfaces were inflamed.
SKELETAL SYSTEM:
Not examined.
PAGE 3 ID NO. BWC-Zc-8746
PARASITE SUMMARY:
No parasites observed.
GROSS SUMMARY:
1. 5 em mass in small bowel
2. greenish-red foul smelling fluid in abdominal cavity
CONCLUSIONS:
A ruptured small bowel abscess resulted in peritonitis and death.
D a t e ~ /f'f'/
Sign d: ~ (f)JL l fif//Frl.
;
SEA WORlD
Facility: Sea World of Texas Prosector: Dr. Leslie Dalton
Genus/Species: Zalophus californianus ID f: SWC-Zc-8747
Age: Pre Act Sex: Female
Date of Death: 6/12/91 Date of Necropsy: 6/12/91
EXTERNAL MORPHOMETRieS: (metric only)
WEIGHT: 141 kg
TOTAL LENGTH: 185 em GIRTH AT AXILLA: 110 em
GIRTH AT ANUS: NA FLUKE WIDTH: lift
GIRTH AT UMBILICUS: DORSAL FIN HEIGHT: NA
HISTORY:
This animal was acquired from Marineland of California in 1987. She had a
cataract removed frc:ra her right eye in April of 1989. Recovery was
uneventful. It was noted that her abdomen appeared distended in February of
1991. A paracentesis was performed and the fluid was submitted for cytology.
The animal was radiographed and ultrasounded on March 2, 1991. Multiple
masses were noted throughout the abdomen. A diagnosis of neoplasia was made
with a grave prognosis. The animal continued to eat well until June 11,
1991. She was re-evaluated using ultrasound and the decision was made to
euthanize her due to the number and size of the masses in the abdomen as well
as due to the animal's behavior.
Superficial abrasion, 4 em X 3 em, over:. dorsal edge of left scapula.
DENTITION: I R L c R L PC R L
1 1 1 1 4-2
0 0 1 a 2 1
All lymph nodes appeared enlarged.
Not examined.
Not examined.
TnO&ACIC CAVITY% (pleura)
No lesions noted.
No lesions noted.
The lungs were a mottled brownish red and heavy.
Slight enlargement of the right ventricle.
All lymph nodes appeared to be greatly enlarged. Multiple white solid
and fluid filled masses were found throughout the abdominal cavity. The
smallest mass was a few grams measuring 5 mm and the largest mass was
35 em in diameter and weighed 23 kg. The main mass was attached to the
root of the mesentery and the greater curvature of the stomach was
adhered to the center of the mass. Numerous masses where found
throughout the mesentery and floating free in the abdominal cavity. The
caudal diaphragm had numerous areas of fibrous tags and 2-4 mm white
nodules on it.
DIGESTIVE SYSTEM: (esophagus, stomach, intestine, cecum, rectum,
lymph nodes)
The stomach was adhered to the center of a 23 kg mass attached to the
mesenteric root.
Pale brown and uniformly mottled.
PANCREAS:
No lesions noted.
SPLEEN:
An old scar, 3 em, in the mid distal third, very little blood in the
spleen and it lacked substance.
I
Follicles were observed on both ovaries.
The kidney's were uniformly pale with multiple light areas observed
throughout.
PAGE 3 ID NO. BWC-Zo Q7i7
ADRENAL GLANt)St
No lesions noted.
SKELET,_L SYSTEM:
The costochondral junctions of ribs 7 and 8 on both the right and left
side were enlarged.
P,_RASITE SUMMARY:
No parasites observed.
SPECIAL TESTS:
Histopathology
left prescapular LN
abdominal mass #1
abdominal mass #2
kidney
GROSS SUMMARY:
liver Mesenteric LN
lung
stomach
left adrenal
1. Dozens of white masses throughout the abdominal cavity.
2. Fibrous tags and small nodules on abdominal diaphragm.
3. Lungs brownish red and heavy.
Chondrosarcoma
This animal had a chondrosarcoma occupying most of the abdominal cavity.
This neoplasm is of cartilage origin and appeared to have metastasized from
the costochondral junctions of ribs 7 and 8.
Department of Laboratory Animal Resources
July 11, 1991
Accession Number: 91T6-70
The University of
Health Science unter at San Antonio
7703 Floyd Curl Drive
San Antonio, Texas 78284-7859
(512) 567-6166
Animal Number: 708177586
Submitted by: Dr. Dalton
Histopathology:
lymph nodes -
kidney -
liver -
adrenal gland -
lung -
stomach -
intraperitoneal
masses -
prescapular and mesenteric. There was
lymphoid hyperplasia in both nodes. There
was edema and erythrophagocytosis in the
mesenteric node.
glomerulonephritis, minimal to moderate,
characterized by thickening of glomerular
basement membranes, increased mesangial
matrix, occasional interstitial
accumulations of mononuclear leucocytes,
and an occasional senescent glomerulus.
Minimal nephrocalcinosis characterized by
an occasional mineralized tubule.
no lesion
no lesion
no lesion
no lesion
these masses were composed of mesenchytr.al
tissues differentiating into neoplastic
cartilage. The cartilage was composed of
large bizarre chondrocytes in a basophilic
chondroid matrix. The cartilage was
hypercellular and some lacunae contained
two chondrocytes. Mitotic figures were
not found. In some areas a tion
from stellate shaped primitive mesenchymal
cells to chondroblasts to chondrocytes
could be seen. There was extensive
necrosis and cystic degeneration within
the deeper portions of the masses.
