1. Female Genital System infection
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2. Natural defenses of genital tract
Vulva
Inherent resistance to infection
Fungicidal
Proper apposition of introitus by of labia
Vagina
Close apposition of vaginal wall
Well developed stratified squamous epithelium
Vaginal flora
Vaginal acidity

3. Contd.. Cervix Uterus Tubes Functional closure of cervix
Thick mucus plug
Immune –abundance of plasma cell in sub epithelial layer and high concentration of cytotoxic T cell
Uterus
Periodic shedding of surface endometrium during menses
Tubes
Peristalsis movement

4. Contents Vulvovaginal infection Cervicitis
Pelvic inflammatory disease (PID)
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5. Section 1 Vulvovaginal infection
Vulvitis
Bartholinitis/Bartholin’s cyst
Trichomonas vaginitis
Candidiasis
Bacterial vaginosis
Atrophic vaginitis
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6. Self-cleaning Thicken vaginal epithelium Resistance↑
Result in large quantities of glycogen in epithelial cells
Kill or inhibit pathogens
Lactobacilli
Produce H2O2
Lactic acid production↑
Acid environment ( )
Promote growth of normal vaginal flora
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7. Bartholinitis/Bartholin’s cyst
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8. Anatomy of Bartholin’s glands
Position: the base of each bulb
Opening
Secretion: viscid, clear and stringy
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9. 2017/4/24

