Abscess formation is not a rapid process and symptoms develop in the course of weeks or even months, particularly if provoked by anaerobic pathogens, Mycobacterium tuberculosis, Nocardia spp. and fungi. Initial LA stages may be asymptomatic, but this highly depends on the underlying disease and possible previous pneumonia. The transition from symptoms that are triggered by active pneumonia to those provoked by an encapsulated LA may not be clearly defined and the clinical picture is usually dominated by symptoms related to the former.

In this context, commonly observed symptoms are fever, night sweats, cough, chest pain, loss of appetite, anorexia and subsequent weight loss [9]. Fever is said to be higher if a lung infection is caused by aerobic pathogens and may exceed 38.5 °C in these patients. The cough may produce foul smelling and tasting sputum, hemoptysis may be observed if blood vessels are compromised [10].

Auscultation may reveal decreased, more bronchial breath sounds and inspiratory crackles. Percussion produces dull sounds. These symptoms are more severe in patients suffering from pleural empyema or pyopneumothorax. Here, breath sounds may even be inaudible.

Periodontal disease and gingivitis are often detected.

Medical history and clinical examination are usually sufficient to diagnose impaired lung function, but cannot confirm the existence of a LA.

Blood samples should be obtained and analyzed for possible indicators of current infection. Leukocytosis and left shift are often detected. Sputum should be analyzed and prepared for bacterial culture and examination for parasite stages. Of note, special culture media are required for mycobacteria. They need to be ordered explicitly. Interferon-γ release assays and other special tests have recently been proven highly valuable for diagnostic of tuberculosis.

Imaging studies are required to confirm the presence of a LA, to assess the extent of tissue damage and possible pleural involvement. LA, potential empyema and lung cancer are generally visible in thoracic radiographic images [11]. LA display in form of an irregularly shaped cavity that is partially filled with air, partially with fluid. Its capsule becomes more clearly defined as inflammation in adjacent lung tissue resolves. If LA result from an aspiration pneumonia, the upper lobes and the superior segments of the lower lobes are most likely to be affected. If pleural involvement cannot be unequivocally determined, computed tomography scans may supplement diagnostics [12]. Ultrasonography may be an option if the patient needs to be examined at the bedside [13].

Treatment of LA depends on the underlying pathological condition.

The vast majority of LA involves bacterial infection and thus requires antibiotic therapy. Although there are some general guidelines regarding parenteral antimicrobial therapy [14], bacterial cultures and corresponding antibiograms should be prepared as early as possible. This procedure gains increasing importance due to rising resistance among causative agents.

Several anaerobic bacteria may produce β-lactamase and thus render β-lactam antibiotics ineffective unless they are combined with β-lactamase inhibitors. Clindamycin has been proposed as a valuable alternative (starting with 600 mg, i.v. tid, then administering up to 300 mg, per os qid). Metronidazole, however, has been reported to be ineffective in the majority of cases [15]. Moxifloxacin and trimethoprim-sulfamethoxazole may also be applied to treat LA.

Methicillin-resistant Staphylococcus aureus requires the application of vancomycin (15 mg per kg body weight, i.v. bid) and linezolid (600 mg, i.v. bid). Doses may be reduced later.

LA due to infection with fungi is often associated with immunodeficiency, either due to HIV infection or long-term glucocorticoid therapy. If possible, the underlying disease should be treated. Mycotic lung infection requires therapy adjusted to the causative agent.

If patients do not respond to pharmacological treatment, surgery may be an option. It is rarely needed for patients presenting with uncomplicated LA but is sometimes carried out in lung cancer patients with associated LA. Before opting for surgery and depending on the patient's overall condition, endoscopic drainage should be considered [16].

Prognosis for LA that occurred due to aspiration pneumonia or bacterial infection is generally favorable. Drug therapy is sufficient to cure more than 90% of these LA patients.

Prognosis is unfavorable for LA that develop secondary to lung cancer.

