J . small Ariirn. Pract. (1977) 18,687-699.

Bacterial endocarditis in the dog

D . B. M U R D O C H *

AND J.

R. BAKER?

Departments ofveterinary Clinical Studies and Clinical Veterinary Pathology?, University of

Liverpool Veterinary Field Station, Leahurst, Neston, Wirral, Merseyside, L64 7TE.

ABSTRACT
The literature on bacterial endocarditis is reviewed. The condition is
illustrated by three cases in which the findings on clinical, radiological,
electrocardiographical, bacteriological and post-mortem examinations
are described. In one case a 2-year-old Boxer, the causal organism was an
atypical Corynebacterium and in another, a 6-year-old Alsatian, it was
Proteus vulgaris. Neither of these organisms have been previously
associated with canine bacterial endocarditis. The third case is an example
of a chronic, long standing lesion, from which no organisms were isolated.
REVIEW OF T H E LITERATURE
Endocarditis in the dog is usually classified under two headings:- (a) Mural (or
parietal) endocarditis is an ulcerative lesion commonly associated with acute
renal failure, the left atrium being most commonly affected (Jubb & Kennedy,
1970); (b) Bacterial endocarditis is a fibrinous, verrucose lesion affecting
primarily the valves of the heart but may also give rise to parietal lesions. The
condition is usually considered secondary to a localized bacterial infection
elsewhere in the body (Detweiler & Patterson, 1966). For the purposes of this
paper, only the valvular condition will be considered.
Incidence
Fregin, Luginbuhl & Guarda (1972) state that bacterial endocarditis is an
important but infrequently diagnosed condition. When compared to valvular
endocardiosis, the disease is relatively uncommon (Pirie, 1967), indeed Jubb &
Kennedy (1970) state that the condition is seldom observed in dogs. Because
many organs may be secondarily affected, a wide range of non-specific clinical
signs may be present, making accurate diagnosis difficult (Ettinger & Suter,
1970). Consequently, most of the incidence figures available are based on
post-mortem surveys, these figures showing wide variations. The highest
687

688
D. B . M U R D O C H A N D 1. R . B A K E R
incidences were 6.6% and 5.8% respectively reported by Shouse & Meier (1956)
and Jones & Zook (1965). Schornagel in 1936 recorded a figure of 2.27% while
Winquist (1949, Lundh (1964) and Detweiler et al. (1961) in their surveys
described an incidence of 0.74%, 0.58% and 0.06% respectively.
Ettinger & Suter (1970) state that such variable results suggest that the
population of dogs from which necropsy material was obtained differed and/or
the criteria used to reach a diagnosis of endocarditis were variable. In many of
these surveys it was not clear whether endocarditis was the cause of death or an
incidental finding on post-mortem examination. It is consequently impossible to
relate these figures to the incidence of the condition as a clinical entity.
Another possible reason for the variation in the above figure is the hypothesis
of Smith & Jones (1966) that the disease is more prevalent in cold climates
although Lundhs figures (0.58%) were acquired from the Stockholm area.
Age incidence
The condition is commoner in older dogs (Jones & Zook, 1976; Pirie, 1967) but
can occur at any age (Fisher, 1972). In Lundhs survey (1964) the mean age was
8.5 years and in the twenty-seven cases described by Shouse & Meier (1956),
twenty-four were over 5 years of age. Ernst, Schneider & Trautwein (1973)
recorded a mean age of 10 years in their nine cases.

