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Neisseria gonorrhoeae
Published in Firza Alexander Gronthoud, Practical Clinical Microbiology and Infectious Diseases, 2020
Infection can disseminate locally. In men, this can lead to epididymo-orchitis or, less frequently, lymphangitis or prostatitis. In about half of infected women, the infection ascends into the female genital tract, and 10%–20% can contract pelvic inflammatory disease (PID) or perihepatitis (Fitz-Hugh–Curtis syndrome).
Obstetrics and Gynaecology
Published in Seema Khan, Get Through, 2020
The patient has Fitz – Hugh – Curtis syndrome, which occurs as a complication to pelvic inflammatory disease. Ascending pelvic infection results in inflammation of the liver capsule and formation of perihepatic adhesions. This syndrome can be caused by Chlamydia spp. or gonorrhoea. The ELISA (enzyme-linked immunosorbent assay) test detects chlamydia antigens.
Infectious diseases (and tropical medicine and sexually transmitted diseases)
Published in Shibley Rahman, Avinash Sharma, A Complete MRCP(UK) Parts 1 and 2 Written Examination Revision Guide, 2018
Shibley Rahman, Avinash Sharma
Disseminated gonococcal infection (DGI) – including gonococcal arthritis – may also occur, with gonococcal infection being the most common cause of septic arthritis in young adults. The pathophysiology of DGI is not fully understood but is thought to be due to haematogenous spread from mucosal infection (e.g. asymptomatic genital infection). Initially there may be a classic triad of symptoms: tenosynovitis, migratory polyarthritis and dermatitis. Later complications include septic arthritis, endocarditis and perihepatitis (Fitz-Hugh-Curtis syndrome).
In vitro fertilization outcome in women with endometrial tuberculosis and tubal tuberculosis
Published in Gynecological Endocrinology, 2020
Wenrong Dai, Linna Ma, Yurong Cao, Di Wu, Ting Yu, Jun Zhai
FGTB is caused by the bacteria and primarily spreads by hematogenous and disseminate from foci outside the genitalia. FGTB is an important cause of pelvic and perihepatic adhesions (Fitz Hugh Curtis Syndrome) with pelvic pain, menstrual irregularities, and infertility as some of the manifestations associated with the disease [10,11]. Antitubercular treatment (ATT) is required after the diagnosis of FGTB and it can significantly relieve patients' pain and symptoms. However, some studies have shown that ATT does not alleviate pelvic or perihepatic adhesions, shrink uterine cavity, and prevent bilateral blockage of tubes, all conditions associated with infertility [12,13]. IVF-ET remains the best method for the treatment of female infertility associated with FGTB [14].
Insight into diagnosis of female genital tuberculosis
Published in Expert Review of Molecular Diagnostics, 2022
Bhawna Dahiya, Ekta Kamra, Danish Alam, Meenakshi Chauhan, Promod K. Mehta
Female genital TB affects the genital organs in the following descending order: fallopian tubes (95–100%), uterine endometrium (50–60%), ovaries (20–30%), cervix (5–15%), uterine myometrium (2.5%), and vagina/vulva (1%) [16]. The clinical features of female genital TB include primary or secondary infertility, pelvic inflammatory disease (PID), and menstrual dysfunctions [7]. Markedly, genital TB causes anatomical and physiological damage to female genital system, thereby affecting the production of hormones and reproduction during active disease [6] but also persist in latent stage. Infection with Mtb causes tubal blockage as well as abdominal adhesions, including perihepatic adhesions (Fitz–Hugh–Curtis syndrome) and shrunken uterine cavity [14,17]. Infertility is the most common sequel, which occurs in 5–16% of Indian women caused by irreversible damage to the fallopian tubes [12], thus leading to exosalpingitis and endosalpingitis, though tubercular hydrosalpinx is another cause of infertility [2,18]. Mostly, fallopian tubes are associated with congestion and miliary tubercles, whereas endometrium is linked with caseation and ulceration in 50–80% cases [7]. Mtb causes disorder of endometrial receptivity and suppresses the sensitivity of endometrium toward ovarian hormones, thus resulting into deficient secretory phase and defective glycogen secretion [19]. This leads to defective implantation of ovum, thereby causing intrauterine synechiae (Asherman’s syndrome) and infertility [2,20]. Oophoritis is another manifestation of genital TB with poor ovarian reserve and increased need of gonadotrophins for ovulation induction that destroys the ovaries [21,22]. To add, latent TB causes recurrent implantation failure and miscarriages owing to endometrial hostility through enhanced production of TNF-α and IL-2 that shifts Th response from Th2 to Th1 [12,23]. Of note, the hypothalamic-pituitary-ovarian axis controls reproduction through cyclic production of gonadotropic and steroid hormones [24], which is negatively regulated during Mtb infection. This causes diminished ovarian reserve or premature ovarian failure with hypergonadotropic-hypogonadic profile and affects about 5% of women with ovulatory dysfunction, thus leading to infertility [21,24].