Page Two
Accession Number:
Animal Number:
91T6-70
708177586
Diagnoses: 1.) chondrosarcoma 2.) glomerulonephritis
Comment:
If a primary skeletal chondrosarcoma cannot be found this neoplasm
should be considered an extraskeletal chondrosarcoma. I consulted
with Dr. T. B. Aufdemorte, Pathology Department, UTHSCSA and he
concurs with the diagnosis of chondrosarcoma.
~ CS::d1.V.M., Ph.D.
RRC:mkh
,
SEA V/ORLD
FACILITY: SEA WORLD OF OHIO PROSECTOR: DR. SAM DOVER
GENUS/SPECIES: Cystophora
ID NUMBER: 910311-07 AGE: approx. 3 years SEX: Female
DATE OF DEATH: 3/11/91 DATE OF NECROPSY: 3/11/91
EXTERNAL MORPHOMETRICS: (r.,etric only}
WEIGHT: apprsx. 350 lbs
TOTAL LENGTH: SEE SHEET GIRTH AT AXILLA:
GIRTH AT ANUS: FLUKE WIDTH:
' GIRTH AT UMBILICUS: DORSAL FIN HEIGHT:
HISTORY
This juvenile female Hooded Seal was found beached at Falmouth, MA. c:-.
7/6/89. She was picked up by the New England Aquarium Marine Manmal
Rescue team and taken to their facility. At that time, she was
dehydrated, and depressed. She tested positive for
microfilaria and lungworc. She was treated with antibiotics
C:-: s:-:e ::as transferred to Sea l-Jorld of .... :..
did well here until 3/5/Sl her appetite began to gradually
decrease. CBC and indicated increased WBC with a
left shift. Treatment was begun with clindamycin BID,
SID, and Banamine every other day for two treatments. She
c l ert and c::ct:. ve ho'..:ever, continued- -tc l::.e anorexic. 0;. 3 11 "?:.
i:Bc .-:as teginnir1g to S.e.:::::ease whil9, l":Er creatine, c:Jd sE:-.:-
levels sig;.ificantly Intravenous fluid
therapy was tegun, she expired after
completed.
,
?P.Gf. 2 ID NO. 910311-07
GENERAL EXTERNAL APPEARANCE:
eyes)
(oral cavity, external nares, skin,
Good weight, no external abnormalities seen.
Adequate blubber layer, no muscular abnormalities seen. Axillary and
mandibular lymph nodes pale.
No visible lesions.
No visible lesions.
, THORACIC CAVITY: (pleura)
No visible lesions.
No visible lesions.
Lungs slightly purple, bilateral pulmonary edema, several multifocal
areas of subcapsular hemorrhage.
Slightly enlarged heart. Myocardium of_right ventricular wall appears
. r_hin ( 5 r:-,;.,) .
ABDOMINAL CAVITY: (lyr:-.ph nodes)
No visible lesions.
DIGESTIVE SYSTEM:
l y:r.lph nodes)
(esophagus, stomach, intestines, cecum, rectum,
,
Several rocks in stomach (in the pylorus) - 4 gastric ulcers in area
of lesser curvature - all actively hemorrhaging, ranging in size from
5 nrn to 25 mm in diameter. Distal jejunun has several areas of mural
hemorrhage and distention. All mesenteric lymph nodes pale.
~ o r m l size, uniform appearance, slightly pale.
PAGE J ID NO. 910311-07
PANCREAS:
No visible lesions.
SPLEEN:
Grossly enlarged, friable, normal color.
No visible lesions.
Kidneys - subcapsular hemorrhage bilateral. No other visible
ADRENAL GLANDS:
Hemorrhagic at cranial pole, pale at caudal pole, bilateral.
SKELETAL SYSTEM:
No visible lesions.
PARASITE SUMMARY:
No visible lesions.
SPECIAL TESTS:
HISTOPATHOLOGY:
CULTURES:
urinalysis
muscle
heart
kidneys
pancreas
lung
kidney
urine
ovaries
blubber
diaphragm
liver
brain
liver
brain
spleen

lungs
adrE:nals
spleen
:!.ntestine
: ::: l- c :.. r, L. E: st. i n e
I D NO. _QJ_ ____
GROSS SUMJI..ARY
Pulmonary edema with multifocal subcapsular hemorrhage, slightly
distended right ventricle, multiple gastric ulcers with foreign bodies
(stones) present, 2 regions of jejunal mural distention and
hemorrhage, enlarged and friable spleen, hemorrhagic adrenal glands,
bilaterally subcapsular renal hemorrhage.
TENTATIVE DIAGNOSIS:
Acute renal failure, gastric ulcers, cardiovascular collapse.
CONCLUSIONS: (after histology and clinical pathology review)
Focal acute pyelonephrltis, suspect bacterial etiology histologically
however no growth on culture. The lack of growth could be a result of
the antibiotic therapy. Mild to severe congestion of spleen, lungs,
liver and brain, all appear to be a result of cardiovascular collapse.
There are several gastric ulcers with resulting hemorrhage visible in
the distal small intestine. These ulcers could also be a result of
the uremia.
DATE: SIGNED:
l l

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