bubble_chart Overview

Pneumococcal pneumonia is caused by Streptococcus pneumoniae, also known as pneumococcal pneumonia, accounting for about half of community-acquired pneumonia cases. It typically has an acute onset, characterized by high fever, shivering, cough, bloody sputum, and chest pain. Chest X-rays show acute inflammatory consolidation of lung segments or lobes. In recent years, due to the widespread use of antibiotics, the onset patterns, symptoms, and X-ray changes have become atypical.

bubble_chart Etiology

Streptococcus pneumoniae is a Gram-positive coccus, often arranged in pairs or short chains. It possesses a capsule, and its virulence is related to the structure and content of polysaccharides in the capsule. Based on the antigenic properties of the capsular polysaccharides, S. pneumoniae can be classified into 86 serotypes. Pathogenic strains in adults mostly belong to types 1–9 and 12, with type 3 being the most virulent, while types 6, 14, 19, and 23 are more common in children. S. pneumoniae can survive for months in dried sputum but is killed by direct sunlight for 1 hour or heating to 52°C for 10 minutes. It is also highly sensitive to disinfectants such as phenol. In individuals with normal immune function, S. pneumoniae is a normal flora residing in the oral cavity and nasopharynx, and its carriage rate varies with age, season, and immune status. When the host's immune function is compromised, virulent S. pneumoniae can invade and cause disease. In addition to pneumonia, a few cases may develop bacteremia or septic shock, with particularly severe conditions in the elderly and infants.

bubble_chart Pathogenesis

The disease is more common in winter and early spring, often paralleling respiratory viral infections. Patients are typically previously healthy young adults, elderly individuals, or infants and young children, with a higher incidence in males. Smokers, individuals with chronic bronchitis, bronchiectasis, congestive heart failure, chronic sexually transmitted diseases, and immunocompromised hosts are all more susceptible to Streptococcus pneumoniae infection. Streptococcus pneumoniae does not produce toxins and does not cause primary tissue necrosis or cavity formation. Its pathogenicity stems from the invasive effect of the polysaccharide capsule on tissues, initially causing alveolar wall edema, followed by the exudation of white blood cells and red blood cells. The bacteria-laden exudate spreads toward the central part of the lung through Cohn's pores, potentially affecting several lung segments or even an entire lobe. Since the lesions begin at the periphery of the lung, the interlobar boundaries are clearly demarcated, and the pleura is easily involved, leading to exudative pleuritis.

bubble_chart Pathological Changes

The pathological changes include the congestion stage, red hepatization stage, gray hepatization stage, and resolution stage. The lung tissue becomes congested and edematous, with serous fluid and red and white blood cells exuding into the alveoli. White blood cells phagocytose bacteria, followed by the dissolution and absorption of fibrin exudate, allowing the alveoli to re-expand. In the hepatization stage, there is no clear boundary between the pathological phases. With the use of antibiotics in advanced stages, such typical pathological staging has become rare. After resolution, the lung tissue structure is mostly undamaged, leaving no fibrous scars. In very rare cases, incomplete absorption of fibrin in the alveoli may occur, and fibroblasts may even form, leading to organizing pneumonia. Infections in the elderly and infants can spread along the bronchial distribution (bronchopneumonia). If antibiotics are not administered promptly, 5–10% of patients may develop empyema, while 15–20% may experience bacterial spread into the bloodstream via lymphatic vessels or the thoracic duct, leading to extrapulmonary infections such as meningitis, pericarditis, endocarditis, arthritis, and otitis media.

bubble_chart Clinical Manifestations

1. Symptoms Before the onset, there is often a history of cold exposure, rain exposure, fatigue, drunkenness, or viral infection, with many cases presenting prodromal symptoms of upper respiratory tract infection. The onset is usually abrupt, with high fever, shivering, and generalized muscle pain. Body temperature typically rises to 39–40°C within a few hours, peaking in the afternoon or evening, or presenting as a continuous fever, accompanied by an accelerated pulse rate. The affected side may experience chest pain, which can radiate to the shoulder or abdomen and worsens with coughing or deep breathing. Sputum is scant, possibly blood-streaked or rust-colored. Appetite sharply decreases, and occasional nausea, vomiting, abdominal pain, or diarrhea may occur, potentially leading to misdiagnosis as an acute abdominal condition.
2. Signs The patient appears acutely ill, with flushed cheeks, flaring nostrils, hot and dry skin, and herpes simplex at the corners of the mouth and around the nose. Cyanosis may appear if the lesions are extensive. In cases of septicemia, petechiae may appear on the skin and mucous membranes, with scleral icterus. Early pulmonary signs may show no significant abnormalities, with only reduced respiratory excursion, grade I dullness on percussion, diminished breath sounds, and pleural friction rub.

Lung Consolidation During consolidation, percussion reveals dullness, tactile fremitus is increased, and bronchial breath sounds may be heard. In the resolution phase, moist rales may be audible. The heart rate increases, sometimes with arrhythmia. Severe cases may present with abdominal distension, and epigastric tenderness is often related to inflammation involving the diaphragmatic pleura. Severe infections may be complicated by shock, acute respiratory distress syndrome, and neuropsychiatric symptoms, such as confusion, dysphoria, dyspnea, drowsiness, delirium, or unconsciousness. If the meninges are involved, neck stiffness and pathological reflexes may appear.

