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INFECTIOUS DISEASES: Edited by Michael S. Niederman and Alimuddin Zumla

Necrotizing pneumonia (aetiology, clinical features and management)

Krutikov, Mariaa; Rahman, Anannab; Tiberi, Simona,c

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Current Opinion in Pulmonary Medicine: May 2019 - Volume 25 - Issue 3 - p 225-232
doi: 10.1097/MCP.0000000000000571
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Community-acquired pneumonia (CAP) accounts for more hospital admissions than any other lung disease, with a 30-day mortality of 5–15% in those admitted [1]. Complications include empyema, pleural effusion, lung abscess, broncho-pulmonary fistulae, pneumothorax, cavities and necrotizing pneumonia. Necrotizing pneumonia was first described in adults in the 1940s and in children 50 years later [2▪]. In the United States, necrotizing pneumonia has been reported in 0.8–7% of children presenting with CAP to a tertiary centre [2▪]. In adults, this figure has been quoted as less than 1%. In view of the rapidly progressing course of the condition that often presents in previously healthy patients, there has been much emphasis on finding a host or pathogen factor contributing to severity of presentation. Several large case series and reviews have been published on necrotizing pneumonia in children [2▪]. However, there has been no review published on the presentation and management of necrotizing pneumonia in adults since 2014 [3]. This review will provide an overview of the condition, including case reports, recent evidence on appropriate management of such patients and the benefit of surgery in severe cases.

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In necrotizing pneumonia, pulmonary infection leads to inflammation and dense consolidation. Toxin release with cytokine response can lead to necrosis and formation of multiple small cavities. In addition, the pulmonary vasculature is often obstructed because of thrombus formation. This reduced blood supply causes necrosis of lung parenchyma and favours uncontrolled bacterial replication, often involving anaerobic bacteria. In such situations, antibiotic delivery is severely impaired because of large volumes of poorly perfused tissue. Eventually, this lung tissue may liquefy and form pulmonary gangrene, a condition that often requires surgical management. This condition can be differentiated from a lung abscess, in which tissue necrosis is localized and therefore an encapsulated abscess is formed [4].


The most common causative organisms have been reported as Streptococcus pneumoniae, Stapylococcus aureus and Klebsiella pneumoniae. Less common pathogens include Haemophilus influenzae, Streptococcus anginosus group, Pseudomonas aeruginosa, Mycoplasma pneumoniae alongside anaerobes like Fusobacterium nucleatum and Bacteroides fragilis, Mycobacterium tuberculosis and less commonly fungi like Aspergillus sp. and Histoplasma capsulatum[5–8]. In children, pneumococcal infection is the most widely seen cause of necrotizing pneumonia [2▪]. Reports from the United States and United Kingdom have suggested rising rates of pneumococcal necrotizing pneumonia since the introduction of the polyvalent pneumococcal vaccine. This 7-valent vaccine protects against seven serotypes of the polysaccharide pneumococcal capsule and its introduction has reduced the incidence of pneumococcal infection. However, serotypes not included in the vaccine, particularly 3, 5, 7F and 19A have been documented in a rising number of necrotizing pneumonia cases [2▪]. In low-income countries where rates of HIV infection are high, reports suggest that M. tuberculosis is the most common cause of necrotizing pneumonia in children. One case series from South Africa included 32 children (9 HIV positive) who were admitted with necrotizing pneumonia to a tertiary centre. About 25% of all those admitted had tuberculosis (TB) infection confirmed as the cause of necrotizing pneumonia [9].

By contrast, in adults necrotizing pneumonia is more commonly caused by community-acquired Staphylococcus aureus, as well as S. pneumoniae and K. pneumoniae. Pulmonary gangrene is seen more commonly with gram-negative organisms like K. pneumoniae and P. aeruginosa[3,10].