Breed incidence
Lundh (1964) reported that the German Shepherd Dog had a statistically
significant predisposition to endocarditis. This finding, however, has not been
confirmed by the other workers.
Clinical signs
Classically, these cases have a history of shifting lameness, dullness and
recurrent pyrexia. Emboli from the basic lesion to other organs (brain, muscle,
lungs, kidney and gastro-intestinal tract) may produce clinical signs related to
dysfunction of these organs (Nielsen & Nielsen, 1954; Ettinger & Suter, 1970;
Fisher, 1972; Robertson & Giles, 1972; Burrows, Gaskell & McGrath, 1972;
Knight, Kelly & Wardley, 1972). As with many cardiac lesions, increasing
exercise intolerance is frequently recorded.
Syncope and convulsive siezures were the presenting signs in a three year old
female Dalmatian with vegetative endocarditis (Robertson & Giles, 1972), and
Fisher (1 967) records fainting as a clinical sign in endocarditis.
The presence of a potential primary lesion has been recorded in many cases, the
commonest sites of infection being subcutaneous abscesses, metritis, pyorrhoea,
pneumonia, infected anal glands and prostatitis (Shouse & Meier, 1956; Burrows
et al., 1972; Darke, 1973). Fisher (1972) considers that the history is suggestive if it
includes evidence of an infected wound. Numerous other clinical signs may

689
develop depending upon the primary site of infection and the eventual destination
of the emboli.
BACTERIAL ENDOCARDITIS IN D O G S

Cardiac examina [ion

The vegetative growths associated with the condition frequently affect the
heart valves, producing both systolic and diastolic murmurs (Pirie, 1967). Systolic
murmurs are very much commoner than diastolic murmurs in the dog (Pirie,
1967), indeed Fisher (1972) states that the presence of a diastolic murmur in the
dog is almost positive evidence of bacterial endocarditis. The location of the point
of maximum intensity of the murmur and its position in the cardiac cycle will
depend upon the site of the endocardia1 lesion. This will be discussed under
post-mortem findings. If the lesion has not progressed beyond the endocardium,
disturbances of conduction and cardiac arrhythmias are uncommon. If an active
myocarditis has developed, ventricular premature contractions are likely to occur
(Ettinger & Suter, 1970). The 3-year-old Dalmatian recorded by Robertson &
Giles (1972) quoted earlier, showed a third degree A-V block with a pulse rate of
forty per minute. Theran, Henry & Thornton (1965) described a complete heart
block with unifocal premature contractions in a 34-year-old male Boxer. As
myocardial infarction is uncommon in the dog, it is interesting to note that the
electrocardiographic changes in the traces from the thoracic leads on a
10-year-old male miniature poodle with endocarditis were typical of those seen in
myocardial infarction in man (Fregin et al., 1972). A continuous murmur was
recorded by Kleine, Bisgard & Lewis ( 1966), arising because the sinus of Valsalva
had ruptured as a sequel to endocarditis of the aortic valve.
Laboratory findings
The condition is frequently associated with an increase in total white blood cell
count, principally polymorphonuclear leucocytes and band cells (Ettinger &
Suter, 1970).
As discussed earlier, a primary focus of infection may be present which can give
rise to a bacteraemia. Kirchoff et af.(1 973) isolated bacteria and/or mycoplasmas
from the hearts of thirty-one dogs (not all suffering from endocarditis). In
twenty-four of these thirty-one cases, the same organism was isolated from
organs other than the heart, most frequently, the tonsils (eighteen cases). Culture
of blood from endocarditis cases, however, does not always give a positive result
(Pirie, 1967), especially if antibiotics have been administered prior to sample
collection. Haemolytic and non-haemolytic streptococci, Staphylococcus aureus,
Erysipelothrix rhusiopathiae, Aerobacter aerogenes, Pseudomonas aeruginosa and
Escherichia coli have all been implicated as causal agents, a1though streptococci
are the organisms most frequently involved (Shouse & Meier, 1956; Lundh, 1964;
Luginbuhl & Detweiler, 1965; Bone, 1970; Fregin et al., 1972; Darke, 1973).
Kirchoff et al. (1973) questioned the significance of post-mortem cultures from

690
D. B . M U R D O C H A N D J . R . B A K E R
the heart, unless the organism had been isolated during life, as contamination of
the valve prior to and during post-mortem examination was highly probable.

