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Elephant
Bibliographic
Database
www.elephantcare.org
References
Updated October 2007
1.
Ruf, T., Valencak, T., Tataruch, F., and Arnold, W. Running Speed in
Mammals Increases with Muscle n-6 Polyunsaturated Fatty Acid Content.
PLoS ONE. 2006 Dec 20;1:e65. 2007.
Ref Type: Electronic Citation
Abstract: Polyunsaturated fatty acids (PUFAs) are important dietary
components that mammals cannot synthesize de novo. Beneficial effects of
PUFAs, in particular of the n-3 class, for certain aspects of animal and
human health (e.g., cardiovascular function) are well known. Several
observations suggest, however, that PUFAs may also affect the
performance of skeletal muscles in vertebrates. For instance, it has
been shown that experimentally n-6 PUFA-enriched diets increase the
maximum swimming speed in salmon. Also, we recently found that the
proportion of PUFAs in the muscle phospholipids of an extremely fast
runner, the brown hare (Lepus europaeus), are very high compared to
other mammals. Therefore, we predicted that locomotor performance,
namely running speed, should be associated with differences in muscle
fatty acid profiles. To test this hypothesis, we determined phospholipid
fatty acid profiles in skeletal muscles of 36 mammalian species ranging
from shrews to elephants. We found that there is indeed a general
positive, surprisingly strong relation between the n-6 PUFAs content in
muscle phospholipids and maximum running speed of mammals. This finding
suggests that muscle fatty acid composition directly affects a highly
fitness-relevant trait, which may be decisive for the ability of animals
to escape from predators or catch prey.
2.
Langbauer W., Philp K., Frydman G. and Galvanek J. 2006.
The effect of
human contact on African elephant heart rate. Proceedings International
Elephant Conservation & Research Symposium., 2006, pp. 253-255.
3.
Suedmeyer W.K. and Fine D. 2006. Indirect oscillometric blood pressure
measurement in four African elephants (Loxodonta africana).
2006 Proceedings American Association of Zoo Veterinarians, pp. 170-172.
Abstract: The elephant is the largest living land mammal and in danger
of extinction. The few literature citations involving blood pressure
(BP) measurements have utilized direct arterial measurement of
immobilized or stationary conditioned elephants. These investigations
determined that BP's in the healthy elephant are generally higher than
most other clinically normal mammals studied but similar to unsedated
domestic cattle and horses, and increased in laterally recumbent
elephants. This project was undertaken to compare cited direct arterial
measurements to indirect oscillometric BP measurement of systolic,
diastolic, and mean arterial pressure (MAP), and heart rate (HR) in four
stationary, non-sedated African elephants. Four female African elephants
ranging in age from 28-38 yr of age were used in this study. One
elephant (E3) had a history of fetal retention of 5 yr and bilateral
scleral injection but was clinically normal in all other regards. The
three remaining elephants had no significant clinical histories. All
four elephants were conditioned to present the tail for placement of a
standard occlusive BP cuff (Cardell™, CAS Medical Systems, Inc.
Branford, Connecticut 06405 USA). Use of this indirect oscillometric
unit has been compared with simultaneous direct arterial measurement in
anesthetized African lions (Panthera leo), and an immobilized African
elephant at the Kansas City Zoo. Blood pressure results in each animal
studied were virtually identical in both techniques. The width of the
cuff was approximately 40% the circumference of the tail (12 cm cuff on
an average 27.5 cm tail circumference) of the elephant, in accordance
with general recommendations for obtaining BP measurements in domestic
animals. Cuff placement was at the distal extent of the caudal tail
fold. Three sets of BP's, heart rates, and respiratory rates were
obtained on three different occasions in each elephant (Table 1). Each
elephant was sampled at the same time of day and had not been exercised.
Blood pressure measurements obtained in three of the four elephants in
this population compared favorably with reference ranges obtained
invasively (direct arterial) in unsedated African elephants. In the
elephant with scleral injection and retained fetal mummy (E3), overall
BP measurements were higher, on average, than the other three elephants
and ranges reported in a previous study of direct arterial pressures in
unsedated African elephants. This may reflect a hypertensive state
related to increased systemic vascular resistance associated with a
retained calf. However, this elephant is the oldest of the four animals
studied, and blood pressure parameters generally increase with age in
humans and this may be the case with this elephant. Further
investigation into the potential causes for a clinical hypertensive
state in this elephant is being pursued. The advantages of this
technique are the non-invasive application, portability, and comparable
results to direct arterial measurement. Disadvantages are that BP
measurement can be altered by cuff size, placement, and movement. In
this study, cuff placement and size was identical in all elephants, and
the only movement was associated with masticatory efforts involved with
positive food enrichment, eliminating two of the three variables.
Additional elephants are being evaluated and refinement of BP
measurement techniques is being completed to help define normal indirect
oscillometric BP values in the African elephant. Use of an indirect
oscillometric measuring device for obtaining BP measurements in African
elephants may prove to be an easily applied valuable ancillary
diagnostic tool when evaluating cardiovascular parameters without the
need for sedation or immobilization.
4.
2002. Large Animal Internal Medicine. Mosby, St.Louis, pp.1-1735.
5.
Cheeran J.V., Chandrasekharan K. and Radhakrishnan K. 2002.
Tranquilization and translocation of elephants.Journal of Indian
Veterinary Association Kerala 7: 42-46.
6.
Geddes L.A. 2002. Electrocardiograms from the turtle to the elephant
that illustrate interesting physiological phenomena.Pacing Clin
Electrophysiol 25: 1762-1770.
Abstract: This article describes a collection of ECGs from many species
obtained over the past 50 years. Presented are ECGs of species in which
the pacemaker is a separate contractile chamber with its own action and
recovery potentials. In such species, pacemaker atrial and AV block can
be produced. Shortening of the atrial refractory period and the negative
inotropic effect can be produced by vagal stimulation. The cardiac
electrogram and stroke volume are recorded from the turtle heart. The
ECG and respiration were recorded from the snake. ECG records were
obtained from the anesthetized and decapitated housefly. ECG records of
the rabbit show slowing when the nose encountered irritating vapors.
