bubble_chart Overview

Pneumococcal pneumonia is an acute alveolar inflammation caused by Streptococcus pneumoniae, the most common type of bacterial pneumonia. It often occurs when the body's resistance suddenly decreases, predominantly affecting young adult males and occurring more frequently in winter and spring. The main clinical features include sudden onset, chills, high fever, chest pain, cough, and bloody sputum. Typical X-ray findings show consolidation of lung segments or lobes. With the widespread use of antibiotics, the classic presentation and lobar distribution have become less common.

bubble_chart Etiology

Pneumococci are arranged in short chains or pairs, belonging to Gram-positive cocci. Currently, 86 subtypes are known, with types 1–9 and 12 being prone to causing pneumonia in adults, and type 3 being the most virulent. The bacterial cell is surrounded by a capsule composed of high-molecular-weight polysaccharide polymers, which serves as a pathogenic substance, protecting the bacteria, resisting phagocytosis by white blood cells, and possessing specific antigenicity. The bacteria are found in the nasopharynx of 40–70% of healthy individuals. They can survive for months in dried sputum but are not heat-resistant; exposure to sunlight for 1 hour or heating to 52°C for 10 minutes can sterilize them.

Although many healthy individuals carry the bacteria in their upper respiratory tract, they usually do not develop illness due to the body's robust local and systemic defense mechanisms. Disease occurs only when the body's resistance is suddenly weakened for some reason. Respiratory viral infections can damage the airway mucosa and impair local defense functions, making pneumococcal pneumonia more likely during the winter and spring seasons when respiratory viral infections are prevalent. Factors such as cold exposure, rain, alcohol intoxication, excessive fatigue, general anesthesia after surgery, or overdose of sedatives can significantly weaken the body's defenses and become important predisposing factors for the disease. Transmission occurs mainly through healthy carriers, with current patients being rare sources of spread.

Depending on the disease course, the typical pathological progression can be divided into four stages: (1) **Congestion stage**: On days 1–2 of illness, bacteria proliferate in the alveoli, causing alveolar congestion, edema, and a small amount of serous exudate, spreading to adjacent areas through alveolar pores (Cohn's pores). (2) **Red hepatization stage**: Around days 3–4, fibrin and neutrophils, particularly a large number of red blood cells, fill the alveolar spaces, leading to consolidation of the affected lung segment or entire lobe, appearing dark red. (3) **Gray hepatization stage**: Around day 5, congestion begins to subside, and the alveoli become filled with large numbers of leukocytes, fibrin, dead bacteria, and cellular debris, turning from red to gray-yellow consolidation. (4) **Resolution stage**: After day 7, fibrin in the alveoli is dissolved by fibrinolysin released by neutrophils, and bacteria and cellular debris are phagocytosed and removed by macrophages, allowing the alveoli to re-expand and recover. Since pneumococci do not produce exotoxins, they do not cause primary lung tissue necrosis or abscess formation, so inflammation typically resolves without scarring. Nowadays, such distinct pathological stages are rare, and the changes in each stage are not always synchronized. Additionally, since the lesions originate in the peripheral alveoli and do not spread via the bronchi, the lobar boundaries remain clear, and the pleura is often involved. The typical disease course lasts 7–12 days.

As lung consolidation occurs, the gas exchange area decreases, leading to venous admixture and toxemia, which may result in hypoxemia and dyspnea.

bubble_chart Clinical Manifestations

Most patients have predisposing factors before the onset of illness, such as exposure to cold, getting caught in the rain, drunkenness, excessive fatigue, or emotional trauma. About half of the cases present with prodromal symptoms like upper respiratory viral infections.

1. Symptoms

   (1) Systemic symptoms: Most patients experience sudden onset while in good health, with shivering and high fever as the initial symptoms. The body temperature rapidly rises to around 40°C, often presenting as a continuous fever, accompanied by generalized body aches and weakness (lack of strength). This is primarily due to the massive proliferation of bacteria releasing toxins, leading to toxemia or bacteremia.

