Staphylococcal pneumonia is an acute suppurative lung inflammation caused by Staphylococcus, predominantly in patients with underlying diseases, such as diabetes, hematopathy, AIDS, hepatopathy, malnutrition, alcoholism, intravenous drug abuse, and bronchopulmonary diseases. Individuals recovered from influenza or viral pneumonia and children with measles are susceptible to the disease. Clinical manifestations include acute onset, high fever, rigors, thoracodynia, and purulent sputum; and circulatory failure may occur in the early stage. Chest imaging shows necrotizing pneumonia, such as lung abscess, pulmonary cyst, and empyema. If not treated properly, the mortality is very high.
Etiology and pathogenesis
Staphylococcus is Gram-positive and can be divided into coagulase-positive staphylococcus, mainly Staphylococcus aureus, and coagulase-negative staphylococcus, such as Staphylococcus epidermidis and Staphylococcus saprophyticus. Its pathogenic substances are mainly toxins and enzymes, such as hemolytic toxins, leukocidins, and enterotoxins, which have the effects of hemolysis, necrosis, destruction of leukocytes, and vasospasm. The pathogenicity of staphylococci can be determined by plasma coagulase, and positive results reveal strong pathogenicity. Coagulase-positive Staphylococcus aureus is the main etiology of purulent infection, but other coagulase-negative staphylococci can also cause infection. With the increase of nosocomial infections, pneumonia caused by coagulase-negative staphylococci has also been increasing. Staphylococcal infection accounts for 11% - 25% of hospital acquired pneumonia (HAP). In recent years, there have been reports of methicillin-resistant Staphylococcus aureus (MRSA) outbreaks in hospital. In addition, the emergence of community-acquired MRSA (CA-MRSA) pneumonia has also attracted great attention.
Pathology
Pneumonia caused by inhaled bacteria through the respiratory tract often presents lobar and/or segmental bronchopneumonia. Bronchial and alveolar rupture can allow gas to enter the pulmonary interstitium and communicate with the bronchi. When necrotic tissue or pus blocks the bronchioles, a one-way valve is formed, resulting in tension pulmonary cyst. If the tension of superficial pulmonary cysts is too high, they may rupture to form pneumothorax or pyopneumothorax, and may form bronchopleural fistulas. Occasionally, purulent pericarditis and meningitis may occur. Staphylococci in skin infections such as furuncles, carbuncles, folliculitis, cellulitis, and wound infections can reach the lungs through the blood circulation, causing pulmonary consolidation, suppuration, and tissue destruction, thereby forming single or multiple lung abscesses.
Clinical manifestations
Patients present with acute onset, rigors, high fever (body temperature often as high as 39℃ - 40℃), thoracodynia, excessive purulent bloody sputum, generalized myalgia and arthralgia, weak constitution, and listlessness. In severe patients, peripheral circulatory failure may occur in the early stage. Hospital-acquired infections usually have insidious onset and gradual rise in body temperature. Symptoms in the older adults may be atypical. Hematogenous staphylococcal pneumonia often presents with skin wounds, furuncles, carbuncles, and central venous catheter placement, as well as less purulent sputum; and there may be a history of intravenous drug abuse.
There may be no signs in the early stage, and then scattered moist crackles may be heard in both lungs. When the lesions are large or fused, there may be signs of pulmonary consolidation; and if pneumothorax or pyopneumothorax occurs, there can be corresponding signs. In hematogenous staphylococcal pneumonia, attention should pay to extrapulmonary lesions. Intravenous drug users often have skin punctures and tricuspid valve vegetations, and heart murmurs may be heard.
Laboratory and auxiliary examinations
The peripheral leukocyte count is significantly elevated, the proportion of neutrophils is increased, and left shift is present. Some patients have a decreased white blood cell count due to infection with Staphylococcus aureus that produces leukocidin. Chest x-ray shows consolidation of segments or lobes, manifested by cavities in the early stage, lobular infiltration, and single or multiple fluid-filled or air-filled cysts. Another characteristic is the variability of x-ray shadows, manifested by the disappearance of inflammatory infiltration in one place and the appearance of new lesions in another place, or small single lesion developing into large opacity. When the treatment is effective, the lesions subside, the opacity gradually vanishes, and the lesions resolve completely in about 2 - 4 weeks, occasionally leaving few irregular linear opacities or increased lung markings.
Diagnosis
Based on cough, bloody sputum, increased white blood cell count, increased neutrophil ratio, left shift, and x-ray imaging, a preliminary diagnosis can be readily established. Bacteriological examination is the basis for definite diagnosis. Cultures of sputum, pleural effusion, blood, and aspiration specimen can be performed.
Treatment
Early clearance and drainage of primary lesions and the selection of sensitive antibiotics are very important. In recent years, the resistance of Staphylococcus aureus to penicillin has reached about 90%. Therefore, penicillinase-resistant semisynthetic penicillin or cephalosporins, such as oxacillin sodium, cloxacillin, and cefuroxime sodium, in combination with aminoglycosides such as amikacin, have good therapeutic effects. Combination preparations consisting of amoxicillin, ampicillin, and enzyme inhibitors are effective against penicillinase-producing Staphylococcus aureus. For MRSA, vancomycin, teicoplanin, and linezolid can be used, and occasionally there are adverse reactions such as drug fever, rash, and phlebitis. Antibiotic sensitivity test in bacterial culture can guide the selection of antibiotics.