Records from a dog with atrial fibrillation exhibit rhythmic
fibrillation frequency changes correlated with respiration. In addition,
in a morphinized dog with atrial fibrillation, impulses crossed the AV
node only during inspiration. The ECGs of a cow and camel exhibit long
P-R intervals and biphasic P waves. Finally the elephant ECG shows a
clear U wave following the T wave.
7.
Pitts N.I., Mitchell G. and Raath C. 2002. Succinylcholine overdose in
the African elephant (Loxodonta africana) and impala (Aepyceros melampus):
pharmacokinetics, pharmacodynamics and physiological responses.South
African Journal of Science 98: 581-588.
Abstract: We investigated the mechanism of the delayed effect of
succinylcholine (SuCh) in elephants, by correlating the plasma
concentration of SuCh with alterations in respiratory and cardiovascular
function and with changes in plasma markers of metabolism. These changes
were compared with those in impalas, following a lethal SuCh dose in
each species. Total entry of SuCh into the circulation (cumulative dose)
and total exposure of neuromuscular receptors to unhydrolysed SuCh (area
under curve of plasma, SuCh vs. time), were determined. Absorption of
intramuscular SuCh was slower, and the cumulative dose lower in elephant
than impala, but exposure to intact SuCh was similar in both. SuCh
produced apnoea, a fall in PaO2 and pH, and rises in the PaCO2 and
plasma catecholamine and cortisol concentrations, and variable
cardiovascular responses. These changes took longer to develop in
elephant than impala, but in both species death was associated with
metabolic consequences of severe hypoxia. We conclude that the delayed
effect of SuCh in elephant does not arise from differences in SuCh
pharmacodynamics between the species but can be attributed to different
pharmacokinetics, the lower mass-specific metabolic rate of the
elephant, and its greater tolerance of severe metabolic changes before
death results.
8.
Sarma K.K. and Pathak S.C. 2001. Cardio vascular response to xylazine
and Hellabrunn mixture with Yohimbine as reversal agent in Asian
elephants.Indian Veterinary Journal 78: 400-492.
Abstract: Xylazine (0.1 mg/kg body weight) produced highly significant
bradycardia and hypotension in recumbent Asian elephants, with a peak
depression observed at the 30th minute for heart rate and 30th minute in
the mean arterial pressure (MAP). Ketamine (1.25 : 1 ratio with xylazine)
mildly marginalised the bradycardia, but remarkably improved the MAP.
Yohimbine, used to reverse the sedation produced by xylazine did not
appear to influence these parameters to any appreciable levels.
9.
Schmitt D.L. and Pace L.W. 2000. Multiple Congenital Cardiac Anomalies
in a Newborn Asian Elephant (Elephas maximus). Proceedings of
the Elephant Managers Association Conference, Oct 6-9,2000 Syracuse, NY,
2000, pp. 13-14.
Abstract: Cardiac anomalies in humans occur in about 1% of human births.
Most are a developmental disorder of the vascular trunk and septum of
the heart, which result in reduced blood circulation to periphery. This
report of a cardiac anomaly in a neonatal elephant is first to the
author's knowledge. A congenital defect known as tetrology of Fallot is
described in a male Asian elephant who lived for 9 hours following
birth.
10.
Victor S. and Nayak V.M. 2000. Evolutionary anticipation of the human
heart.Ann R Coll Surg Engl 82: 297-302.
Abstract: We have studied the comparative anatomy of hearts from fish,
frog, turtle, snake, crocodile, birds (duck, chicken, quail), mammals
(elephant, dolphin, sheep, goat, ox, baboon, wallaby, mouse, rabbit,
possum, echidna) and man. The findings were analysed with respect to the
mechanism of evolution of the heart.
11.
1999. Equine Medicine and Surgery. Mosby, St. Louis MO USA, pp.1-2076.
12.
Mikota S.K. 1999. Diseases of the Elephant: A
Review.Verh.ber.Erkrg.Zootiere 39: 1-15.
13.
Endo H., Yamada T.K., Suzuki N. et al. 1995.
Ultrastructure of cardiac myocyte in the Asian elephant (Elephas
maximus).Journal of Veterinary Medical Science 57: 1035-1039.
Abstract: Cardiac myocytes of an Asian elephant (Elephas maximus) were
observed by transmission electron microscopy. Typical ultrastructural
features of cardiac myocytes are exhibited in the musculature of both
the left and right atria, and left ventricle of the heart. Myofibrils,
mitochondria, T-system and sarcoplasmic reticulum are well-developed
within the cytoplasm. Many mitochondria are characteristically
concentrated is some myocytes. Cardiac musculature is also distributed
in the root of the caudal vena cava. Many atrial granules are detected
not only in atrial myocytes, but also in the myocytes of the caudal vena
cava. Atrial natriuretic polypeptide may be secreted from the caval
venous wall in the elephant.
14.
Schumacher J., Heard D.J., Caligiuri R., Norton T. and Jacobson E.R.
1995. Comparative effects of etorphine and carfentanil on
cardiopulmonary parameters in juvenile African elephants (Loxodonta
africana). Journal of Zoo and Wildlife Medicine 26: 503-507.
Abstract: Fourteen African elephants (Loxodonta africana) were
immobilized with either etorphine hydrochloride (3.2 ± 0.5 µg/kg i.m.)
or carfentanil citrate (2.4 µg/kg i.m.). Induction time with etorphine
was significantly longer (30 ± 21 min) than with carfentanil (8 ± 2
min). Immediately following immobilization all elephants were placed in
lateral recumbency and respiratory rate, heart rate, and rectal body
temperature were monitored every 5 min throughout the immobilization
period. Arterial blood samples, collected from an auricular artery,
were taken 10 min after immobilization and every 15 min thereafter for
up to 1 hr. At the first sampling, mean values for arterial blood gas
variables for etorphine immobilized elephants were pHa, 7.29 ± 0.03;
PaCO2, 53.4 ± 5.2 mmHg; PaO2, 71.8 ± 13.8 mmHg;
standard base excess (SBE), -1.6 ± 2.9 mEq/L; and HCO3, 25.7 ± 2.7 mEq/L.
