Rapidly progressive necrotizing pneumonia: remember the Streptococcus anginosus group!

Acute necrotizing pneumonia in an immunocompetent host is uncommon and usually caused by Staphylococcus aureus infection. Streptococcus anginosus group (SAG) is a less recognized cause of rapidly destructive lung infection resulting in significant patient morbidity and mortality. Unlike many other bacterial infections, SAG can cross fascial planes and cause fulminant infections. Necrotizing pneumonia and lung abscesses due to SAG often fails conservative therapy with antimicrobials and requires definitive surgical intervention. Consideration of SAG as a potential etiology might help to institute definitive therapy earlier and prevent complications.


Patient and observation
A 45-year old male presented to the ED with mild fever, sneezing, rhinorrhea, cough, right-sided dull chest pain and shortness of breath.
He was recently exposed to a co-worker suffering from 'flu' and started experiencing upper respiratory tract infection symptoms two days ago. He was nauseous, vomited several times and suffered from diarrhea. The persistent dull chest pain and worsening exertional shortness of breath for a day prompted the ED visit. His past medical history was significant for Crohn´s disease for which he was not on any medication. The patient was a smoker of about half a pack per day and denied any history of alcohol or recreational drug abuse. He Cavitary pneumonia with a fungal pathogen and lung malignancy were other possibilities, but no significant risk factors, such as prolonged neutropenia, chronic steroid use or prior structural lung disease were present. The patient was started on linezolid and meropenem. Highflow oxygen was used to achieve acceptable oxygen saturation level.
Repeat chest X-rays on day one, two and three are shown in Figure   2. A repeat CT scan was obtained on day three to identify the

Discussion
Rapidly evolving necrotizing pneumonia (NP) complicated by lung abscess and empyema formation is a rare complication of communityacquired bacterial pneumonia. Even though it is rare, the disease progression can be extremely rapid with the virtual destruction of the lung parenchyma in a matter of days. In most reported cases, Panton-Valentine leukocidin (PVL) toxin-producing S. aureus (both methicillin sensitive and resistant SA) was found to be the culprit organism [1][2][3]. The incidence of community-acquired pneumonia (CAP) due to SA is only about 1.6% among all cases of CAP [4]. However, necrotizing pneumonia, especially in the setting of co or prior influenza infection is predominantly due to superimposed SA infection. Viruses other than influenza, such as rhinovirus and respiratory syncytial virus have been shown to increase upper airway colonization by SA transiently, but whether these viruses make the patient more susceptible to SA pneumonia, is unclear [5]. The other reported bacteria include Streptococcus pneumoniae, Klebsiella pneumoniae, group A Streptococcus and Pseudomonas aeruginosa [6][7][8][9]. In clinical practice, patients from the community who present with NP, SA infection is almost universally considered to be the likely etiology. Members of SAG are often associated with pharyngitis and endodontic infections [10]. Suppurative infection, either local or distant, is a common complication. Local suppurative infection in the form of head and neck abscess, jugular vein thrombophlebitis [11], peritonsillar abscess [12] and cervical necrotizing fasciitis [13], have been described. SAG bacteremia in the absence of any apparent infection has also been reported [14]. Identification of SAG bacteremia should prompt a workup for metastatic abscesses [15]. In contrast to NP, due to SA, patients with SAG pneumonia appear less toxic, at least on presentation. Very high fever is usually uncommon [16]. Risk factors include male sex, alcoholism, cancer and cystic fibrosis. Our patient had a co-existent coronavirus infection. Whether that played a role in the pathogenesis of the disease is uncertain. SAG causes invasive lung infection either alone or as a part of polymicrobial infection, including oral anaerobes. Aspiration of oropharyngeal content is the likely inciting event.
Necrotizing pneumonia, lung abscess, empyema, mediastinitis resulting in septic shock and death have been reported [17,18]. SAG has the unique ability to extend beyond fascial planes and has been reported to cross interlobar fissures, diaphragm or even erode through the chest wall [19] and should be considered as a potential etiology in such situations. Management of thoracic infection due to SAG is quite different from the norm. In general, there is no established surgical guideline regarding the management of acute bacterial necrotizing pneumonia. Surgical intervention is usually considered in the setting of septic shock as a source control measure [20]. Lung abscesses that develop from necrotizing pneumonia, communicate with an airway and undergo auto-drainage and usually only require long term antibiotic therapy. But due to the SAG´s ability to cross fascial planes, the lung abscess is often complicated by empyema due to rupture of the abscess in the pleural cavity. In one study, 67% of patients failed antibiotic therapy and required surgical intervention for definitive management [21]. The progression of the disease could be explosive, as was in this case. Four weeks of an intravenous antibiotic such as ceftriaxone with anaerobic coverage or a combination of betalactam and a beta-lactamase inhibitor, in addition to surgical intervention is considered optimal therapy.

Conclusion
Necrotizing pneumonia in the modern era of antibiotic is a rare event.
Most common causes include SA or a pneumococcal lung infection.

Competing interests
The author declares no competing interests.