Vegetative valvular endocarditis and septicemia in a beef cow
Amanda MH. Breuer
Abstract – A Limousin beef cow was evaluated for progressive weight loss and poor doing following premature
calving. Traumatic reticuloperitonitis was suspected and treated accordingly. The cow died two weeks following
initial assessment and treatment. Post mortem examination revealed vegetative valvular endocarditis involving the
left atrioventricular valve and ventricular wall.
Case Description
An 8-year-old Limousin beef cow presented
for the evaluation of progressive weight loss and poor
doing, 3 weeks following premature calving. Weight
loss commenced in the 7th month of gestation and the
cow gave birth to a premature but otherwise normal
calf. Following calving, the cow continued to lose 200300 lbs over the course of three weeks, until at which
point veterinary care was sought by the client.
Physical examination revealed marked weight
loss, an abnormal response to withers pinch, increased
lung sounds, poor rumen motility and dry feces. A
remnant of an old abscess on the skin overlying the left
tuber coxae was noted. Slight favouring of the left hind
foot was observed, which was consistent with a recent
episode of footrot treated several weeks previously. The
remainder of the physical exam was unremarkable.
Traumatic reticulopericarditis (TRP) was suspected and
a course of antibiotics, an antiinflammatory and a
magnet were instituted as treatment. In response, the
cow showed moderate signs of improvement, but
deteriorated rapidly thereafter, resulting in death.
A post mortem examination was performed 12
hours following death. The abdomen was explored and
no discernable lesions consistent with TRP were
evident; the diaphragm was clear of puncture wounds,
fibrin and adhesions. In addition, no sharp objects were
found in the rumen or reticulum. The magnet given
previously was recovered from the reticulum and found
to have minimal filings attached. A large amount of
serous, amber coloured fluid was observed in the
pleural space upon entry into the thorax. Severe
pulmonary edema was present in the lungs and the lung
tissue exuded fluid from the cut surface. The heart did
not appear to be enlarged and had a normal right to left
ventricular ratio of 1:3. Upon dissection a large, yellow,
fibrous, vegetative mass approximately 4cm x 4cm x
5cm was found within the left ventricle, involving both
the mitral valve and ventricular wall. The cut surface of
the mass revealed a fibrinonectrotic center filled with
purulent material.
Tissue samples of the heart, vegetative mass,
trachea, lung, uterus, spleen, liver and kidney were
submitted for histopathology. Histopathology of the
heart muscle revealed random multifocal areas of
fibrosis throughout the myocardium and the
Figure 1. Photograph of the vegetative mass found in the left
ventricle involving the mitral valve and ventricular wall.
endocardium was extremely thickened with maturing
granulation and fibrous tissue. The vegetative mass on
the affected valve was found to be composed of
laminated fibrinonecrotic debris containing many
bacterial colonies and scattered infiltrates of degenerate
leukocytes. Colonies of bacteria and fibrin were present
on the eroded surface of the lesion. The
bronchoalveolar lumina in the diffusely congested and
edematous lung contained variable amounts of
proteinaceous edema. Mild and acute pulmonary
hyaline membranes and alveolitis were also present.
The kidney had mild to moderate multifocal interstitial
fibrosis and showed small numbers of focally
mineralized tubules. The liver sample displayed mild
hepatic lipidosis, consistent with metabolic imbalance.
The remaining tissues were markedly autolyzed and
provided no other useful diagnostic information.
Bacterial culture on samples of pleural fluid,
mediastinal lymph node and purulent material within
the mass revealed presence of Pseudomonas spp.
A diagnosis of terminal septicemia and
endotoxemia due to Pseudomonas spp., valvular
endocarditis and myocardial fibosis in addition to mild
hepatic lipidosis was made based on the post mortem
and pathology reports.
Discussion
Bacterial endocarditis (BE) is a major cause of
heart disease in adult cattle. However, it often goes
undiagnosed or is frequently misdiagnosed in practice
(1). BE may cause showering of bacteria from the heart
and disseminated sepsis, in addition to being a potential
cause of heart failure as a consequence of valvular
insufficiency. In cattle, BE most commonly involves
the tricuspid valve. However, the second site of
predilection is the mitral valve (2). As seen in this case,
the mitral valve was affected with BE due to
Pseudomoas spp. colonization. Death was not a direct
result of heart failure, as gross cardiac changes
consistent with congestive heart failure were not
evident. Instead, the histopathological report concluded
death was the result of bacterial showering of
Pseudomonas spp. from the vegetative lesion.
Disseminated septicemia and endotoxemia from septic
emboli originating from the vegetative lesion on the
mitral valve lead to terminal, multi-organ failure.
The clinical signs associated with heart disease
resulting from BE are non-specific and infrequently
observed in cattle (3). A systolic cardiac murmur, thrill,
tachycardia, thoracic pain, intermittent or constant
fever, polypnea, ill thrift, diarrhea, constipation and
shifting lameness are all clinical signs which may be
present but are not necessarily unique to BE. For a
general practitioner in the field, auscultation of a
cardiac murmur is the most specific clinical sign of BE,
while the others listed are vague and may be present
with other conditions common to cattle (1). This
ambiguity of clinical signs ultimately interferes with
obtaining an accurate diagnosis. For example, in a
recent study, of 52 cows afflicted with endocarditis only
13 had an obvious murmur (4). Another previous study
speculates that closer to half of cattle with BE will fail
to have an auscultable murmur (5).
