A Comparison of Surface Infrared with Rectal Thermometry in Dogs.

Abstract

This article is a review on Infectious Endocarditis in dogs.

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INFECTIVE ENDOCARDITIS IN DOGS: A REVIEW
Omobowale T.O.*1, Otuh P.I.2, Ogunro B.N.2, Adejumobi O.A.1 and Ogunleye A.O.3
1Department of Veterinary Medicine, University of Ibadan, Ibadan.
2Veterinary Teaching Hospital. University of Ibadan, Ibadan.
3Department of Veterinary Microbiology and Parasitology, University of Ibadan, Ibadan.
Article Received on 12/06/2017 Article Revised on 02/07/2017 Article Accepted on 22/07/2017
EPIDEMIOLOGY
The epidemiology of endocarditis in companion animals
has not been extensively studied (Bruce, 2002).
However, difficulty in diagnosis and underreporting of
IE in dogs contribute to the reported low prevalence rate
of the disease. This disease is relatively uncommon,
occasionally observed in dogs but rarely in cats (Larry
and John, 2001).
IE is one of the more significant of the endocardial
alterations with increased occurrence in middle-aged,
large-bred, male dogs are most often affected. Pure-bred
dogs are more affected (Maark, 2013).
PATHOGENESIS AND PATHOPHYSIOLOGY
Based on experimental studies, the following factors
have been suggested to be important in the pathogenesis
of IE (Larry and John, 2001).
1. Endocardial damage(which may result from valvular
insufficiency, stenosis, or a stunting lesion)
2. Activation of clothing factors
3. Bacteremia and colonization of a noninfective
thrombus
It is believed that endothelial damage must be present for
infective endocarditis to develop. It is virtually
impossible to induce endocarditis in experimental
animals unless the valvular endocardium is first
traumatized with a polyethylene catheter inserted into the
right or left side of the heart (Garrison and Freedman,
1970). High velocity regurgitant vortices and jets from
turbulent blood flow may mechanically damage the
endocardium (Woodfield and Sisson, 1989; Kasari and
Roussel, 1989). The resultant exposure of underlying
collagen activates platelet aggregation and the
coagulation cascade, and formation of platelet-fibrin
matrix. Deposition of fibrin and platelets, is a part of the
normal healing process which forms a non-infective
thombus (Yok-Ai and Philippe, 2011). The development
of such noninfectious thombus is the first step in the
establishment of infectious endocarditis. Episodes of
bacteremia can result in the colonization process that
result in infection of the thrombus and the initiation of
the process that results in distortion and destruction of
the valve leaflets and their associated structures (Larry
and John, 2001). The valve colonizing organisms may
originate from disrupted oral, gastrointestinal, or
urogenital mucosal surfaces, or from any other localized
SJIF Impact Factor 4.161
Review Article
ISSN 2394-3211
EJPMR
EUROPEAN JOURNAL OF PHARMACEUTICAL
AND MEDICAL RESEARCH
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ejpmr, 2017,4(8), 103-109
*Corresponding Author: Dr. Omobowale T.O.
Department of Veterinary Medicine, University of Ibadan, Ibadan.
INTRODUCTION
Endocarditis has been defined as exudative and proliferative inflammatory alterations of the endocardium,
characterized by the presence of vegetations on the surface of the endocardium or in the endocardium itself, and
most commonly involving the heart valves, but also affecting the inner lining of the cardiac chambers or the
endocardium elsewhere (Blood et al., 2007). Bacterial endocarditis is an infection of the valvular and or mural
endocardium and it may have both cardiac and extra-cardiac sequelae (Brown, 2004). The term, Bacterial
Endocarditis (BE) has been replaced with Infectious Endocarditis (IE) since non bacterial isolates have been
incriminated in its pathogenesis. BE refers to endocarditis that is caused by infection with various bacteria.
