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Year : 2010  |  Volume : 53  |  Issue : 4  |  Page : 899-900
Native valve endocarditis caused by a non-toxigenic strain of Corynebacterium diphtheriae

1 Department of Microbiology, Dr. A.L. Mudaliar Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai, India
2 Department of Cardiology, Madras Medical College & General Hospital, Chennai, India

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Date of Web Publication27-Oct-2010

How to cite this article:
Menon T, Senthilkumar S, Pachaiyappan P. Native valve endocarditis caused by a non-toxigenic strain of Corynebacterium diphtheriae. Indian J Pathol Microbiol 2010;53:899-900

How to cite this URL:
Menon T, Senthilkumar S, Pachaiyappan P. Native valve endocarditis caused by a non-toxigenic strain of Corynebacterium diphtheriae. Indian J Pathol Microbiol [serial online] 2010 [cited 2021 Nov 27];53:899-900. Available from: https://www.ijpmonline.org/text.asp?2010/53/4/899/72056


Infective endocarditis in children can occur as a complication of congenital heart disease and is usually caused by Streptococci or Staphylococci. Corynebacterium diphtheriae is the causative agent of diphtheria and an uncommon cause of endocarditis.

A five year old girl was admitted to a hospital in Chennai, India in August 2008, with fever of one-month duration. She had a history of congenital cyanotic heart disease, with tricuspid atresia, ventricular septal defect, atrial septal defect and transposition of great vessels. On physical examination her blood pressure was 90/70 mmHg and a hematological investigation showed a total leucocyte count of 9000 cells/mm 3 with neutrophils 60%, lymphocytes 34% and eosinophils 6%, hemoglobin 11.1 gm/dL, platelet count 54,000 cells/mm 3 and an erythrocyte sedimentation rate of 19 mm/h. A transthoracic echocardiogram showed vegetation attached to the anterior mitral leaflet; severe pulmonary hypertension, dilated left atrium and left ventricle and pulmonary arteries arising from the left ventricle.

Blood culture of three consecutive samples of 5 ml of venous blood grew non-hemolytic, smooth, opaque colonies which were gram-positive coryneform bacteria. Metachromatic granules were demonstrated by Albert's staining technique and the organism produced characteristic black colonies on blood tellurite agar. It was biochemically characterized as Corynebacterium diphtheriae var gravis, since it produced catalase and nitrate, fermented glucose, maltose and starch, did not ferment lactose or sucrose, did not liquefy gelatin and did not produce urease. The identification was confirmed by 16S rRNA sequence analysis which showed 99% homology with C. diphtheriae. The strain was found to be non-toxigenic when tested by the guinea pig lethal test.

The isolate was found to be sensitive to ampicillin, erythromycin, amikacin, levofloxacin, ceftriaxone, cephotaxime, vancomycin, resistant to gentamicin and showed intermediate sensitivity to penicillin G. Minimum inhibitory concentration (MIC) of penicillin (benzyl penicillin G, Alembic, Vadodara) by the broth microdilution method was found to be 0.25 μg/ml. The minimum bactericidal concentration (MBC) was found to be 1 μg/ml.

Initially therapy was started with intravenous cefotaxime and gentamicin. The patient continued to be febrile and gentamicin was replaced by amikacin. On the 12 th day after admission the patient had an embolic stroke with left hemiplegia. A computed tomography (CT) scan found hypodensities involving right caudate nucleus, lentiform nucleus and internal capsule with adjacent sulcal effacement and edema.

The antibiotic regimen was changed to include ampicillin, physiotherapy was initiated and the patient was discharged after 45 days of hospitalization with residual hemiparesis.

Diphtheria has become uncommon as a result of widespread immunization; however non-toxigenic strains of C. diphtheriae have been increasingly reported as causes of invasive diseases.[1],[2] Infections caused by non-toxigenic C. diphtheriae are not preven table by vaccination. Pathogenic mechanisms of non-toxigenic C. diphtheriae are not well known and a possible mechanism may be related to an increased ability to adhere to vascular endothelium.

The clinical features of our patient such as underlying structural heart disease, history of previous immunization, no evidence of nasopharyngeal or cutaneous diphtheriae and lack of toxic manifestations were similar to pediatric cases of C. diphtheriae reported in the past. [3] The patient did not show clinical improvement after treatment with penicillin which correlated with the laboratory finding that the strain was only intermediately sensitive to penicillin. Corynebacteria are often found on human skin and mucus membranes and in a clinical setting, the detection of coryneform bacteria in blood cultures is often dismissed as contamination. Hence, species identification of coryneform bacteria, as well as toxin testing if the species proves to be C. diphtheriae is important since identification of illness caused by these organisms has wide reaching consequences for the therapy of the patient as well as public health authorities.

   References Top

1.Alexander D. Splenic abscess caused by Corynebacterium diphtheriae. Clin Pediatr (Phila) 1984;23:591-2.  Back to cited text no. 1
2.Belko J, Wessel DL, Malley R. Endocarditis caused by Corynebacterium diphtheriae: Case report and review of the literature. Pediatr Infect Dis J 2000;19:159-63.  Back to cited text no. 2
3.Pennie RA, Malik AS, Wilcox L. Misidentification of toxigenic Corynebacterium diphtheriae as a corynebacterial species with low virulence in a child with endocarditis. J Clin Microbiol 1996;34:1275-6.  Back to cited text no. 3

Correspondence Address:
Thangam Menon
Department of Microbiology, Dr. A.L. Mudaliar Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani, Chennai - 600 113
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.72056

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