bubble_chart Overview

Bacterial pneumonia accounts for 80% of all pathogen-induced pneumonias in adults. Since the advent of the antibiotic era, the prognosis of bacterial pneumonia has significantly improved, particularly for grade I cases, but the mortality rate has remained high since the 1960s. Currently, bacterial pneumonia exhibits some new characteristics, including shifts in pathogen profiles, notably a significant increase in the proportion of Gram-negative bacilli in hospital-acquired pneumonia. Although *Streptococcus pneumoniae* still dominates as a pathogen in community-acquired pneumonia, its clinical manifestations are increasingly atypical. The rise in bacterial resistance has made so-called "refractory" pneumonia increasingly common, with particularly high mortality rates among children, the elderly, and immunocompromised patients. Enhancing etiological diagnosis, rational antibiotic use, preventing the emergence of resistant strains, and improving supportive care are urgent issues that need emphasis and resolution in the clinical management of pneumonia.

bubble_chart Pathogen

Anatomically, pneumonia can be classified into lobar, lobular, and interstitial types. For treatment purposes, it is now more commonly classified by disease cause, primarily into infectious and physicochemical types (such as radiation, toxic gases, drugs) and allergic types (e.g., hypersensitivity pneumonitis). Clinically, the vast majority of cases are infectious pneumonia caused by bacteria, viruses, chlamydia, mycoplasma, rickettsia, fungi, and Chinese Taxillus Herb parasites, with bacterial infections being the most common.

The pathogens causing pneumonia vary significantly depending on the host's age, underlying diseases, immune status, and mode of acquisition (community-acquired or hospital-acquired pneumonia) (see Table 1). Common pathogens for community-acquired pneumonia include Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus, Streptococcus pyogenes, Legionella, anaerobes, as well as viruses, mycoplasma, and chlamydia. In contrast, hospital-acquired pneumonia is often caused by Pseudomonas aeruginosa and other pseudomonads, Klebsiella pneumoniae, large intestine bacilli, Enterobacter cloacae and other Enterobacteriaceae, Proteus, methicillin-resistant Staphylococcus aureus (MRSA), and fungi. Aspiration pneumonia is mostly caused by anaerobic infections.

Table 1 Common Pathogens and Antibiotic Choices for Bacterial Pneumonia

Population	Clinical Scenario	Common Pathogens *	First-Line Drugs **	Second-Line Drugs **
Neonates	≤5 days >5 days	Large intestine, Group A or B Streptococcus Group A or B Strep, S. aureus, large intestine, Pseudomonas	Ampicillin, combined penicillin Penicillinase-resistant penicillin + 2nd/3rd gen cephalosporin	3rd gen cephalosporin Vancomycin (for MRSA)
Infants and Young Children (≤5 years)	Mild to Grade II Grade III	Often viral S. pneumoniae, H. influenzae, S. aureus	Antibiotics not necessary Ceftriaxone, cefotaxime, cefuroxime	Penicillinase-resistant penicillin + Amg
5–40 years	Community-acquired, no underlying lung disease	Viruses, mycoplasma, chlamydia, S. pneumoniae, Lp	Penicillin, macrolides	Doxycycline
>40 years	No underlying lung disease Alcoholism, diabetes, heart failure Stroke, intoxication, drug abuse, unconsciousness	S. pneumoniae, Group A Strep, H. influenzae S. pneumoniae, H. influenzae, Enterobacteriaceae, chlamydia, S. aureus S. pneumoniae, anaerobes, Enterobacteriaceae	Newer penicillin, penicillin G or ampicillin (if no GNB on smear) Macrolides + (2nd/3rd gen cephalosporin, combined penicillin, IMP) Clindamycin, cefoxitin, combined penicillin	2nd/3rd gen cephalosporin, combined penicillin, SMZCo Macrolides + SMZCo Clindamycin + Amg, IMP
All ages	NP, AA#, broad-spectrum antibiotics granulocytopenia, chemotherapy, organ transplantation post-influenza AIDS	Enterobacteriaceae, Pseudomonas, Acinetobacter, S. aureus, Lp Enterobacteriaceae, Pseudomonas, Acinetobacter, S. aureus, Lp, Fungus S. pneumoniae, S. aureus, H. influenzae (rare) CP, S. pneumoniae, subcutaneous node, H. influenzae, Hc	IMP, (AP-Penicillin or AP-Cephalosporin) + Amg Vancomycin + (AP-Penicillin or AP-Cephalosporin) + Amg, IMP (If fungus is detected, add Amphotericin B) Cefuroxime, Penicillinase-resistant Penicillin SMZCo + Ampicillin or 2nd/3rd Gen Cephalosporin	Fluoroquinolone + Ampicillin, Aztreonam replaces Amg (AP-Penicillin or AP-Cephalosporin) + Amg, AP-Penicillin + AP-Cephalosporin, Aztreonam replaces Amg Vancomycin (for MRSA) Pentamidine + Clindamycin + 2nd/3rd Gen Cephalosporin