Pathology
The lesions affecting the valves or the mural endocardium are friable or firm,
and small vegetations can be broken off completely to leave a granular, eroded
surface. The vegetations are yellowish-red or yellowish-grey (Jubb & Kennedy,
1970). Early lesions may resemble dry plaques (Pirie, 1967), whereas advanced,
long standing lesions appear as a dense, non-vascular, scar-like mass (Smith &
Jones, 1966). In the sixty-seven cases surveyed by Lundh (1964), the valves
affected were as follows: Mitral54.8%; Aortic 19.4%; Tricuspid 6.5%. Pulmonary
0%; Mitral and Aortic 12.9%; Mitral and Tricuspid 4.8%. Mitral and Aortic and
Tricuspid 1-6%.
Many authors have noted that a higher percentage of cases have lesions of the
left valves rather than right valves, Schornagel (1936)-82.4%; Winquist
(1945)-97.8%; Shouse & Meier (1956); Pirie (1967) and Detweiler (1968). Ernst
et al. (1973) recorded lesions on the tricuspid valve in only two of the nine cases.
Parietal lesions are much less common. In Lundhs survey quoted earlier, only
five dogs had parietal fibrinous plaques, three of these affecting the left ventricle.
That there is a link between endocarditis and nephritis has been suspected for
some time (Stunzi, 1962; Luginbuhl & Detweiler, 1965; Smith & Jones, 1966).
Ernst et al. (1973) recorded interstitial nephritis as an accompanying disease in
three of their nine cases. It should be pointed out, however, that nephritis is a
common condition in the dog; Valtonen & Oksanen (1972) recorded an incidence
at 55.1% in their fifty-eight randomly selected dogs (mean age 7.54 years).
CASE HISTORIES

Case I. A 2-year-old Boxer bitch

The dog had been presented to the general practitioner 4 weeks previously with
a history of sudden onset of shivering and reluctance to bear weight on the
left-hind leg. The dogs temperature was 103F. and treatment consisted of
antibiotics and cortico-steroids. The dog recovered for a few days then developed
anorexia, an ocular discharge, bouts of sneezing and a lameness in the right hind
leg, accompanied by a temperature of 105F. Following several relapses during
which a vulva1 discharge and a painful right fore limb developed, the dog was
referred to the University of Liverpool Veterinary Field Station.

Case II. A 6-year-old Alsatian bitch

Seven weeks before admission to the University of Liverpool Veterinary Field
Station, the dog had been presented to the general practitioner with a history of
vomiting, dullness and persistent panting. During the next 4 weeks, it developed

69 1

BACTERIAL ENDOCARDITIS IN DOGS

swelling and pain in both carpal and both hock joints at different times.
Temperature fluctuated between 102F and 105"F., although the temperature
reverted to normal after administration of antibiotics. Three weeks before
admission, an exploratory laparotomy was performed by the practitioner, but no
abnormalities were recorded.

Case III. a 3-year-old Dalmatian bitch

Eighteen months previously the dog had been involved in a road accident and
suffered trauma to the left shoulder. A haematoma developed which was
subsequently drained by the practitioner. Oestrus had not been observed in the
last 18 months. Ten days before admission, the dog had become lethargic and
dull. She appeared reluctant to move and was unsteady on her feet when walking.
The owners remarked that during this period the dog was tripping over objects
and bumping into doors. Once, on the evening before admission, and twice, on
the morning of admission, the dog had collapsed.
Clinical examination
In addition to the findings summarized in Table 1 , the Alsatian had an enlarged
turgid vulva with a haemorrhagic discharge. A bilateral, mucopurulent ocular
discharge was present in the Boxer. The Dalmatian's pupillary light reflex was
slow in both eyes as was the eye protective reflex.
Electrocardiography
Fig. 1 is the trace from case I on admission. Fig. 2 shows the phonocardiographic recording from it. Within 3 hours of admission, the heart returned to
TABLE
1. Clinical examination