Endocarditis (both the term and the disease) is pathophysiologically and epidemiologically unrelated to the most
common form of chronic valvular heart disease in dogs known as endocardiosis (Bruce, 2002). Endocardiosis of
which there is no specific etiology is characterized by chronic fibrosis and nodular thickening of the free edges of
the atrioventricular valves (Blood et al., 2007). IE is an infection of the valvular or mural endocardium with
microbe, which may have both cardiac and extracardiac sequelae. (Valerie, 2004) It is a disease that commonly
occurs in dogs. The mitral and aortic valves are the worst affected. Common causative microbial agents include
Staphylococcus spp, Streptococcus spp, Escherichia coli, and Bartonella spp. Congestive heart failure, immune-
mediated disease, and thromboembolism are the major complications of IE. Diagnosis of IE by echocardiography
and long-term treatment with broad-spectrum antibiotics may contribute to the timely detection and treatment of
the disease.

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source of infection (Calvert, 1982; Anderson and
Dubielzig, 1984). The manner by which bacteria localize
on a valve is not completely clear. The production
extracellular polysaccharides, such as dextrans by some
bacteria, has been shown to be important in their
adherence to the constituents of non-bacterial thrombotic
endocarditis and may play a role in the pathogenesis of
bacterial endocarditis (Michael et al., 1977; Anderson,
1984; Kasari and Roussel, 1989). Also, the contribution
of gelatinase to the pathogenesis of endocarditis caused
by Enterococcus faecalis in rabbit models have been
shown (Lance et al., 2010). Subacute and chronic
bacteremia often followed integumentary infections such
as abscesses, cellulitis, and infected wounds and was
usually the result of gram-positive microbes. Peracute
and acute bacteremia was associated with internal
infections and was usually the result of E coli. (Calvert et
al., 1985).
BACTERIAL ISOLATES
The most common isolates include Staphylococcus
aureus, Escherichia coli, β-hemolytic streptococci,
Corynebacterium spp., Pseudomonas aeruginosa, and
Erysipelothrix rhusiopathiae (Calvert, 1982; O’Grady,
2000). It has been speculated that these organisms may
originate from disrupted oral, gastrointestinal or
urogenital mucosal surfaces or from other sources of
infection (Calvert, 1982, Anderson and Dubielzig, 1984).
The primary difference between the types of organisms
isolated in humans and dogs with infective endocarditis
is that dogs have a higher incidence of gram negative
infections. In four studies, Staphylococcus aureus
accounted for approximately 25% of the organisms
isolated, hemolytic and non hemolytic Streptococci for
20% and Escherichia coli for 25%. Corynebacterium
was isolated in 10% and Pseudomonas in 6%.
Erysipelothrix sp. accounted for 3% of the cases (Mark,
2013). This unusual organism has been reported
elsewhere and has recently been determined to be E.
tonsillarum, not E. rhusiopathiae, the swine pathogen.
Bartonella vinsonii, a rickettsial organism, has been
reported in dogs with culture negative vegetative
endocarditis. PCR-restriction fragment length
polymorphism, sequence and phylogenetic analyses have
identified Bartonella rochalimae involvement in
endocarditis in dogs (Jennifer, 2009). A novel Bartonella
species, Bartonella vinsonii subsp. berkoffii subsp. nov
which can induce endocarditis in dogs, was reported by
Edward et al. (1995) using PCR DNA amplification,
DNA hybridization and sequencing. Similar techniques
were also used by Patrick et al. (2006) to identif
Bartonella Quintana as an isolate also associated with
endocarditis in dogs. Nosocomial cases involving
Pseudomonas sp., Proteus sp., or other unusual (and
often highly antibiotic resistant) isolates as well as
anaerobic bacteria (e.g., Bacteroides sp.) also
occasionally cause infective endocarditis (Dow, 1988).
NON BACTERIA ISOLATES
Candida albicans, is associated with endocarditis in IV
drug users and immunocompromised patients (Badley et
al., 2008). Histoplasma capsulatum and Aspergillus are
other fungi demonstrated to cause endocarditis(Lamas
and Eykyn, 2003). Endocarditis with Tricosporon asahii
has also been reported in a case report (Izumi et al.,
2009).