[Note]^*Enterobacteriaceae: Enterobacteriaceae (including E. coli, Klebsiella pneumoniae, Enterobacter cloacae, etc.); Pseudomonas: Pseudomonas (including P. aeruginosa, etc.); S. pneumoniae: Streptococcus pneumoniae; H. influenzae: Haemophilus influenzae; E. coli: Escherichia coli; Acinetobacter: Acinetobacter; Lp: Legionella pneumophila; CP: Pneumocystis carinii; Hc: Histoplasma capsulatum
**IMP: Imipenem; AP-Penicillin, AP-Cephalosporin: Penicillins and cephalosporins with anti-Pseudomonas activity; 1st/2nd/3rd Gen Cephalosporin: First, second, third generation cephalosporins; Amg: Aminoglycosides; Penicillinase-resistant: Penicillinase-resistant penicillins; Compound Penicillin: Broad-spectrum penicillins combined with enzyme inhibitors; New Macrolides: New macrolides such as Clarithromycin, Roxithromycin, etc. #NP: Nosocomial pneumonia; AA: Artificial airway

bubble_chart Pathogenesis

The immune defense mechanisms, such as the filtration and dampness transformation of inhaled gases, the epiglottis and cough reflexes, the bronchial ciliary mucus excretion system, and the roles of humoral and cellular immune functions, maintain the sterility of the trachea, bronchi, and alveolar tissues. Pneumonia is prone to occur when immune function is impaired (e.g., due to cold exposure, hunger, fatigue, drunkenness, unconsciousness, toxic gas inhalation, hypoxemia, pulmonary edema, uremia, malnutrition, viral infections, or the use of glucocorticoids, artificial airways, nasogastric tubes, etc.) or when the virulence or quantity of pathogens entering the lower respiratory tract is high. The primary modes of bacterial invasion are aspiration of colonized bacteria from the oropharynx and inhalation of bacteria-laden aerosols, with the former being the most important mechanism of disease, particularly in hospital-acquired pneumonia and Gram-negative bacillary pneumonia. Direct bacterial seeding, spread from adjacent infections, or hematogenous dissemination from other sites are rare.

The typical pathological changes of pneumococcal pneumonia are divided into four stages: the early stage is mainly characterized by edema fluid and serous exudation; the intermediate stage [second stage] involves red blood cell exudation; the late stage [third stage] features massive accumulation of leukocytes and phagocytes, with consolidation of lung tissue; finally, the pneumonia resolves and dissipates. With the use of antibiotics, progression to full lobar inflammation is now uncommon, and typical lung excess changes are even rarer, replaced instead by segmental inflammation. A key pathological feature is the absence of alveolar wall or other lung structural destruction or necrosis throughout the course of the disease, allowing complete restoration of lung tissue post-resolution without fibrosis or lung qi distension. Although other bacterial pneumonias may exhibit similar pathological processes, most are accompanied by varying degrees of alveolar wall destruction. In Staphylococcus aureus pneumonia, the bacteria produce coagulase, forming a protective membrane outside the bacterial cells to resist phagocytic killing, while the release of various enzymes can lead to lung tissue necrosis and abscess formation. If the lesions invade or penetrate the pleural membrane, empyema or pyopneumothorax may develop. During resolution, lung qi cysts may form. Gram-negative bacillary pneumonia often presents as bilateral lobular pneumonia, frequently with multiple necrotic cavities or abscesses, and some patients may develop empyema. Resolution is often incomplete, potentially leading to fibrosis, residual suppurative foci, and bronchiectasis.

