Streptococcus pneumoniae sepsis

Introduction to Streptococcus pneumoniae sepsis Can be secondary to pneumococcal pneumonia, otitis media, mastoiditis, pharyngitis, most of the pathogens are drained by the lungs through the thoracic duct blood, otitis media and mastoiditis when the pneumococcal can enter the blood through the sinus, 20% to 30% of patients with pneumococcal pneumonia are positive for blood culture, and the positive rate increases with age. Type II Streptococcus pneumoniae is more likely to cause. Patients with splenectomy have more symptoms, which may be related to the spleen mononuclear-phagocytic system with strong phagocytosis and the function of killing the encapsulated S. pneumoniae. Other serious diseases such as sickle cell anemia and immunocompromised patients , are prone to pneumococcal sepsis. basic knowledge The proportion of sickness: 0.0052% Susceptible people: no special people Mode of infection: non-infectious Complications: meningitis osteomyelitis peritonitis

The cause of pneumococcal sepsis

Causes:

The bacteria are spear-headed and often arranged in pairs, so they can also be called pneumococci. They can be short-chain in liquid culture. On the solid medium, grass green rings can appear around the colonies, and the central part of the colonies can be autolyzed. The role of the umbilical or volcanic mouth, using the gene classification method belongs to the third group, namely the light streptococcus group, the bacteria have three antigens, the cell membrane composed of lipids and teichoic acid is F The cell wall composed of antigen, non-specific, peptidoglycan, teichoic acid and choline phosphate is a C polysaccharide antigen, which is species-specific and shared by various types of Streptococcus pneumoniae. The capsular polysaccharide antigen is type-specific. Sex, there are currently 90 serotypes, the United States called 1,2,3...90, while Danish is named according to the similarity of antigens, the first discoverer is called F(first), and then the discoverer is A. , B, C, etc., for example, 19A, 19B and 19C, which are corresponding to 19, 57, 58 and 59 in the American nomenclature, and the capsule resists the phagocytosis of the host, which is an important virulence factor of the bacteria. This bacterium can produce autolysin, pneumolysin, Neuramindase, as well as cell surface protein A, surface adhesion protein A, choline-binding protein, etc., have certain pathogenic effects during infection, and the bacteria are resistant to physical and chemical factors in the external environment. Not strong, can be killed under direct sunlight for 1h. Currently, commonly used disinfectants such as 0.2% povidone iodine (iodine) solution, chlorine disinfectant (containing effective chlorine 500mg/L) can be killed in 10min, but in no It can survive for more than 1 month in the dry sputum of sunlight.

Pathogenesis:

In normal people, although there are bacteria in the nasopharynx, but not in the disease, the cilia of the tracheal mucosa, the macrophages in the alveoli can remove the invading bacteria, but when the body's defense function is reduced, the bacteria can be colonized, multiplied, causing local tissue. Inflammatory reaction, leading to solid degenerative lesions in the lungs; such as bacteria entering the bloodstream, causing sepsis, causing purulent meningitis through the blood-brain barrier; occasionally endocarditis, osteoarthritis and other suppurative reactions, in The most important mechanism in the process of onset is that the bacteria can multiply in the host tissue and cause a strong suppurative inflammatory response. The surface protein A of Streptococcus pneumoniae, adhesion protein A and choline-binding protein can make the bacteria adhere to On the host, neuraminidase can lyse the sialic acid of the mucosal cells, allowing the bacteria to colonize. The capsular polysaccharide can resist the phagocytosis of the host, and the bacteria can multiply. The autolysin can bind the cell wall of teichoic acid and peptidoglycan. Released to activate complement (classical and bypass pathways), pneumolysin also activates the alternative pathway of complement, causing a strong inflammatory response, not only It is now organized with congestion, edema, inflammatory cells and fibrin exudation, and accompanied by a large number of interleukin-1, tumor necrosis factor alpha, etc., aggravating the inflammatory response, the severity of the disease and the inflammatory response program are closely related.

Streptococcus pneumoniae sepsis prevention

1. Active immunization: There are two kinds of vaccines for prevention. The capsular polysaccharide vaccine containing 23 serotypes (types causing more infections) has good immunity in adults, especially young people, but only maintains 5 In the year, the injection must be strengthened, and the elderly should be kept for a shorter period of time. The injection should be boosted once every 3 to 4 years. The vaccine has a poor immune effect on small infants, so the protein such as capsular polysaccharide and tetanus or diphtheria toxoid will be used. The covalently combined conjugate vaccine, which is vaccinated three times in a row, can produce antibodies in small infants under 18 months, which not only protects the baby, but also reduces the incidence of adults and effectively reduces the number of resistant strains. infection.