After 1 hr of immobilization, mean arterial blood gas values were pHa,
7.32 ± 0.06; PaCO2 , 57.2 ± 9.6 mm Hg; and PaO2 ,
53.8 ± 10.5 mm Hg; SBE, 2.7 ± 1.4 mEq/L; and HCO3-, 30.6 ±
1.6 mEq/L. For carfentanil immobilized elephants, blood gas values at
the first time of collection were pHa, 7.28 ± 0.04; PaCO2,
52.1 ± 2.8 mmHg; PaO2, 78.3 ± 14.7 mmHg; SBE, -2.3 ± 24 mEq/L;
and HCO3-, 24.3 ± 2.1 mEq/L. Sixty minutes after the first
sampling, blood gas values of one elephant were pHa, 7.38; PaCO2,
48.7 mmHg; PaO2, 52 mmHg; SBE, 3.4 mEq/L, and HCO3-,
28.8 mEq/L. Over time there was a progressive decline in arterial PO2
in all elephants. It is concluded that elephants immobilized with
either etorphine HCl or carfentanil developed hypoxemia (PaO2
< 60 mmHg) after 30 min of immobilization. It is recommended that the
administration of one of these opioid drugs be accompanied by
supplemental oxygen, or followed by an inhalant anesthetic in 100%
oxygen for prolonged procedures. Diprenorphine or nalmefene reversal
was rapid and uneventful in both the etorphine and carfentanil group.
No cases of renarcotization were noted. Additional excerpt: All
elephants in the etorphine group (n=8) received diprenorphine at a mean
dosage of 8.3 ± 1.1 µg/kg IV. Two elephants in the carfentanil group
(n=6) were administered diprenorphine at a dosage of 8.9 µg/kg IV and
IM. Three elephants in this group received nalmefene hydrochloride.
One of the three elephants was given nalmefene 166.7 µg/kg both IV and
SC. Two of the three elephants were given nalmefene IV and IM. The
dosage was 88.9 µg/kg IV and IM in one elephant and 53.3 µg/kg IV and IM
in the other. One elephant in the carfentanil group was administered
nalmefene (88.9 µg/kg IV) followed by diprenorphine (8.9 µg/kg IM).
15.
Brain C. and Fox V.E.B. 1994. Suspected cardiac glycoside poisoning in
elephants (Loxodonta africana).Journal of the South African
Veterinary Association 65: 173-174.
Abstract: Two young (< 2 years old) elephants (Loxodonta africana)
died suddenly and simultaneously at Ongava Game Reserve bordering on the
Etosha National Park, Namibia. Both elephants showed lung congestion,
epi- and endocardial haemorrhages and hyperaemic areas in the mucosa of
the stomach and small intestine. Histopathology of the myocardium showed
multifocal degeneration and necrosis of muscle fibres accompanied by
haemorrhages. Parts of the leaves of the alien plant Cryptostegia
grandiflora (Asclepiadaceae) were found in the intestinal tracts of
the elephants. These findings suggested that the elephants died from
heart failure after ingesting this plant which contains cardiac
glycosides.
16.
Dunlop C.I., Hodgson D.S., Cambre R.C., Kenny D.E. and Martin H.D. 1994.
Cardiopulmonary effects of three prolonged periods of isoflurane
anesthesia in an adult elephant.Journal of the American Veterinary
Medical Association 205: 1439-1444.
Abstract: Department of Clinical Sciences, College of Veterinary
Medicine and Biomedical Sciences, Colorado State University, Fort
Collins 80523.
An adult 3500-kg female African elephant (Loxodonta africana) was
anaesthetized 3 times for treatment of subcutaneous fistulas over the
lateral aspect of each cubitus (anaesthesia 1 and 2) and for repair of a
fractured tusk (anaesthesia 3). Lateral recumbency and anaesthesia were
achieved with etorphine (anaesthesia 1 and 2) or etorphine and azaperone
(anaesthesia 3). The trachea was intubated and anaesthesia was
maintained by isoflurane and oxygen delivered through 2 standard large
animal anaesthesia machines joined in parallel. The range of total
recumbency time was 2.4 to 3.3 h. Breathing and heart rates, systemic
arterial pressure, rectal temperature, PaO2, pH and end-tidal gases were
monitored. After administration of etorphine, measurements were made
while the elephant was recumbent and breathing air, then every 5 min
(cardiovascular) or 15 min (blood gases) after the start of
administration of isoflurane and oxygen. Tachycardia and hypertension
were detected after administration of etorphine, but heart rate and
systemic arterial pressure decreased to within normal ranges after
administration of isoflurane and oxygen. The elephant remained well
oxygenated while anaesthetized and breathing a high oxygen mixture. The
elephant had an uneventful recovery from each anaesthesia.
17.
Chakraborty A. and Chaudhury B. 1993. Spontaneous aortic lesions in
captive wild herbivores.Indian Journal of Veterinary Pathology 17:
36-40.
18.
Honeyman V.L., Pettifer G.R. and Dyson D.H. 1992. Arterial blood
pressure and blood gas values in normal standing and laterally recumbent
African (Loxodonta africana) and Asian (Elephas maximus)
elephants.Journal of Zoo and Wildlife Medicine 23: 205-210.