Case I1
Alsatian

Case I
Boxer
Demeanour
Temperature
Pulse rate/min.
Pulse Volume
Gait
Examination of heart
Murmur on the lefi
Type
Maximum Intensity
Precordial Thrill
Murmur on rhe right
type
Maximum intensity

Case 111
Dalmatian

Dull
Normal
120
Poor
Stiff

Poor
Normal

Dull
Normal
140
Very Poor
Normal

Systolic/diastolic
Fourth Intercostal
No

Systolic/diastolic
Fifth Intercostal
No

Systolic/diastolic
Fourth Intercostal
Present

Systolic
Fourth Intercostal

Systolic
Third Intercostal

Dys tolic
Third Intercostal

Dull
Normal

I50

692

D. B . M U R D O C H A N D J . R . B A K E R

FIG.1. Multiple premature ventricular contractions with capture and fusion, Beat 2 is a
capture beat where an impulse from the A-V node has reached the ventricle while it is not
refractory. Beats 1, 9 and 10 may be termed fusion beats as they have a configuration
between the normal capture beat and the premature ventricular systoles (3,4,5,6,7,8,1 I).
Trace taken from case number one on admission.

FIG.
2. Phonocardiogram recording ofcase number one. A pansystolic (S)and a diastolic
(d) murmur is present. The E.C.G. is showing multiple premature ventricular
contractions.

693

BACTERIAL ENDOCARDITIS IN DOGS

normal sinus rhythm, although no anti-arrhythmic therapy had been used. The
trace showed deep negative T waves (1.4 m.v. deflection) with depression of the
S-T segment.
Case TI showed multiple premature ventricular contractions on admission,
with deviation of the S-T segment and deep T-waves. Within 24 hours of
admission, no premature extra-systoles were visible on the trace although the
T-wave abnormalities were still present.
The rest of the findings are summarized in Table 2.

Radiography
Radiographs of the thorax of all three cases failed to reveal any significant
abnormalities.
TABLE
2. Electrocardiographical traces

Rhythm
P-waves (Lead 11)
Height
Duration
P-Q Interval
QRS Complexes (Lead 11)
Height
Duration
T-Waves (Lead 11)

Case I
Boxer

Case I1
Alsatian

Multiple premature
ventricular systoles

Premature ventricular
systoles

Regular

Not present
Not present
Not measurable

0.3 m.v.
0.04 S ~ C S
0.10 secs

0.4 m.v.
0.04 S ~ C S
0.12 secs

1.8 m.v.
0.06 secs
Large 1.3 m.v.

1.2 m.v.
0.06 secs
Large 0.6 m.v.

0.04 secs

Case 111
Dalmation

I - ? m.v.
Large 0.7 m.v.

TABLE
3. Laboratory examinations

Packed Cell Volume %

Total red blood cells 106/mm3
Haemoglobin G/100 ml
Total white cell count/mm3
Band cells/mm3
Polymorphs/mm3
Monocytes/mm3
Lymphocytes/mm3
Eosinophils/mm3
Serum urea mg/ 100 ml
Venous blood culture

Case I
Boxer

Case I1
Alsatian

Case I11
Dalmatian

41
4.6

44
5.1
13.2
33 000
1485
27 060
1815
2310
330
66
-ve

48
6.9
19.1
9700
339
742 1
339
1455
97
45
- ve

13.4
21 900
541
18 834
986
1533
0
98
Corynebacterium sp.