Panton–Valentine leucocidin (PVL) is a staphylococcal exotoxin that was first described in 1932 and can be found in methicillin-resistant and methicillin-sensitive S. aureus. It potently activates macrophages, neutrophils and monocytes which in turn cause a large amount of cell death but is also rapidly inactivated by serum antibodies [11]. In 1999, Lina et al.[12] described the association of PVL toxin with severe necrotizing pneumonias and with soft tissue infections. A subsequent study compared 16 cases of PVL-positive staphylococcal community-acquired necrotizing pneumonia with 36 PVL-negative cases and found more rapidly progressive severe infection with lower survival rate, in the PVL-positive cases [13]. A meta-analysis in 2013 by Shallcross et al.[14] showed that patients with staphylococcal pneumonia were less likely to be infected with a PVL-positive strain than those with a staphylococcal skin and soft tissue infection (pooled odds ratio 0.28, 95% confidence interval 0.14–0.55). Other staphylococcal toxins have also been described in the pathogenesis of severe necrotizing pneumonia; for example, toxic shock syndrome toxin-1 was identified in the genetic analysis of a clinical isolate and is likely to also contribute to severity [15].


Necrotizing pneumonia usually develops over a few days and presents acutely with severe sepsis. Leukopenia, haemoptysis and high fevers are hallmarks with radiological evidence of necrosis and microabscesses. Pulmonary gangrene is often present; large cavities are formed when small abscesses coalesce. Clinically, necrotizing pneumonia can be differentiated from pulmonary abscess which tends to present with a long history (weeks) of fevers and night sweats.

There is some evidence that necrotizing pneumonia is often overlooked. One retrospective study of 136 patients with pneumococcal pneumonia, none of which were reported as necrotizing pneumonia, found that computed tomography (CT) imaging showed radiological evidence of necrotizing pneumonia in 11% of patients [16]. A retrospective study in Korea of patients presenting with CAP over 4 years found 103 (12%) had necrotizing changes on CT. When comparing the groups, chest pain was more common in the necrotizing pneumonia group (P < 0.001) and patients with necrotizing pneumonia had significantly higher inflammatory markers (erythrocyte sedimentation rate, C reactive protein and white cell count), lower serum albumin and required pleural drainage. They also found a significantly longer median length of hospital admission (14 versus 8 days) in the necrotizing pneumonia group with no difference in use of mechanical ventilation and 30-day mortality between the groups [7]. A case series of Pseudomonal necrotizing pneumonia suggested that cases presented with predominantly upper lobe cavities, likely related to the strict anaerobic properties of the organism [10].

Risk factors for necrotizing pneumonia involve the host inflammatory response and development of thrombi in pulmonary vasculature. In addition, there is evidence that delay in seeking treatment may contribute to development of pulmonary necrosis [4]. The Korean study found that smokers were more likely to develop necrotizing pneumonia (P < 0.001), those with heavy alcohol use (P = 0.031) and those who have had a gastrectomy [7]. A further case series of 93 patients with community-acquired SNP found that median age of presentation was 35.1, only 28.9% had any underlying disease, 12.4% were ever-smokers and 11.2% had a history of drug abuse or HIV/AIDS. In this case series, 71 out of 73 samples tested were positive for PVL toxin. Using logistic regression, factors associated with death were leukopenia (P = 0.0002), influenza-like illness (P = 0.011) and haemoptysis (P = 0.024) [17].


Influenza coinfection is a major risk factor for development of necrotizing pneumonia. There is clear evidence that influenza increases host susceptibility to bacterial infections. In a case series of 43 cases of staphylococcal necrotizing pneumonia, 86% were PVL-positive, 28% had confirmed and 37% had suspected viral coinfection [11]. The main mechanisms for this have been demonstrated in studies of influenza and S. pneumoniae coinfection, in which the virus impairs macrophage-mediated bacterial clearance through damage to epithelium and subsequent build-up of debris and secretions that obstruct small airways and prevent removal of bacteria. During influenza infection, viral neuraminidase removes sialic acid from respiratory cells therefore increasing bacterial adherence and the virus induces lysis of respiratory epithelial cells with subsequent destruction of the muco-ciliary escalator and diminished pulmonary alveolar macrophages [18,19]. Rapidly progressing necrotizing pneumonia has been widely described with influenza coinfection as viral infection results in a large number of inflammatory cells in the airways which are then activated by even a small dose of PVL-toxin to cause massive cell death and necrosis [11].