Abstract: Normal cardiopulmonary data in seven African (Loxodonta
africana) and eight Asian (Elephas maximus) elephants were
documented in conscious animals standing and in left lateral (LL)
recumbency. In the standing position, arterial blood pressures, heart
and respiratory rates, and blood gas values did not differ (P > 0.05)
over time or between species. Systolic, diastolic, and blood pressure
means (+/- SEM) were 178.6 (+/- 2.94), 118.7 (+/- 3.10), and 144.6 (+/-
2.90) mm Hg, respectively, in unsedated standing elephants. Arterial
blood pressures increased (P </= 0.05) with time in LL recumbency and
were highest (179.83 +/- 9.32) by the last reading at 16.5 +/- 0.41
min. Arterial PO2 values decreased (P </= 0.05) from 96.2 (+/- 1.55) mm
Hg while standing to 83.8 (+/- 3.37) mm Hg by 13.6 (+/- 6.8) min in LL
recumbency. Lateral recumbency increased (P < 0.05) arterial pH,
adjusted base excess, and HCO3- content; however, these changes were not
considered clinically significant. Clinically healthy unsedated
laterally recumbent elephants may be at risk of developing clinically
significant hypoxemia and hypertension in the absence of alteration in
more readily measured cardiopulmonary parameters.
19.
Yathiraj S., Choudhuri P.C., Rao D.S.T. and Reddy P.K. 1992.
Clinico-haematological observations on Indian elephant (Elephas maximus
indicus).Indian Veterinary Journal 69: 995-997.
Abstract: In 3 apparently healthy elephants (a male aged 40, and 2
females aged 20 and 60) the mean values for heart rate, respiratory rate
and body temperature, respectively, were 34.66±1.08/min, 7.88±0.09/min
and 35.25±0.07°C in the mornings, and 36.22±1.07/min, 8.33±0.15/min and
35.75±0.06°C in the afternoons. Haemoglobin values averaged 11.65±0.49
g%, and PCV 33.25±0.46%. Various erythrocyte and leukocyte counts and
indices are presented.
20.
Loypetjra P. 1991. Electrocardiography of the wildlife animals.Thai
Journal of Veterinary Medicine 21: 175-186.
Abstract: The electrocardiogram of wildlife animals was recorded using
hexaxial lead system. The animals were seventeen crocodiles, one
gibbon, three lorises, three tigers, four elephants and one binturong.
All of them were conscious during the measurement. The Lead II of
electrocardiogram was used in evaluating heart rate, rhythm and
measuring the amplitude, time interval and segment. Standard limb leads
were employed to calculate mean electrical axis of the ventricles.
Electrocardiographic features of P, QRS and T waves in all species were
normal without slurring or notching. The values of heart rate per
minute of crocodile, gibbon, loris, tiger, elephant, and binturong were
43-65, 166, 125-214, 90-154, 35-49 and 150, respectively. The duration
of P wave in crocodile was between 0.051-0.179 sec, QRS wave was
0.108-0.158 sec, P-R interval was between 0.24-0.42 sec, and Q-T
interval was between 0.282-0.454 sec. P wave duration in gibbon, loris,
tiger, elephant and binturong were nearly the same which were 0.04 to
0.08 sec. The mean electrical axes were between 66 deg-72 deg, 57 deg,
110 deg, 70 deg-85 deg, 40 deg-90 deg and 120 deg in crocodile, gibbon,
loris, tiger, elephant and binturong, respectively. The large
variation of ECG values within species was thought to be the
unrestrained and exciting effects. However, this was considered to be
normal and could be found in each species.
21.
Sreekumar K.P., Nayar K.N.M., Pillai M.G.R. et al. 1991.
Electrocardiographic studies before, during and after athirathra yajna
in animals.Journal of Veterinary and Animal Sciences 22: 112-115.
22.
Wells S.K., Gutter A.E., Soike K.F. and Baskin G.B. 1989.
Encephalomyocarditis virus: Epizootic in a zoological collection.Journal
of Zoo and Wildlife Medicine 20: 291-296.
Abstract: Encephalomyocarditis virus (EMCV) was isolated from eight
nonhuman primates, one Thomson's gazelle (Gazella thomsoni), and
one dromedary camel (Camelus dromedarius) that died peracutely
between January 1985 and October 1987 at Audubon Park Zoo, New Orleans,
Louisiana. Gross pathology consisted of excessive pericardial fluid,
epicardial hemorrhages, and pale foci within the myocardium.
Microscopic changes included myofiber necrosis, edema, and mononuclear
cell infiltration within the myocardium. Anti-EMCV antibody was
found in a variety of species including a capybara (Hydrochoerus
hydrochaeris), which subsequently died of a necrotizing myocarditis
but from which virus was not isolated. Although one hospital staff
member had a high anti-EMCV antibody titer, all primate keepers were
seronegative. Encephalomyocarditis virus was recovered from 38 wild
rodents, one opposum (Didelphis virginiana), and one rabbit (Sylvilagus
sp.) collected on the zoo grounds. Fifty-five percent of the positive
samples were found in areas where confirmed deaths had occurred or
antibody-positive animals were housed. A killed vaccine was developed
and administered to six domestic cats, 12 primates, and one camel.
Antibody response to vaccination was variable.
23.
Gaskin J.M. 1988. Encephalomyocarditis: A potentially fatal virus
infection of elephants. Proc.Ann.Elephant Workshop 9, pp. 133-136.
24.
Gaskin J.M., Andresen T.L., Olsen J.H. et al. 1987.
Encephalomyocarditis in zoo animals: Recent experiences with the disease
and vaccination.Proceedings of the 1st International Conference on
Zoological and Avian Medicine: 491.
Abstract: Encephalomyocarditis (EMC), a specific viral infection caused
by a group of antigenically related viruses in the family
Picornaviridae, a genus of Cardiovirus, continues to be a
source of sporadic mortality loss in zoo animals in Florida. Deaths in
a young Nyala antelope, 2 chimpanzees, 3 llamas, a two-toed sloth, 3
ringtail lemurs, a ruffed lemur, and an orangutan have recently been
confirmed by virus recovery. Experimental vaccine trials were initiated
in pygmy goats, Barbados sheep, and white mice using B-propiolactone
inactivated virus preparations. Various adjuvants, including aluminum
hydroxide, mineral oil, and dimethyl dioctadecyl ammonium bromide (DDAB)
were used to enhance the immune responses to inactivated virus. The
vaccine preparations produced varying levels of hemagglutinations-inhibition
(HI) antibodies in the immunized animals. Experimental challenge of
unvaccinated weaned pigs, pygmy goats, and Barbados sheep demonstrated
that, although they seroconverted, they did not become ill when exposed
to the virulent EMC virus strains used in this study. Laboratory mice,
however, proved to be very susceptible when exposed to these same
strains, and either died acutely or developed posterior paresis and
paralysis subsequent to challenge. All experimental vaccine
preparations protected mice against challenge. In vaccinated goats and
sheep, the oil-emulsion-adjuvanted and DDAB-adjuvanted vaccines produced
the highest and most persistent HI antibody titers. Sera obtained from
African elephants were screened for HI antibodies to EMC virus.