2. Passive immunization: For HIV-infected patients, patients with malignant tumors, who do not produce antibodies when vaccinated, can be injected with immunoglobulin regularly.

3. Drug prevention: When there is a risk of infection, oral penicillin drugs can be prevented.

Streptococcus pneumoniae sepsis complications Complications meningitis osteomyelitis peritonitis

1, meningitis: concurrent purulent meningitis is more common, to be vigilant, early cerebrospinal fluid examination.

2, pneumonia or lung abscess: followed by pneumonia or lung abscess, respiratory symptoms.

3, migratory lesions: such as cellulitis, osteomyelitis, pyelonephritis can occasionally occur.

4, multiple organ dysfunction syndrome: the serious result of infection spread is often MODS.

Symptoms of Streptococcus pneumoniae Septicemia Common symptoms High fever, septicemia, hemoptysis, skin and mucous membrane hemorrhage, chills, Sanfeng fever, coma, nausea

Sepsis can only cause sepsis of the bacteria when the systemic immune function is seriously damaged. For example, lymphatic malignancies, liver, kidney failure, splenectomy and HIV infection, all organs can be invaded and inflammation occurs. Pneumonia, meningitis, pericarditis, osteomyelitis, peritonitis, etc., patients may have chills, high fever, headache, body aches, nausea, vomiting, irritability, convulsions, lethargy, coma, but also the performance of circulatory failure: fast heart rate, The pulse is weak, the lips are cyanotic, the blood pressure is decreased, the urine volume is reduced, etc. If there are migratory lesions, such as meningitis, osteomyelitis, etc., the corresponding clinical manifestations may appear.

The clinical manifestations and blood changes of pneumonia, meningitis, sepsis caused by pneumococcal infection, the results of routine examination of CSF, the chest radiographs of patients with pneumonia, and other non-specific differences caused by other purulent bacteria, so the diagnosis and determination The differential diagnosis must be based on the results of bacteriological examination, especially the results of bacterial culture, as far as possible before the application of antibiotic treatment.

Examination of pneumococcal sepsis

1. Blood: When the systemic infection, the white blood cells can be significantly increased (20 ~ 30) × 109 / L, neutrophils accounted for about 90%, the elderly and immune function is low, the white blood cell increase is not obvious, but the classification is still neutral More than 80%.

2. Bacteriology examination: the patient's discharge of purulent lesions (such as sputum, pus, cerebrospinal fluid) smear Gram staining to find bacteria, and bacterial culture, fever patients should still do blood culture, get S. pneumoniae as the basis for diagnosis.

3. Cerebrospinal fluid examination: CSF in patients with meningitis is a purulent-like change, the appearance is rice soup, the protein is often above 1g/L, the white blood cells are more than 500×106/L, the multinucleus is the majority, and the sugar and chloride are reduced.

4. Immunological examination: The detection of capsular polysaccharide antigen in serum neutralizing CSF by latex agglutination test or convection electrophoresis is helpful for the diagnosis of negative bacteria culture.

X-ray examination: chest X-ray examination should be performed on the lungs. Only the lung texture is thickened and the local light is infiltrated. The perspective is easy to be ignored. The film should be examined. The lobe or segmental can be seen after the lungs are solidified. The sheet is densely shadowed, and the brightness is increased during the dissipating period. It takes 2 to 3 weeks for the shadow to completely dissipate.

Diagnosis and identification of pneumococcal sepsis

Should be differentiated from fulminant pneumococcal sepsis. The onset of fulminant pneumococcal sepsis is rapid, with high fever, often in the short term, the whole body appears extensively sputum, the lips and the fingertips are cyanotic, the limbs are cold, the skin is patterned, the blood pressure drops, and even undetectable. The number of cells is normal or slightly increased, and blood culture is often positive. Can be complicated by heart failure, jaundice, liver failure, acute renal failure, respiratory distress and DIC, etc., individual patients may have more serious hemolytic anemia and renal failure, but also complicated with endocarditis, meningitis and so on.

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