Necrotizing pneumonia is often called cavitating pneumonia, but not all cases are characterized by pulmonary cavitation [20]. Chest X-rays are often reported as showing no evidence of necrosis. However, in one study, retrospective analysis of chest X-rays reported evidence of necrosis in 2% of cases [21]. The main distinction between these conditions is radiological and can be difficult to distinguish on plain radiograph; however, these findings are more evident on a chest computed tomography (CT) scan with contrast, which usually shows patchy or diffuse consolidation in multiple lobes of the lung [22]. Other findings include destruction of lung parenchyma, loss of parenchymal enhancement (indicating liquefaction), air/fluid-filled thin-walled cavities or thick-walled cavity (lung abscess) [16]. Early CT findings may include the development of a pleural effusion, which may be followed by the development of multiple cavities a few days later [22]. This is thought to occur because of development of pulmonary gangrene, followed by tissue liquefaction and necrosis [22]. In most patients, the chest X-ray shows complete resolution or minimal residual fibrotic changes in 1–3 months after treatment completion [23].

Case 1

A previously healthy 16-year-old boy presented to hospital with fever, night sweats, pleuritic chest pain and occipital headache, associated with epistaxis, neck pain, dysuria, swollen left knee, nausea and vomiting.

His vital signs at admission revealed a temperature of 38.2°C, heart rate of 134 beats/min and blood pressure of 119/64. He was at hypoxic, dehydrated and his left knee was swollen limiting his movement. His chest was clear on auscultation, his heart sounds were normal and his abdomen was soft and nontender with no evidence of organomegaly. Initial blood investigations revealed a white blood cell count (WBC) of 16 (neutrophils 14.6, lymphocytes 0.7) with normal platelets, haemoglobin, electrolytes, renal and liver function. C - reactive protein (CRP) was elevated at 361. Chest X-ray (Fig. 1) was unremarkable.

Anteroposterior chest X-ray of case 1 showing left lower lobe consolidation.

A CT pulmonary angiogram scan (Fig. 2) reported no evidence of pulmonary embolus but multiple cavitating lesions affecting the upper lobes of both lungs with paratracheal lymphadenopathy.

CT scan image of case 1 showing large ulcerating necrotic nodule and central cavity.

An ultrasound of his liver reported mildly enlarged liver with steatosis, biliary sludge, spleen 15.5 cm. Cultures of urine and knee aspirate samples taken at time of admission did not yield any organisms. His methicillin resistant staphylococcus aureus (MRSA) throat and skin swabs were negative. A head CT was normal. A transoesophageal echocardiogram did not reveal any vegetations.

Cultures of blood and sputum taken on day of admission yielded a methicillin susceptible S. aureus, later identified as PVL toxin producing. He received a 21-day course of linezolid and clindamycin, and anticoagulation for a left leg deep vein thrombosis. He was monitored in the intensive care unit (ICU) and made a good recovery.

Case 2

A previously healthy 25-year-old woman presented to her local hospital with acute breathlessness and flu-like symptoms.

Her vital signs at time of admission revealed a temperature of 39°C, heart rate of 123 beats/min and blood pressure of 90/50, respiratory rate of 70 breaths a minute. On auscultation, there was evidence of reduced air entry at both lung bases. Initial blood investigations revealed a WBC count of 1.9, with normal platelets, haemoglobin, electrolytes, renal and liver function. Lactate dehydrogenase was elevated at 888 and CRP at 153. Chest X-ray on admission (Fig. 3) showed bilateral pneumonia.

Chest X-ray of Case 2 demonstrating bilateral pulmonary consolidation.

A chest CT (Fig. 4) reported extensive cystic changes affecting the lower lobes bilaterally consistent with severe cavitating pneumonia with added widespread consolidation and moderate pleural effusions. She was transferred to the ICU with hypoxic respiratory failure where she was mechanically ventilated.

CT scan image of case 2, note the multifocal consolidation, necrosis and cavitation.

Cultures of blood and sputum taken on day of admission yielded methicillin S. aureus. Viral swab yielded H3N1 virus.

She was commenced on oseltamivir, piperacillin/tazobactam and linezolid, which was then rationalized to oseltamivir, flucloxacillin and clindamycin on identification of PVL S. aureus. Following antibiotic therapy and respiratory support, she made a good recovery.