Ninety-three African elephant sera from the Kruger National Park in the
Republic of South Africa had titers of less than 10 hemagglutination-inhibition
units (HIU) while 4 of 76 imported juvenile African elephants had titers
from 10-40 HIU and the rest had no titer. EMC virus infections are
apparently acquired in Florida from reservoir hosts and HI titers of 40
HIU or higher indicate subclinical infection with the virus.
Experimental vaccines may help prevent EMC in susceptible species; HI
responses to vaccination in various exotic species are being evaluated.
25.
Seaman J.T. and Finnie E.P. 1987. Acute myocarditis in a captive African
elephant (Loxodonta africana).Journal of Wildlife Diseases 23:
170-171.
26.
Meijler F.L. and van der Tweel L.H. 1986. Electrocardigrams of 10
elephants and a killer whale in Harderwijk.Ned Tijdschr Geneeskd 130:
2344-2348.
27.
Meijler F.L. 1985. Atrioventricular conduction versus heart size from
mouse to whale.J Am Coll Cardiol 5 (Pt 2): 363-365.
28.
Poupa O. and Brix O. 1984. Cardiac beat frequency and oxygen supply: a
comparative study.Comp Biochem Physiol A 78: 1-3.
Abstract: The length of diastole in mammals varies between approx 1 s
(elephant) and 38 ms (shrew) which makes oxygen supply in high speed
cardiac pumps in very small mammals precarious. High capillary density
and high blood P50 are reported in mammals with high frequency cardiac
cycle. Both are probably insufficient when cardiac frequency is
exceedingly high (shrew: 1000 min-1). High respiratory efficiency due to
large relative mitochondrial volume per cell (greater than 50%) seems to
be preferential solution to maintain sufficient O2-gradient. Similar
strategy, i.e. high relative cardiac mitochondrial volume was reported
in analogous situation in ice-fish (Chaenocephalus aceratus) where O2
cardiac cell supply is difficult due to the absence of hemoglobin and
cardiac myoglobin.
29.
Bain O., Baker M. and Chabaud A.G. 1982. New data on the Dipetalonema
lineage (Filarioidea, Nematoda).Ann Parasitol Hum Comp 57: 593-620.
Abstract: The evolutionary line of Dipetalonema can apparently be
divided into four groups: I: Australian species; II: paleoendemic South
American species; III: the Tetrapetalonema group; IV: the
Acanthocheilonema group. Loxodontofilaria at present insufficiently
known to be classified and several species belonging to the
Acanthocheilonema group are the object of the present study.
Descriptions are given of Loxodontofilaria asiatica n. sp., parasite of
Elephas indicus in Burma, Cercopithifilaria degraaffi n. sp., parasites
of Papio ursinus in South Africa, C. cephalophi n. sp., parasite of
Cephalophus dorsalis and C. gabonensis n. sp., parasite of Atherurus
africanus in Gabon. Additional morphological data are given on
Cercopithifilaria didelphis, C. rugosicauda, Acanthocheilonema
pachycephalum, A. viteae, Molinema dessetae, Dipetalonema gracile,
Orihelia sp., Skrjabinofilaria skrjabini, Breinlia (B.) spratti,
Litomosa sp., Loxodontofilaria hippopotami. Yatesia n. gen. with type
species Yatesia hydrochoerus (Yates, 1980), is proposed, distinguished
by specialized characters of the posterior extremity. The genus
Cercopithifilaria is used to accomodate species considered as
specialized Acanthocheilonema. Chenofilaria is placed in synonymy with
Acanthocheilonema. Loxodontofilaria includes the three filarid species
from elephants, L. loxodontis, L. gossi, L. asiatica n. sp. and the
species from the Hippopotamus, L. hippopotami; D. okapiae is considered
a species inquirenda. The interpretation given for the neotropical fauna
is the following: --Skrjabinofilaria, Orihelia, Dasypafilaria and
Dipetalonema may be true paleoendemics in South America. --Molinema and
Ackertia on the one hand and Yatesia on the other may be forms of
African origin introduced at the end of the Eocene during the migration
of African rodents into South America. The capture in American reptiles
(the genus Macdonaldius) could have occurred during this period.
--Surprisingly, the two species of Dipetalonema in Didelphis may be late
captures of neartic origin: A. pricei from Acanthocheilonema in
carnivores and C. didelphis from a Cercopithifilaria in eutherian
mammals.
30.
Paynter D. 1982. Death of Shingwidzi.African Wild Life 36: 70.
31.
Murname T.G. 1981. Encephalomyocarditis. In: Steele JH (ed), CRC
Handbook Series in Zoonoses, Section B: Viral Zoonoses pp. 137-147. The
Iowa State University Press, Ames, Iowa.
32.
Gaskin J.M., Jorge M.A., Simpson C.F. et al. 1980. The tragedy of
encephalomyocarditis virus infection in zoological parks of
Florida.Proceedings American Association of Zoo Veterinarians: 1-7.
33.
Mill J. and Kuntze A. 1978. ECG studies in healthy elephants and in one
diseased elephant (Elephas maximus).Erkrankungen der Zootiere 14:
315-326.
34.
Tesh R.B. and Wallace G.D. 1978. Observations on the natural history of
encephalomyocarditis virus.American Journal of Tropical Medicine and
Hygiene 27: 133-143.
