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 Table of Contents  
Year : 2019  |  Volume : 26  |  Issue : 1  |  Page : 65-68

Severe necrotising pneumonia in a toddler: A rare presentation with dual bacterial aetiology

1 Department of Paediatrics, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria
2 Department of Paediatrics, Federal Medical Centre, Gusau, Nigeria

Date of Web Publication12-Mar-2019

Correspondence Address:
Maria Ahuoiza Garba
Department of Paediatrics, Ahmadu Bello University Teaching Hospital, Shika, Zaria
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/npmj.npmj_1_19

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Necrotising pneumonia (NP) is a rare complication of bacterial pneumonia which is associated with severe morbidity and mortality. Pneumonia of polymicrobial aetiology predicts worse pathology with fulminating clinical course. Reports of necrotising pneumonia from multiple bacterial infections are scanty in published literature. We report a case of a toddler with NP in whom Klebsiella pneumonia and Staphylococcus aureus, two pathogens which are well documented in its aetiopathogenesis, were isolated concurrently from his sputum and blood. Severe pneumonia, which shows slow response to recommended antibiotics treatment, should raise the suspicion of NP and possibly one of the polymicrobial origins. Even in resource-constrained settings, prompt institution of antibiotics and supportive care can result in resolution of pulmonary lesions.

Keywords: Child, Klebsiella pneumoniae, necrotising pneumonia, Staphylococcus aureus

How to cite this article:
Garba MA, Umar LW, Akeredolu FD, Mayaki S. Severe necrotising pneumonia in a toddler: A rare presentation with dual bacterial aetiology. Niger Postgrad Med J 2019;26:65-8

How to cite this URL:
Garba MA, Umar LW, Akeredolu FD, Mayaki S. Severe necrotising pneumonia in a toddler: A rare presentation with dual bacterial aetiology. Niger Postgrad Med J [serial online] 2019 [cited 2020 May 30];26:65-8. Available from: http://www.npmj.org/text.asp?2019/26/1/65/253972

  Introduction Top

Necrotising pneumonia (NP) is defined as the consolidation of a lung segment with necrosis in its periphery, forming multiple cavities.[1],[2] NP was previously believed to be rare in children,[1],[2],[3] but there has been an increase in the number of reports in the last two decades.[2] It has been proposed that the increasing prevalence is due to temporal changes in bacterial serotypes.[2],[4] NP lies within the continuum of a spectrum between pulmonary abscess on one side and pulmonary gangrene on the other.[1] In a review of case reports and case series, the organisms usually implicated include Pneumococcus (59%) and Staphylococcus aureus (23%);[2] however, some of the other reported causes include Streptococcus pyogenes, Haemophilus influenza, Pseudomonas aeruginosa, Mycoplasma pneumonia, Legionella pneumophila, Aspergillus spp. and Klebsiella pneumonia.[2] Although K. pneumonia is a rare cause in children, it may occur in the setting of immunosuppression, severe malnutrition and in hospitalised children.[5]

  Case Report Top

A 3-year-old nursery school pupil was referred to the emergency paediatric unit of the Ahmadu Bello University Teaching Hospital, Zaria, on the May 5, 2017, with a foul-smelling right ear discharge of 3 weeks, high-grade intermittent fever of 10 days, cough with progressive breathlessness of 5 days and a 2-day history of recurrent haemoptysis. He had suffered from a similar episode of right ear discharge 12 months earlier that was successfully treated with antibiotics. There was no history of foreign body insertion in the ear. He had no previous episode of difficulty with breathing. He had three bouts of haemoptysis within this period with the loss of approximately 20 ml of blood per bout. There was no bleeding from other bodily orifices. He had been growing well and had no history of previous hospitalizations. His haemoglobin phenotype was AA. Although he had received some vaccination, his parents were unsure of which ones precisely and a vaccination card was not available. His past medical history was not contributory. His father has tertiary level education and works in an administrative capacity in a clinical department of a hospital, while his mother has a secondary school education but is unemployed. Both parents and other three siblings were apparently well.

He was admitted for 2 days in the course of the illness in a private hospital where he received a blood transfusion and some parenteral drugs whose names were unknown to the parents. He was brought to our facility because of worsening of the symptoms.