As the airways are colonized with multiple bacterial pathogens, it can be difficult to isolate a causative organism on microbiological culture often inhibited by concurrent antimicrobial therapy [21]. The advent of polymerase chain reaction (PCR) allows for detection of respiratory viruses and PVL toxins. Multiplex PCR assays accurately identify several pathogens simultaneously from sputum and endotracheal aspirates in patients on antimicrobial therapy [24]. However, PCR is unable to differentiate between airway colonization and infection and remains relatively expensive [25].

Initial management of necrotizing pneumonia requires a suspicion of necrotizing pneumonia and every possible opportunity for isolating the causing pathogen should be made followed by prompt delivery of antimicrobials within 4 h of presentation to hospital [26,27]. Diagnostics should include blood cultures, sputum for microscopy and culture, and if available molecular tests, urinary antigens for Legionella pneumophila and Pneumococcus, and HIV status should be determined [28]. Sputum for acid-fast bacilli should be obtained if TB a possibility, if the patient is unable to expectorate an induced sputum or bronchoscopy could be considered if TB a possibility, but not recommended in pneumonia in children or adults [29]. In intubated patients, blind sampling should be performed [30]. Isolation of the pathogen may allow for tailored narrow spectrum therapy that may be more effective and better tolerated by the patient; therefore, sampling may be key to better outcomes in severe infections, whereas they are of little utility in mild infections. Administration of appropriate broad-spectrum empirical antimicrobials for lower respiratory tract infections should be in accordance with local therapy guidelines tailored with the most likely pathogen and antimicrobial susceptibility data [26–28].

The addition of antitoxin antimicrobials like clindamycin [31] and rifampicin may have a role in reducing toxin-mediated disease in pneumonias caused by gram-positive toxin-producing bacteria, for example PVL producing S. aureus or in Group A Streptococcal and Pneumococcal pneumonia [32▪].

Corticosteroid therapy has been shown to reduce mortality of CAP by 3% in hospitalized patients, reduce mechanical ventilation by 5% and reduce length of stay by 1 day [33]. In a Cochrane review, corticosteroids were found to reduce mortality and morbidity in severe CAP, saving an additional patient per 18 patients treated [34].

There may be a role for the use of intravenous immunoglobulin (IVIG) in necrotizing pneumonias, especially in S. aureus pneumonias[35,36,37▪▪].

Inhaled antibiotics may also be considered in adjunct to systemic therapy and may be more effective than systemic antimicrobials particularly when blood supply to the affected tissue is reduced, that is pulmonary gangrene. Clinical case reports have reported use of nebulized vancomycin in MRSA pneumonia [38], and colistin and tobramycin in Pseudomonal pneumonia [39]. However, a recent randomized trial with use of nebulized amikacin and fosfomycin in gram-negative ventilator associated pneumonia showed no efficacy [40▪▪]; the efficacy of nebulized therapy remains unknown and technically administration and bronchospasm can present as challenges.

Empyema should be managed with drainage. Surgery is restricted to the management of empyema, broncho-pleural fistulas and recalcitrant necrotizing infection leading to gangrene [41,42]. Conversely, pulmonary abscess does not usually require surgical intervention as drainage through an adjacent bronchus can occur over a period of weeks.


Necrotizing pneumonia is a severe form of CAP associated with admission to intensive care and is characterized by a higher morbidity and mortality. A high index of suspicion and CT chest imaging is required to confirm the diagnosis. Isolation of the causing agent can give additional information on whether the damage may be toxin-mediated and provide antimicrobial susceptibility, after which aggressive specific antimicrobial therapy can lead to better outcomes. Use of IVIG and clindamycin may be warranted with a toxin-producing strain. Surgery is reserved for cases not improving on medical therapy.



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Conflicts of interest

There are no conflicts of interest.


Papers of particular interest, published within the annual period of review, have been highlighted as:

  • ▪ of special interest
  • ▪▪ of outstanding interest


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intravenous immunoglobulin; necrotizing pneumonia; Panton–Valentine leukocidin; pulmonary gangrene; Staphylococcus aureus

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