35.
White P.T. and Brown I.R.F. 1978. Haematological studies on wild African
elephants, Loxodonta africana.Journal of Zoology (Lond) 185:
491-503.
36.
Cmelik S.H.W. and Ley H. 1977. A further contribution to the knowledge
of the blood lipid fractions from the African elephant Loxodonta
africana.Comparative Biochemistry and Physiology [B] 58: 205-209.
Abstract: 1. Plasma lipids from 5 African elephants were extracted and
fractionated into cholesterol esters, free fatty acids, triglycerides,
phosphatidylcholine, phosphatidylethanolamine, phophatidylinositol,
sphingomyelin, and glycosphingolipids. The fatty acids of various
individual fractions were investigated by gas-chromatography. 2. All
animals, except one, had a high linoleic acid content in cholesterol
esters indicating an adequate supply of linoleic acid in the diet. 3.
Phosphatidylcholine had a strong saturated character originating from
the presence of unusually high quantities of stearic acid. 4.
Phosphatidylethanolamine was present in small quantities and was
characterized by a low content of arachidonic acid. 5. Sphingomyelin
did not contain any long chain saturated acids. Instead it contained
10.2-47.0% of a long chan acid which was most likely monounsaturated.
6. The presence of significant quantities of glycosphingolipids was
established.
37.
Simpson C.F., Lewis A.L. and Gaskin J.M. 1977. Encephalomyocarditis
virus infection of captive elephants.Journal of the American Veterinary
Medical Association 171: 902-905.
Abstract: Four Asian elephants at each of 2 widely separated zoologic
gardens in Florida died following a fulminating illness. Tissue
suspensions obtained from an elephant from each of the zoologic gardens
were inoculated into newborn mice, 3- to 4-week-old mice, buffalo green
monkey and baby hamster kidney cell cultures. Encephalitis and
myocarditis developed in the mice. The cell cultures were destroyed
within 24 to 72 hours, and intracytoplasmic viral inclusions were
observed in infected cells by electron microscopy. The viral agent was
neutralized by known antiserum to encephalomyocarditis virus.
38.
Bartels H. 1976. Comparative aspects of respiration and circulation in
mammals.Pneumonologie Supplement: 1-9.
39.
Cave A.J.E. 1975. Postcava structure in the elephant and
rhinoceros.Journal of Zoology (Lond) 176: 559-565.
Abstract: The mammalian postcava is vulnerable to lumen diminution or
collapse under sudden increase of intra-abdominal pressure. Against
such collapse its dorsal wall receives an extrinsic protection from the
abdominal parietes. Its ventral wall, however, develops an intrinsic
protective mechanism in the form of a specialization of its histological
architecture. This specialization is most readily noticeable in
large-bodied mammals and the details of it are given for four such
forms, viz., Asiatic elephant (Elephas), Sumatran rhinoceros (Didermocerus),
Black rhinoceros (Diceros) and White rhinoceros (Ceratotherium).
40.
Huber D., Kardum P. and Gomercic H. 1975. Blood vessels of the fore limb
in Indian elephant, Elephas maximus.Veterinarski Arhiv 45:
311-320.
41.
McCullagh K.G. 1975. Arteriosclerosis in the African elephant: Part 2.
Medial sclerosis.Atherosclerosis 21: 37-59.
Abstract: Summary: A type of spontaneous arteriosclerosis, described as
medial sclerosis and quite distinct from atherosclerosis, was found in
the aortas, coronary arteries and aortic branch arteries of free-living
elephants (Loxodonta africana) in Uganda and Kenya. The lesions took the
form of calcified fibrotic plaques in the inner tunica media. The
calcification appeared to commence in the internal elastic lamina and
was associated with atrophy of medial smooth muscle fibres and their
replacement by fibrous tissue. In the aorta, medial sclerosis was found
to be associated with aortic dilatation, decreased wall thickness and
decreased extensibility. These changes were shown to result in
substantial increases in the tangential stresses carried by the tissues
of the aorta and coronary arteries. As with atherosclerosis, medial
sclerosis increased progressively with age; and the approximate
involvement of the aorta at different ages could be predicted from
linear regression equations. There was no difference in the severity of
lesions between male and female animals. Biochemically, the lesions of
medial sclerosis were associated with decreased amounts of elastin and
increased amounts of collagen in arterial walls. Arterial tissue showing
medial calcification always contained less than 30% elastin by weight.
In addition, the severity of medial sclerosis in individual elephants
was found to be positively correlated with the concentration of calcium
in their sera. The pathogenesis of these lesions is discussed and it is
suggested that mechanical stress, medial anoxia and high serum calcium
levels all contribute to the aetiology of medial sclerosis.
42.
McCullagh K.G. 1973. Studies on elephant aortic elastic tissue. I. The
histochemistry and fine structure of the fiber.Experimental Molecular
Pathology 18: 190-201.
Abstract: Elephant arterial elastic laminae were shown to be refractory
to staining by orcein or the resorcin dyes, both normally regarded as
routine elastic tissue stains. To investigate this more thoroughly,
elastin was isolated from the arterial tissue by alkaline hydrolysis and
studied in vitro. Compared to elastin from other species,
elephant elastin was found to resist alkaline hydrolysis to a greater
extent, to possess a greater UV absorption at 275 nm, and to shown an
unusual fluorescence at 415 nm. Electron micrographs of elastic fibers
in situ demonstrated the presence of large amounts of
microbibrillar sheath surrounding the amorphous core. These results are
interpreted to indicate the presence, in elephant arterial elastic
tissue, of unusually large amounts of a nonelastin component which
interferes with the normal staining reactions.
43.
McCullagh K.G., Derouette S. and Robert L. 1973. Studies on elephant
aortic elastic tissue. II. Amino acid analysis, structural
glycoproteins and antigenicity.Experimental Molecular Pathology 18:
202-213.
44.
McCullagh K.G. 1972. Arteriosclerosis in the African elephant. I.