694
D. B . M U R D O C H
Laboratory findings
These are summarized in Table 3.

A N D J. R. BAKER

Treatment
All three dogs received fluid therapy (Hartmanns solution) and 250 mg of
soluble Ampicillin i.v. four times daily. In cases with arrythmias, no quinidine
compounds were used as difficulties were experienced in obtaining these
preparations and none was in stock at that time.
All three cases died within 48 hours of admission.
POST-MORTEM EXAMINATIONS
Case I
The bitch weighed 22.7 kg and was in average bodily condition. There was
about 150 ml. of fluid in the pleural cavities containing considerable amounts of
blood and some fibrin clots. The pericardial sac was dilated with about 40 ml of
clear fluid, again containing some poorly contracted fibrin clots. The heart
appeared to be slightly enlarged and a branching, filamentous vegetation was
present on all cusps of the aortic valves, the large piece being about 8 mm long. A
flat plaque-like vegetation, 6 mm across, was present on the endocardium close to
the apex of the left ventricle. The lungs were very congested and oedematous, and
there was much froth in the major airways. Numerous renal infarcts were present
in both kidneys, some of these were shrunken and fibrotic but others were raised
above the surface of the kidney with recent haemorrhage at the point of
infarction. The spleen was large and all the body lymph nodes were slightly
haemorrhagic. The gastro-intestinal tract was empty. Histological examination
showed that the vegetations were composed of oedematous fibrous tissue close to
their bases but with the bulk of the lesion being of fibrin containing many
inflammatory cells, mainly polymorphs, many of which were dead. Colonies of
Gram + ve coccobacillary organisms were present in the lesions. In the kidneys,
there were typical macroscopic changes of old and recent infarcts and the lung
showed congestion and oedmea. On bacteriological examination a corynebacterium was grown from the vegetations. The liver, kidney and spleen were sterile.
This organism could not be identified as to species; it gave the following reactions;
it fermented glucose, maltose, sucrose, fructose, dextrin and arabinose, but did
not ferment lactose or mannite. It failed to produce changes in litmus milk, did
not liquify solid serum, failed to split urea, and was indole-negative.
Case II

The bitch weighed 32.7 kg and was in thin bodily condition. There was a
healing mid-line, ventral, abdominal incision associated with which were a
number of omental adhesions. In the dorsal tip of the spleen there were

69 5
approximately one dozen abscesses up to 1 cm across and this part of the organ
was wrapped in omentum. The liver was large and congested. Both ventricles
were dilated, especially the right. There were vegetations of a friable nature
involving all the left atrio-ventricular valve with a large, 1 cm diameter mass on
the cusp close to the aortic valve. There were multiple renal infarcts in both
kidneys. The vegetations gave growths of an organism having the typical features
of Proteus vulgaris and the splenic abscesses gave very heavy, mixed growths
which included Proteus sp.
BACTERIAL ENDOCARDITIS I N D O G S

Case III
The bitch weighed 22.7 kg and was in average bodily condition. A large, firm
vegetation, 2 cm x 2 cm, was present on the cusps of the aortic valve virtually
occluding the lumen (see Fig. 3). This lesion appeared to be chronic in nature, in
that the centre of the lesion was fibrocartilage with peripheral areas composed of
dense or myxomatous fibrous tissue. A few foci of calcification were present. No
inflammatory reaction was seen and no organisms were detected histologically.

FIG.3. Case 111. a large, vegetative growth is present on the aortic valve.

696
D. B. MURDOCH A N D J. R. BAKER
A firm mass, 1.5 c m x 1 cm present in left mid-brain appeared to be an
astrocytoma histologically.
There were haemorrhages in the kidneys and both lungs were slightly
congested.

