URINARY TRACT INFECTIONS RISK FACTORS URINARY TRACT INFECTIONS RISK FACTORS
Infections of the Genital Tract
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Transcript of Infections of the Genital Tract
Infections of the Genital Tract
Karl BolintiamFrancine 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– Actinomyces Infection– Tuberculosis
TOXIC SHOCK SYNDROME
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
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
• Nonmenstrual TSS may be a sequela of focal staphylococcal infection of the skin and subcutaneous tissue– often following a surgical procedure
Classical TSS(1) the woman must be colonized or infected with S. aureus(2) the bacteria must produce TSS toxin-1 (TSST-1) or related
toxins(3) 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.
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.
• Exotoxin is believed to be absorbed directly from the vagina, as blood cultures are rarely positive for S. aureus in a woman with TSS– microulcerations produced by use of tampons systemic circulation
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– forme fruste: low-grade fever and dizziness rather than
hypotension
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
Clinical Manifestations
• tenderness of the external genitalia and vagina on pelvic exam
• Myalgia, vomiting, and diarrhea
Diagnosis
• CBC, Urinalysis, PT/PTT• Blood chem– Crea, FBS, BUN, transaminases
• cervical, vaginal, and blood cultures for S. aureus
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
Treatment
• clindamycin 600 mg IV every 8 hours – PLUS: nafcillin or 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. aureus culture
• Include aminoglycoside for gram negative coverage (sepsis), if diagnosis is questionable
ENDOMETRITIS
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
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.
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
Pathogens
• C. trachomatis, N. gonorrhoeae, bacterial vaginosis, M. genitalium, and Trichomonas vaginalis
• 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.
Treatment
• same as outpatient salpingitis treatment• should last 14 days. • Addition of metronidazole if with bacterial
vaginosis.
2010 CDC guidelines for PID
TUBERCULOSIS
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
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.
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
Clinical Manifestations
• May be asymptomatic, could also have normal pelvic exam findings
• PE: mild adnexal tenderness and bilateral adnexal masses– inability to manipulate the adnexa because of
scarring and fixation.
Diagnosis
• Suspect in patients not responding to conventional antibiotic therapy for acute bacterial PID.
• Positive tuberculin skin test• +/- CXR findings
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
Diagnosis
• Characteristic changes on laparotomy: distal ends of the oviduct remain everted, producing a “tobacco pouch” appearance
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