Intimal artherosclerosis and its possible causes.Atherosclerosis 16:
307-335.
45.
Basson P.A., McCully R.M., de Vos V., Young E. and Kruger S.P. 1971.
Some parasitic and other natural diseases of the African elephant in the
Kruger National Park.Onderstepoort Journal of Veterinary Research 38:
239-254.
46.
Dillman J.S. and Carr W.R. 1970. Observations on arteriosclerosis, serum
cholesterol and serum electrolytes in the wild African elephant.Journal
of Comparative Pathology 80: 81-87.
47.
McKinney B. 1970. Hyaline arteriolosclerosis in wild animals.Journal of
Comparative Pathology 80: 275-279.
48.
Gainer J.H. 1969. Encephalomyocarditis virus infections in Florida,
1960-1966.Journal of the American Veterinary Medical Association 151:
421-425.
49.
Sikes S.K. 1969. Habitat and cardiovascular diseases, observations made
on elephants (Loxodonta africana) and other free-living animals
in East Africa.Transactions of the Zoological Society of London 32:
1-104.
Abstract: A field survey to investigate the ecology of cardiovascular
disease in free-living East African wild animals is described. Its aim
was to assess the susceptibility of such animals to arteriosclerosis,
and particularly to atherosclerosis, and to examine in greater detail
the ecology of cardiovascular disease in a single, naturally-susceptible
species in relation to dietary change and stress in naturally occurring
situations. A total of 201 specimens, representing 43 species of
mammals and 25 of birds, was examined: 37 species of mammals had
uncomplicated lipid deposits in the arterial intima, thought to
represent a normal physiological occurrence; ten had atheroma-like
lesions of the intima, and a number had medial sclerosis and/or other
arteritides. Twenty species of birds had intimal lipid deposits. The
African elephant was selected for special study. The ecology of its
cardiovascular disease patterns was studied in three different habitat
types: one "natural" (the "control") and two degenerate ("stressed" or
"disturbed"). Atherosclerosis and medial sclerosis were not found in
elephants living in the "natural" habitat type, but were correlated with
habitat degeneration in the other two "stressed" or "disturbed" ranges,
where potential "stress" factors included excessive continuous exposure
to sunlight, dietary changes, frustration of the migratory habit,
disrupted calving patterns, and over-population. Neither disease was
found to be directly related to age, and each had a distinct
intra-arterial development pattern: the aetiology of each is therefore
thought to be basically independent, although in advanced cases
interaction had occurred. Incidental original observations include
comparisons, in various species, or the functional anatomy of the
arterial supportive thickenings at ostia, bifurcations and regions of
mechanical strain in relation to the normal intra-aortic distribution of
intimal lipid deposits; a note on the nutrition of the Spring hare; a
note on the formulation of a new field technique for assessing relative
age in the African elephant; notes on abnormalities other than
cardiovascular disease, and discussion on ecological data collected
which may have practical relevance to current problems of wildlife
management.
50.
Gainer J.H., Sandifur J.R. and Bigler W.J. 1968. High mortality in a
Florida swine herd infected with encephalomyocarditis virus. An
accompaning epizootiologic survey.The Cornell Veterinarian 58: 31-47.
51.
McCullagh K.G. 1968. Essential fatty acids and atheroma.The Lancet 2:
353.
52.
Sikes S.K. 1968. Observations on the ecology of arterial disease in the
African elephant (Loxodonta africana) in Kenya and
Uganda.Procedings of the Zoological Society of London 21: 251-273.
Abstract: Complete aortae, and samples of selected arteries, were
recently collected for detailed study from forty African elephants (Loxodonta
africana) in Kenya and Uganda. In every case a wide range of
additional data was obtained, relating to the status of each individual
elephant from which the material was collected and its ecological
background. These elephants were collected from three distinct habitat
types, and a correlation is indicated between the occurrence of certain
arterial abnormalities which have been found in the elephants and
ecological differences in the habitat types. It seems possible that the
effects of the modern human pressures, which frequently directly affect
the vegetational cover, soil character and animal migrations in a given
environment, may also indirectly influence the behaviour patterns and
physiological rhythms of the elephants. Such combined pressures may
also result in nutritional imbalance, influencing calcium and lipid
metabolism, and producing associated changes in the arterial structure.
53.
Sikes S.K. 1968. The disturbed habitat and its effect on the health of
animal populations, with special reference to cardiovascular disease in
elephants.Proceedings of the Royal Society of Medicine 61: 160-161.
54.
Sikes S.K. 1968. Habitat stress and arterial disease in elephants.Oryx
9: 286-292.
Abstract: Elephant management in East African reserves and national
parks has become one of the urgent conservation problems of today. In
this study of the African savanna elephant, Dr. Sikes shows that two
diseases of the heart and arteries, found only in lowland elephants,
were directly associated with the degeneration of the habitat when
elephant numbers began to build up in the Tsavo National Park in Kenya
and the Queen Elizabeth and Murchison Falls National Parks in Uganda.
The two diseases thus appear to be natural factors tending to limit the
elephant populations in these reserves, and she suggests four lessons to
be drawn from this discovery by those concerned with elephant management
in national parks.
55.
Geddes L.A., Hoff H.E. and Cohen B.S. 1967. The electrocardiogram of an
elephant.The Southwestern Veterinarian 20: 211-216.
56.
McCullagh K. and Lewis M.G. 1967. Spontaneous arteriosclerosis in the
wild African elephant.The Lancet 2: 492-495.
Abstract: Two distinct lesions which arise spontaneously in the arteries
of wild African elephants resemble uncomplicated arteriosclerosis and
Monckeberg's sclerosis in man. Such lesions can develop in the absence
of dietary or tissue lipid.
57.
Moore J.H. and Sikes S.K. 1967. The serum and adrenal lipids of the
African elephant (Loxodonta africana).Comparative Biochemistry
and Physiology [A] 20: 779-792.