DISCUSSION
For many years it was postulated that bacterial endocarditis developed when a
bacteraemia was present which allowed colonization of the affected areas of the
heart. The lesions which were assumed to be the primary focus of infection occur
commonly in the dog. Bacterial endocarditis on the other hand is an uncommon
condition in the dog. It is clear, therefore, that other factors must be involved.
The possible link between nephritis and endocarditis mentioned earlier may be
of significance. Madewell & Norrdin (1975) noted that of 150 dogs with renal
disease, eleven had pericardial lesions and postulated that the toxic damage to the
epicardial capillary endothelium allowed a fibrinous lesion to develop. This
argument could apply to the parietal ulcerative lesions described in renal failure
but are unlikely to be of importance in valvular endocarditis as vascularisation of
the normal valve is confined to its basal attachments (Jubb & Kennedy, 1970).All
three dogs described had serum urea levels of less than 100 mg/l00 ml and the
only renal lesion present was an embolic nephritis. Another possible aetiological
link between endocarditis and nephritis is the increase in systolic blood pressure
recorded in the latter condition (Anderson & Fisher,1968; Valtonen & Oksanen,
1972). This increased blood pressure may provide the stress situation which
predisposes the valve to bacterial colonization. Lillehei, Bobb & Visscher (1950)
produced the condition by inducing arterio-venous fistulas experimentally which
give rise to a volume overload. The concept of stress on the valve itself may
account for the observation by Jubb & Kennedy (1970) that the lesions tend to
occur at the lines of apposition on the surfaces exposed to the forward flow of
blood. Angrist, Oka & Nakao (1969) induced changes in the heart valves of rats
by differing stress situations (A.C.T.H.,high altitude, cooling and arterio-venous
anastomosis) and concluded that the primary changes in the heart valves are
always of a biochemical nature and not of an infectious or inflammatory nature.
This work has been repeated by Trautwein et al. (1973) who reported a diffuse
oedematous swelling in the heart valves in dogs subjected to stress.
The role of bacteria in the pathogenesis of the condition is of considerable
interest. Blahd, Frank & Saphir in 1939 produced the condition by single or
multiple intravenous injections of bacteria, a finding which would appear to
conflict with current theories on aetiology. In a series of elegant experiments,
Gould et al. (1 975) showed that the adherence of various bacteria to heart valves
in vitro varied markedly. They noted that the Gram-negative cocci had the highest
adherence ratio closely followed by Pseudomonas aeruginosa. It is interesting to
observe that these organisms are those most commonly isolated from naturally

69 7
occurring cases in dogs. The same authors also found that adherence was much
greater when the valve sections were agitated.
Neither of the organisms isolated from the first two cases described in this
paper have been recorded previously as the causal agent of bacterial endocarditis
in the dog.
In conclusion then, it would appear that a primary stimulus, possibly
endocrinological, is necessary before colonisation of the heart valves can take
place. Further a bacteraemia is necessary, the ease with which the bacteria adhere
to the valve being an inherent characteristic of the organism.
Several theories have been advanced to explain paroxysmal tachycardia, the
ectopic pacemaker being the most likely. This supposes the presence of an ectopic
focus in the ventricular myocardium (normally kept under control by the sinus
pacemaker), which suddenly gains control of the heart. It is thought that this
focus may develop from damaged heart muscle. The fibres adjacent to the ectopic
focus will themselves be more excitable if damaged by disease (Katz & Pick,
1956). This theory would explain why premature ventricular contractions are
uncommon if the lesion does not involve the myocardium. Case I had a large
parietal lesion which could account for the arrythmia recorded in this dog.
The absence of myocardial infection does not rule out the possibility of an
ectopic focus being present. The capacity of certain fibres to produce impulses
may be temporarily or permanently altered by local metabolic conditions e.g.
electrolyte imbalances. These fibres may then initiate premature ventricular
systoles.
That both cases showing arrythmias reverted to sinus rhythm without the use
of anti-arrhythmia therapy may be explained by: (a) rest; (b) fluid therapy
corrected any metabolic imbalances present: (this is purely a hypothesis as serum
electrolytes were not measured), although hyperkalaemia is commonly associated with T-waves of increased amplitude; (c) the use of intra-venous ampicillin
decreased the irritability of the myocardium, a conclusion for which there is no
pharmacological evidence.
Finally, the systolic-diastolic murmur in the Boxer can be explained by the
presence of a lesion on the aortic valve producing both stenosis and incompetence. The Alsatian had a lesion on the mitral valve which would account for the
left sided systolic murmur, the diastolic component being due to aortic
incompetence as it is doubtful if the mitral lesion was giving rise to a stenosis of
the valve, sufficient to produce a diastolic murmur. The Dalmatian is a good
example of a chronic, long standing lesion. It is interesting to speculate if there is
any connection between the lesion and the surgical interference 18 months
previously. It is unfortunate that the presence of the astrocytoma would tend to
confuse any conclusions about clinical behaviour although the size of the aortic
lesion explains the systolic/diastolic murmur and the fact that the dogs femoral
pulse was barely palpable.
BACTERIAL E N D O C A R D I T I S IN D O G S