   (2) Respiratory symptoms: Cough and expectoration. In the typical initial stage [first stage], the cough is dry or accompanied by a small amount of sticky sputum. After 2–3 days of onset (corresponding to the red hepatization stage), due to the breakdown of a large number of red blood cells filling the alveoli, which release hemosiderin, thick, rust-colored sputum or bloody sputum is often observed. By days 4–5, the sputum turns into mucopurulent sputum, corresponding to gray hepatization. During the resolution stage, it becomes a large amount of thin, pale yellow sputum. If the pleura is involved, chest pain may occur, often presenting as stabbing pain on one side of the chest, which worsens with coughing or deep breathing but can be alleviated by lying on the affected side. Involvement of the diaphragmatic pleura may lead to persistent hiccups and severe upper abdominal pain or shoulder and back pain.

   (3) Other symptoms: Sharp loss of appetite, nausea, vomiting, and abdominal bloating. In cases of right lower lobe pneumonia, severe abdominal pain may be mistaken for acute abdomen. A few patients may develop jaundice. Neurological symptoms such as apathy, dysphoria, restlessness, delirium, unconsciousness, and meningeal irritation signs may also occur.

2. Signs: Due to differences in the severity and course of the disease, the signs can vary greatly. Mild cases often lack or show few positive signs. Typical cases present with a high fever appearance, dry and hot skin, and about one-third of patients develop herpes simplex on the nose and lips.

Severe cases may exhibit dyspnea, cyanosis, and typical signs of lung consolidation, including weakened respiratory movement on the affected side, increased vocal fremitus, dullness on percussion, and pathological bronchial breath sounds, which are typical manifestations of the red and gray hepatization stages. During the congestion and resolution stages, small to medium moist rales may be heard, and some patients may have pleural friction rubs.

[Laboratory and auxiliary examinations]

Peripheral blood leukocyte count is significantly elevated, mostly between 10–30×10⁹/L, with neutrophils accounting for over 80%, often accompanied by a left shift and toxic granules in the cytoplasm. In about 20% of elderly patients, the leukocyte count may be normal or reduced, but the proportion of neutrophils remains elevated. Gram staining of sputum smears may reveal paired or short-chain cocci, and the presence of intracellular bacteria is particularly valuable. Sputum culture may yield pneumococcal growth, with an early blood culture positivity rate of about 20%. Severe cases may be accompanied by hypoxemia and acid-base imbalance.
X-ray findings: In the early stage, only increased lung markings or faint, blurred shadows in the affected segments or lobes are observed. During the consolidation stage, large, uniform, dense shadows consistent with the distribution of lung segments or lobes are visible, often demarcated by the interlobar pleura with clear edges. Since the lesions are confined to the alveoli without bronchial involvement, bronchial air bronchograms may be seen within the shadows. Currently, such typical consolidation manifestations are less common. During the resolution stage, the consolidation shadows gradually absorb, presenting as scattered, irregular small patches, followed by linear shadows, which usually resolve completely in about three weeks. Occasionally, incomplete resolution may lead to organizing pneumonia. Additionally, blunting of the costophrenic angle and a small amount of pleural effusion may be observed.

bubble_chart Diagnosis

(1) Presence of predisposing factors such as exposure to cold, getting caught in the rain, or intoxication; (2) Sudden onset with shivering and high fever; (3) Cough, shortness of breath, expectoration of bloody sputum, and chest pain; (4) Signs of lung consolidation; (5) Chest X-ray reveals homogeneous lobar or segmental opacities, peripheral blood leukocytes and neutrophils are significantly elevated, and diagnosis is confirmed by isolation of Streptococcus pneumoniae in sputum or blood cultures.

