CERVICITIS II—GONORRHEA, CHLAMYDIAL INFECTIONS - pediagenosis
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Monday, September 27, 2021

CERVICITIS II—GONORRHEA, CHLAMYDIAL INFECTIONS

CERVICITIS II—GONORRHEA, CHLAMYDIAL INFECTIONS

CERVICITIS II—GONORRHEA, CHLAMYDIAL INFECTIONS


Infection by the obligate intracellular organism Chlamydia trachomatis is the second most common sexually transmitted disease (STD) and most common bacterial STD. More common than Neisseria gonorrhoeae by threefold, infections by C. trachomatis can be the source of significant complications and infertility. Twenty percent of pregnant patients and 30% of sexually active adolescent women experience chlamydial infections. Up to 40% of all sexually active women have antibodies, suggesting prior infection. The most common age for chlamydial infections is 15 to 30 years (85%), with a peak age of 15 to 19 years. The Centers for Disease Control and Prevention recommends screening all sexually active women younger than 26 years. Chlamydia has a long incubation period (average 10 days) and may persist in the cervix as a carrier state for many years.

Gonorrheal infection is a common cause of clinically acute cervicitis. It is important to realize that this specific infection invades the lower reproductive tract first before ascending to the upper tract and pelvis. Infection by this gram-negative intracellular diplococcus remains common, with a rate of infection that is roughly 3 per 1000 sexually active women and as many as 7% of pregnant patients.

Acute infection of the deeply branching cervical and endocervical glands causes an outpouring of thick, tenacious, yellowish, mucopurulent discharge from a fiery red external os (leukorrhea). Skene glands near the urethral meatus are also commonly involved at this time, producing burning, frequency, and nocturia, whereas acute bartholinitis may be responsible for inflammation and edema of the vulva. These symptoms may appear singly or in any combination. Not infrequently, however, they are so mild as to pass unrecognized as danger signals—at the very time that treatment offers the most favorable prognosis.

Ascending, the organisms reach the tubes, which become swollen, inflamed, and tortuous. The endosalpinx is particularly vulnerable to specific infection, and pus drips from the edematous fimbriae into the posterior cul-de-sac, causing pelvic peritonitis. Lymphatic involvement in the mesosalpinx may be the forerunner of bacteremia or septicemia.

Although endometritis commonly coexists with salpingitis, endometritis is a distinct clinical syndrome. Chronic endometritis (not illustrated) is quite common. It accompanies all chronic adnexal infections, although its clinical significance is minor, particularly in view of the more significant symptoms and implications of tubal disease. Lower genital tract infections with

C. trachomatis, N. gonorrhoeae, bacterial vaginosis, and Trichomonas vaginalis all increase the risk of histologically diagnosed endometritis. The ultimate diagnosis of endometritis is based on endometrial biopsy. The presence of plasma cells in the endometrial stroma combined with neutrophils in the superficial endometrial epithelium comprises the histopathologic criteria for endometritis. In severe cases, diffuse lymphocytes and plasma cells in the endometrial stroma or stromal necrosis may be present.

The classic example of acute endometritis is the puerperal infection following delivery or infection after abortion. Mechanical irritation from pessaries and chemical irritation from caustic solutions and lesions after curettage may be followed by cervical or uterine infections. When pathogenic bacteria invade the myometrium, the uterus in acute endometritis or metritis is enlarged and very tender. The patients feel ill and complain of nausea and abdominal pains, and a thin, sanguineous, sometimes purulent, secretion appears at the external cervical os. Because many of the symptoms and signs associated with endometritis are subtle and non-specific, a high degree of suspicion and a low threshold for performing an endometrial biopsy are required to establish the diagnosis. Treatment for endometritis is the same as that for outpatient salpingitis.

Because of the common coexistence of upper tract disease, the sequelae of endometri is distinct from salpingitis are difficult to determine.

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