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Case Reports

Indian Pediatrics 2002; 39:388-392  

Infective Endocarditis in a Child Due to Abiotrophia Defectivus


Munni Ray

C. Subramanian
Pallab Ray*

Pratibha Singhi

From the Departments of Pediatrics and Microbio-logy*, Post Graduate Institute of Medical Education and Research, Chandigarh 160 012, India.

Correspondence to: Dr. Pratibha D. Singhi, Additional Professor, Department of Pediatrics, Post Graduate Institute of Medical Education and Research, Chandigarh 160 012, India.

E-mail: [email protected]

Manuscript received: June 11, 2001;

Initial review completed: July 10, 2001;

Revision accepted: September 18, 2001.

Infective endocarditis is one of the most dreaded complications of structural heart disease. It is a common infection in adult; however, it is a less common infection in children(1). The genus Abiotrophia refers to fastidious Gram-positive bacteria earlier classified as nutritionally variant streptococci (NVS). The recovery of this species from the normal flora i.e., the oral cavity and from the intestinal and urogenital tract is well described. Recently these relatively avirulent microbes have attracted attention because they have caused invasive disease in immunocompetent hosts in a variety of clinical settings(2). Numerous reports have implicated Abiotrophia species in adults in variety of systemic infections but little is known about the pathogenesis and clinical presentations of disease caused by these organisms in children. We present what is to our knowledge the first report in Indian literature of a case of infective endocarditis in a child due to Abiotrophia defectivus.

Case Report

A 10-year-old boy was admitted to the hospital for evaluation of fever, fatigue, and listlessness of two weeks duration. He had good oral hygiene and there was no recent dental manipulation. On examination he had clubbing and his temperature was 39.5ºC and pulse rate was 130 beats/min. He did not have any petechiae or any other cutaneous signs of infective endocarditis. Fundii were normal. The lung fields were clear. Cardiac examination revealed a systolic thrill over the aortic area and a harsh grade 4/6-ejection systolic murmur over the same area radiating to the carotids. The spleen was palpable 2 cm below the left costal margin.

His hemoglobin was 11.4 g/dl, a total leukocyte count of 16,400/mm3 with normal differential count and erythrocyte sediment-ation rate was 40 mm/h. His serum electrolyes, renal function tests and repeated urinalysis were normal. Echocardiography showed severe aortic stenosis with moderate aortic regurgitation with a vegetation at the aortic valve. A subaortic membrane was also detected. The left ventricular function was normal. Three sets of blood cultures on blood agar after 48 hours of inoculation showed minute alpha hemolytic colonies which showed satellitism around a Staphylococcus aureus streak routinely applied for isolation of Haemophilus influenzae. Smear showed highly pleomorphic coccobacilli in small chains. The isolate failed to grow on unsupplemented blood agar but grew as small alpha-hemolytic colonies on sheep blood agar supplemented with 1-Cysteine (100 µg/ml) and pyridoxal hydrochloride (10 µg/ml). The organism was optochin resistant. Susceptibility testing was done on Muelber Hinton sheep blood agar supplemented with 1-cysteine and pyridoxal hydrochloride. These findings were suggestive of growth of nutritionally variant streptococci, which was subsequently characterized by biochemical tests as A. defectivus. The antibiotic sensitivity for the strain was tested on sheep blood plate by NCCLS disc diffusion method. They were sensitive in vitro to the following drugs: penicillin, ampicillin, amoxycillin, cephalexin, all aminoglycosides and quinolones. MIC testing was not undertaken because of laboratory constraints.

The boy was started initially on penicillin G, cloxacillin and gentamicin as culture negative endocarditis and on receiving the blood culture sensitivity report cloxacillin was omitted. He was continued on penicillin G for 6 weeks and gentamicin for 2 weeks. Two cultures collected prior to discharge were sterile. The boy was thereafter referred for corrective surgery. The patient was well when reevaluated six months following discharge.

Discussion

Streptococci requiring either pyridoxal or 1-cysteine for growth were first observed 40 years ago as organisms forming satellite colonies adjacent to colonies of "helper" bacteria (3). Although they were previously considered as nutritional mutants of viridans streptococcal species, the NVS are currently thought to belong to a distinct species of the genus Streptococcus. Since then, knowledge has accumulated regarding their unique nutri-tional requirements, biochemical properties, morphological variability and antimicrobial susceptibility(2). Current taxonomy states that there are 3 species of NVS: Abiotrophia defectivus, Abiotrophia ajacens and Abiotrophia elegans(4). Low recovery rate of Abiotrophia species in clinical specimens can be because of the paucity of organisms, delay in transportation to the laboratory, relatively slow growth rate and variable efficacy of microbiologic media to support the growth of these fastidious organisms(5).