Pulmonary inflammation and LA formation is usually triggered by bacteria that are inhaled into the lungs. Potential causative agents are commensal germs that may be present in the oral cavity and in the upper respiratory tract [2]. These bacteria do not cause inflammation in the lower respiratory tract as long as sufficient oxygen is inhaled and inhibits metabolism and growth. If lung tissue is damaged, e.g., due to trauma, there may be parts that remain inadequately ventilated that facilitate replication of the aforementioned bacteria.

This same chain of events may apply to obligate pathogens such as Mycobacterium tuberculosis and bacteria causing periodontal disease. In these cases, however, no primary lesion is necessary for infection to take place. The infection is, however, facilitated by immunodeficiency. Other causative agents of LA pertain to the genus Streptococcus and Staphylococcus. Methicillin-resistant Staphylococcus aureus may cause a severe infection that is difficult to treat [3].

Pulmonary embolism generally provokes tissue necrosis and secondary infection. However, in rare cases, septic emboli may become trapped in pulmonary vessels and may directly cause vessel occlusion and tissue infection. Septic pulmonary embolism is often associated with drug abuse and utilization of unsterile needles. It may also result from bacterial endocarditis or peripheral septic thrombophlebitis [4].

Other than bacteria, fungi, parasites as well as mechanical disturbances may lead to LA formation. In this context, mucus secreted in bronchial tubes and bronchioles that are located below the point of airway obstruction, cannot be moved upwards to be eliminated. Bacteria may be present in this accumulation of mucus and may trigger pulmonary inflammation and LA formation.

Patients with weakened reflexes, possibly due to alcohol or drug use, sedation or comorbidities, may be unable to eliminate bacteria, gastric content or foreign bodies from the trachea by coughing. They are therefore more prone to develop pneumonia and subsequent LA.

The worldwide incidence of LA has been declining since antibiotics are readily available in large parts of the world. Also, retrospective analysis has shown that oral surgery and tonsillectomy in a sitting position may lead to LA formation. Such surgical approaches have thus been abandoned and LA incidence could be decreased further [5]. However, local trends do not necessarily reflect this development. Indeed, immunodeficiency facilitates pulmonary infection and LA formation and is becoming increasingly common in developing countries. Other explanations have to be found to account for the local increase in LA incidence in pediatric patients that has recently been observed in France [6].

Increasingly weakened immune systems and higher incidence rates of lung cancer may account for the fact that LA are most frequently seen in the elderly. Almost half of all LA detected in patients aged 50 years and older are related to lung tumors. Here, they are often preceded by pneumonia [7]. Despite of higher incidence rates among the elderly, people at any age may be affected by LA. 

Men are affected more often than women.

One of the more common triggers for LA formation is aspiration pneumonia. Reduced consciousness is accompanied by blunt reflexes. Gastric content, foreign bodies and pathogens - although the latter may always happen involuntarily - cannot be coughed up in states of alcoholic delirium, drug abuse, seizures, stroke and other neurologic dysfunctions [8]. Neurologic or muscular disorders may also cause dysphagia, a condition that predisposes for inhalation of food particles and subsequent aspiration pneumonia.

Gastric content and food particles do not only carry pathogens into the lungs, they may also be considered foreign bodies in a broader sense of the term. They will trigger a necrotising infection, accumulation of remaining parts of the inhaled foreign bodies, tissue debris, immune cells and bacteria that will finally be demarcated by a thick, fibrous wall, the capsule of the LA.

Pathogenesis of LA also determines whether patients present with single or multiple LA. Typical causes for single LA are airway obstruction and lung tumors. Primary bacterial infection and septic pulmonary embolism often evoke formation of multiple focuses of inflammation and subsequent demarcation.

Most abscesses rupture eventually and generally empty their content into bronchioles or bronchial tubes. The patient will then cough up purulent sputum. LA may empty into the interpleural space, thus causing an empyema that is associated with dyspnea and chest pain. Rarely, greater blood vessels are damaged during abscess maturation and rupture. If this is the case, hemorrhages occur and may be visible as hemoptysis.