PREDISPOSING FACTORS
Predisposing factors for canine infective endocarditis
include congenital aortic valve disease and probably
other congenital heart diseases that cause disturbances of
blood flow and subsequent changes in the endocardium
(Bruce, 2002). Prior valvular endocardial damage is one
of the most significant factors increasing the chances of
endocardial infection (Anderson, 1984). Dogs with
congenital heart abnormalities are at a higher risk of
developing valvular BE, because altered blood flow
favors endocardial trauma (Kasari and Roussel, 1089).
Approximately 25% of dogs with BE have some form of
congenital heart disease (Calvert, 1982; Kasari and
Roussel, 1989). Still, many dogs with valvular BE have
no prior history of valvular disease or congenital heart
defect (Calvert, 1982). In these cases, BE may be caused
by bacteria, such as S. aureus or β-hemolytic
streptococci, that produce -proteases that damage
endothelial surfaces, subsequently exposing the
subendothelial matrix (Sisson and Thomas, 1986).
Corticosteroid administration has also been known to be
a very common predisposing factor. It may be that the
immunosuppressive effect of such drugs encourages
bacteremia that preludes infective endocarditis. Infection
with potentially immunosuppressive organisms (e.g.,
Bartonella sp., Ehrlichia sp.) appears to enhance the risk
of endocarditis in dogs. (Bruce, 2002).
Many cases of endocarditis appear to have a nosocomial
origin. Infected intravenous catheters, prosthetic heart
valves, openheart surgery and interventional cardiac
catheterization (e.g., aortic balloon valvuloplasty) all
appear to enhance the risk of endocarditis in dogs. There
is actually little evidence that periodontal disease is a
frequent source of infective endocarditis in dogs. This is
in contrast to humans. Other predisposing factors for
endocarditis in dogs include other chronic sources of
bacteremia (e.g., urinary tract infection, diskospondylitis)
or systemic illness that facilitates bacterial infection
(e.g., diabetes mellitus, Cushing’s disease). (Bruce,
2002). Interestingly, chronic valvular heart disease
(endocardiosis) does not appear to predispose to infective
endocarditis.
CLINICAL PRESENTATION
Clinical signs observed in cases of bacterial endocarditis
are not limited to cardiac disease and such may result
from sepsis, septic embolization and immune mediated
complications. Clinical signs associated with septic
embolization may vary depending on the location of the
embolization, the degree of vascular obstruction and the

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degree of collateral circulation remaining (O’Grady,
2000). In the dog, the kidney and the spleen are the
commonest sites of embolization (Anderson and
Dubielzig, 1984, O’Grady, 2000). With a prolonged
course of the condition, deposition of immune complexes
in the glomeruli and synoviae of joints may occur
(Brown, 2004).
Owners commonly present Patients because they appear
ill systemically. Weakness, depression, anorexia (or
inappetence) and weight loss are common presenting
signs (Mark, 2013). Other dogs have signs of left heart
failure. The owners often note respiratory abnormalities
(tachypnea, dyspnea, cough) in this situation.
Concomitant discospondylitis is a common problem
(Mark, 2013).
Infective endocarditis can produce a wide spectrum of
clinical signs, including primary cardiovascular effects or
signs related to the nervous system, GI tract, urogenital
system, or joints. This is because infected thrombi
released from the infected aortic or mitral valves enter
the circulation and can embolize other organs and limbs
(Cynthia et al., 2010). A chronic, intermittent or
continuous fever is usually present.
Arrhythmia or sudden death may be caused by very
small emboli which may take the first exit that, off the
aorta and so travel down a coronary artery, creating a
small, septic myocardial infarct (Mark, 2013). Slightly
larger emboli may take the brachiocephalic trunk travel
through the right subclavian artery and lodge in the right
front leg. This causes a right front leg lameness (Mark,
2013). Lameness is a common clinical sign in dogs with
IE (Cynthia et al., 2010). Two types of arthritis have
been described in dogs with IE (Mark, 2013). One is
septic arthritis, presumably secondary to bacteremia or
embolization. The other is a sterile arthritis, thought to be
due to immune complex deposition that occur secondary
to the bacterial antigenemia. The lameness may be stable
or shift from leg to leg.
Acute to subacute mitral or aortic valve regurgitation can
result in left heart failure (ie, pulmonary edema) and
clinical signs of tachypnea, dyspnea, and cough. If the
tricuspid valve is affected, ascites and jugular pulsations
may be present. (Cynthia et al., 2010).