69 8

D. B . M U R D O C H A N D J . R . B A K E R
ACKNOWLEDGMENTS

The authors are grateful to Mr H. E. Ritchie for his advice and assistance.
REFERENCES
ANDERSON,
L.J. & FISHER,
E.W. (1968) The blood pressure in canine interstitial nephritis. Res. vet.
Sci. 9, 304.
ANGRIST,
A., OKA,M. & NAKAO,
R. (1969) Interstitial oedema in valvular endocarditis. Ann. N. Y.
Acad. Sci. 156,480.
BONE,W.J. (1970) L-form of Pseudomonas aeruginosa the aetiologic agent of Bacterial
endocarditis in a dog. Vet. Med. 65,224.
BLAHD,M., FRANK,
I. & SAPHIR,
B.(1939) Experimental endocarditis in dogs. Archs. Path. 27,423.
BURROWS,C.F., GASKELL,
C.L. & MCGRATH,J.T. (1 972) Clinico-pathologic Conference
(vegetative endocarditis). J. Am. vef.rned. Ass. 161,926.
DARKE,
P.G.C. (1973) Acquired cardiac disorders in the dog. In: The Veterinary Annual, Fourteen
Year--1973. John Wright, Bristol.
DETWEILER,
D.K., PATTERSON,
D.F., HUBBER,K. & BOTTS,R.D. (1961) The prevalence of
spontaneously occurring cardiovascular disease in dogs. Am. J. publ. Hlth. 51,228.
DETWEILER,
D.K. & PATTERSON,
D.F. (1966) Bacterial endocarditis. In: Current Veterinary Therapy
1966-1967. Ed. by R.W. Kirk) W. B. Saunders, Philadelphia.
DETWEILER,
D.K. (1968) Bacterial endocarditis. In: Canine Medicine, 1 st Catcott edn. American
Veterinary Publications Inc., Santa Barbara, California.
ERNST,E., SCHNEIDER,
P. & TRAUTWEIN,
G. (1973) Untersuchungen zur atiologie und pathogenese
der Endokardiose und Endokarditis des hundes. Teil 11-Pathologisch-anatomischeBefunde.
Dtsch. Tierarztl. Wschr. 80, 322.
ETTINGER,
S.J. & SUTER,
P.F. (1970) Bacterial endocarditis. In: Canine Cardiology. W.B. Saunders
Co. Philadelphia.
FISHER,E.W. (1967) Clinical signs and differential diagnosis of heart disease in the dog. J. small.
Anim. Pract. 8, 15 1.
FISHER,E.W.(1972) Heart disease in the dog. J. small. Anim. Pract. 13,553-560.
FREGIN,
G.F., LUGINBUHL,
H. & GUARDA,
F. (1972) Infarction in a dog with bacterial endocarditis.
J . Am. vet. rned. Ass. 160,956.
GOULD,
K., RAMIREZ-RONDA,
C.H., HOLMES,
R.K. & SANDFORD,
J.P. (1975) Adherence of bacteria
to heart valves in vitro. J. clin. Invest. 56, 1364.
JONES,
T.C. & ZOOK,B.C. (1965) Aging changes in the vascular system of animals. Ann. N. Y. Acad.
Sci. 127,671.
JUBB,K.U.F. & KENNEDY,
P.C. (1970) In: Pathology of Domestic Animals (2nd Edn.) Academic
Press, New York.
KATZ,L.N.& PICK,A. (1956) In: Clinical electrocardiography-Part I, The Arrythmias. 1st Edn.
Lea & Febiger, Philadelphia.
KIRCHOFF,
VON H., AMTSBERG,
G., BISPING,
W. & BASU,A. (1973) Untersuchungen zur atiologie
und pathogenese der Endokardiose und Endokarditis des hundes-Teill 1 1 1 : Mikrobiologische
Befunde. Dtsch. Tierarztl Wschr. 80,428.
KLEINE,L.H., BISGARD,G.F. & LEWIS,R.E. (1966) Rupture of the aortic sinus and aortic
insufficiency in a dog. J. Am. vef.med. Ass. 149, 1050.
KNIGHT,O.H., KELLY,
A.M. & WARDLEY,
R.C. (1 972) Clinico-Pathological Conference (endocarditis). J. Am. vet. med. Ass. 160, 212.
LILLEHEI,
C.W., BOBB,J.R.R. & VISSCHER,
M.B. (1950) Occurrence of endocarditis with valvular
deformities in dogs with arteriovenous fistulae. Proc. SOC.exp. Biol. Med. 75,9.