Aspiration pneumonia, periodontal disease and infection with mycobacteria may be prevented to a certain degree.

Preventive measures for aspiration pneumonia include endotracheal intubation or elevated, possibly lateral positioning of patients with blunted reflexes or high risk of vomiting. Good oral hygiene may decrease the prevalence of periodontal disease. Appropriate hygiene measures should be taken when interacting with patients suffering from tuberculosis, although this may not always be possible.

An abscess forms after tissue necrosis and demarcation and typically consists of a previously not existing, pus-filled cavity and a solid capsule. While the cavity is filled with tissue debris, immune cells and bacteria, if the latter triggered inflammation and abscess formation, the capsule mainly consists of fibroblasts and macrophages. If such an abscess forms in the pulmonary parenchyma, it is called lung abscess (LA).

Sterile LA exist, but the vast majority of LA develops with the involvement of anaerobic bacteria [1]. Tissue damage may originate from primary infection, aspiration pneumonia, pulmonary embolism, trauma or neoplasm, but even though the primary lesion is not infected, microorganisms may colonize necrotic tissue. Secondary bacterial infection often provokes further tissue damage, stimulates an immune response and formation of pus.

A patient may present one or multiple LA that do not necessarily are not at the same stage of development and maturation. If LA rupture, their content will drain into pre-existing cavities, i.e. into the bronchial tubes or the interpleural space. Patients may thus expectorate pus or show symptoms of pleural empyema.

The human body disposes of several defense mechanisms to assure its integrity and to eliminate pathogens. If bacteria or foreign bodies, e.g., food components, are inhaled into the pulmonary parenchyma, immune cells will try to kill pathogens and to demarcate the area of tissue damage. This process results in the formation of an abscess, a pus-filled cavity that is encapsulated with a fibrous membrane. If these events occur in lung tissue, the abscess is called lung abscess (LA).

Causes

Most cases of LA are triggered by bacteria that reach the pulmonary parenchyma through the upper airways. They may originate from the environment, as is the case for Mycobacterium tuberculosis, or from oral focuses of infection such as periodontal disease and gingivitis.

Pathogenic agents may be carried into the lungs with food components. People with blunted reflexes, e.g., those who are abusing alcohol or drugs, who are suffering from neurological problems or are sedated, are more prone to swallow the wrong way and subsequently develop aspiration pneumonia and LA.

In rare cases, bacteria are carried to lung vessels with the blood stream. This may be the case if the patient suffers from bacterial endocarditis or septic thrombophlebitis.

Symptoms

Because LA often develop in the late stages of pneumonia, symptoms provoked by the latter may not always be distinguishable from those caused by the abscess itself.

Infections cause fever, night sweats, loss of appetite and subsequent weight loss. Lung infections account for productive cough. The expectorated sputum may contain pus, sometimes even blood, smells and tastes foully.

Diagnosis

Medical history and clinical examination are usually not sufficient to identify the cause of lung problems. In order to do so, blood and sputum need to be analyzed and chest X-rays have to be obtained.

Laboratory analysis of blood samples will reveal elevated white blood cell counts that indicate infection. The causative pathogens may be isolated from sputum samples and grown in bacterial cultures. This procedure is also very useful to identify antibiotics that are effective against these pathogens. Finally, chest X-rays will confirm the presence of a LA. They also allow for an evaluation of the overall condition of the lung and its surrounding space, the interpleural space. Questionable findings may be verified in computed tomography scans.

Treatment

Treatment depends on the underlying disease. Since bacteria are involved in the majority of LA cases, antibiotics are most frequently prescribed. The specific antimicrobial compound should be chosen in consideration of resistance results obtained from bacterial cultures. Antibiotic therapy of LA is a long-term treatment that starts with intravenous application and later switches to oral medication. Similarly, mycotic lung infections require anti-fungal treatment.

Surgery is usually not necessary but may be considered if patients do not respond to drug therapy.

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