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| Journal of the New Zealand Medical Association,
24-September-2004, Vol 117 No 1202
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Erysipelothrix
rhusopathiae causing infective endocarditis in a female patient requiring
valve replacement
Biju Paul, Wazir Baig
We present a female with infective endocarditis due to
Erysipelothrix rhusopathiae. Extensive
aortic valve damage was present so she was treated surgically by aortic valve
replacement. We present the case report and literature review.
E. rhusopathiae is
a Gram-positive, non-spore forming catalase-negative bacillus. It affects swine,
turkey, ducks, and sheep and is communicable from animals to humans. It causes
an occupational disease (Rosenbach’s disease in its mild cutaneous form or
Klauder’s syndrome in its severe systemic form), and is predominantly seen
in men.1 Treatment before 1945 with hyperimmune
serum resulted in 100% mortality.2
Case reportA
63-year-old female was admitted in December, to the Doncaster Royal Infirmary,
UK due to worsening shortness of breath. She was an ex-smoker, abstained from
alcohol, and avoided animal contact due to eczema. On examination, she was
afebrile, pulse 80/min, respiratory rate 16/min, and blood pressure 117/51 mmHg.
Bilateral basal crepitations were present on auscultation of the lung fields.
Chest X-ray showed an increased cardiothoracic ratio and prominent vascular
markings. Chronic heart failure was diagnosed and anti-failure therapy including
diuretics and ACE inhibitors was initiated.
In the ward, she developed a
low-grade fever and early diastolic murmur in the aortic area. An echocardiogram
revealed severe aortic regurgitation and a large vegetation on the aortic valve.
Biventricular systolic function was good. Blood culture grew a Gram-positive
bacillus presumed to be Streptococcus,
and was highly sensitive to penicillin. A diagnosis of infective endocarditis
was made, and treatment initiated with penicillin and gentamycin.
Her breathlessness responded
to treatment. However, she continued to have a wide pulse pressure and low-grade
fever. An oesophageal echocardiogram done 2 weeks later revealed large bulky
vegetation on the aortic valve, left ventricular dilatation, and global systolic
impairment. She was transferred to the cardiothoracic centre for an aortic valve
replacement.
Pathological examination of
the aortic valve showed signs of active inflammation. The organism grown from
blood culture was sent to the reference laboratory in London and identified as
E. rhusopathiae and confirmed by
examination of 16srRNA.
DiscussionE.
rhusopathiae was first isolated in 1880 by Koch and demonstrated to be a
pathogen in humans by Rosenbach in 1909. It is a slightly curved, pleomorphic,
catalase-negative bacillus.1
E. rhusopathiae
causes Rosenbach’s disease/Klauder’s syndrome—an occupational
disease affecting butchers, fishermen, farmers, and veterinarians. Alcohol abuse
is the most commonly encountered underlying medical
condition.3
It presents during the summer and autumn months’, with an
incubation period of 1 to 4 days.
It is differentiated from bacillus species by the absence of
spores. However, it is commonly misidentified as
Streptococcus viridans and is often
dismissed as a contamination.
The clinical presentation ranges from a mild cutaneous form
(erysipeloid) to severe septicaemia. The septic form is usually associated with
subacute endocarditis.3 It causes extensive
damage of the native valves with a predilection for the aortic valve. Despite
appropriate therapy, the mortality rate for disease caused by
E. rhusopathiae is 38%.
The organism is extremely sensitive to penicillin, and
highly susceptible to cephalosporins, erythromycin and
clindamycin1—but it is resistant to
vancomycin. The recommended therapy for E.
rhusopathiae endocarditis is 12–20 million units/day of intravenous
penicillin in divided doses over 4 to 6 weeks.5
Penicillin-sensitive patients can be treated with erythromycin or clindamycin.
Valve replacement is required in 36% of cases and relapses
can occur. It should be considered in the presence of progressive congestive
failure, recurrent emboli, persistent bacteraemia (despite therapy), development
of heart block, and presence of large vegetations. Prevention of infection for
those in high-risk occupations can be achieved by the use of preventive gear
such as gloves. A live attenuated vaccine is available for veterinary
use.6
Our case is unique because the infection is rarely seen in
females or in the winter months. Furthermore, extensive valve destruction
requiring surgery is not common and the patient was not an alcoholic and did not
have extensive exposure to the organism.
Author information:
Biju Paul, Medicine Registrar, Department of Medicine, Flinders Medical
Centre, Adelaide, Australia; Wazir W Baig, Consultant Cardiologist, Department
of Cardiology, Leeds General Infirmary, Leeds, UK
Correspondence:
Dr Biju Paul, Department of
Medicine, Flinders Medical Centre, Adelaide, SA 5050, Australia. Fax: +61 (0)8
8204 5450; email: Biju.Paul@fmc.sa.gov.au
References:
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