bubble_chart Clinical Manifestations

It is often triggered by factors such as exposure to cold or overexertion, or accompanied by underlying conditions like chronic obstructive pulmonary disease or heart failure. One-third of patients have a history of upper respiratory tract infections prior to the illness. Most cases have an acute onset. Some cases of Gram-negative bacillus pneumonia, pneumonia in the elderly, and hospital-acquired pneumonia may have an insidious onset. Fever is common, typically presenting as persistent high fever, though the fever pattern may become atypical after antibiotic treatment. Cough and sputum production are prominent, with an initial dry cough gradually progressing to productive cough of varying severity. The sputum is often purulent; typical manifestations include yellow purulent sputum in Staphylococcus aureus pneumonia, rusty sputum in pneumococcal pneumonia, brick-red gelatinous sputum in Klebsiella pneumonia, and pale green sputum in Pseudomonas aeruginosa pneumonia. Anaerobic infections are often accompanied by foul-smelling sputum. However, such classic sputum presentations are less common after antibiotic therapy. Hemoptysis is rare. Some patients experience chest pain, which may manifest as sharp, stabbing pain if the pleura is involved. Inflammation of the lower lobe irritating the diaphragmatic pleura may cause referred pain to the shoulder or abdomen, the latter of which can be misdiagnosed as acute abdominal disease. Systemic symptoms include headache, muscle aches, and lack of strength, while a minority may present with gastrointestinal symptoms such as nausea, vomiting, abdominal distension, or diarrhea. Severe cases may exhibit neurological symptoms like drowsiness, impaired consciousness, or convulsions.

On examination, patients appear acutely ill with rapid, shallow breathing, and some may exhibit nasal flaring. Varying degrees of cyanosis and tachycardia are common. A small number of patients, particularly the elderly, may develop shock (with blood pressure plummeting below 10.6/6.7 kPa or even undetectable within 24 hours, accompanied by dysphoria, pallor, cold extremities, oliguria, tachycardia, and weakened heart sounds). Pneumococcal pneumonia is often associated with herpes labialis. Early chest signs may be unremarkable or limited to a few crackles. As the disease progresses, classic signs emerge. Unilateral pneumonia may present with weakened respiratory movement on the affected side, dullness to percussion, diminished breath sounds, and moist rales. Signs of consolidation often suggest bacterial infection. In elderly patients, Gram-negative bacillus pneumonia, or pneumonia secondary to chronic bronchitis, bilateral involvement is common, with physical examination revealing bilateral basal crackles.

Total white blood cell count and neutrophils are usually elevated. In elderly or debilitated patients, the white blood cell count may remain normal, but the neutrophil percentage is still high. Significant pulmonary inflammation without leukocytosis often indicates severe disease. Arterial blood gas analysis typically shows decreased oxygen partial pressure.

bubble_chart Diagnosis

The clinical diagnosis of pneumonia can often be established based on typical symptoms, signs, and X-ray examinations.