Without a
discernable murmur, a practitioner may fail to recognize
BE as a differential diagnosis when performing an
initial evaluation, and as a result, a misdiagnosis of
pneumonia or TRP is frequently made. When a murmur
is ascultated, ancillary tests such as echocardiography
and a blood culture would permit a definitive diagnosis
of BE to be made (6). In this case, both vague clinical
signs similar to TRP and the absence of an auscultable
heart murmur interfered with obtaining an accurate
initial differential diagnosis of BE.
A key component of the pathophysiology of
BE is persistent bacteremia, which is often the result of
a chronic septic process at a distant site in the body or a
low-grade infection. Possibilities include, but are not
limited to septic mastitis, chronic metritis, foot abscess,
musculoskeletal abscessation, cellulitis, venipuncture of
the jugular or milk vein, or the presence of an
indwelling intravenous catheter for an extended period
of time (5,7). Arcanobacterium pyogenes is one of the
most commonly isolated pathogenic agents from
endocardial lesions and/or blood (6). Other common
isolates
include
-hemolytic
streptococci,
Arcanobacterium
pyogenes,
Corynebacterium
pyogenes, Micrococcus and Staphylococcus spp.,
Clostridium
chauvoei,
Mycoplasma
mycoides,
Erysipelothrix rhusiopathiae and as seen in the case of
this cow, Pseudomonas spp. In large animals, BE does
not require pre-existing trauma to the cardiac
endothelium to initiate the disease process of
endocarditis. Instead, it is believed that the ability of
some pathogens to adhere to normal endothelium in
conjunction with persistent bacteremia can be sufficient
cause (7). No direct inciting cause was identified in this
case, however it is speculated the scar of a previously
ruptured abscess observed over the tuber coxae is most
probable. The other two possibilities of footrot and a
metritis post-calving occurred after the initial onset of
clinical signs, and can therefore be excluded from the
possible causes. The cow likely became bacteremic
with Pseudomonas spp. as a result of the ruptured
abscess, resulting in the colonization of the mitral valve
and the development of valvular BE.
Treatment options for those cases of BE that
are diagnosed ante-mortem are limited by both
feasibility and economics. The minimum length of
recommended antimicrobial treatment is 21 days, but is
often prolonged past 4 weeks (6). When developing a
treatment regime, blood culture and sensitivity is
recommended. An appropriate antimicrobial providing
high concentrations in the serum relative to the
minimum bactericidal concentration should be selected
based on culture and sensitivity results (7). Inadequate
antibiotic distribution and activity within the lesions as
the result of thick fibrous tissue and pyonecrotic debris
are likely to be problematic in regards to treatment
efficacy (1,7). Not only the quantity of drug required
for treatment, but also the difficulty of administering
treatment to animals, such as beef cattle, over a
prolonged period of time often makes treatment
impractical for clients. However, an exception may be
made in some cases where the animal is of particular
value. In addition, the prognosis for animals with BE is
generally guarded to poor, despite attempted treatment,
as most cases are identified and diagnosed late in the
course of the disease. (7). Marginal improvement of
prognosis with early diagnosis and early initiation of
treatment has been documented. Ultimately, informed
clients often opt for euthanasia or salvage for slaughter
rather than a course of treatment due to the high
financial cost, length of treatment and the overall
guarded to poor prognosis associated with BE (1). In
the case of this cow, diagnosis of BE was not obtained
in a timely manner, and a treatment regime specific to
BE was not an option.
This case emphasizes the challenges which can
complicate diagnosing BE in the field. Often clinical
signs are non-specific making a definitive diagnosis
difficult to obtain. Regardless of a timely diagnosis and
treatment, the prognosis and practicality of treating
cases of BE is an additional challenge, as prognosis
remains guarded to poor, and is additionally
complicated by finances.
3.
4.
Acknowledgements
The author would like to thank Dr. Reg Clinton for his
guidance, and Dr. Charlotte Winder and Dr. Katharine
Found for their support.
5.
6.
References
1.
2.
Dowling PM, Tyler JW. Diagnosis and treatment of
bacterial endocarditis in cattle. J Am Vet Med Assoc
1994;204:1013-1016.
Reef VB, McGuirk SM. Diseases of the cardiovascular
system. In: Smith BP, ed. Large Animal Internal Medicine.
7.
4th ed. St. Louis, Missouri: Elsevier-Saunders, 2008:453–
489.
Buczinski S, Rezakhani A, Boerboom D. Heart disease in
cattle: diagnosis, therapeutic approaches and prognosis.
Vet J 2010;184:258-263.
Bexiga R, Mateus A, Philbey AW, et al.
Clinicopathological presentation of cardiac disease in
cattle and its impact on decision making. Vet Rec
2008;162:575–580
Power HT, Rebhun WC. Bacterial endocarditis in adult
dairy cattle. J Am Vet Med Assoc 1983;182:806-808.
Divers TJ, Peek SF. Cardiovascular Diseases. In:
Rebhun’s Diseases of Dairy Cattle 2nd ed. St. Louis,
Missouri: Elsevier-Saunders, 2008: 53-56.
Radostits OM, Gay CC, Hinchcliff KW, et al. Diseases of
the cardiovascular system In: Veterinary medicine – a
textbook of the diseases of cattle, horses, sheep, pigs and
goats 10th ed. Philadelphia: Elsevier-Saunders, 2007: 42443.