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| CASE REPORT |
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| Year : 2021 | Volume
: 18
| Issue : 2 | Page : 62-65 |
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Infective endocarditis due to Acinetobacter baumannii in an infant with complex congenital heart disease
Ibrahim Ahmadu1, Nuhu Abubakar Garba2, Muhammad Shakur Abubakar1, Halima Kabir3, Peter David Igoche4, Apollos Daniel5, Ismail Mohammed Inuwa6, Ibrahim Aliyu3, Mustafa O Asani3
1 Department of Paediatrics, Aminu Kano Teaching Hospital, Kano, Nigeria
2 Department of Paediatrics, Federal Medical Centre, Nguru, Yobe State, Nigeria
3 Department of Paediatrics, Aminu Kano Teaching Hospital/Bayero University, Kano, Nigeria
4 The Limi Children Hospital, Abuja, Nigeria
5 Department of Paediatrics, Federal Teaching Hospital, Gombe, Nigeria
6 Department of Surgery, Cardiothoracic Unit, Aminu Kano Teaching Hospital, Kano, Nigeria
| Date of Submission | 06-Feb-2021 |
| Date of Decision | 09-Dec-2021 |
| Date of Acceptance | 08-Jan-2022 |
| Date of Web Publication | 10-Dec-2022 |
Correspondence Address:
Dr. Ibrahim Ahmadu
Department of Paediatrics, Aminu Kano Teaching Hospital, Kano
Nigeria
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/njc.njc_1_21
Infective endocarditis (IE) due to Acinetobacter baumannii is rare in children, however associated with significant morbidity and mortality. Congenital heart diseases are among the major risk factors for IE. We report a case of IE in an infant caused by A. baumannii. The patient is a 2-month-old infant with complaints of recurrent cough and breathlessness since birth which worsened 2 days before admission, associated with fever. There is difficulty in breastfeeding and occasional forehead sweating with associated darkening of the lips, palms and soles. She has been failing to thrive since birth. Significant findings on physical examination include respiratory distress with hypoxia, pyrexia, severe wasting, tachycardia, tachypnea, tender hepatomegaly, widespread coarse crepitation, displaced apex beat and a pan-systolic murmur. Full blood count was suggestive of sepsis, blood culture yielded A. baumannii, chest X-ray revealed dextrocardia with cardiomegaly and increased vascular markings while transthoracic echocardiography showed complex congenital heart disease with vegetation. The patient was commenced on intravenous antibiotics and supportive managements, however died while on admission.
Keywords: Acinetobacter baumannii, complex congenital heart disease, infant, infective endocarditis
How to cite this article:
Ahmadu I, Garba NA, Abubakar MS, Kabir H, Igoche PD, Daniel A, Inuwa IM, Aliyu I, Asani MO. Infective endocarditis due to Acinetobacter baumannii in an infant with complex congenital heart disease. Nig J Cardiol 2021;18:62-5 |
How to cite this URL:
Ahmadu I, Garba NA, Abubakar MS, Kabir H, Igoche PD, Daniel A, Inuwa IM, Aliyu I, Asani MO. Infective endocarditis due to Acinetobacter baumannii in an infant with complex congenital heart disease. Nig J Cardiol [serial online] 2021 [cited 2023 May 30];18:62-5. Available from: https://www.nigjcardiol.org/text.asp?2021/18/2/62/363142 |
| Introduction | |  |
Infective endocarditis (IE) is an uncommon life-threatening condition that is usually caused by Gram-positive cocci including Streptococci, Staphylococci, and enterococci.[1],[2],[3] It is less common in children and adolescent when compared to adult, however associated with significant morbidity and mortality.[2],[4] Congenital heart disease, cardiac surgery, central venous access device, and immunodeficiency were found to be the predisposing factors for IE in 80%–90% of cases in the postantibiotic era.[5] Acinetobacter baumannii is a Gram-negative bacilli which is responsible for the majority of nosocomial Acinetobacter infections, because of its ability to survive much longer on inanimate surfaces than other Gram-negative bacilli.[6] However, IE due to Acinetobacter spp. are very rare.[7]
| Case Report | | |
A 2-month-old female infant, product of term gestation, presented with recurrent cough and breathlessness since birth which worsened 2 days prior to admission, associated with fever. There is difficulty in breastfeeding and occasional forehead sweating with associated darkening of the lips, palms, and soles. She has been failing to thrive since birth. There is history of similar illness in the elder sibling who died at the age of 1 year.
Physical examination revealed severe respiratory distress with hypoxia (SPO2 = 82%), severe wasting, low grade pyrexia (temperature = 37.9°C), tachycardia (heart rate = 170 beats/min) and tachypnea (respiratory rate = 96 breaths/min), blood pressure = 80/50 mmHg. There was widespread coarse crepitation bilaterally. The apex beat was located on the right 5th intercostal space, anterior axillary line; heart sounds were S1, S2 and S3 gallop with grade 4/6 Pan-systolic murmur. The liver was palpable on the left hypochondrium and was tender.