bubble_chart Treatment Measures

1. Strengthen nursing care and supportive therapy. Bed rest should be ensured, with adequate supply of protein, vitamins, calories, and fluids. Monitor respiration, blood pressure, temperature, pulse, and urine output closely to detect early signs of shock. For high fever, physical cooling is preferred, and antipyretics that induce profuse sweating should generally be avoided. For severe dry cough or chest pain, oral codeine phosphate 15–30 mg may be administered to alleviate discomfort. Supplement fluids and electrolytes appropriately, aiming for a urine specific gravity <1.020 and serum sodium not exceeding 145 mmol/L. Provide oxygen promptly for patients with dyspnea and hypoxia.
2. Antibiotics should be administered as early as possible without waiting for bacteriological results. Most pneumococci are highly sensitive to penicillin, so penicillin G is the first choice. For milder cases, 800,000 units intramuscularly 3–4 times daily is sufficient, while severe cases require 8–12 million units daily, divided into 2–4 intravenous infusions. To maintain effective concentrations, each infusion should be completed within 1 hour. For penicillin-allergic patients, erythromycin 1.2–1.5 g/day or lincomycin 1.8 g/day may be administered intravenously. Severe cases may require first-generation (cefazolin, cephalothin) or second-generation (cefuroxime) cephalosporins, but allergy testing is still necessary. Fever typically subsides in 3–4 days, with a treatment course of 7–10 days or until 3 days after fever resolution, followed by oral formulations such as compound sulfamethoxazole 1.0 g twice daily.

   Additionally, Chinese medicinal formulas—such as Heartleaf Houttuynia Herb, common dayflower herb, and Barbated Skullcup Herb, 30 g each—can be used. For high fever, add wild buckwheat root and Giant Knotweed, 15 g each. These have notable heat-clearing and detoxifying effects, often reducing fever within 2–3 days, and can be used in conjunction with antibiotics.

3. Treatment for shock-type pneumonia: Patients complicated by shock have severe pneumonia and must receive timely, intensive care.

   (1) Elevate the foot of the bed, ensure warmth, and provide high-flow oxygen. Closely monitor respiration, blood pressure, heart rate, rhythm, and temperature changes. Promptly assess acid-base balance, electrolytes, and oxygen partial pressure. Record fluid intake and output, particularly urine volume.

   (2) Restore blood volume: Rapidly infuse 500–1000 mL of dextran or 706 plasma substitute within 1–2 hours to maintain urine output at 30–40 mL/hour and quickly raise blood pressure. Fluid replacement should follow the principles of "fast first, then slow," "saline first, then glucose," "crystalloids first, then colloids," and "potassium supplementation after urine output is observed." Maintain fluid and electrolyte balance based on intake/output and electrolyte levels. If possible, monitor central venous pressure (CVP). If CVP is <0.49 kPa (50 mmH ₂ O), fluid replacement can be liberal; if >0.98 kPa, proceed cautiously.

   (3) Correct acidosis: Shock is often accompanied by metabolic acidosis. If acidemia is present, infuse 200 mL of 5% sodium bicarbonate and periodically reassess acid-base status to determine if additional alkali therapy is needed.

   (4) Administer vasoactive drugs: If peripheral circulation or urine output does not improve after volume expansion and acidosis correction, it may be due to intense vasoconstriction and circulatory stagnation from septic shock. Vasodilators such as 654-2 (10–20 mg) or higher doses intravenously, phentolamine, or isoproterenol may be added. If ineffective, dopamine, dobutamine, or metaraminol can be used. However, vasoactive drugs are only effective after adequate volume replacement and can prevent hypotension from vasodilation.

   (5) Administer sufficient antibiotics: Penicillin G should exceed 10 million units daily. If necessary, ampicillin 8–10 g/day or cephalosporins may be used, or combination therapy may be considered.

4. Three broad-spectrum antibiotics. Due to peripheral circulatory disorders, all should be administered intravenously.

(6) Glucocorticoids In cases of severe illness or when shock remains uncorrected after the above treatments, hydrocortisone 100–200 mg or dexamethasone 5–10 mg should be added as early as possible via intravenous drip. The dose may be increased if necessary, which helps alleviate toxic symptoms, improve the condition, and restore blood pressure. However, it should be used for a short duration.