Abstract: 1. The serum and adrenal lipids of the African elephant were
fractionated by chromatography on columns of silicic acid into
cholesterol esters, cholesterol, triglycerides, unesterified fatty acids
and phospholipids. The fatty acid compositions of the various lipid
fractions were determined by gas-liquid chromatography. 2. The results
obtained from the African elephant were compared with the results
reported in the literature for other species of mammals. In many
respects the composition of the serum lipids of the African elephant was
similar to that of the rat and rabbit but was markedly different from
that of the ox and man. 3. Unlike the serum cholesterol esters and
phospholipids of other animals, these two lipid fractions in the serum
of these elephants contained appreciable concentrations of
delta-8,11,14-eicosatrienoic acid. 4. The total lipid content of the
African elephant adrenal galnd was particularly high (63 per cent of the
dry tissue). Cholesterol esters accounted from almost half of the
adrenal lipid. Delta-8,11,14-eicosatrienoic acid was present in
substantial amounts in the adrenal cholesterol esters and phospholipids.
58.
Sikes S.K. 1967. A survey of cardiovascular disease in free-living wild
animals with particular reference to the African elephant. Ph.D. Thesis,
London University, England.
59.
Sikes S.K. 1966. The African elephant, Loxodonta africana: a
field method for the estimation of age.Journal of Zoology (Lond) 150:
279-295.
Abstract: The need for a field method of determining and describing the
relative age of African elephants collected in their natural habitat
arose during a recent research project, and has led to an attempt to
formulate a laminary age standard for use in the field, based upon
direct observations and measurements on the lower right molars. For
this purpose a series of 31 African elephants of both sexes, covering
almost the complete potential age range of an elephant's life, and of
known body condition, locality and size, have been used as the basis for
constructing a reference chart of molar laminary age. Eye lens weights
were also obtained for 26 of these specimens, but, although indicative
of a direct correlation with laminary age, they were obtained in
insufficient numbers to provide an adequate sequence. Each of the
specimens used was first observed alive, then shot and examined post
mortem during the course of a research project on cardiovascular
disease, in which the determination of relative age formed an integral
part.
60.
Finlayson R. 1965. Spontaneous arterial disease in exotic
animals.Journal of Zoology (Lond) 147: 239-343.
61.
French J.E. 1964. Atherosclerosis. In: Florey H (ed), General pathology
pp. 418-446. Loyd-Luke, London.
62.
Jayasinghe J.B., Fernando S.D.A. and Brito-Babapulle L.A.P. 1964. The
electrocardiogram of a baby elephant.American Heart Journal 67: 388-390.
63.
Jayasinghe J.B., Fernando S.D.A. and Brito-Babapulle L.A.P. 1963. The
electrocardiographic patterns of Elephas maximus -- the elephant
of Ceylon.British Veterinary Journal 119: 559-564.
64.
Evans G.H. 1961. Elephants and Their Diseases: A Treatise on Elephants.
Government Printing, Rangoon, Burma, pp.1-323.
65.
Gainer J.H. and Murchison T.E. 1961. Encephalomyocarditis virus
infection of swine.Vet.Med. 56: 173-175.
66.
Jayasinghe J.B. and Brito-Babapulle L.A.P. 1961. A report on the
electrocardiogram of the Ceylon elephant.Ceylon Veterinary Journal 9:
69-70.
67.
Lindsay S., Skahen R. and Chaikoff I.L. 1956. Arteriosclerosis in the
elephant.Arch.Pathol. 61: 207-218.
68.
Hill W.C.O. 1938. Studies on the cardiac anatomy of the elephant: II --
the heart and great vessels of a foetal Asiatic elephant.Journal of
Science 21: 44-61.
69.
King R.L., Burwell C.S. and White P.D. 1938. Some notes on the anatomy
of the elephant's heart.American Heart Journal 16: 734-743.
70.
White P.D., Jenks J.L. and Benedict F.G. 1938. The electrocardiogram of
the elephant.American Heart Journal 16: 744-750.
Abstract: An analysis has been made of the electrocardiograms of nine
circus elephants with heart rates ranging from 24 to 53 per minute
(average of 35 to 40). Relatively low amplitude of the P-, QRS, and
T-waves was found in the three classical leads (with greatest excursions
in Lead I), despite accurate standardization which was made easy by the
remarkably low resistance invariably found (often only 200 to 300 ohms
in any given lead). The various time intervals (P-R of 0.28 to 0.41
sec, QRS of 0.12 to 0.18 sec, and Q to T time -- duration of systole --
of 0.59 to 0.79 sec) were beyond the measurements to be expected at slow
heart rates in the case of mammals of average size like man, and may be
explained by the immense size of the elephant's heart with its longer
paths of impulse conduction and its greater bulk of contracting muscle.
71.
Forbes A., Cobb S. and Cattell M. 1921. An electrocardiogram and an
electromyogram in an elephant.American Journal of Physiology 55:
385-389.
72.
Putter A. 1918. Studien uber physiologische
Xhnlichkeit.Arch.f.d.ges.Physiol. 172: 367-412.
73.
Evans G.H. 1910. Elephants and Their Diseases: A Treatise on Elephants.
Government Printing, Rangoon, Burma.
74.
Bruce D. and Hamerton A.E. 1909. A note on the occurrence of a
trypanosome in the African elephant.Proc.Roy.Soc.Lond.[B] Biol.Sci. 81:
414-416.
75.
Colin G. 1888. Traite de physiologie comparee des animaux. Paris.
Abstract: Cited in Benedict, 1936.
76.
Miall L.C. and Greenwood F. 1879. The anatomy of the Indian elephant.
Part III alimentary canal and its appendages.Journal of Anatomy and
Physiology 13: 17-50.
77.
Watson M. 1875. Contributions to the anatomy of the Indian elephant,
Part IV. Muscles and blood vessels of the face and head.Journal of
Anatomy and Physiology 9: 118-133.
78.
Watson M. 1872. Contributions to the anatomy of the Indian elephant.
Part I. The thoracic visera.Journal of Anatomy and Physiology 6: 82-94.
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