Examination revealed an acutely looking, pale, underweight toddler (weight = 11 kg, height = 92 cm, WFH -3 to -2 standard deviation) who was tachypnoeic with a respiratory rate of 72/min and chest wall indrawing. His oxygen saturation was 86% in room air. There was no tracheal deviation, and chest excursions were equal on both sides. He had dull percussion notes with reduced air entry in the area of the middle lobe of the right lung as well as coarse crepitations bilaterally. His pulse rate was 160/min and blood pressure of 94/60 mm/Hg. His apex was displaced to the 5th intercostal space lateral to the mid-axillary line with the first and second heart sounds accompanied by an S3 gallop. He had a tender hepatomegaly of 8 cm below the right costal margin with a span of 14 cm. An initial clinical diagnosis of severe bronchopneumonia with congestive cardiac failure was made, and he was commenced empirically on intravenous antibiotics (ceftriaxone and gentamicin), oxygen therapy and other supportive care including a transfusion of 20 ml/kg of fresh whole blood.

His full blood count showed packed cell volume 30%, white blood cell 13.5 × 109/L, granulocytes 57%, lymphocytes 39.4% and platelets 103 × 109/L, while the blood film revealed toxic granulations and a left shift. A chest X-ray [Figure 1] showed widespread homogeneous opacities in both lung fields with thin-walled cavities noted in both the right lower and left upper zones. A right lamellar effusion was noted with obliteration of right the costophrenic angle. A culture of his sputum yielded K. pneumoniae which was sensitive to amoxicillin clavulanate, gentamicin, ampicillin and ciprofloxacin, while the right ear swab yielded Candida spp. The isolation of S. aureus from the blood prompted repeat samples to be taken. However, the initial isolate was sensitive to ceftazidime and chloramphenicol. Lung puncture was not deemed safe and was thus not done. Tests for HIV and tuberculosis were negative.
Figure 1: Posteroanterior view of chest radiograph at presentation showing homogeneous opacities with thin-walled cavities in the right lower and left upper zones

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Following persistent hypoxaemia, recurrent haemoptysis and progressive lung parenchymal destruction on imaging by the 5th day on admission [Figure 2], his diagnosis was reviewed to that of a NP, and antibiotics cover was broadened accordingly to include ceftazidime, amoxicillin-clavulanate. Clindamycin and fluconazole based on the available sensitivity patterns from the culture results. A cardiothoracic surgical review suggested a non- operative approach (to avoid the surgical risk of development of a bronchopleural fistula), with continued conservative management. He remained pyrexic and oxygen dependent by the 20th day on admission. Ventilatory support was unavailable. A chest computed tomography revealed reduced right lung volume with consolidation within which were cavities with no fluid collection within them. Streaky changes were also noted within the left lung. Lung function test could not be done due to his age and the cooperation required.
Figure 2: Posteroanterior view of chest radiograph showing progressive parenchymal destruction, pneumatoceles and emphysema predominantly right-sided with left mediastinal shift

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With gradual stabilisation of his vital signs, he was weaned off oxygen by the 4th week. The chest X-ray done at the point of discharge [Figure 3] showed right-sided pneumothorax with lung collapse. He was discharged on the 42nd day on admission, and he continued to maintain improvement with full reexpansion of the right lung over the next 4 weeks [Figure 4].
Figure 3: Posteroanterior view of chest radiograph at discharge showing persistent right-sided pneumothorax with lung collapse

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Figure 4: Posteroanterior view of chest radiograph at 4-week follow-up showing reexpansion of the right lung with restoration of mediastinal position

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  Discussion Top

While majority of cases of NP are seen in previously well children, undernutrition in our case may have been a strong predisposing factor to co-infection with S. aureus and Klebsiella spp., two organisms that are well documented in the aetiology of NP. It is also possible that S. aureus might have been acquired as a nosocomial infection sequel to the initial interventions.

The initial delay in altering antibiotics was borne out of the consideration that the isolated S. aureus might have been a contaminant as its coagulase status was not determined necessitating a repeat blood culture request, but with continued poor response to antibiotic treatment and even progression of the disease, it became paramount to reflect on its significance as an aetiological pathogen. However, the repeat blood culture yielded the same pathogen. As documented in the literature, bacteraemia in the presence of pneumonia is a pointer to the causative agent, and this is obtained in about 30% of cases.[6] It is worthy of note that S. aureus and K. pneumonia have emerged as important pathogens of community-acquired pneumonia (CAP) in developing countries in recent times.[6]

Most cases of co-infections reported in the literature are viral–viral or viral–bacterial.[6],[7],[8],[9] Although bacteria–bacteria co-infections have been described to occur in up to a third of cases of CAP in other climes,[7],[8] a literature search using keywords and the search engines EMBASE, Google Scholar, African Journals Online and PubMed yielded only a case study of mixed anaerobic primary infection with Clostridium welchii, coliforms and anaerobic streptococci in a 2-year old in Ibadan.[10]