(7) Other precautions include the prevention and treatment of impaired cardiac function, renal insufficiency, adult respiratory distress syndrome (ARDS), and disseminated intravascular coagulation (DIC).

bubble_chart Prognosis

Most cases of pneumococcal pneumonia have a good prognosis and can recover within about two weeks with proper treatment. However, the prognosis is poorer in elderly or debilitated individuals, those with pre-existing chronic diseases, or those with severe conditions complicated by shock.

bubble_chart Prevention

Preventive measures include: (1) Preventing upper respiratory infections by regularly engaging in cold resistance training; (2) Avoiding triggers such as exposure to rain and cold, excessive alcohol consumption, and overexertion; (3) Actively treating underlying conditions such as chronic cardiopulmonary diseases, chronic liver disease, diabetes, and oropharyngeal disorders. If possible, pneumococcal vaccines should be administered.

bubble_chart Complications

Concurrent infection with toxic shock is not uncommon, with main manifestations including cold and clammy extremities, cyanosis, oliguria, decreased blood pressure, and peripheral circulatory disturbances; a sudden drop in body temperature below normal or persistently low; impaired consciousness, dysphoria, restlessness, delirium, or even unconsciousness. This syndrome is referred to as toxic pneumonia or shock-type pneumonia. Its mechanism may be related to the high virulence and large quantity of pathogenic bacteria, combined with low body resistance, leading to microcirculatory disturbances and ischemia or hypoxia in vital organs.

Some patients may develop fibrinous or serous exudative pleuritis, occasionally empyema; a few may experience toxic myocarditis, presenting with tachycardia, extrasystoles, atrioventricular block, gallop rhythm, hepatomegaly, and other signs of heart failure; rarely, meningitis and suppurative pericarditis may occur. Due to the widespread use of antibiotics, these complications have become increasingly rare.

bubble_chart Differentiation

With the widespread use of antibiotics, typical cases have gradually decreased. Some early-stage, mild, and elderly patients often present atypically and require differentiation from the following diseases.

1. Caseous pneumonia, also known as lobar infiltrative pulmonary subcutaneous node, sometimes closely resembles pneumococcal pneumonia. The differences are: a prolonged course, the presence of subcutaneous node toxic symptoms; frequent involvement of the upper lobe with cavity formation and bronchial dissemination; and positive acid-fast bacilli on sputum smear.
2. Early acute lung abscess In the early stages, the symptoms and X-ray findings of lung abscess patients are similar to those of pneumococcal pneumonia, but they exhibit: the appearance of copious foul-smelling purulent sputum, often accompanied by hemoptysis during the course; the formation of cavities and air-fluid levels in the lungs; and a prolonged course, requiring more than 6 weeks for complete resolution.
3. Other infectious pneumonias Staphylococcus aureus pneumonia is severe, often accompanied by sepsis, with multiple metastatic sexually transmitted disease foci and large amounts of purulent sputum; Gram-negative bacillary pneumonias, such as Klebsiella, Pseudomonas, and large intestine bacillus pneumonias, mostly occur in patients with chronic cardiopulmonary diseases, the elderly and debilitated, and those with compromised immune systems, and are often nosocomial infections. Definitive diagnosis relies on bacterial isolation from sputum and blood cultures; Mycoplasma pneumonia is more common, generally milder, and serological testing and pathogen isolation have important differential value.
4. Lung cancer Bronchogenic carcinoma can complicate obstructive pneumonia, often presenting with segmental or lobar distribution. Its characteristics include: recurrent inflammation in the same location with slow resolution; frequent mass shadows near the hilum, prone to atelectasis; repeated sputum examinations may reveal cancer cells; fiberoptic bronchoscopy can visualize endobronchial neoplasms, and biopsy often confirms the diagnosis.
5. Other diseases Lesions involving the diaphragmatic pleura membrane can cause severe abdominal pain vomiting and should be differentiated from acute liver abscess, cholecystitis, pancreatitis, etc.; those with chest pain require exclusion of pulmonary infarction, subcutaneous node pleuritis membrane, and other conditions, generally distinguishable through X-ray and comprehensive examinations.