Changes in pathogens and the frequent emergence of multidrug-resistant strains have made etiological diagnosis of pneumonia more important. However, due to contamination by normal flora from the oropharynx in expectorated sputum, unselected single routine sputum cultures are unreliable. Sputum smear microscopy aids in early preliminary pathogen diagnosis and helps eliminate "unqualified" sputum specimens heavily contaminated with oropharyngeal flora, selecting "qualified" specimens (with <10 squamous epithelial cells and >25 white blood cells per low-power field, or a squamous epithelial cell-to-white blood cell ratio <1:2.5) for examination, which should be emphasized. The presence of G⁺ and G^- cocci or polymorphic short G^- bacilli (possibly Haemophilus influenzae) within phagocytes on smears is highly diagnostic, whereas the presence of G^- bacilli has limited etiological diagnostic value. Sputum washing and quantitative culture are also effective methods to improve the accuracy of sputum cultures. Pathogens with concentrations exceeding 10⁷ CFU/ml in sputum are mostly causative agents of pneumonia, while those below 10⁴ CFU/ml are usually contaminants. For severe, complex cases, or pneumonia in immunocompromised hosts, direct sampling from the lower respiratory tract can be employed for precise pathogen diagnosis, including transtracheal aspiration (TTA) via cricothyroid membrane puncture, lung aspiration (LA) via transthoracic puncture, protected specimen brush (PSB) sampling, and protected bronchoalveolar lavage (PBAL). Blood and pleural fluid samples, which have lower contamination risks, should not be overlooked in pathogen diagnosis. Additionally, immunological and molecular biological methods are applicable for diagnosing pneumonia, such as Legionella infections, especially when conventional culture methods are complex and cannot rapidly detect pathogens. A limitation is the inability to perform drug sensitivity testing.

I. History and Symptoms:

Predisposing factors may include exposure to cold, fatigue, alcohol consumption, medication use, or chronic diseases. Common symptoms include fear of cold, fever, cough, sputum production, and chest pain, with a few cases presenting hemoptysis and dyspnea. Other symptoms may include nausea, vomiting, general malaise, and muscle aches. The history should inquire about the progression of these symptoms, treatment received, and its effectiveness.

II. Physical Examination Findings:

Flushed face (Rebing appearance), with a few cases showing respiratory distress and cyanosis. Severe patients may have a high fever (39–40°C) and signs of hypotension or shock. Chest examination may reveal reduced respiratory movement on the affected side, increased or decreased tactile fremitus, dullness on percussion, bronchial breath sounds or moist rales on auscultation, and occasionally pleural friction rubs or diminished breath sounds.

III. Auxiliary Examinations:

(1) Chest X-ray: The most common finding is bronchopneumonic changes, which usually do not aid in identifying the causative pathogen. However, certain features may provide diagnostic clues, such as lobar consolidation, cavity formation, or significant pleural effusion, which are more common in bacterial pneumonia. Staphylococcal pneumonia can cause significant lung tissue necrosis, pneumatoceles, lung abscesses, and empyema. Gram-negative bacillary pneumonia often presents as lower lobe bronchopneumonia, with a tendency to form multiple small abscesses. Chest X-rays are highly valuable for pneumonia diagnosis, as the location and extent of inflammatory infiltrates, the presence of cavities or pleural effusion, etc., are related to the causative pathogen.

X-ray Findings of Pneumonia Caused by Different Pathogens

(2) Bacteriological examination: Sputum or pleural fluid smear examination, culture of pathogenic bacteria, and antibiotic sensitivity testing. If the same bacteria grow in 2 or 3 consecutive tests, the likelihood of it being pathogenic is high. A single positive result or multiple tests showing different bacteria indicate low reliability. A bacterial concentration of ≥10^7 CFU/ml suggests pathogenic bacteria, while 10^5–10^7 CFU/ml is suspicious. <105cfa/ml多為污染菌。

(3) Blood tests: Leukocyte count and neutrophil levels are generally elevated, with possible left shift. In elderly, frail, or severe cases, leukocyte count may not increase.

(4) Immunological tests: Detection of serum pathogen antigens or antibodies using immunofluorescence, enzyme-linked immunosorbent assay (ELISA), or counterimmunoelectrophoresis can aid diagnosis. Polymerase chain reaction (PCR) has certain significance in pathogen detection.

(5) Other tests: Seasonal epidemic blood gas analysis, liver and kidney function, serum electrolytes, and related examinations may be necessary.

IV. Differential diagnosis: A few non-infectious sexually transmitted diseases may present similarly to pneumonia, such as acute respiratory distress syndrome (ARDS), congestive heart failure, pulmonary embolism, chemical gas inhalation, hypersensitivity pneumonitis, drug-induced pneumonia, radiation pneumonitis, connective tissue diseases involving the lungs, pulmonary tuberculosis, leukemia, or other malignant tumor infiltration or metastasis in the lungs. Careful differentiation is required, and diagnostic treatment may be used if necessary to clarify the diagnosis.

bubble_chart Treatment Measures

Antimicrobial therapy is the key factor determining the prognosis of bacterial pneumonia. Table 1 lists common pathogens of acute pneumonia and commonly recommended medication options for reference.