Polymicrobial infections in pneumonia are promoted by immune dysregulation caused by viral factors such as cytotoxic accessory protein (PB1-F2) and bacterial factors (pneumolysin and Panton–Valentine leucocidin [PVL]) which result in vasculitis and intravascular thrombosis.[2],[11] Implicated in the pathogenesis of NP is PVL, a pore-forming virulent factor produced by S. aureus and Streptococcus pneumoniae which destroys host cells.[2] Although coagulase testing was not done, available reports show that up to 12% coagulase-negative S. aureus produce this factor.[2]

The management of NP centres on the control of the infective process, limitation of the pathological process, healing and parenchymal tissue regeneration facilitated by prolonged antibiotic therapy, provision of supplemental oxygen and fluid and electrolyte management as well as adequate nutrition[3] as was done in this case. The multiple antimicrobial agents resorted to was borne out of the need to cover for all organisms isolated. The use of clindamycin has been shown to ameliorate the effect of PVL by binding to the 50s subunit of the microbial ribosome, thereby diminishing toxin production.[12] Other drugs with similar effect include linezolid, rifampicin and fusidic acid.[12]

Our patient required oxygen therapy for 28 days; he had multiple blood transfusions and a hospital stay of 42 days. Intravenous immunoglobulins and extracorporeal membrane oxygenation are beneficial in children with bilateral lung disease, pulmonary haemorrhage or ventilatory and circulatory abnormalities.[2] These modalities are, however, currently unaffordable or unavailable in our setting.

In conclusion, although necrotising pneumonia has a severe course, resolution of pulmonary lesion may be achieved if diagnosed early and antibiotics and supportive care is instituted promptly. Severe pneumonia with initial poor response to recommended antibiotic therapy should raise the suspicion of a necrotising pneumonia, a polymicrobial aetiology or both.

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.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Chatha N, Fortin D, Bosma KJ. Management of necrotizing pneumonia and pulmonary gangrene: A case series and review of the literature. Can Respir J 2014;21:239-45.  Back to cited text no. 1
Masters IB, Isles AF, Grimwood K. Necrotizing pneumonia: An emerging problem in children? Pneumonia (Nathan) 2017;9:11.  Back to cited text no. 2
Lemaître C, Angoulvant F, Gabor F, Makhoul J, Bonacorsi S, Naudin J, et al. Necrotizing pneumonia in children: Report of 41 cases between 2006 and 2011 in a French tertiary care center. Pediatr Infect Dis J 2013;32:1146-9.  Back to cited text no. 3
Wojsyk-Banaszak I, Bręborowicz A. Pneumonia in children. In: Vats M, editor. Respiratory Disease and Infection – A New Insight. London: IntechOpen; 2013. [doi: 10.5772/54052].  Back to cited text no. 4
Jarvis WR, Munn VP, Highsmith AK, Culver DH, Hughes JM. The epidemiology of nosocomial infections caused by Klebsiella pneumoniae. Infect Control 1985;6:68-74.  Back to cited text no. 5
Johnson WB, Abdulkarim AA. Childhood pneumonias in developing countries. Afr J Respir Med 2013:8;2. Available from: http://www.africanjournalofrespiratorymedicine.com/articles/march_2013/AJRM%20%20Mar%2013%204-9.pdf. [Last accessed on 2018 Nav 05].  Back to cited text no. 6
Cillóniz C, Ewig S, Polverino E, Marcos MA, Esquinas C, Gabarrús A, et al. Microbial aetiology of community-acquired pneumonia and its relation to severity. Thorax 2011;66:340-6.  Back to cited text no. 7
de Roux A, Ewig S, García E, Marcos MA, Mensa J, Lode H, et al. Mixed community-acquired pneumonia in hospitalised patients. Eur Respir J 2006;27:795-800.  Back to cited text no. 8
Johnson BR, Osinusi K, Aderele WI, Tomori O. Viral pathogens of acute lower respiratory infections in pre-school Nigerian children and clinical implications of multiple microbial identifications. West Afr J Med 1993;12:11-20.  Back to cited text no. 9
Seriki O, Adeyokunnu A, De la Cruz TO. Destructive pulmonary disease due to mixed anaerobic infection. Thorax 1970;25:41-5.  Back to cited text no. 10
Hsieh YC, Hsiao CH, Tsao PN, Wang JY, Hsueh PR, Chiang BL, et al. Necrotizing pneumococcal pneumonia in children: The role of pulmonary gangrene. Pediatr Pulmonol 2006;41:623-9.  Back to cited text no. 11
Hodille E, Rose W, Diep BA, Goutelle S, Lina G, Dumitrescu O, et al. The role of antibiotics in modulating virulence in Staphylococcus aureus. Clin Microbiol Rev 2017;30:887-917.  Back to cited text no. 12


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]


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