| disease | Uncomplicated Gonorrhea in Women |
| alias | Gonorrhea |
Gonorrhea is a purulent infection of the urogenital system caused by Neisseria gonorrhoeae. It is one of the most common sexually transmitted diseases, primarily manifesting as gonococcal urethritis and cervicitis. The gonococcus can also spread locally from the urethra or cervix, causing epididymitis and pelvic inflammation, or disseminate hematogenously, leading to disseminated gonorrhea. Additionally, it can cause infections of the eyes, throat, and rectum. Some individuals, despite being infected with gonococcus, exhibit no clinical symptoms, a condition known as asymptomatic gonorrhea. The emergence of drug-resistant strains, such as penicillinase-producing variants, has posed significant challenges to the prevention and control of this disease. Traditional Chinese medicine documented gonorrhea as early as the 2nd–3rd century BCE in the Huangdi Neijing﹒Suwen. In the 7th century CE, during the Sui Dynasty, Chao Yuan-fang described the disease in his work Zhubing Yuanhou Lun. By the 10th century CE, during the Song Dynasty, the terminology for gonorrhea became more varied, though later, the conditions of "lin" (淋), "long" (癃), and "zhuo" (濁) were often conflated. "Zhuo" referred to seminal disorders, akin to modern descriptions of leukorrhea. Galen (130 CE) used the Greek term "Gonorrhea" (from "gono" meaning seed and "rhea" meaning flow) to describe the disease, reflecting the historical confusion between semen and urethral pus.
In 1767, John Hunter conducted a bold experiment by inoculating himself with pus from a gonorrhea patient who also had syphilis. Consequently, he contracted both gonorrhea and syphilis and ultimately died from syphilitic aortitis. At the time, gonorrhea was believed to be an early stage of syphilis, and until the mid-19th century, the two diseases were considered identical.
In 1897, Albert Neisser identified the gonococcus in the pus from patients' urethras, vaginas, and newborns' eyes, naming it Neisseria gonorrhoeae. Three years later, Leistikow and Loffler successfully cultured the bacterium in vitro. In 1885, Bumm grew the bacterium on coagulated serum from humans, cows, or sheep and demonstrated its pathogenicity by inoculating it into healthy human urethras, reproducing the same symptoms. This confirmed the gonococcus as the causative agent of gonorrhea. However, in the early 20th century, gonorrhea and chlamydial infections were still confused. Cases with mild symptoms and thin urethral discharge were misclassified as chronic gonorrhea until penicillin treatment distinguished gonorrhea from other sexually transmitted urethritides.Humans are the sole host of Neisseria gonorrhoeae. The bacterium lacks pathogenicity in lower animals; repeated attempts to induce gonococcal conjunctivitis in rabbits by transplanting human urethral pus containing gonococci were unsuccessful, indicating humans' unique susceptibility. Thus, gonococci exclusively infect humans and cannot invade lower animals.
Research on gonorrhea advanced after the 1970s. In the 1980s, studies focused on the genetic structure and pathogenic mechanisms of Neisseria gonorrhoeae, aiming for immunological control, though success remains elusive.
The treatment of gonorrhea has evolved over time. Early methods included intraurethral drug instillation. Sulfonamides were introduced in 1935, followed by penicillin from 1938 to 1940. By 1945, cases of penicillin-resistant gonococcal urethritis were reported in the U.S. Sensitivity testing for penicillin resistance began in 1960. In 1976, penicillinase-producing Neisseria gonorrhoeae (PPNG) was officially isolated in the U.S. Recent reports also highlight strains resistant to spectinomycin.
