Gonorrhea (gonorrhea) is the abbreviation for gonorrheal urethritis. It is an ancient and common sexually transmitted disease. It occurs mostly in young men and women. It was discovered by man in ancient times and described in the Bible, and in the 17th century Boswell described vividly his own illness, recurrent infections, complications and treatment. John Hunter (1728-1793) believed that the type of disease could be determined by the site of infection, for example, gonorrhea occurred on the mucous membranes, while syphilitic chancre occurred on the skin. According to this hypothesis, he transplanted the pus of a gonorrhea patient into himself, and since this patient also had syphilis, John Hunter contracted both gonorrhea and syphilis and died of syphilitic aortitis. In China, in the 2nd-3rd century B.C., the Yellow Emperor’s Classic of Internal Medicine Su Wen stated, “The bladder is not in harmony with the retention of urine.” In the second century AD, Zhang Zhongjing described gonorrhea like this in the Jin Kui Essentials: “Urine is like pulp, the small abdomen is stringent and urgent, and pain leads to the umbilicus.” In the 7th century AD, Chao Yuanfang of the Sui Dynasty divided gonorrhea into seven gonorrhea, namely, stone gonorrhea, gas gonorrhea, cream gonorrhea, consumption gonorrhea, hot gonorrhea, blood gonorrhea and cold gonorrhea, and classified cream gonorrhea as acute gonorrhea and consumption gonorrhea as chronic gonorrhea. Before liberation, the incidence rate of gonorrhea in some cities in China was about 20%. After liberation, the early stage patients were nearly extinct in 1953, and the census and treatment of late stage patients were basically completed in 1960, and gonorrhea had basically disappeared in 1964. Since gonorrhea is the most prevalent sexually transmitted disease in the world, the rate of infection among contacts is high and the incubation period is short, so the number of cases can multiply in a short period of time. Since the emergence of penicillin-resistant gonococcal strains in West Africa and East Asia in 1976, there has been a clear trend of increase in gonorrhea in the world. Since 1975, gonorrhea has returned to China, and the number of patients has increased linearly year by year, and it is the main disease of STD. For example, gonorrhea is the main STD in Shanghai, accounting for more than 90%. The pathogen of gonorrhea is Neisseria, which was isolated by Neisseria for the first time in 1879, so it is also called Neisseria gonorrhoeae (Neisseria gonorrhoeas). Neisseria gonorrhoeae is kidney-shaped, with two concave surfaces opposite each other and the same size, about 0.7 µm long and 0.5 µm wide. It is a carbon dioxide-loving aerobic bacterium, gram-staining negative, best suited for growth in a humid, 35°C, 2.5-5% CO2 environment. It is often present in multinucleated leucocytes, elliptical or spherical, often arranged in pairs, without flagella, without pods, not shaped in the budding spores, poor resistance to external physical and chemical conditions, the most fear of dryness, in a dry environment can die in 1 – 2 hours. In high or low temperature conditions are prone to death. Resistance to various chemical disinfectants is also very weak. The normal adult male urethra is 15-18 cm long, and the mucosa of the navicular fossa is composed of squamous cells, the mucosa of the anterior urethra is composed of columnar cells, and the mucosa of the posterior urethra and bladder is composed of migrating epithelial cells. The arrangement and level of cells vary according to the resistance of bacteria. The navicular fossa is composed of overlapping layers of squamous cells and has the greatest resistance to S. gonorrhoeae. The anterior urethral columnar cells are arranged in rows and have a single layer structure, and in case of infection, the bacteria can enter the submucosa from the cellular space and cause serious lesions. The migrating epithelium of the posterior urethra and bladder triangle is also susceptible to invasion because it cannot stretch freely due to anatomical limitations. The bladder wall, except for the triangle, is very stretchable and the migratory epithelium can act as a squamous cell and is never affected by S. gonorrhoeae. After entering the urethra, gonococcus enters the urethra, with the help of bacterial hairs, protein II and lgAl decomposition enzymes quickly bond with the urethral epithelium, the protein of the outer membrane of gonococcus is transferred to the epithelial cell membrane of the urethra, and then gonococcus is engulfed by the columnar epithelial cells, and then transferred to the submucosa of the cells, and through the synergistic effect of endotoxin lipopolysaccharide and complement, lgm, etc., the inflammatory reaction is caused there. 36 hours later, it causes severe After 36 hours, it causes severe mucosal erythema and the appearance of pus, with leukocytes concentrated around the bacterial flora. After entering the urethral glands and crypts, the bacteria can also penetrate from the mucosal layer to the underlying tissue. The glandular fossa and the opening of the sleeve are the main entry points for bacteria and the pathological changes are more serious than in other areas. The glandular ducts and fossa openings are often blocked and secretions cannot escape, resulting in abscesses in the glands and fossa. After the inflammatory reaction, most of the urethral mucosa is necrotic, and in severe cases, the submucosal tissue and even the corpus cavernosum are affected, resulting in periurethritis, chorioretinitis, lymphadenitis, and inguinal lymphadenitis. During repair all the destroyed cells are replaced by squamous cells and the repaired mucosa thickens, hardens and bleeds easily. When the submucosa, glandular fossa and other surrounding tissues are invaded, they are mostly replaced by connective tissue. In severe or recurrent infections, fibrosis may develop and cause urethral stricture. In the 1950s, local irrigation therapy was advocated to treat gonococcal anterior urethritis, but local irrigation is not effective and may spread the anterior urethritis to the posterior urethra, resulting in acute posterior urethritis. The bacteria mainly invade the openings of the urethral crest, prostate and seminal vesicles, and from these ducts, gonococci enter the prostate and seminal vesicles. The so-called posterior urethritis is actually acute gonococcal prostatitis and seminal vesiculitis, and in a few patients, it is combined with epididymitis. The bacteria that lurk in these glandular tissues become the main focus of chronic gonorrhea.