BACTERIAL ENDOCARDITIS I N DOGS

699

LUGINBUHL,
H. & DETWEILLER,
D.L. (1965) Cardiovascular lesions in dogs. Ann. N. Y. Acad. Sci.
127, 517.
LUNDH,
T. (1964) Fibrinous endocarditis in dogs. Acta. vet. scand. 5, 17.
NIELSEN,
S.W. & NIELSEN,
S.B. (1954) Coronary embolism in valvular bacterial endocarditis in two
dogs. J. Am. vet. rned. Ass. 125, 376.
MADEWELL,
B.R. & NORRDIN,
R.W. (1975) Renal failure associated with pericardial effusion in a
dog. J. Am. vet. med. Ass. 167, 1091.
PATTERSON,
D.F., DETWEILLER,
D.K., HUBBEN,
K. & BOTTS,R.P. (1961) Spontaneous abnormal
cardiac arrythmias and conduction disturbances in the dog. Am. J. vet. Res. 22,355.
PIRIE,H.M. (1967) The pathology of heart disease in the dog. J. small Anim. Pract. 8, 175.
ROBERTSON,
B.T. & GILES,H.D. (1972) Complete heart block associated with vegetative
endocarditis in a dog. J. Am. vet. rned. Ass. 161, 180.
SCHORNAGEL,
H. (1936) Endocarditis. Tijdschr. diergeneesk. 63,57 and 143.
SHOUSE,
C.L. & MEIER,H. (1956) Acute vegetative endocarditis in the dog and cat. J . Am. vet. rned.
Ass. 129,278.
SMITH,
H.A. &JONES,T.C. (1966) In: Veterinary Pathology, 3rd Edn., Lea & Febiger, Philadelphia.
STUNZI,
H. (1962) Zur Pathogenese der Endocarditis valvularis. Schweiz. Arch. Tierheilk 104, 135.
THERAN,
P., HENRY,W.B. & THORNTON,
G.W. (1965) Case Records of the Angel1 Memorial
Hospital (Bacterial endocarditis). J. Am. vet. rned. Ass. 146, 54.
TRAUTWEIN
VON G., BRASS
W., KERSTEIN,
V., ERNST,
E., SCHNEIDER,
P., SCHULZ,
L-CL.,AMTSBERG,
G., BISPING,W., KIRCHOFF,
H. & SCHOLE,J. (1973) Untersuchungen zur aetiologie und
pathogenese der Endokardiose und Endokarditis des hundes. Teil V. Synopsis der Ergebnisse
Dtsch. Tierarztl Wschr. 80, 507.
VALTONEN,
M.H. & OKSANEN,
A. (1972) Cardiovascular disease and nephritis in dogs. J. small
Anim. Pract. 13,687.
WINQUIST,
G. ( I 945) Topografisk och etiologisk sammanstailning av de fibrinosa och ulcerosa
endokarditerna hos en del av vora husdjur. Skand. Vet Tidskr. 35,515.