Corynebacterium striatum endocarditis masquerading as connective tissue disorders

B. Stoddart, J. A. T. Sandoe and M. Denton

Medical Microbiology, Leeds Teaching Hospitals NHS Trust, Leeds, UK

Correspondence to: B. Stoddart. E-mail: bethanstoddart{at}hotmail.com

SIR, Stimulation of both humoral and cellular immunity occurs in bacterial endocarditis. The constant intravascular antigenic challenge results in development of several classes of circulating antibody [1]. Deposition of immune complexes in subendothelial tissues, with associated acute inflammatory injury, leads to renal impairment and arthritis in a similar manner to some vasculitides. Treatment with antibiotics leads to a rapid fall in immune complex concentration and a clinical improvement. Immunosuppressive agents transiently have the same effect.

Anti-neutrophil cytoplasmic antibodies (ANCA) are associated with a spectrum of necrotizing small vessel vasculitides, and have been demonstrated in infective endocarditis [2]. cANCA, which is normally considered to be specific for Wegener's granulomatosis, has been reported previously in bacterial endocarditis with renal involvement [3].

We present two patients with endocarditis caused by Corynebacterium striatum in whom there were diagnostic difficulties due to the ambiguous nature of their presentation.

Case 1 was a 72-yr-old retired teacher who presented to her general practitioner with a 6-week history of non-specific symptoms, including weight loss, malaise, sweats, dizziness and arthralgia. Her medical history included childhood rheumatic fever, mitral valvotomy in 1960 and prosthetic mitral valve replacement in 1990. She had made an uneventful recovery from culture-negative endocarditis 18 months previously at another hospital.

Initial examination was unremarkable, with no fever or stigmata of endocarditis. Investigations on admission revealed normochromic anaemia, haemoglobin 9.8 g/dl, white cell count 6.97 x 109/l, platelets 204 x 109/l, acute renal failure (creatinine 842 µmol/l) and a CRP of 19 mg/l. Immunological investigations showed ANA weakly positive at 1/40, cANCA 1/640 and rheumatoid factor 22.

A diagnosis of a systemic vasculitic syndrome was made. She was commenced on haemodialysis and given 10 days of cyclophosphamide, with 3 days of methylprednisolone 500 mg. Her renal function began to improve, so a renal biopsy was not undertaken. However, she later developed a fever and a cerebrovascular event, following which blood cultures were obtained. Corynebacterium striatum was subsequently isolated from four sets of blood cultures. A transoesophageal echocardiogram was equivocal due to acoustic shadowing, which was attributed to calcified vegetations from the previous episode of endocarditis.

A diagnosis of endocarditis was made. The patient was treated with a 6-week course of vancomycin and rifampicin. After 2 weeks (four dialysis sessions), her renal function improved sufficiently to cease renal replacement therapy. She made a full recovery.

Case 2 was a 61-yr-old lady who was admitted feeling unwell for a few weeks, experiencing dizziness, nausea, back pain, palpitations and lethargy. Her past history included cutaneous lupus, multiple pulmonary emboli, hypothyroidism and ischaemic heart disease. As a child she had had rheumatic fever. Her medications on admission included prednisolone.

Clinical examination revealed skin changes consistent with cutaneous lupus, normal heart sounds, vague abdominal tenderness and a low-grade fever, always <38°. Ophthalmoscopy revealed bilateral retinal haemorrhages. Twelve-lead and 24-h ECG findings were consistent with ischaemic heart disease. She had normochromic anaemia, haemoglobin 9.9 g/dl, CRP initially >100 mg/l and a normal white cell count throughout her admission (4.5–7.6 x 109/l). ANA, rheumatoid factor, C3 and C4 and double-stranded DNA antibodies were negative or normal. cANCA was weakly positive at 1/40.

The episode was thought to represent a transformation from cutaneous lupus to a systemic sclerosis/lupus erythematosus overlap syndrome. She was treated with thalidomide, cyclophosphamide and increased doses of prednisolone, to which she initially responded. However, she later failed to improve and had intermittent low-grade fevers, and blood cultures were obtained. A coryneform organism isolated from the first blood culture set was dismissed as a skin contaminant. When second and third blood culture sets again grew coryneforms 2 months into her admission, the diagnosis of endocarditis was entertained.

The isolate was identified as Corynebacterium striatum. A transthoracic echocardiogram revealed a partially calcified vegetation on the mitral valve. She was treated with vancomycin for 4 weeks and gentamicin for 1 week. She made an uneventful recovery from her endocarditis but remains under rheumatology follow-up.

Coryneforms, or non-diphtheria corynebacteria, also called ‘diphtheroids’, form part of the normal commensal flora of the skin and mucous membranes. They are frequently isolated from blood cultures and are often dismissed as skin contaminants. Coryneform endocarditis can be difficult to diagnose because of its insidious nature and non-specific presentation, and it is not uncommon for cases to present with immunological phenomena [4–7].

In these two cases, the diagnosis of endocarditis was delayed due to presentation and investigation findings thought to be consistent with an autoimmune vasculitis of non-infectious aetiology, and dismissal of the blood culture findings as contaminants. Both were treated with immunosuppressive agents, and made a partial response before deteriorating and the correct diagnosis being made. Neither patient had a convincing fever or a leucocytosis. Nevertheless, Duke's diagnostic criteria [1] for endocarditis were met by both patients: both had consistent blood cultures, a predisposing cardiac condition, suggestive echocardiograms and immunological phenomena, and both recovered following appropriate endocarditis treatment.

The authors have declared no conflicts of interest.

References

  1. Weatherall DJ, Ledingham JGG, Warrell DA, eds. Oxford Textbook of Medicine, 3rd edn. Oxford: Oxford University Press, 1996.
  2. Choi HK, Lamprecht P, Niles JL, Gross WL, Merkel PA. Subacute bacterial endocarditis with positive cytoplasmic antineutrophil cytoplasmic antibodies and anti-proteinase 3 antibodies. Arthritis Rheum 2000;43:226–31.[CrossRef][ISI][Medline]
  3. Subra JF, Michelet C, Laporte J et al. The presence of cytoplasmic antineutrophil cytoplasmic antibodies (C-ANCA) in the course of subacute bacterial endocarditis with glomerular involvement, coincidence or association? Clin Nephrol 1998;49:15–8.[ISI][Medline]
  4. Rufael DW, Cohn SE. Native valve endocarditis due to Corynebacterium striatum: case report and review. Clin Infect Dis 1994;19:1054–61.[ISI][Medline]
  5. Arnold AZ. Corynebacterium endocarditis. Difficult diagnosis in an elderly woman. Postgrad Med 1987; 81:283–7.
  6. Juurlink DN, Borczyk A, Simor AE. Native valve endocarditis due to Corynebacterium striatum. Eur J Clin Microbiol Infect Dis 1996;15:963–5.[ISI][Medline]
  7. Melero-Bascones M, Munoz P, Rodriguez-Creixems M, Bouza E. Corynebacterium striatum: an undescribed agent of pacemaker-related endocarditis. Clin Infect Dis 1996;22:576–7.[ISI][Medline]
Accepted 12 November 2004





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