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Osteomyelitis and possible endocarditis secondary toLactococcus garvieae: a first case report

Abstract

Although osteomyelitis is commonly caused by staphylococcal infection, the first case of a lumbar osteomyelitis secondary to Lactococcus garvieae is reported. The case was complicated by possible endocarditis of an aortic valve prosthesis.

  • Lactococcus garvieae
  • osteomyelitis

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Lactococci are often believed to be of low virulence. We report a first case of osteomyelitis secondary toLactococcus garvieae in a previously well, middle aged woman.

Case report

A 56 year old woman was referred to a rheumatology clinic with a nine week history of lower back pain and a five week history of rigors and night sweats. She was anorexic and had lost approximately 3.5 kg in weight in six weeks. Systems review was unremarkable. Her past medical history included a xenograph aortic valve replacement for aortic stenosis 12 years earlier (Ionesu-Shiley valve) and she was known subsequently to have mild aortic regurgitation. She took no prescribed medication and until this illness had been fit and well. Examination was unremarkable other than tenderness over L5/S1 and a soft early diastolic murmur at the left sternal edge in keeping with the aortic regurgitation. Results of routine tests were as follows: haemoglobin 99 g/l (mean corpuscular volume 92 fl), white cell count 6.1 × 109/l, erythrocyte sedimentation rate 74 mm/hour, and C reactive protein 12.6 mg/l; urea, electrolytes, creatinine, liver function tests, and a bone profile were all normal. The urine culture was negative, the chest radiography was normal, an electrocardiogram showed sinus rhythm with a normal axis and deep T wave inversion in the inferolateral territory. This was unchanged from earlier electrocardiograms (previous history of aortic stenosis). Thoracic and lumbar spine radiographs showed a thoracolumbar scoliosis with loss of disc height at L2/L3 and subchondral bone loss. A bone scan revealed increased tracer activity in the mid-lumbar region (fig1).

Figure 1

Bone scan showing increased tracer uptake in mid-lumbar region.

Three days later she was admitted with increasing back pain and spiking temperatures. A diagnosis of presumed osteomyelitis was made and she was treated with analgesics and bed rest, while blood cultures were repeatedly taken during temperature spikes. A computed tomographic guided vertebral biopsy was arranged.

On day 6 after admission, pale splinter haemorrhages were noted in several nails of her hands and toes, not previously documented. There was no splenomegaly or microscopic haematuria and there was no other evidence of embolic phenomena. The murmur of aortic regurgitation was unchanged. A transthoracic echocardiogram revealed a well seated valve replacement in the aortic position, with thin mobile leaflets and mild to moderate transvalvular aortic regurgitation. Other valves appeared normal and no vegetations were identified. In view of the high suspicion of infective endocarditis, a transoesophageal echocardiogram was undertaken. No vegetations or changes consistent with an aortic root abscess were identified. The aortic regurgitation remained unchanged in severity and no further splinter haemorrhages subsequently developed.

All blood cultures, in addition to the biopsied bone, grew Gram positive cocci growing in chains on blood agar. They were identified asLactococcus garvieae and were found to be indistinguishable from one another by API Strep (bioMerieux, Basingstoke, Hants, UK), sensitivity testing and their identity was confirmed by the Streptococcal Reference Laboratory (Respiratory and Systemic Infection Laboratory, London, UK). Vancomycin had been started after the bone biopsy, which was subsequently replaced by teicoplanin to which the organism was sensitive. With antibiotic treatment her clinical course improved and her remaining admission was uneventful. She was discharged after one month of intravenous treatment, with a temperature chart, to complete a further two months of teicoplanin at home via a Hickman line. She has remained well and continues under active follow up.

Discussion

This is the first report of osteomyelitis secondary to infection with L garvieae, an emerging zoonotic pathogen.1 Although first isolated from bovine sources, mainly involving cases of mastitis,2 L garvieae has subsequently been isolated from both fish and humans.1 Lactococci are facultatively anaerobic, catalase negative, Gram positive cocci that occur singly, in pairs, or in chains. They are most often confused with enterococcus species but can be differentiated by biochemical tests.3 In contrast to streptococci and enterococci, lactococci are unusual pathogens and are considered to be opportunistic and of low virulence in humans. They have previously been recovered from urine and blood.4 We are unaware, however, of any previous reports of osteomyelitis secondary to L garvieae, a condition whereStaphylococcus aureus remains the commonest causative organism.

The complicating issue in this case was the finding of splinter haemorrhages in the presence of bacteraemia and a prosthetic heart valve. There should be a high index of suspicion for infective endocarditis in the presence of heart valve replacements, but there was no evidence on transthoracic or transoesophageal echocardiography of valve prosthesis or aortic root infection. The aortic regurgitation had previously been noted and was transvalvular rather than paraprosthetic. Using the criteria published by the Duke endocarditis service, the diagnosis of endocarditis in this case remains possible (see boxes 1 and 2).5 This method for assessing the likelihood of infectious endocarditis employs clinical, microbiological, serological, and echocardiographic parameters as major and minor criteria rather similar to the Jones criteria used in the diagnosis of acute rheumatic fever. This yields a high specificity and hence a low chance of a false negative result5.

Acknowledgments

We should like to acknowledge the help of Dr Andrew Mackay MRCP, MRCPath, MA, MSc, Consultant Microbiologist and Lead Clinician in Pathology, Microbiology Department, Greenwich District Hospital, Vanbrugh Hill, London for his assistance with this report.

References

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