A cardiac murmur is a common finding (Cynthia et al.,
2010). Discovering a new heart murmur in a patient that
is febrile is the classic finding to make one suspicious of
IE. Of course, most clinicians realize that classic findings
usually do not occur in most cases (Mark, 2013). A
systolic heart murmur is the most common (Mark, 2013).
The murmur associated with mitral valve endocarditis is
that of mitral regurgitation. If the murmur is grade III or
louder and can be documented to be new and the patient
is febrile, IE must be a primary differential diagnosis.
Being certain that a systolic heart murmur has only
occurred recently, however, is often difficult (Mark,
2013). A loud heart murmur in a young dog with a fever
examined previously by a veterinarian, however, should
be considered a new murmur until proven otherwise. A
loud systolic murmur in a small breed, geriatric dog
(even one with a fever) is most commonly due to
myxomatous mitral valve degeneration, not to IE (Mark,
2013). A soft systolic murmur in large dog can also be
due to IE but can also occur with numerous other
cardiovascular lesions or increased stroke volume
secondary to fever.
In dogs with aortic valve endocarditis, a diastolic heart
murmur (which is difficult to identify) due to aortic
regurgitation is commonly present (Mark, 2013). The
murmur is heard with maximal intensity over the left
cardiac base (Cynthia et al., 2010). It is blowing in
character. It starts immediately after the second heart
sound and decreases in intensity through diastole.
Infective endocarditis is by far the most common cause
of an audible diastolic heart murmur secondary to aortic
regurgitation in the dog and cat (Mark, 2013).
A soft systolic heart murmur caused by increased stroke
volume may also be observed. In this situation, a
bounding arterial pulse is noted due to increased pulse
pressure caused by diastolic run-off and increased stroke
volume (Cynthia et al., 2010).
Lesions of bacterial endocarditis are usually located in
those areas where high pressure and velocity gradients
exist such as are found in both the mitral and aortic
valves (Brown, 2004). One of the most significant
factors for the development of endocardial infection is a
prior valvular damage (Anderson and Dubielzig, 1984,
Kasari and Roussel, 1989). High velocity regurgitant
vortices and jests of blood from turbulent blood flow
may damage the endocardium mechanically (Kasari and
Roussel, 1989, Woodfield and Sisson, 1989). The
resultant exposure of sub-endeothelial collagen activates
the aggregation of platelets and the cascade of events that
are involved in coagulation and bacteria are able to
adhere to the platelet fibrin matrix (Brown, 2004).
Animals that have a congenital cardiac defect are more
likely to develop bacterial endocarditis because altered
blood flow favours endocardial trauma (Kasari and
Roussel, 1989). It has been reported that about 25% of
dogs with bacterial endocarditis have some form of
congenital heart disease (Calvert, 1982, Kasari and
Roussel, 1989). However, bacteria like Staphylococcus
aureus and β-haemolytic streptococci which produce
proteases that are capable of damaging endothelial
surfaces and subsequently exposing the subendothelial
matrix (Sisson and Thomas, 1986). Once bacterial
endocarditis has been established, resolution is difficult
because the bacterial colonies become tightly enmeshed
in an avascular network of platelets and fibrin that host
humoral factors and blood phagocytes cannot traverse
(Brown, 2004). The rate of propagation of the vegetative
lesion varies with the virulence of the infecting
organism. Highly virulent organisms cause rapid necrosis

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of the valvular stroma and may even perforate the valve
(Woodfield and Sisson, 1989). Conversely, organisms of
lower virulence damage the valvular stroma to a lesser
degree and produce a slowly enlarging vegetative lesion
that evolves over weeks to months (Kittleson and Kienle,
1998). Hyalinization or calcification of the vegetative
lesion may be observed in older lesions (Kasari and
Roussel, 1989, Woodfield and Sisson, 1989). There
could be perforation, tearing or valvular leaflet distortion
due to vegetative lesions which alter valvular leaflet
coaptation and cause valvular insufficiency. If the
regurgitant blood flow is small and develops slowly, the
heart can adapt through compensatory measures. If
severe regurgitation is however present, the heart cannot
compensate and congestive heart failure develops
(Brown, 2004).