Laboratory investigations revealed leukocytosis (white blood cell count = 14,200 cells/mm3, neutrophils = 67.4%, lymphocytes = 29.6%), metabolic acidosis (bicarbonate = 16 mmol/L), Chest X-ray revealed dextrocardia with cardiomegaly, increased vascular markings and patchy opacities [Figure 1]. Blood culture grew Gram-positive bacilli, which was confirmed to be A. baumannii (Sensitive to ciprofloxacin, ceftazidime, cefepime, and piperacillin/tazobactam but resistant to tetracycline). Transthoracic echocardiography revealed complex congenital heart disease (dextrocardia, hypoplastic left atrium/ventricle, dilated right atrium/ventricle, large muscular ventricular septal defect, small secundum atrial septal defect and a double outlet right ventricle) with vegetation along the ventricular septal defect measuring 6.6 mm × 5.0 mm in size [Figure 2],[Figure 3],[Figure 4]. | Figure 1: Chest X-ray showing dextrocardia with increased vascular markings and patchy opacities
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 | Figure 2: Transthoracic echocardiography: Apical 4 chamber view showing ventricular septal defect and hypoplasia of the left heart chambers
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 | Figure 3: Transthoracic echocardiography: Apical 4 chamber view showing vegetation on the left side of the ventricular septal defect
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 | Figure 4: Transthoracic echocardiography: Subcostal view showing the pulmonary artery and aorta (MPA – Main pulmonary artery; RPA – Right pulmonary artery; LPA – Left pulmonary artery; Ao – Aorta)
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She was commenced on intranasal oxygen, diuretics (intravenous furosemide and oral spironolactone), nasogastric tube feeding with express breast-milk and empirical antibiotics (intravenous amoxicillin at 150 mg/kg/day divided 8 hourly and gentamicin 5 mg/kg/day divided 12 hourly) after blood culture was taken. However, 3 days into admission, body temperature rose to 39.9°C and repeat full blood count showed increasing leukocytosis (white blood cell count = 16,400 cells/mm3, neutrophils = 72.8%, and lymphocytes = 22.6%).
The antibiotic was changed based on the sensitivity to intravenous ceftazidime at 150 mg/kg/day divided 12 hourly. Peripheral blood film was positive for malaria parasite and she was treated for malaria with intravenous artesunate at 3 mg/kg/dose at 0, 12, and 24 h followed by oral Artemisinin-based combination therapy. However, fever persisted; hence, the antibiotics was changed to intravenous meropenem at 20 mg/kg/day divided 8 hourly and amikacin at 15 mg/kg/day divided 12 hourly. Other supportive managements were continued; however, the patient died 4 weeks into admission.
| Discussion | | |
The diagnosis of IE in neonate and small infants may be challenging, as they do not have the typical features.[1] Hence, it requires a high index of suspicion to diagnose IE in this group of patients. The main predisposing factor for pediatric IE is the presence of a preexisting heart disease including complex congenital heart disease.[8] Most cases are caused by Gram-positive cocci and in rare cases by Acinetobacter species. Several Acinetobacter species have been described in the literature including A. baumannii, Acinetobacter haemolyticus, Acinetobacter calcoaceticus, Acinetobacter johnsonii, Acinetobacter junii, and Acinetobacter lwoffii.[9] These micro-organisms which may be isolated from human specimens such as sputum, feces, urine and vaginal secretions, have enhanced capability to survive on human skin.[6] Published guidelines recommend the used of prolonged antibiotic for the treatment of IE, usually 4–6 weeks; however, certain indications for surgical intervention include valvular dysfunction, highly resistant micro-organisms, and presence of complications such as heart block or abscess.[1] Previous studies revealed that resistance to currently used antimicrobial agents, such as ampicillin-sulbactam, cefepime, and ciprofloxacin occur in over 50% of A. baumannii isolates.[10] However, in the case, we report, the A. baumannii isolated was sensitive to ciprofloxacin, ceftazidime, cefepime, and piperacillin/tazobactam but resistant to tetracycline. Study by Olut and Erkek in Turkey isolated A. baumannii was sensitive to levofloxacin and netilmicin but resistant to carbapenems, amikacin, and β-lactam-β-lactamase combinations.[6] Martinez et al. in Spain reported a case of Acinetobacter haemolyticus IE of the interventricular patch which was sensitive to ampicillin, third generation cephalosporins, aminoglycosides, and imipenem. Mortality following Acinetobacter infection is high. A case series of Actinetobacter pneumonia and/or bacteremia showed a considerably high mortality rate of 56%.[11]
| Conclusion | | |
In conclusion, we report a case of IE caused by A. baumannii in a 2-month-old infant with complex congenital heart disease, which is associated with significant morbidity and mortality. This highlights the needs for routine screening for IE in infants with congenital heart diseases.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4]
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