Streptococcal pneumonia is a type of pneumonia caused by Streptococcus pneumoniae (SP), also known as pneumococcus, accounting for about half of community acquired pneumonia (CAP), and is characterized by acute onset, high fever, rigors, cough, bloody sputum, and thoracodynia. Chest imaging shows acute inflammatory consolidation of lung segments or lobes. Due to the widespread use of antibacterials, the onset, symptoms and x-ray imaging changes of this disease are atypical.
Etiology and pathogenesis
SP is a Gram-positive coccus, mostly arranged in pairs or short chains, with capsule. Its virulence is related to the structure and content of polysaccharides in the capsule. According to the antigenic characteristics of the capsular polysaccharide, SP can be divided into 86 serotypes. Pathogens in adults are mostly type 1 - 9 and 12, type 3 is the most virulent; while in children are mostly type 6, 14, 19, and 23. SP can survive for several months in dry sputum, but can be eliminated by direct sunlight for 1 hour or heating to 52°C for 10 minutes. It is also very sensitive to disinfectants such as phenol. When the immune function is normal, SP is a normal flora colonizing the oral cavity and nasopharynx, and the carrier rate varies with age, season, and immune status. When the immune function is impaired, virulent SP invades the human body and causes disease. In addition to pneumonia, SP may cause bacteremia or septic shock, and the condition is particularly serious in the older adults and infants. SP does not produce toxins, and does not cause tissue necrosis or cavities. Its pathogenicity is due to the invasion of the capsular high-molecular polysaccharides on tissues. Alveolar wall edema causes leukocytic and erythrocytic extravasion, and the bacterial exudate spreads to the central lung through pores of Kohn, involving several lung segments or the entire lung lobe. Because the lesions start from the peripheral lung, the boundaries between the lobes are clear. The pleura is easily involved, causing exudative pleurisy.
Pathology
Pathological changes include congestion, red hepatization, grey hepatization, and resolution, and are manifested by pulmonary congestion and edema, intraalveolar serous exudation and infiltration of erythrocytes and leukocytes, and bacterial phagocytosis by leukocytes; followed by dissolution and absorption of fibrin exudate, and reinflation of alveoli. After the lesions subside, the structure of lung tissue is mostly undamaged without leaving fibrous scars. In few patients, the resorption of fibrin in the alveoli is incomplete, and even fibroblasts are formed, forming organizing pneumonia. Infection in older adults and infants can be distributed along the bronchi (bronchopneumonia). If not treated properly, 5% - 10% of patients may have complications such as empyema; and 10% - 20% of patients may have extrapulmonary infections such as meningitis, pericarditis, endocarditis, arthritis, and otitis media due to bacteria entering the bloodstream through lymphatic vessels and thoracic ducts.
Clinical manifestations
The disease is more common in winter and early spring, often accompanied by respiratory viral infection, mostly in healthy young adults or older adults and infants. Smokers, patients with dementia, chronic bronchitis, bronchiectasis, congestive heart failure, or chronic disease, and immunosuppressed individuals are susceptible to SP infection.
There is often a history of cold exposure, rain exposure, fatigue, alcohol intoxication, or viral infection. Prodromal symptoms of upper respiratory tract infection are often present. The manifestations include acute onset, rigors, and generalized myalgia, high fever (body temperature up to 39 - 40°C within few hours, with a peak in the afternoon or evening, with or without continuous fever), tachycardia, thoracodynia on the affected side radiating to the shoulder or abdomen (aggravated after cough or deep breath), little but probably bloody or rusty sputum, and anorexia. Occasionally, patients present with nausea, emesis, abdominal pain, and diarrhea, which can be easily misdiagnosed as acute abdomen.
Patients present with acute fever, flushed cheeks, nasal flaring, xeroderma, and angular and perinasal herpes simplex. Cyanosis may occur when the lesions are extensive. In patients with sepsis, cutaneous and mucosal petechiae and scleral icterus may occur. There are no obvious abnormalities in early pulmonary signs, only a decrease in the amplitude of chest respiratory movement, slightly dullness can be detected in percussion, and decreased breath sounds and pleural friction sounds may be heard on auscultation. In the case of pulmonary consolidation, percussion reveals dullness, tactile fremitus is enhanced, and bronchial breath sounds can be heard. Moist crackles may be heard during the resolution phase. Tachycardia and sometimes arrhythmia are present. Severe patients have intestinal flatulence, and upper abdominal tenderness, which is mostly related to inflammation involving the diaphragmatic pleura. Severe infection may be accompanied by shock, acute respiratory distress syndrome, and neuropsychiatric symptoms. The natural course of the disease is about 1 - 2 weeks. 5 - 10 days after onset, the body temperature may drop suddenly or gradually. After effective antibacterial treatment, the body temperature can return to normal in 1 - 3 days. Other symptoms and signs also gradually resolve.
