disease | Staphylococcal Pneumonia |
alias | Staphylococal Pneumonia |
Staphylococcal pneumonia is a suppurative lung inflammation primarily caused by Staphylococcus aureus (S. aureus). It accounts for approximately 5% of community-acquired bacterial pneumonia and 10% of hospital-acquired bacterial pneumonia. It predominantly affects infants, the elderly, and individuals with pre-existing chronic diseases, while healthy individuals are less susceptible. The condition can be classified into primary and hematogenous types. It manifests with sudden onset, characterized by high fever, copious purulent bloody sputum, rapid deterioration, and a high tendency to form lung abscesses.
bubble_chart Etiology
Staphylococcus is a Gram-positive coccus that is aerobic or facultatively anaerobic, often arranged in clusters resembling irregular grape-like bunches. It is primarily classified into Staphylococcus aureus and Staphylococcus epidermidis, with the latter generally being non-pathogenic. Most cultured colonies of Staphylococcus produce a golden-yellow pigment, known as Staphylococcus aureus, which is highly pathogenic. Based on pigment production, there are also white and lemon-yellow staphylococci, which are less pathogenic. The strong pathogenicity of Staphylococcus aureus is attributed to its production of coagulase, which forms a fibrin barrier around the bacterial cells, protecting them from phagocytosis. Even if phagocytosed, the bacteria can survive within phagocytes for some time. Additionally, it produces α-toxin, which delays neutrophil aggregation, leukocidin that destroys white blood cells, hemolysin causing hemolysis, and enzymes like tissue-dissolving enzyme and hyaluronidase that facilitate tissue destruction and bacterial spread. In recent years, it has been found that most Staphylococcus aureus strains produce penicillinase, with over 90% being penicillin-resistant.
This bacterium can be detected in the nasopharynx of healthy individuals and is also present in the external environment, particularly in hospital settings. Infections mainly occur in young children after measles or influenza virus infection; patients with chronic diseases such as chronic obstructive pulmonary disease, lung heart disease, diabetes, and cirrhosis; hospitalized patients receiving corticosteroids, anticancer drugs, or broad-spectrum antibiotics; and those undergoing mechanical examinations or surgeries like aerosol inhalation, uterine curettage, assisted delivery, or cystoscopy. Infections can be categorized into hospital-acquired and community-acquired types. Staphylococcus aureus invades primarily through respiratory inhalation, such as nasal secretions or aerosolized pathogens entering the lungs, or hematogenously, such as through squeezing boils, wounds, or surgical and instrumental procedures, leading to bacteremia and dissemination to the lungs.Primary inhalation infections are typically located in the posterior segment of the upper lobe and the basal segment of the lower lobe, starting as suppurative bronchiolitis and then spreading to adjacent airways and alveoli, potentially affecting several lung segments, lobes, or even an entire lung. Early-stage lesions are exudative inflammation, but due to the highly destructive nature of Staphylococcus aureus, it can lead to suppurative necrosis and abscess formation. Hematogenous infections first cause multiple bacterial or septic emboli in small pulmonary arteries, followed by hemorrhagic edema, inflammatory cell infiltration, and fibrin exudation in the pulmonary interstitium and alveoli, progressing to suppurative necrosis and the formation of multiple small abscesses. As pus is expelled, cavities form. Due to air entering the cavities through a valve-like obstruction in the bronchioles, tension pneumatoceles often develop, a hallmark feature of this disease. During inflammation resolution, bronchial obstruction eases, and the accumulated air in the cavities is expelled through the airways or collateral alveolar ventilation, causing the tension pneumatoceles to disappear. If the pleura is involved, empyema, pyopneumothorax, or interlobar abscesses may form, and it can also lead to suppurative pericarditis, suppurative meningitis, or brain abscesses.
Most cases have an acute onset, with shivering, high fever, often presenting as remittent or irregular fever. Anemia and systemic exhaustion can develop rapidly, and peripheral circulatory failure is prone to occur. In cases of respiratory inhalation infection, symptoms include cough, copious purulent or bloody sputum, often accompanied by chest pain, dyspnea, and cyanosis. Signs such as lung excess changes, pulmonary internal damp rales, and pleural friction rubs may be present. Patients with hematogenous infections exhibit marked systemic exhaustion and toxic symptoms, often with apathy, dysphoria, restlessness, delirium, or unconsciousness, while respiratory symptoms and signs are usually less pronounced. Hemorrhagic rashes are common, and during the convalescent stage, extensive bran-like skin desquamation is frequently observed. In patients with chronic diseases complicated by nosocomial Staphylococcus aureus pneumonia, the onset is usually more insidious. The course of Staphylococcus aureus pneumonia is prolonged, and even with aggressive treatment, recovery often takes more than 4 to 6 weeks.
bubble_chart Auxiliary Examination
The peripheral blood white blood cell count is significantly elevated, reaching 30–50×109/L, with neutrophils often exceeding 90%, accompanied by a left shift and toxic granules in the cytoplasm. Hemoglobin and red blood cell counts are often reduced. Gram staining of sputum smears reveals a large number of neutrophils and Gram-positive cocci, with the presence of phagocytosed cocci within leukocytes being of significant importance. Sputum and blood cultures grow plasma coagulase-positive Staphylococcus aureus, and drug sensitivity tests often show resistance to multiple commonly used antibiotics.
bubble_chart Treatment Measures
General treatment and nursing care include bed rest, diet, fluid replacement, antipyretics, cough expectoration, oxygen supply, and supportive therapy, which are the same as for pneumococcal pneumonia.
For the selection of antibacterial drugs, sputum and blood bacterial cultures and drug sensitivity tests should be performed as early as possible before treatment. Most Staphylococcus aureus, especially hospital-acquired infections, are resistant to penicillin G, so β-lactamase-resistant β-lactam antibiotics should be the first choice. Commonly used drugs include oxacillin (new penicillin II) or cloxacillin at 4–6 g/day, administered in two divided doses via intramuscular injection or intravenous drip, or cephalosporin antibiotics such as cefazolin (cefamezin V) or cephalothin (cefamezin I) at 4–8 g/day via intravenous drip. Cefuroxime (Zinacef) or ceftriaxone can also be used. The optimal regimen is to select highly sensitive antibiotics based on bacterial culture and drug sensitivity test results, and the treatment course often requires 4–6 weeks or longer. For patients with empyema or abscesses in other locations, pus drainage should be performed.
Most patients can recover with early diagnosis and active, effective treatment, while a few with severe conditions, advanced age, pre-existing chronic diseases, or serious complications have a very poor prognosis.
Common complications include empyema and pyopneumothorax, while less frequent ones are suppurative arthritis, pericarditis, meningitis, brain abscess, and liver abscess.
It should be differentiated from other bacterial pneumonias, especially Klebsiella pneumoniae. Although the clinical and X-ray findings of Klebsiella pneumoniae share many similarities with Staphylococcus aureus pneumonia, Klebsiella pneumoniae often presents with thick, reddish-brown, jelly-like sputum. X-rays frequently reveal downward displacement of the interlobar fissure. Sputum smear shows Gram-negative bacilli, and diagnosis can be confirmed by culturing Klebsiella pneumoniae from the sputum.