Under normal circumstances, urine should be sterile. The continuous flushing of the urethra by urine makes it difficult for invading microorganisms to settle in the urinary tract. However, Neisseria gonorrhoeae can easily colonize the urinary tract Chinese Taxillus Herb, primarily because the gonococcus has pili, which make it highly sensitive to single-layer columnar epithelial cells and transitional epithelial cells, such as those in the anterior urethra, cervix, posterior urethra, and bladder mucosa, allowing it to adhere easily to these cells. In acidic urine (pH<5.5）很快殺死，因而膀胱和腎臟不易被感染，而前列腺液含有精胺及鋅，故可受淋球菌感染。
), the Chinese Taxillus Herb flora in the urethra and vagina has a certain inhibitory effect on the growth of gonococci. The presence of these flora provides some natural resistance to the body. The mucosal surface contains lactoferrin, and iron is essential for the growth and reproduction of gonococci. When iron levels in the environment are low, the growth of gonococci is restricted. Gonococci exhibit varying sensitivity to different cells, being most sensitive to the columnar epithelial cells of the anterior urethral mucosa. Thus, the anterior urethra is most susceptible to infection. The posterior urethra and bladder mucosa are composed of transitional epithelium, to which gonococci are less sensitive than columnar cells, making these areas less prone to gonococcal infection. The navicular fossa mucosa consists of stratified squamous cells, which are less likely to be infected by gonococci. Gonococci rapidly adhere to urethral and cervical epithelial cells using pili, protein II, and IgA protease. The outer membrane protein I of gonococci transfers to the epithelial cell membrane of the urethra, after which the gonococci are engulfed by columnar epithelial cells and then translocated beneath the submucosa. There, through the synergistic action of endotoxin lipopolysaccharide, complement, and IgM, they trigger an inflammatory response. Around 30 hours later, widespread mucosal edema and adhesion occur, accompanied by purulent discharge. During urination, the adhered urethral mucosa stretches, stimulating local nerves and causing pain. Due to the inflammatory response and mucosal erosion and shedding, the typical urethral purulent discharge forms. The inflammatory stimulation also causes spasmodic contraction of the urethral sphincter, leading to frequent and urgent urination. If small mucosal blood vessels rupture, terminal hematuria may occur. When bacteria enter the urethral glands and crypts, they can also invade the submucosa from the mucosal layer, blocking the openings of the gland ducts and crypts, leading to local abscess formation. During this process, the body produces local and systemic antibodies. The immune response to gonococci manifests in various ways, with host defense primarily relying on IgG and IgM, while IgA also plays a preventive role on the mucosal surface. In males with gonococcal urethritis, urethral secretions often exhibit an antibody response to the infecting gonococci, known as the mucosal antibody response. These antibodies include not only IgA but also IgG and IgM. In terms of serum antibody response, after gonococcal infection, serum levels of IgG, IgM, and IgA increase. IgA, as a secretory antibody, enters the bloodstream from the mucosal surface. These antibodies are crucial for serum antibody-complement-mediated bactericidal effects and provide protection against gonococcal bacteremia caused by serum-sensitive strains. Generally, the inflammation does not spread systemically. If treated with Yaodui in a timely and adequate manner, local inflammation will gradually subside. After the inflammation subsides, the necrotic mucosa is repaired, replaced by squamous epithelium or connective tissue. Severe or recurrent infections can lead to connective tissue fibrosis, causing urethral stricture. If treatment is delayed, gonococci can enter the posterior urethra or cervix, spreading upward and causing inflammation in the urogenital tract and nearby organs, such as paraurethral glanditis, bulbourethral glanditis, prostatitis, seminal vesiculitis, epididymitis, endometritis, etc. In severe cases, the bacteria can disseminate systemically via the bloodstream. Gonococci can also remain latent in the deep tissues of glands for extended periods, becoming a cause of recurrent chronic gonorrhea. After the inflammation in these infected organs subsides, connective tissue fibrosis can lead to strictures or obstruction of the vas deferens or fallopian tubes, resulting in ectopic pregnancy and sterility.
The primary site of primary gonococcal infection in women is the cervix. Gonococci can attach to stratified squamous epithelium, and electron microscopy reveals that the infection site is at the squamous-columnar epithelial junction of the cervix. The nature of the disease: Patients with cervicitis often have no early symptoms, making the incubation period difficult to determine. Symptoms include cervical congestion, tenderness, increased purulent discharge, frequent vulvar itching and burning sensations, and occasionally lower abdominal pain and lumbago. These atypical symptoms often lead to delayed medical attention, making patients a major source of infection. Gonococcal urethritis typically occurs 2-5 days after intercourse, presenting with urethral orifice congestion, tenderness, and purulent discharge, accompanied by grade I urinary frequency, urgency, dysuria, and a burning sensation during urination. Pressing the urethra may produce purulent discharge. Gonococcal bartholinitis is usually unilateral, with redness and swelling at the gland opening, severe pain, and possible abscess formation in severe cases. Systemic symptoms such as fever may occur. Gonococcal vaginitis is relatively rare. In chronic cases, symptoms are mild, with some patients experiencing abdominal heaviness, lower back pain, increased leucorrhea, lower abdominal pain, or hypermenorrhea. Gonococcal vulvovaginitis in women manifests as inflammation of the vulva and vagina, with abundant purulent vaginal discharge. Yellow-green discharge may sometimes be observed in the vagina and urethra, accompanied by painful urination and vulvar redness and swelling. The discharge may spread to the anus, causing irritation. In severe cases, it can infect the rectum, leading to gonococcal proctitis.