TREATMENT
The goal of therapy is to control clinical signs of
congestive heart failure, resolve any significant
arrhythmias, sterilize the lesion, and eliminate the spread
of infection. (Cynthia et al., 2010) Ideally, the choice of
antibiotic therapy should be based on culture of the
offending organism from blood and on identifying an
antibiotic to which the organism is sensitive. Before
antibiotic therapy is instituted, blood culture should be
carried out on every patient suspected of having IE
(Mark, 2013). Parenteral antibiotics are indicated
initially for 1–2 wk. This uneconomical start is followed
by oral antibiotics for at least 6–8 wk. (Cynthia et al.,
2010) Initial broad-spectrum bactericidal antibiotics (a
combination of ampicillin plus gentamicin or
enrofloxacin, or cephalothin plus gentamicin) should be
used and changed, if antibiotic sensitivity studies
indicate. (Cynthia et al., 2010) Renal function should be
monitored when gentamicin is used because it is
nephrotoxic. Antibiotics selected to treat a patient with
IE must be bactericidal because bacteria are growing
slowly within the vegetations and the vegetations prevent
leukocytes from phagocytizing cells. Consequently, a
bacteriostatic agent will not successfully sterilize the
vegetation (Mark, 2013). Antibiotic prophylaxis is
indicated in dogs with subaortic stenosis when any type
of procedure that can result in significant bacteremia is
performed (Cynthia et al., 2010). Routine dental
prophylaxis is not warranted with other types of cardiac
disease and especially not in dogs with myxomatous
mitral valve degeneration; because there is no evidence
that these dogs are at increased risk of infective
endocarditis (Cynthia et al., 2010).
Dogs that respond to antibiotic therapy often require long
term cardiac medications for heart failure and frequent
reevaluations (Cynthia et al., 2010). The choice of
cardioactive agents is guided by radiographic and
echocardiographic findings (Larry and John, 2001).
Controlling heart failure often requires the use of
diuretics such as furosemide, an ACE inhibitor and when
myocardial failure is present, pimobendan (Cynthia et
al., 2010). In addition, a more potent arteriolar dilator,
such as hydralazine, can be very beneficial in a patient
that has acute, severe pulmonary edema or that is
refractory to the other drugs (Mark, 2013). Hydralazine
reduces peripheral vascular resistance and so reduces the
amount of regurgitation in both aortic and mitral
regurgitation (Mark, 2013). This results in decreased
diastolic intracardiac pressures and a rapid reduction in
pulmonary edema formation (Mark, 2013). Care must be
taken not to produce profound hypotension when
administering hydralazine along with an angiotensin
converting enzyme inhibitor. This complication can be
prevented by monitoring.
Corticosteroid administration is contraindicated IE
patients (Mark, 2013). Its use may result in exercitations
of the clinical signs and worsening of the prognosis
(Mark, 2013). Moreover, Patients with occult IE will
usually develop clinical signs rapidly following
corticosteroid administration (Mark, 2013).
PROGNOSIS
The prognosis for dogs with active IE is poor. By the
time of diagnosis, most cases of IE have reached such an
extent that there is irreversible damage to the valve
(Larry and John, 2001). In one study, of 45 dogs proven
to have IE either by fulfillment of clinical diagnostic
criteria or by necropsy, only 20% survived (Mark, 2013).
Congestive heart failure, common sequelae of IE, may be
severe and intractable if the aortic valve is significantly
involved; the prognosis is grave in these cases (Cynthia
et al., 2010). The prognosis is much more favorable
when infection is mild and limited to one of the AV
valves (Cynthia et al., 2010).
Severe left heart failure commonly develops in dogs with
large aortic valve lesions which is fatal (Mark, 2013).
Dogs with severe mitral valve endocarditis may follow a
similar course but generally have a better prognosis,
depending on the severity of regurgitation. (Mark,
2013).No definitive treatment for valve destruction such
as prosthetic valve replacement exists in veterinary
medicine. Consequently, once severe regurgitation is
produced heart failure and death are ultimately the
expected result (Mark, 2013).
