Staphylococcal pneumonia is an acute suppurative lung inflammation caused by staphylococci. It often occurs in individuals with underlying conditions such as diabetes, blood disorders, Acquired Immune Deficiency Syndrome, liver disease, or pre-existing bronchopulmonary diseases. Children are also susceptible during influenza or measles infections. The onset is usually abrupt, with high fever, shivering, chest pain, and purulent sputum, and circulatory failure may occur early. X-ray findings typically show necrotizing pneumonia, such as lung abscesses, pneumatoceles, and empyema. If treatment is inadequate or inappropriate, the mortality rate is very high.

bubble_chart Etiology

Staphylococci are Gram-positive cocci that can be divided into coagulase-positive staphylococci (primarily Staphylococcus aureus, abbreviated as S. aureus) and coagulase-negative staphylococci (such as Staphylococcus epidermidis and Staphylococcus saprophyticus, among others). The pathogenic substances of staphylococci are mainly toxins and enzymes, such as hemolysins, leukocidins, enterotoxins, etc., which have effects including hemolysis, necrosis, leukocyte destruction, and vasospasm. The pathogenicity of staphylococci can be measured by plasma coagulase, with positive strains being more pathogenic. S. aureus is coagulase-positive and is the primary cause of purulent infections, but other coagulase-negative staphylococci can also cause
infections. With the increase in nosocomial infections, pneumonia caused by coagulase-negative staphylococci has also been on the rise. Staphylococcal infections account for 11% to 25% of hospital-acquired pneumonia cases. In recent years, there have also been reports of outbreaks of methicillin-resistant Staphylococcus aureus (MRSA) in hospitals.

Pneumonia caused by inhalation through the respiratory tract often presents as lobar distribution or extensive, confluent bronchopneumonia. The rupture of bronchi and alveoli allows gas to enter the pulmonary interstitium and communicate with the bronchi. When necrotic tissue or pus obstructs the bronchioles, a one-way valve effect is formed, creating a tension lung qi cyst. If the tension in a superficial lung qi cyst is too high, it may rupture, leading to pneumothorax or pyopneumothorax, and may also form a bronchopleural membrane fistula. Occasionally, it may be complicated by suppurative pericarditis, brain membrane inflammation, etc.

Staphylococci from skin infections (such as boils, carbuncles, folliculitis, cellulitis, or wound infections) can reach the lungs through the bloodstream, causing multiple areas of lung excess changes, suppuration, and tissue destruction, forming single or multiple lung abscesses (hematogenous infection).

bubble_chart Clinical Manifestations

1. Symptoms: The onset of this disease is often abrupt, with shivering, high fever (temperature usually reaching 39-40°C), chest pain, and copious purulent sputum, which may be streaked with blood or appear purulent-bloody. Signs of toxemia are prominent, including generalized muscle and joint pain, constitutional weakness, and mental fatigue. In severe cases, peripheral circulatory failure may occur early. Hospital-acquired infections typically have a more insidious onset, with a gradual rise in temperature. Symptoms in elderly patients may be atypical. Hematogenous staphylococcal pneumonia often involves a history of skin wounds, boils, carbuncles, central venous catheter placement, or intravenous drug use, with purulent sputum being less common.
2. Signs: Early signs may be absent and often appear disproportionate to the severe toxic symptoms and respiratory manifestations. Later, scattered moist hiccup sounds may be heard in both lungs. Larger or consolidated lesions may present with lung excess signs. Pneumothorax or pyopneumothorax will exhibit corresponding signs. For hematogenous staphylococcal pneumonia, attention should be paid to extrapulmonary lesions; intravenous drug users often have tricuspid valve vegetations, and cardiac murmurs may be audible.

bubble_chart Auxiliary Examination

Chest X-ray shows segmental or lobar consolidation, which may form cavities or present as lobular infiltrates with single or multiple air-fluid levels. Another characteristic is the variability of X-ray shadows, manifested as the disappearance of one inflammatory infiltrate and the appearance of a new lesion elsewhere, or the progression of a small single lesion into a large shadow. With effective treatment, the lesions resolve, and the shadow density gradually decreases, usually disappearing completely in about 2 to 4 weeks, occasionally leaving behind minor linear shadows or increased lung markings.

bubble_chart Treatment Measures

Emphasis should be placed on early drainage of the primary lesion and the use of sensitive antibacterial drugs. In recent years, the resistance rate of *Staphylococcus aureus* to penicillin G has reached as high as 90%. Therefore, penicillinase-resistant semi-synthetic penicillins or cephalosporins, such as oxacillin sodium, cloxacillin, and cefuroxime sodium, can be selected. Combining these with aminoglycosides like amikacin also yields good therapeutic effects. Compound formulations of amoxicillin
and ampicillin combined with β-lactamase inhibitors are effective against enzyme-producing *Staphylococcus aureus* and can also be used.

For MRSA, vancomycin or teicoplanin should be selected. In recent years, streptogramins and oxazolidinones have also been used abroad. Vancomycin is administered intravenously at 1–2 g/day, or teicoplanin is given at 0.8 g intravenously on the first day, followed by 0.4 g/day thereafter. Adverse reactions such as drug fever, rash, and phlebitis may occasionally occur. When selecting antibacterial drugs clinically, drug sensitivity tests from bacterial cultures can serve as a reference.