Alpha hemolytic streptococci requiring pyridoxal or thiol group for their growth are grouped as NVS. They grow as small satellite colonies around a staphylococcus streak on sheep blood agar plate. They are pleomorphic and show variable morphology on routine gram staining. So, wherever, NVS are suspected as the offending organism, the subculture plate should be cross streaked with Staphylococcus aureus or the medium should be supplemented with 0.001% pyridoxal or a chocolate agar plate should be used for all subcultures. Biochemically, A. defectivus isolates are bile esculin negative and ferment glucose, lactose, sucrose and trehalose. They do not ferment arabinose, rafinose, inulin, starch and mannitol nor do they decarboxy- late arginine. Unlike pneumococci they are optochin resistant. These biochemical tests should be done after adding 20 µg of pyridoxal hydrochloride per ml of broth base(6).

Abiotrophia species have been implicated as a cause of corneal ulcers and conjunctivitis, liver cirrhosis, pancreatic abscess, wound infection, iatrogenic meningitis, osteomyelitis and brain abscess in adults(7). They are likely to be responsible for most blood culture negative endocarditis and account for more than 4% of Streptococcal strains isolated from blood cultures during this disease(8,9). But in several pediatric series of infective endo-carditis these organisms have not been implicated as a causative agent(1,10). In children occasional case reports are only available of this organism causing infective endocarditis(11-13).

In adults, cases of infective endocarditis due to these group of organisms have a higher morbidity and mortality. They also have more frequent complications like embolization, congestive cardiac failure and increased rate of surgical intervention. The cases reported in children have a lesser rate of complications like congestive cardiac failure(11,12). Our child also had a rather benign course of the disease and became asymptomatic within 5 days of starting of appropriate therapy. Yet the importance of identifying these organisms lies in the fact that a longer duration of therapy is essential and shorter courses may result in treatment failure or relapse, which has also been noted in children. Literature documents a bacteriological failure and relapse rates in these cases to be 41% and 17% cases, respectively(14). The slow growth rate of the bacteria and production of large amounts of exopolysaccharide in vivo may account for the difficulties encountered in therapy and suggest that a longer course of antimicrobial therapy may be required for successful cures.

In experimental models different antibiotic treatment regimens have been compared for treatment of infective endocarditis due to these organisms. It was found that pencillin and gentamicin or amikacin was more effective than penicillin alone. Vancomycin with or without aminoglycoside was at least as effective as the penicillin gentamicin combination. Thus it is recommended that these cases be treated with high dose penicillin at least for four weeks and an aminoglycoside for at least two weeks. Unfortunately, even with this regime relapse is known to occur(14,15). Minimal inhibitory concentra-tions of antibiotics should be determined in all cases when facility is available. In cases where this combination is ineffective or contra-indicated, Vancomycin should be used as an alternative therapy.

The rare etiological diagnosis and the successful treatment in our case prompted us to report this case. A nutritionally variant streptococcus should also be considered as a possible etiology in all cases of suspected endocarditis with negative blood cultures and appropriate media employed to isolate these fastidious organism.

Contributors: MR and CS carried out the clinical workup and also drafted the manuscript. PR was responsible for the microbiological aspects and co-drafted the manuscript. PS was the consultant in charge of the patient and also supervized the drafting of the paper; she will act as the guarantor for the manuscript.

Funding: None.

Competing interests: None declared.

Key Messages

• Nutritionally variant streptococci should be suspected as a causative agent in all patients with endocarditis in whom routine blood cultures are negative.

• Communication between the microbiologist and the clinician is of crucial importance for identification of these microorganisms early during the course of the infection before complications such as embolization or valvular failure occur.

• Endocarditis caused by nutritionally variant streptococci is often difficult to eradicate; combination of penicillin and an aminoglycoside for prolonged periods are recommended for treatment.


 References


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2. Ruoff KL. Nutritionally variant streptococci. Clin Microbiol Rev 1991; 4: 184-190.

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11. Narasimhan SL, Weinstein AJ. Infective endocarditis due to a nutritionally variant streptococcus. J Pediatr 1980; 96: 61-62.

12. Feder HM, Olsen N, McLaughlin J, Bartlett RC, Chameides L. Bacterial endocarditis caused by Vitamin B6 - dependent viridans group streptococcus. Pediatrics 1980; 66: 309-312.

13. Poyart C, Quesne G, Acar P, Berche P, Trieu-Cuot P. Characterization of the Tn916-like transposon Tn3872 in a strain of Abiotrophia defectiva (Streptococcus defectivus) causing sequential episodes of endocarditis in a child. Antimicrob Agents Chemother 2000; 44: 790-793.

14. Stein DS, Nelson KE. Endocarditis due to nutritionally variant streptococci: Therapeutic dilemma. Rev Infect Dis 1987; 9: 908-916.

15. Bouvet A, Cremieux C, Contrepois A, Vallois JM, Lamesch C, Carbon C. Comparison of penicillin and vancomycin, individually and in combination with gentamicin and amikacin, in the treatment of experimental endocarditis induced by nutritionally variant streptococci. Antimicrob Agents Chemother 1985; 30: 607-611.

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