Renal infarction and failure are embolic complications
that may result in death of IE patients (Mark, 2013).
DIAGNOSIS
Clinical signs and abnormal heart sounds may help to
suggest IE. A Complete Blood Count often shows a
neutrophilic leukocytosis (Cynthia et al., 2010). Active
infection may be associated with the presence of band
neutrophils, and upto 90% chronic infection with a
monocytosis (Cynthia et al., 2010). Anemia of chronic
disease is frequently present (Cynthia et al., 2010).
Serum analysis may reveal abnormalities reflecting
organ involvement secondary to infective emboli and
may include increases in liver enzymes, BUN, and
creatinine. In animals that develop immune complex

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glomerulonephritis, significant urinary protein loss and
hypoalbuminemia may develop (Cynthia et al., 2010).
Blood cultures must be obtained to try to identify the
offending organism and subsequently to identify the
appropriate antibiotic in patients with IE. Critically ill
animals frequently develop sepsis and have positive
blood culture results. Dogs with discospondylitis can
have clinical signs that closely mimic IE (Mark, 2013).
To increase the chance of successful identification of
bacteremia through the use of blood cultures in a patient
with IE, more than one blood culture should always be
taken (Mark, 2013). Preferably the patient should not be
on antibiotic therapy at the time of culture but positive
blood cultures can still be obtained and so antibiotic
therapy is not an absolute contraindication (Mark, 2013).
It is preferable to draw 2 or 3 blood samples, each 1–2 hr
apart, in a 24-hr period (Cynthia et al., 2010). If the
patient has already been administered antibiotics, three
more cultures can be taken over the following week.
Strict aseptic blood collection procedures should be
followed (Cynthia et al., 2010). Blood cultures are never
used definitively to make a diagnosis of IE due to lack of
specificity as blood cultures are also positive in other
diseases. In one study, of 165 dogs with positive blood
cultures, only 45 were diagnosed as having IE (Mark,
2013). Cultures should be incubated for at least three
weeks and Gram stains should be made at intervals, even
if no growth is apparent (Mark, 2013).
Radiographic findings in IE are variable (Larry and John,
2001). Radiography may demonstrate cardiac chamber
enlargement, depending on the location and degree of
insufficiency of the involved valve (Cynthia et al., 2010).
If the aortic or mitral valve is severely affected, there
will be left atrial and left ventricular chamber dilatation
(Cynthia et al., 2010). Evidence of left heart failure may
be seen as an increase in interstitial density or, in severe
Congestive heart failure, an alveolar pattern in the
pulmonary parenchyma. If the tricuspid or pulmonic
valve is affected, right-sided chamber enlargement is
expected (Cynthia et al., 2010).
Echocardiography is the diagnostic test of choice
because findings using this technique are distinctive
(Larry and John, 2001). It is however not 100% sensitive
or specific (Mark, 2013). Besides identifying
vegetations, dogs with destructive lesions of their valves
but without vegetations can be diagnosed with IE based
on the presence of a regurgitant lesion and the
echocardiographic appearance of the valve, especially
when the aortic valve is involved (Mark, 2013). The
affected valve is usually easily detected—the involved
area is hyperechoic (bright), thickened, and often
vegetative (ie, looks like a cauliflower). Erosive lesions
may predominate in some animals (Cynthia et al., 2010).
Doppler echocardiography will confirm insufficiency of
the valve, and chamber enlargement on the side of the
affected valve is expected when significant insufficiency
is present (Cynthia et al., 2010).
Electrocardiographic findings in IE are not diagnostic
(Larry and John, 2001). Electrocardiography may
demonstrate atrial and ventricular premature complexes
(Cynthia et al., 2010). Ventricular tachyarrhythmias,
including ventricular tachycardia, are relatively common,
and supraventricular tachyarrhythmias including atrial
fibrillation, are also observed (Larry and John, 2001).
The height of the R wave may be increased (suggestive
of left ventricular enlargement) and the width of the P
wave increased (suggestive of left atrial enlargement)
(Cynthia et al., 2010).

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