The natural course of the disease is approximately 1–2 weeks. Within 5–10 days of onset, the fever may resolve abruptly or gradually. With effective antibiotic treatment, the fever typically normalizes within 1–3 days, and other symptoms and signs gradually subside.

bubble_chart Auxiliary Examination

The white blood cell count is (10-20)×10⁹/L, with neutrophils accounting for over 80%, showing a left shift and toxic granules within the cells. In elderly, debilitated, alcoholic, or immunocompromised patients, the white blood cell count may not increase, but the percentage of neutrophils remains high. Direct Gram staining and capsule staining of sputum smears under microscopy can reveal typical Gram-positive diplococci or streptococci with capsules, providing a preliminary pathogen diagnosis. Sputum culture within 24-48 hours can identify the pathogen. Polymerase chain reaction (PCR) and fluorescent-labeled antibody testing can improve the etiological diagnosis rate. Sputum samples should be collected in clean, sterile containers after rinsing the mouth and before antibiotic use, preferably deep-coughed purulent or rust-colored sputum. Approximately 10-20% of patients have concurrent bacteremia, and blood cultures should be performed in severe infections. If pleural effusion is present, it should be actively aspirated for bacterial culture.

Early imaging may only show thickened lung markings or slight blurring of the affected lung segment or lobe. As the disease progresses, the alveoli fill with inflammatory exudate, appearing as large areas of inflammatory infiltration or consolidation shadows, with air bronchograms visible within the consolidation and possible small pleural effusions at the costophrenic angles. During the resolution phase, X-rays show gradual absorption of the inflammatory infiltrates, with some patchy areas resolving faster, presenting as "pseudocavitation." Most cases resolve completely within 3-4 weeks after onset. In elderly patients, lesion resolution is slower, and incomplete absorption may lead to organizing pneumonia.

bubble_chart Diagnosis

Based on typical symptoms and signs, combined with chest X-ray examination, a preliminary diagnosis can be easily made. For elderly and debilitated patients, those with secondary conditions, or those showing focal pneumonia changes, clinical manifestations are often atypical and require careful differentiation. Pathogen detection is the main basis for confirming the diagnosis.

bubble_chart Treatment Measures

1. Antibiotic Therapy: Antibiotic treatment should be administered immediately upon diagnosis without waiting for bacterial culture results. For pneumococcal pneumonia, penicillin G is the first-line treatment. The route of administration and dosage depend on the severity of the condition and the presence of complications. For adult patients with mild illness, 2.4 million units per day can be given, divided into three intramuscular injections, or procaine penicillin can be administered at 600,000 units intramuscularly every 12 hours. For moderately severe cases, penicillin G at 2.4–4.8 million units per day is recommended, administered intravenously in divided doses every 6–8 hours. For severe cases and those complicated by meningitis, the dose can be increased to 10–30 million units per day, divided into four intravenous infusions. For patients allergic to penicillin, those with penicillin-resistant or multidrug-resistant strains, alternatives such as fluoroquinolones (levofloxacin, gatifloxacin, moxifloxacin), cefotaxime, or ceftriaxone may be used. For infections caused by multidrug-resistant strains, vancomycin may be administered. The standard course of antibiotic therapy is typically 14 days, or the treatment may be discontinued three days after fever subsides, or switched from intravenous to oral administration for a few additional days.
2. Supportive Therapy: Patients should rest in bed and ensure adequate intake of protein, calories, and vitamins. Close monitoring of the patient's condition is essential, with attention to preventing shock. For severe chest pain, a small dose of analgesics such as codeine (15 mg) may be considered. Aspirin or other antipyretics should be avoided to prevent excessive sweating, dehydration, and interference with the true fever pattern, which could lead to clinical misjudgment. Encourage fluid intake of 1–2 liters per day. Patients with mild illness do not require routine intravenous fluids, but those with dehydration may need fluid replacement to maintain urine specific gravity below 1.020 and serum sodium below 145 mmol/L. For moderate or severe cases (PaO₂<60mmHg或有發紺)應給氧。若有明顯麻痺性腸梗阻或胃擴張，應暫時禁食、禁飲和胃腸減壓，直至腸蠕動恢復。煩躁不安、譫妄、失眠者酌用地西泮5mg或水合氯醛1～1.5g，禁用抑制呼吸的鎮靜藥。
3. Management of Complications: After antibiotic treatment, high fever usually subsides within 24 hours or gradually decreases over several days. If the fever recurs after subsiding or persists beyond three days, consider complications such as extrapulmonary pneumococcal infections (e.g., empyema, pericarditis, or arthritis). Other causes of persistent fever include penicillin-resistant Streptococcus pneumoniae (PRSP), mixed bacterial infections, drug fever, or coexisting conditions. If pneumonia resolves but the underlying cause (e.g., bronchial obstruction due to tumors or foreign bodies) remains untreated, pneumonia may recur. Approximately 10–20% of pneumococcal pneumonia cases are accompanied by pleural effusion, and pleural fluid should be examined as needed to determine its nature. If improperly treated, about 5% of cases may develop empyema, requiring active pus drainage.