Complications
The complications are less common. Severe patients, particularly older adults, are susceptible to septic shock, manifested by hypotension, cold extremities, diaphoresis, cyanosis, tachycardia, and arrhythmia. However, high fever, thoracodynia, and cough are not prominent. Other complications include pleurisy, empyema, pericarditis, meningitis, and arthritis.
Laboratory and auxiliary examinations
The white blood cell count is elevated, and the neutrophil count is mostly above 80%, with left shift. The white blood cell count in the older, infirm, alcoholic, and immunocompromised individuals may not increase, but the percentage of neutrophils is still increased. Sputum smear in Gram staining and capsule staining in microscopy revealing typical Gram-positive, capsulated diplococci or streptococci suggests preliminary etiological diagnosis. Sputum culture for 24 - 48 hours can determine the pathogen. Polymerase chain reaction (PCR) and fluorescent-labeled antibodies can improve etiological diagnostic yield. Urine SP antigen can be positive. About 10% - 20% of patients have bacteremia, so blood culture should be performed in severe pneumonia. If pleural effusion, the effusion should be extracted for bacterial culture. In the early stage, chest imaging shows thickened lung markings or slightly hazy involved lung segments and lobes. As the disease progresses, the manifestations are massive inflammatory infiltration or consolidation. Bronchial inflation signs can be seen in the consolidation, and there may be little pleural effusion in the costophrenic angle. In the resolution stage, the inflammatory infiltration gradually subsides, and there may be false cavities resulting from quick regression. Most symptoms resolve completely 3 - 4 weeks after onset. The lesions in the older patients regress slowly, and incomplete resolution may result in organizing pneumonia.
Diagnosis
Based on typical symptoms and signs, in combination with chest x-ray, a preliminary diagnosis can be readily established. In older, infirm patients, and in patients with pneumonia secondary to other diseases or with focal pneumonia manifestations, the clinical presentation is often atypical and careful differentiation is needed. Pathogen detection is the main basis for the definite diagnosis of this disease.
Treatment
Antibiotic treatment
Penicillin is preferred, and the route of administration and dose depend on the severity of the disease and the presence or absence of complications. The treatment plan is penicillin intramuscularly 2.4 million U/d in 3 divided doses or penicillin G procaine intramuscularly 600,000 U once every 12 hours in mild patients, penicillin intravenously 2.4 million - 4.8 million U/d once every 6 - 8 hours in moderate patients, and penicillin intravenously 10 million - 30 million U/d in 4 divided doses in severe patients and patients with meningitis. In view of the current increased insensitivity of penicillin and increased sensitivity threshold of penicillin MIC, high-dose penicillin treatment is recommended. In suspected pneumonia patients, penicillin (MIC ≤ 8 mg / L) 3.2 million U once every 4 hours is effective against SP, and can prevent the transmission of antibiotic-resistant SP, methicillin-resistant staphylococcus aureus (MRSA), and clostridium difficile caused by abuse of broad-spectrum antibiotics. In patients allergic to penicillin or infected with penicillin-resistant strains, respiratory fluoroquinolones, cefotaxime, and ceftriaxone can be administered. In patients infected with MDR strains, vancomycin, teicoplanin, and linezolid can be given.
Supportive therapy
Bed rest is required, and shock should be monitored and prevented. In patients with severe thoracodynia, little analgesic can be used if needed. Aspirin and other antipyretics, analgesics, and anti-inflammatory drugs can cause diaphoresis, dehydration, and interference with the true fever, leading to clinical misdiagnosis. Dehydrated patients can receive intravenous infusion. Patients with hypoxemia and severe patients (Pa02 < 60mmHg, or with cyanosis) should receive oxygen therapy. If there is obvious paralytic ileus or gastric dilatation, food and water should be temporarily withheld and gastrointestinal decompression should be performed until intestinal motility is restored. Sedatives should be used if needed in patients with dysphoria, delirium, and insomnia, but sedatives containing respiration inhibitors are contraindicated.
Treatment of complications
After antibiotic treatment, high fever usually subsides within 24 hours or gradually decreases within few days. If the body temperature drops and then rises again or does not drop in 3 days, extrapulmonary infections such as empyema, pericarditis, and arthritis can be considered. If fever persists, other causes should be sought. In 10% - 20% of SP patients, pleural effusion is complicated, and pleural fluid should be aspirated for examination and culture. If not treated properly, about 5% of patients can be complicated by empyema, and drainage and purulent discharge should be conducted.