I am Streptococcus pneumoniae, a Gram-positive diplococcus and anaerobic bacterium, isolated by Sternberg and Pasteur in 1881. I have several names such as: Basidiococcus, Pneumococcus, S. pneumoniae, until 1974 when I was officially called Streptococcus pneumoniae. Since I am wrapped with a layer of podococcal polysaccharide outside, the podococcal polysaccharide is pathogenic, which is often called antigen, and the podococcal polysaccharide determines the serotype of pneumococcus, so that I have a big family, there are ≥ 90 serotypes. This causes a lot of trouble for everyone, and trying to prevent all my siblings is impossible. Fortunately for everyone, studies have found that 7 major serotypes cause more than 80% of invasive cases. The antibodies produced against these podoconjugates provide protection against the body, and the vaccine was developed and produced on this basis – the 7-valent conjugate vaccine, as it is often called. I is one of the leading causes of death in children under 2 years of age, killing approximately 1.2 million children worldwide each year, accounting for 9% of all deaths in developing countries, with a mortality rate greater than any vaccine-preventable pathogen. In 1977, Overturf et al. found that I was particularly fond of patients with functional or anatomical splenic deficiency, especially children with sickle cell anemia, who were at high risk for invasive systemic infections caused by me, and thus considered this systemic disease caused by me as Invasive pneumococcal disease (IPD). I am very powerful, often colonizing the throat and nasopharynx of healthy people, and can directly disseminate to adjacent mucosal tissues, causing infections such as otitis media, sinusitis and pneumonia; a small percentage of bacteria also invade the mucosa to reach the bloodstream causing invasive infections such as bacteremia, meningitis, septic arthritis and osteomyelitis. Asymptomatic nasopharyngeal carriage of pathogens is the most common in clinical practice and is the main source of infection causing IPD epidemics. Asymptomatic carriage of pathogens is also high (≥50%) in infants and preschool children, especially in children in daycare facilities and crowded places. The carrier rate decreases with age. Pathogenic bacteria are usually collected in the first few days of life, but the peak age tends to be 2 to 3 years after birth. I prefer children under 2 years of age, elderly people over 65 years of age, as well as children in group care (kindergartens/nurseries), premature and low birth weight infants, children with chronic heart and lung disease, especially cyanotic congenital heart disease and children with heart failure, diabetes, immunodeficiencies such as: those with diseases requiring immunosuppressive therapy or radiation therapy, such as malignancies, renal failure or nephrotic syndrome, and People with congenital immunodeficiency disease (HIV infection). The typical presentation of pneumonia caused by me is sudden onset of chills, high fever, chest pain, and rust-colored sputum, however, the clinical presentation is highly variable. Respiratory symptoms may or may not be present, especially in patients with simple bacteremia. Gastrointestinal symptoms such as nausea, vomiting, and diarrhea are present in 15-20% of patients and may sometimes even be the main clinical manifestation. Infants and elderly patients are even more lacking in specific signs and symptoms, which can lead to missed or misdiagnosis. Many patients can have no fever, and pneumonia is only suspected when local signs are abnormal and respiratory rate increases . Prior to antibiotic application, systemic septic lesions caused by me were more common. Laboratory tests suggest elevated peripheral blood leukocytes, most with leftward nuclear shift and toxic granules, but some patients have normal total leukocyte counts. Elevations in serum bilirubin, creatinine, and transaminases may occur due to hypoxia, hemolysis, and myocardial and hepatic damage. Penicillin has been used clinically for more than half a century as the standard drug for the treatment of my infection. Oral penicillin V (3-4g/d, Tid or Qid) can treat mild Streptococcus pneumoniae infections, while patients with severe disease require intravenous penicillin G (1-3g, q6-8h,iv). However, since the first discovery of penicillin-resistant me in Australia in 1967, resistant strains to β-lactams, erythromycin, tetracycline, sulfamethoxazole, chloramphenicol, and clindamycin have been continuously identified in many parts of the world, and increasing multi-drug resistance has been observed. The resistance rate of 1856 strains of Streptococcus pneumoniae isolated from 14 centers in Europe and the United States to erythromycin was 8.3% and 12.2% in 1992 and 1993, respectively, and increased to 19.3% in 1997 and 1998. Most of the strains with reduced susceptibility to penicillin are sensitive to the third and fourth generation cephalosporin antibiotics, such as cefotaxime sodium, bacteriophage, Masparin, but there are always some strains that are cross-resistant to β-lactam antibiotics, and thus the resistant strains to these drugs are increasing. In terms of oral antibiotics, amoxicillin has good pharmacokinetics, good absorption, long half-life, lower protein binding compared to penicillin V [30], and oral cephalosporins are less effective than penicillin antibiotics, thus amoxicillin is another good option for treating strains with reduced penicillin sensitivity. So scary! Don’t be afraid I’m not which is unreasonable, just don’t underestimate me on the line.