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Infective Endocarditis Due
to Streptococcus Pneumonia
Al Suob H. and Saif A.S.
Department of Medicine, Hamad Medical Corporation
Doha, Qatar
Abstract:
A young patient with a ventricular septal defect
presented with Streptococcus pneumoniae pneumonia
complicated by endocarditis. The presentation
was acute with high fever, hypotension, leukocytosis,
and renal impairment. The organism was penicillin
sensitive. Treatment with ampicillin for four
weeks produced a successful outcome. Endocarditis
due to Streptococcus pneumoniae has become rare
in recent years and the association with a ventricular
septal defect has not been reported before. Pertinent
literature is reviewed.
Key words: Endocarditis, Streptococcus pneumoniae,
pneumococcal endocarditis.
 Introduction:
Infective endocarditis is an uncommon manifestation
of Streptococcus pneumonia infection(1). In the
pre-antibiotic era, Streptococcus pneumonia caused
approximately ten per cent of all cases of native
valve endocarditis but the introduction of penicillin
and other antibiotics substantially reduced the
incidence of pneumococcal endocarditis to less
than one per cent (1). Aronin et
al(2) in a review
of the English literature published from 1966
to 1996 found 197 reported cases. There is a strong
association with alcohol consumption(1). The usual
portal of entry for infection is the lung(2).
Pneumococcal endocarditis characteristically presents
as an acute illness often accompanied by meningitis,
rapid destruction of heart valves, congestive
heart failure, and is associated with a high
mortality(3).
We describe a patient with a ventricular septal
defect who developed pneumococcal pneumonia complicated
by endocarditis, and the successful outcome.
  Case
Report:
A 14-year-old male was admitted to Hamad General
Hospital in December 2000 with the complaints
of fever, shortness of

Figure 1:
breath, and a productive
cough of three days duration. He was a known case
of Down’s syndrome with ventricular septal defect
(VSD) diagnosed when he was four years old. Physical
examination on admission revealed an ill-looking
patient, with a blood pressure of 80/60 mm Hg,
pulse rate 120/minute, respiratory rate 35/ minute,
temperature 39.2 oC, and bilateral coarse crepitation
at both bases although more on the left side.
Heart examination revealed a palpable thrill and
a pansystolic murmur at the left sternal border.
The rest of the physical examination was unremarkable.
Laboratory investigations revealed: haemoglobin
13.4 gm/dL, platelets 178,000/mm3, white blood
cell count 24,000/mm3, with 93% polymorphonuclear
neutrophils, 5 % lymphocytes, and 2 % monocytes;
serum creatinine 163 umol /L, alanine aminotransferase
31 IU/L, aspartate aminotransferase 77 IU/L, alkaline
phosphatase 21 U/L, lactic acid 5.7 mmol/L; arterial
blood gases: pH 7.36, Pco2 34 mm Hg, Po2 58 mm
Hg. Chest radiograph showed a non-homogenous infiltrate
at the left base. Two sets of blood culture grew
Streptococcus pneumonia colonies sensitive to
penicillin (MIC 0.6 µg/mL ). The patient
was admitted to the intensive care unit, given
intravenous fluids and intravenous ceftriaxone
and erythromycin (later changed to ampicillin
as penicillin was not available in the hospital
at that time). He improved in response to treatment.
In view of the presence of VSD and the positive
blood culture, a transthoracic echocardiogram
(TTE) was done. This showed vegetations attached
to the right ventricular side of the VSD. A diagnosis
of infective endocarditis was made. He had an
uneventful hospital course and was discharged
home after four weeks of treatment with intravenous
antibiotics. Repeat TTE on discharge showed residual
vegetations.
  Discussion:
Our patient fulfilled Dukes’s criteria for definite
infective endocarditis (4); he had a predisposing
condition for endocarditis (ventricular septal
defect), fever (temperature > 38oC), two positive
blood cultures growing Streptococcus pneumonia,
and an echocardiogram demonstrating vegetations.