The diagnosis must be confirmed through comprehensive analysis based on exposure history, clinical manifestations, and laboratory tests.
(1) Exposure history: The patient has a history of extramarital sexual behavior or prostitution, the spouse has a history of infection, shared items with gonorrhea patients (especially household members with gonorrhea), or the newborn's mother has a history of gonorrhea.
(2) Clinical manifestations: The main symptoms of gonorrhea include frequent urination, urgency, dysuria, purulent discharge from the urethral orifice or cervical/vaginal orifice, or manifestations of gonococcal conjunctivitis, enteritis, pharyngitis, or symptoms of disseminated gonorrhea.
(3) Laboratory tests: Microscopic examination of urethral discharge in male acute gonococcal urethritis has preliminary diagnostic significance, while for females, it serves only as a reference. Culture should be performed to confirm Neisseria gonorrhoeae infection. In well-equipped facilities, genetic diagnostic methods can be used for definitive diagnosis.
bubble_chart Treatment Measures
Gonorrhea is an extremely contagious and easily reinfected sexually transmitted disease. It is often complicated by infections such as chlamydia. The gonococcus is prone to developing drug resistance. It is also prone to complications and sequelae, warranting sufficient attention in treatment. Since the use of sulfonamides in 1935 and penicillin in 1944 to treat gonorrhea, relatively good therapeutic outcomes have been achieved. However, the emergence of penicillin-resistant, tetracycline-resistant, and other drug-resistant strains has posed challenges in the treatment of gonorrhea.
Principles of treatment:
(1) Early diagnosis and early treatment; (2) Timely, adequate, and standardized medication; (3) Tailored treatment approaches based on different conditions; (4) Partner tracing and simultaneous treatment; (5) Follow-up and re-examination after treatment; (6) Attention to concurrent infections such as chlamydia, mycoplasma, and other STDs.
Review 1-2 weeks after treatment. The criteria for cure are: (1) clinical symptoms disappear; (2) urine is clear without purulent threads; (3) two consecutive negative results for gonococcus in prostate massage fluid or cervical secretion smears and cultures, indicating recovery.
- Prevention:
- Promote knowledge about sexually transmitted diseases, advocate for high moral standards, and strictly prohibit prostitution.
- Using condoms can reduce the incidence of gonococcal infections.
- Prophylactic use of antibiotics can lower the risk of infection. Taking norfloxacin or amoxicillin before and after sexual intercourse can effectively prevent sexually transmitted disease infections.
- Treat sexual partners simultaneously.
- Patients should pay attention to personal hygiene and isolation, avoiding sharing beds or baths with family members, especially children, particularly girls.
- Implement a system of applying silver nitrate solution or other antibiotic eye drops to newborns to prevent gonococcal conjunctivitis.
- Prognosis:
For gonorrhea patients, timely and correct treatment during the acute phase can lead to a complete cure. Uncomplicated gonorrhea treated with a single high-dose medication has a cure rate of 95%; incomplete treatment can lead to complications, including infertility, ectopic pregnancy, pelvic inflammation, urethral stricture, blindness, or disseminated gonorrhea. Therefore, it is crucial to seize the opportunity to thoroughly cure gonorrhea during the acute phase.
(1) Nongonococcal urethritis: The incubation period is relatively long, ranging from 7 to 21 days. Urethral discharge is minimal or absent, appearing as serous or mucous secretions that are thin and sparse. Symptoms are mild with no systemic manifestations. The primary pathogens are Chlamydia trachomatis and Ureaplasma urealyticum.
(2) Candidal vaginitis: The main clinical symptoms include vulvar and vaginal cutaneous pruritus, increased leucorrhea, which appears white and watery or gel-like. The vaginal mucosa shows congestion, edema, and adherent white membranes. Areas where the white membranes detach exhibit grade I erosions. Microscopic examination of the white membranes reveals spores and hyphae.
(3) Trichomonal vaginitis: The main clinical symptoms are vaginal cutaneous pruritus, with discharge often appearing frothy. The vaginal mucosa and cervix exhibit marked congestion and characteristic strawberry-like hemorrhagic spots. The vaginal mucosa frequently bleeds, resulting in bloody discharge. Trichomonads can be detected in the secretions.
(4) Bacterial vaginosis: Leucorrhea increases, appearing gray and homogeneous with an elevated pH and a fishy odor. Microscopic examination shows a reduction in lactobacilli and an increase in Gram-negative bacteria.
