Staphylococcal pneumonia is an acute suppurative inflammation of the lungs caused by staphylococci. It often occurs in patients with underlying conditions such as diabetes, hematological disorders, AIDS, liver disease, malnutrition, alcoholism, intravenous drug use, or pre-existing bronchial or pulmonary diseases. It is also common following influenza, non-influenza viral pneumonia, or during measles in children. The disease typically has an abrupt onset, presenting with high fever, rigors, chest pain, purulent sputum, and early signs of circulatory failure. Chest imaging often reveals necrotizing pneumonia, such as lung abscesses, pneumatoceles, and empyema. If treatment is delayed or inappropriate, the mortality rate is very high.
Etiology and Pathogenesis
Staphylococci are Gram-positive cocci and can be classified into coagulase-positive staphylococci (mainly Staphylococcus aureus, often referred to as S. aureus) and coagulase-negative staphylococci (e.g., Staphylococcus epidermidis and Staphylococcus saprophyticus). The pathogenicity of staphylococci is largely attributed to toxins and enzymes, such as hemolysins, leukocidins, and enterotoxins, which cause hemolysis, necrosis, leukocyte destruction, and vasospasm.
The virulence of staphylococci can be assessed using the coagulase test, with coagulase-positive strains demonstrating stronger pathogenicity. S. aureus is coagulase-positive and is the main cause of suppurative infections; however, coagulase-negative staphylococci can also lead to infections. With the increasing prevalence of hospital-acquired infections, pneumonia caused by coagulase-negative staphylococci is becoming more common. Staphylococcal infections account for 11%-25% of hospital-acquired pneumonia (HAP). In recent years, outbreaks of methicillin-resistant Staphylococcus aureus (MRSA) in healthcare settings have been reported. Additionally, community-acquired MRSA (CA-MRSA) pneumonia has garnered significant attention.
Pathology
Pneumonia caused by respiratory tract inhalation often displays a lobar distribution or involves multiple lobular segments as bronchopneumonia. The rupture of bronchi and alveoli can allow air to enter the pulmonary interstitium, forming a communication with the bronchi. When necrotic tissue or pus obstructs the bronchioles, a one-way valve effect can occur, resulting in tension pneumatoceles. Superficial pneumatoceles under high tension may rupture, leading to pneumothorax or pyopneumothorax, and in some cases, bronchopleural fistula formation. Occasionally, complications such as purulent pericarditis and meningitis may occur. Staphylococci from skin infections (e.g., boils, carbuncles, folliculitis, cellulitis, or wound infections) can spread to the lungs through the bloodstream, causing multiple areas of lung consolidation, suppuration, and tissue destruction, ultimately forming single or multiple lung abscesses.
Clinical Manifestations
Symptoms
The onset is often abrupt, with rigors, high fever (commonly 39-40°C), chest pain, and copious purulent sputum, which may contain blood streaks or appear as purulent-bloody sputum. Systemic symptoms of infection are severe, including generalized muscle and joint pain, physical weakness, and lethargy. In severe cases, peripheral circulatory failure may develop early. Hospital-acquired infections often have an insidious onset, with a gradual rise in temperature. Symptoms in older patients may be atypical. Hematogenous staphylococcal pneumonia is often associated with skin wounds, boils, carbuncles, central venous catheterization, or a history of intravenous drug use, and purulent sputum may be less common.
Signs
Early in the disease, physical signs may be absent and are often disproportionate to the severity of systemic infection and respiratory symptoms. Scattered moist rales may later develop in both lungs. In cases of extensive or confluent lesions, signs of lung consolidation may be present. Pneumothorax or pyopneumothorax will exhibit corresponding physical signs. For hematogenous staphylococcal pneumonia, attention should be paid to extrapulmonary lesions. Intravenous drug users often present with skin puncture marks and tricuspid valve vegetations, with associated cardiac murmurs.
Laboratory and Other Examinations
Peripheral blood tests typically show a significant increase in white blood cell counts, with a higher proportion of neutrophils and a left shift in the nuclear index. In some patients, infection with leukocidin-producing S. aureus may result in leukopenia. Chest X-rays reveal pulmonary segment or lobe consolidation, with early cavitation or lobular infiltrates containing single or multiple air-fluid levels. A characteristic feature is the variability of X-ray findings, where inflammatory infiltrates in one area may resolve while new lesions appear elsewhere, or a small solitary lesion may rapidly progress into a large opacity. When treatment is effective, lesions gradually resolve, with opacity density decreasing, and complete resolution typically occurs within 2-4 weeks. Occasionally, residual fibrotic streaks or increased pulmonary markings may persist.
Diagnosis
A preliminary diagnosis can be established based on systemic symptoms of infection, cough with purulent or bloody sputum, elevated white blood cell counts, an increased proportion of neutrophils with a left shift and toxic granulation, and characteristic X-ray findings. A definitive diagnosis relies on bacteriological tests, including cultures of sputum, pleural effusion, blood, or lung aspirates.
Treatment
Early removal and drainage of the primary focus of infection, along with the selection of sensitive antibiotics, are emphasized. In recent years, the resistance rate of S. aureus to penicillin G has reached approximately 90%. Therefore, penicillinase-resistant semi-synthetic penicillins or cephalosporins, such as oxacillin, cloxacillin, or cefuroxime, are commonly used, often in combination with aminoglycosides like amikacin, which has shown good efficacy. Combination formulations of amoxicillin or ampicillin with enzyme inhibitors are effective against beta-lactamase-producing S. aureus. For MRSA, vancomycin, teicoplanin, and linezolid are recommended. For example, vancomycin can be administered at 1.5-2.0 g/day via intravenous infusion, though adverse reactions such as drug fever, rash, and phlebitis may occur. The choice of antibiotics should be guided by bacterial culture and drug sensitivity testing.