To our knowledge this is only the second case
of infective endocarditis due to S. pneumonia
seen in our hospital over the last 18 years. Hamad
hospital is the only hospital providing acute
medical care for the whole of Qatar. This finding
is in accordance with the international literature
which indicates that infective endocarditis due
to S. pneumonia is rare(1,2,5,6). Aronin et
al(2)
in a review of the English language literature
from 1966 to 1996 found 197 cases of S. pneumonia
infective endocarditis. Lefort et al(6) reported
30 cases of S. pneumonia infective endocarditis
from France between 1991 and 1998. Infective endocarditis
due S. pneumonia usually has an acute presentation,
with fever, septicaemia, and rapidly progressive
congestive heart failure(3). Subacute presentations
have been described occasionally(7). Typically
the disease follows pneumonia in the setting of
alcoholism(2). Some patients, especially the elderly,
have the typical Osler’s triad of pneumonia, endocarditis,
and meningitis(2). Less commonly it follows primary
infections at other extrapulmonary sites(2). Underlying
valvular heart disease is not a prerequisite for
pneumococcal endocarditis, and normal valves are
frequently affected(1). S. pneumonia infective
endocarditis is associated with a high morbidity
and a mortality variously reported between 28%
and 67%(2,5-6). The poor prognosis has been attributed
to both host and microbial factors, including
older age, and concomitant diseases as well as
the organism’s propensity to infect and rapidly
destroy left-sided heart valves(2).
The portal of entry of the organism in our patient
was the lung. The presentation was acute with
pneumonia and endocarditis but no meningitis.
He was not alcoholic and had none of the other
conditions known to predispose to pneumococcal
sepsis. An interesting feature in our patient
is the association of pneumococcal endocarditis
and ventricular septal defect which has not been
reported before although rupture of the ventricular
septum has been reported as a complication of
pneumococcal endocarditis(9). Fortunately the
S. pneumonia in our patient was sensitive to penicillin
although more than 50% of S. pneumonia isolates
in our hospital are resistant. Accordingly he
was treated with parenteral ampicillin alone for
four weeks with a successful outcome. The persistence
of vege-tations as determined by echocardiography
is common after successful medical treatment of
infective endocarditis and is not associated with
later complications(10). There is no formal recommendation
regarding the optimal empiric antibiotic therapy
for patients with pneumococcal endocarditis, however
one of the third generation cephalosporins such
as ceftriaxone with or without vancomycin depending
on the prevalence of resistance to penicillin
in the area seems to be reasonable(2). This regimen
should be modified according to the organism’s
final susceptibility pattern. The optimal therapy
of pneumococcal endocarditis is unknown but a
combined medical-surgical approach employing a
prolonged course of parenteral antibiotics plus
early surgery appears to result in a lower rate
of attributable mortality(2,6).
 References:
1. Taylor SN, Sanders CV. Unusual
manifestation of invasive pneumococcal infection.
AM J Med 1999; 107: 12S-27S.
2. Aronin SI, Mukherjee SK, Wesst JC, Cooney EL.
Review of pneumococcal endocarditis in adults
in the penicillin era. Clin Infect Dis 1998; 26:
1165-71.
3. Austrian R. Pneumococcal endocarditis, meningitis,
and rupture of the aortic valve. Arch Intern Med
1957; 99: 539-44.
4. Durack DT, Lukes AS, Bright DK. New criteria
for diagnosis of infective endocarditis: Utilization
of specific echocardio- graphic findings. Dukes
Endocarditis Service. Am J Med 1994; 96: 200-9.
5. Bruyn GAW, Thompson Jvan der Meer JW. Pneumococcal
endocarditis in adult patients. A report of five
cases and review of the literature. Br Heart J
1983; 50: 513-19.
6. Lefort A, Mainardi JL, Selton-Suty C, Casassus
P, Guillevin L, Lortholary O. Streptococcus pneumoniae
endocarditis in adults. The pneumococcal endocarditis
group. Medicine (Baltimore); 79: 327-37.
7. Gelfand MS, Threlkeld MG. Subacute bacterial
endocarditis secondary to Streptococcus pneumoniae.
Am J Med 1992; 93: 91-3.
8. Powderly WG, Stanley SL Jr, Medoff G. Pneumococcal
endocarditis: Report of a series and review of
the literature. Rev Infec Dis 1986; 8: 786-91.
9. Louagie Y, Charles S, Marchandise B, et al.
Pneumococcal aortic valve endocarditis with atrio-ventricular
perforation. J Cardivasc Surg 1982; 23: 338-43.
10. Vuille C, Nidrof M, Weyman AE, Picard MH.
Natural history of vegetations during successful
medical treatment of endocarditis. Am Heart J
1994; 128: 1200-9.
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