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Infections of the Genital Tract

Infections of the Genital Tract. Karl Bolintiam Francine Lu Roberto Sioco. Outline. Infections of the lower genital tract Infections of the Vulva Vaginitis Toxic Shock Syndrome Cervicitis Infections of the upper genital tract Endometritis Pelvic Inflammatory Disease

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Infections of the Genital Tract

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  1. Infections of the Genital Tract Karl Bolintiam Francine Lu Roberto Sioco

  2. Outline • Infections of the lower genital tract • Infections of the Vulva • Vaginitis • Toxic Shock Syndrome • Cervicitis • Infections of the upper genital tract • Endometritis • Pelvic Inflammatory Disease • Actinomyces Infection • Tuberculosis

  3. Toxic Shock Syndrome

  4. Toxic shock syndrome (TSS) • an acute, febrile illness produced by a bacterial exotoxin, with a fulminating downhill course involving dysfunction of multiple organ systems • abrupt onset and rapidity • may develop rapid onset of hypotension associated with multiorgan system failure • develop from a site of bacterial colonization rather than from an infection

  5. Toxic shock syndrome (TSS) • used to be related to menstruation and tampon use • more likely with use of higher absorbency tampons, several cycle days of tampons, and kept a single tampon in for a longer period of time • NonmenstrualTSS may be a sequela of focal staphylococcal infection of the skin and subcutaneous tissue • often following a surgical procedure

  6. Classical TSS • the woman must be colonized or infected with S. aureus • the bacteria must produce TSS toxin-1 (TSST-1) or related toxins • the toxins must have a route of entry into the systemic circulation. • Interestingly, approximately 85% of adult females have antibodies against TSST-1 • women with menstrual-related TSS do not respond immunologically to TSST-1 as do women with nonmenstrual-related TSS.

  7. Pathophysiology • signs and symptoms of TSS are produced by the exotoxin named toxin-1 • toxins act as “superantigens.” • activate up to 20% of T cells at once, resulting in massive cytokine production. • primary effects of toxin-1: • increased vascular permeability and thus profuse leaking of fluid (capillary leak) from the intravascular compartment into the interstitial space • profound loss of vasomotor tone, resulting in decreased peripheral resistance. • Exotoxinis believed to be absorbed directly from the vagina, as blood cultures are rarely positive for S. aureus in a woman with TSS • microulcerationsproduced by use of tampons systemic circulation

  8. Clinical Manifestations • Wide range of symptoms but should have high index of suspicion for TSS in a woman who has an unexplained fever and a rash during or immediately following her menstrual period • prodromal flu-like illness for the first 24 hours. • days 2-4 of the menstrual period: • abrupt onset of a high temperature • headache, myalgia, sore throat, vomiting, diarrhea, a generalized skin rash, and often hypotension • formefruste: low-grade fever and dizziness rather than hypotension

  9. Clinical Manifestations • Skin changes: most characteristic manifestation • first 48 hours: rash appears similar to an intense sunburn. • Next few days: the erythema will become more macular and look like a drug-related rash. • Days 12 to 15: fine, flaky, desquamation of skin over the face and trunk with sloughing of the entire skin thickness of the palms and soles • vaginal mucosa is hyperemic during the initial phase of the syndrome

  10. Clinical Manifestations • tenderness of the external genitalia and vagina on pelvic exam • Myalgia, vomiting, and diarrhea

  11. Diagnosis • CBC, Urinalysis, PT/PTT • Blood chem • Crea, FBS, BUN, transaminases • cervical, vaginal, and blood cultures for S. aureus

  12. Management • First eliminate the hypotension produced by the exotoxin • IVF given while pressure and volume dynamics are monitored with a pulmonary artery catheter. • Mechanical ventilation is required for women who develop adult respiratory distress syndrome. • wash out the vagina with saline or dilute iodine solution to diminish the amount of exotoxin that may be absorbed into the systemic circulation • Drain and debride skin infection if that is the focus

  13. Treatment • clindamycin 600 mg IV every 8 hours • PLUS: nafcillinor oxacillin 2 g IV every 4 hours, • and most experts recommend a 1- to 2-week course of therapy with an antistaphyloccocal agent such as clindamycin or dicloxacillin even in the absence of positive S. aureusculture • Include aminoglycoside for gram negative coverage (sepsis), if diagnosis is questionable

  14. Endometritis

  15. Endometritis • Usually coexists with salpingitis • But patients with endometritis alone had distinct risk factors: • douching in last 30 days • current IUD in place • in days 1 to 7 of menstrual cycle

  16. Endometritis • Gold standard diagnosis: endometrial biopsy. • At least one plasma cell per 120× field of endometrial stroma combined with five or more neutrophils in the superficial endometrial epithelium per 400× field • In severe cases: diffuse lymphocytes and plasma cells in the endometrial stroma or stromal necrosis may be present.

  17. Endometritis • May be subclinical • May not have signs of salpingitis as well (no cervical motion or adnexal or uterine tenderness) • High clinical suspicion • Risk factors: • young age (20 to 22 years old in most studies) • abnormal uterine bleeding (menorrhagia or metrorrhagia) • menstrual cycle day less than 14 • douching in last 30 days • history of prior PID

  18. Pathogens • C. trachomatis, N. gonorrhoeae, bacterial vaginosis, M. genitalium, and Trichomonasvaginalis • in women with current N. gonorrhoeae or C. trachomatis infection, endometritis was apparent in 43% of women with a history of prior PID and 23% in women without prior PID. • suggestive of possible immunologic memory. • may not have an isolated pathogen.

  19. Treatment • same as outpatient salpingitistreatment • should last 14 days. • Addition of metronidazole if with bacterial vaginosis.

  20. 2010 CDC guidelines for PID

  21. Tuberculosis

  22. Tuberculosis • primarily chronic salpingitis and chronic endometritis • frequent cause of chronic PID and infertility in other parts of the world • Usually in premenopausal women • either Mycobacterium tuberculosis or M. bovis

  23. Tuberculosis • primary site of infection: usually the lung. • spread hematogenouslyoviduct. • Primary and predominant site of pelvic TB • Subsequent spread to the endometrium and less commonly to the ovaries.

  24. Clinical Manifestations • insidious or rapidly progressing • similar to the chronic sequelae of nontuberculous acute PID • Usually infertility and abnormal uterine bleeding • Mild-to-moderate chronic abdominal and pelvic pain • Ascites

  25. Clinical Manifestations • May be asymptomatic, could also have normal pelvic exam findings • PE: mild adnexal tenderness and bilateral adnexalmasses • inability to manipulate the adnexa because of scarring and fixation.

  26. Diagnosis • Suspect in patients not responding to conventional antibiotic therapy for acute bacterial PID. • Positive tuberculin skin test • +/- CXR findings

  27. Diagnosis • endometrial biopsy late in the secretory phase of the cycle • Portion sent for culture and animal inoculation • remaining portion examined histologically. • classic giant cells, granulomas, and caseous necrosis confirm the diagnosis

  28. Diagnosis • Characteristic changes on laparotomy: distal ends of the oviduct remain everted, producing a “tobacco pouch” appearance

  29. Management • chest radiographic examination, IV pyelogram, serial gastric washings, and urine cultures • Treatment: 5-drug regimen for MDR-TB • Surgery reserved for: • persistent pelvic masses, • some women with resistant organisms, • women older than 40 • women whose endometrial cultures remain positive

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