If there is no improvement or even worsening of the condition after 2–3 days of anti-infective treatment, the anti-infective drugs should be changed. If pathogen test results are available, sensitive drugs should be selected based on drug susceptibility testing. In the absence of etiological data, the possible pathogens of pneumonia should be re-evaluated, and a new round of empirical treatment should be initiated. For mild or grade II pneumonia, the total treatment course can be concluded 3–7 days after symptoms such as fever are controlled. For more severe cases, the course should be 1–2 weeks. For Staphylococcus aureus pneumonia or pneumonia in immunocompromised patients, the treatment course should be appropriately extended. For aspiration pneumonia or lung abscess, the total treatment course may require several weeks to months.

Other treatments should be selected based on the condition, such as oxygen therapy, cough and phlegm resolution, fluid infusion, and anti-shock therapy.

1. General treatment:

Bed rest, consumption of easily digestible foods rich in protein, electrolytes, and vitamins, and attention to hydration. For high fever, physical cooling measures should be applied, and antipyretic drugs may be administered if necessary. For severe chest pain, Fenbid 0.3g can be taken orally twice daily, or codeine tablets 15mg can be taken orally. For severe cough, Ke Bi Qing 25mg or Tussol 100mg can be taken orally three times daily, or codeine can be used if necessary.

2. Promoting expectoration:

Encourage the patient to cough, turn over, or pat the back to promote expectoration. Administer phlegm-resolving and antispasmodic drugs. If necessary, nebulize with 10ml of normal saline mixed with 5mg α-chymotrypsin, 5mg dexamethasone, and a small amount of antibiotics twice daily.

3. Antibiotic application:

For cases where the pathogen is unidentified, the following empirical treatments may be used.

(1) For Gram-positive cocci, use penicillin, cefazolin, erythromycin, or compound sulfamethoxazole. For Gram-negative bacteria or mixed infections, use cefazolin, amoxicillin, cefuroxime, etc. For more severe cases, third-generation cephalosporins, β-lactams + aminoglycosides, or compound sulfamethoxazole may be selected.

(2) For nosocomial infections: Mild or grade II cases may use piperacillin, cefazolin plus gentamicin, cefuroxime, cefamandole, cefotaxime, ceftizoxime, ciprofloxacin, ofloxacin, etc. Augmentin (β-lactam antibiotics with enzyme inhibitors) may also be used. For patients with a history of aspiration or major thoracic/abdominal surgery, metronidazole or clindamycin should be added. For Staphylococcus aureus infections, oxacillin, nafcillin, or vancomycin may be used. For patients on long-term steroids or antibiotics, third-generation cephalosporins, imipenem, or ciprofloxacin plus aminoglycosides should be used. For fungal co-infections, fluconazole should be added. Once the pathogen is identified, antimicrobial drugs should be adjusted based on the results of sputum culture and drug susceptibility testing.

4. Immunotherapy:

Immunomodulators such as immunoglobulins, transfer factor, and thymosin may provide auxiliary benefits. Pseudomonas aeruginosa antiserum and endotoxin antibodies are still in the experimental stage.

5. Complication treatment:

For concurrent respiratory failure, provide oxygen therapy and respiratory support. For electrolyte imbalances or liver/kidney dysfunction, administer corresponding treatments. For empyema, drainage or surgical intervention should be performed.

bubble_chart Prognosis

The prognosis of pneumonia is poorer in the elderly, those with severe underlying diseases, and immunocompromised hosts. After the widespread use of antibiotics, the mortality rate of pneumococcal pneumonia has decreased from the previous 30% to about 6%. However, pneumonia caused by Gram-negative bacilli, Staphylococcus aureus, especially MRSA, still has a relatively high mortality rate. Strengthening constitution, avoiding upper respiratory tract infections, and selective vaccination in high-risk patients are of certain significance in preventing pneumonia.