10. Etiology Infection Congenital narrowing of duct
Obstruction of main duct of bartholin
Retention of secretions and cystic dilatation
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11. Clinical findings Bartholinitis Bartholin’s cyst Pain Tenderness
Dyspareunia
Surrounding tissues become edematous and inflamed
Fluctuant, tender mass
Bartholin’s cyst
No system
Fluctuant mass can be palpable
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12. Clinical findings
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13. Treatment Drain the abscess
Marsupialization for preservation of the gland function
Antibiotics (Ampicillin) in the early stage
Excision for recurrent cases or postmenopausal patient
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14. Trichomonas vaginitis
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15. Etiology Trichomonad A flagellate protozoan Best living environment
Moist
Anaerobic
pH:
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16. Pathogenesis
The trichomonad lives on glycogen and iron of the host cell
Direct contact and damage of the target cell
Arose immune reaction resulting in inflammation
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17. Transmission Sexual contact (70% male infection, asymptomatic carrier)
Nonsexual transmission
Iatrogenic
Contact-soap
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18. Clinical findings latent period: 4-28 days Asymptomatic: 25-50%
Symptoms
Main: Profuse vaginal discharge thin,creamy orslightly green in colour irritating and frothy.and pruritus ,inflamation of vulva.
Occasional: odor, pain, dyspareunia, dysuria, infertility.
Signs
Multiple small putate Strawberry spot on vagina and cervix.
Tiny, punctuate hemorrhages on the mucosa
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19. Characteristics of the vaginal discharge 
Profuse
Purulent
Gray to yellow color
Malodorous
Frothy
Anaerobic glycolysis
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21. Diagnosis Microscopic identification of trichomonad (60%-70%)
Precautions for the examination
Avoid
Intercourse 1-2 days before examination
Washing and medication
Lubricant
Heat preservation
Culture for suspected cases
Refractory case
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22. Treatment Systemic therapy : Oral metronidazole
2g single dose
400mg, twice or 3 times a day, for 7 days
Side effect
Topical application (≤50%)
Effervescent tablets of metronidazole 200mg/day, 7-10 days
Acidify vagina with 1% lactic acid or 0.5% acetic acid
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23. Treatment
Criterion for cure: Negative finding in postmenstrual examination of vaginal discharge for three times
Failure rate: 5%-10%
Poor compliance
Repeated infection
To avoid repeated infection
Sterilize underwear, towels, etc
Treat the sexual partner
Metronidazole
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24. Candidiasis
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25. Etiology Very common The etiologic agent is Candida
About 1/3 of vaginitis cases are caused by fungal infection
About 75% of women develop candidiasis at least once in life
The etiologic agent is Candida
Candida albicans is responsible
for 80-90% of VVC.
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26. Etiology Candida albicans is an opportunistic pathogen
Suitable environment: acid (＜4.5), warm, and moist
Can be isolated from 10-20% Nonpregnant and 30% pregnant women (asymptomatic)
Treatment is not indicated unless symptoms are present
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27. Pathogenesis Yeast spores (Asymptomatic parasitism)
Two phases of candida albicans
Proper environment
Pseudohypha (Pathogenic)
Penetrate vaginal epithelium for nutrients
Release proteolytic enzymes and toxins etc
Result in inflammatory reaction
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28. Predisposing factors Pregnancy DM Immunosuppressant
Broad-spectrum antibiotics: suppress the vaginal normal flora (esp. lactobacillus)
Others
Restrictive synthetic underwear
Obesity
Contraceptive medication
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29. Transmission Endogenous infection (most often) Sexual contact
Vagina, oral cavity, intestinal tract
Sexual contact
Contact fomites
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30. Clinical findings Vulvovaginal pruritus (main) Vaginal discharge↑
Usually intense, coincident with menses or intercourse
Vaginal discharge↑
white, thick, curd-like discharge,
forming patches adhere to vaginal walls
Vulvar erythema
Systems may worse just prior to menses
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31. Diagnosis Microscopic identification of candida albicans
Saline: 30-50%
10% KOH: 70-80%
Gram’s stain: 80%
Culture: higher sensitivity and drug test
Measurement of pH value
pH<4.5 simple infection
pH>4.5 combined infection
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32. Treatment Only for symptomatic patients.
Eliminate predisposing factors
Control DM
Discontinue complicating medications
Long-term, regular, multiple topical therapy
Treatment of sexual partner
Asymptomatic: No treatment
15% should be treated
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33. Treatment Topical application of antifungal agents Miconazole
200mg/day for 7days
400mg/day for 3 days
Clotrimazole ( cream)
150mg/day for 7 days
150mg, twice a day for 3 days
500mg single dose
Nystatin: 500,000 units/day for days
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34. Treatment Fluconazole: 150mg, single use. Itraconazole
Systemic medication: for cases who can’t be treated with topical application of antifungal drugs
Fluconazole: 150mg, single use.
Itraconazole
200mg/day for 3-5 days
400mg for 1 day divided in two doses
Ketoconazole: 200mg, once or twice/day until culture result is negative
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35. Points of note for treating VVC
Treatment should be followed-up with a premenstrual examination of vaginal discharge
Approximately 10% of cases will not respond to initial therapy→prolong treatment up to 14 days
Identify and eliminate predisposing factors
RVVC (5%)should be treated with oral therapy followed by prophylactic doses
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36. Bacterial Vaginosis
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37. Etiology Imbalance of normal vaginal flora
Lactobacilli is decreased
Other bacteria are increased (anaerobic bacteria—Gardnerella)
Causative factors of the imbalance are unknown
Vaginal douching
Frequent sexual relationship
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38. Clinical findings Signs Systems
Asymptomatic: 10-40%
Mild pruritus or burning sensation
Increased vaginal discharge and fishy odor
Signs
Discharge: fishy, gray-white, homogenous, but not sticky
No inflammation
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39. Diagnosis
Identification of clue cells *together with 2 of the following 3 items
Vaginal discharge: homogenous, thin and white
pH>4.5: in virtually all cases ( )
Positive Whiff test (with 10% KOH)
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40. Clinical pictures
Clue cells: Desquamated epithelial cells covered with clumps of coccobacili especially Gardnerella vaginalis→ gives the cells a speckled appearance
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41. Treatment Antibiotics Systemic therapy (oral) Topical therapy
Metronidazole: 400mg, 2-3 times a day for 7d
Clindamycin : 300mg, twice a day for 7d
Topical therapy
Effervescent tablets of metronidazole: 200mg/day, for 7-10 days
2% Clindamycin cream, once a day for 7 days
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42. Criteria for cure
Absence of clue cells with at least 1 of the following items
Normal vaginal discharge
pH≤4.5
Whiff test
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43. Points of note for treating BV
Systemic or topical treatment has the same cure rate (80%).
Patients who are asymptomatic, but scheduled to have a gynecologic surgical procedure should be treated.
Patients who are pregnant can be treated with oral metronidazole.
Follow-up examination should be given after the treatment (postmenstrual)
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44. Differential diagnosis of vaginitis
Trichomonias
Candidiasis BV
Complaints
discharge↑ mild pruritus
severe pruritus burning
Vaginal discharge
thin , purulent frothy
white
curd-like
White, fishy homogenous
Vaginal
epithelium
punctuated hemorrhage
edema erythematic
normal
Vaginal pH
＞5 ( )
＜4.5
＞4.5 ( )
Whiff test - +
Microscopic
examination
Trichomonad WBC many
Candida
WBC some
Clue cells WBC rare
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45. Atrophic vaginitis
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46. Etiology Ovarian function decreaseE Vaginal mucosa is thin
PH of vagina is abnormal high
→ Normally acidogenic flora are replaced by mixed flora
Vaginal epithelium is more susceptible to infection and trauma
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47. Clinical findings Symptoms Signs Vaginal discharge↑ Vulvar itching
Dyspareunia
Signs
Vaginal mucosa is thin ,vaginal folds are few or absent
Spotting hemorrhage
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48. Treatment Intravaginal application of E cream Intravaginal antibiotics
1/3 of vaginal E is systemically absorbed
Contraindication: women with a history of breast or endometrial cancer
E tablet intravaginally daily for two weeks twice per week for at least 3-6 months
Intravaginal antibiotics
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49. Cervicitis
Section2
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50. General consideration
In direct contact with vagina
Common: 50% women of reproductive age
May lead to pelvic infection
Need to identify a venereal disease and differentiate from malignancies
Classification
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51. Part I Acute Cervicitis
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52. Etiology Past Now Staphylococcus, streptococcus, enterococcus
Cause infection after an abortion, puerperium, cervical injury, foreign bodies
Now
Neisseria gonorrhea; Chlamydia trachomatis
Cause superficial infection of the cervical columnar mucosa
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53. Histopathology
Gross examination: The cervix becomes swollen and reddened
Microscopically
Stromal edema
Infiltration by polymorphonuclear leukocytes
Focal loss of overlying mucous membrane
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54. Clinical findings Purulent vaginal discharge: variable
Thick and creamy—in gonorrheal infection
Mucopurulent –in chlamydia infection
Cervix is reddened, congestive
Be indistinguishable from gonorrheal infection
Intermenstrual bleeding, postcoital bleeding
Asymptomatic
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55. Clinical findings
Signs: Inflammation of the cervix with mucopurulent discharge
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56. Diagnosis Gram’s stain of the cervical discharge for leukocyte≥30/HP
Tests for gonococcus and chlamydia
Wet mount microscopy for trichomonads
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57. Treatment According to different pathogens
Gonorrhea infection: Third generation cephalosporins
Ceftriaxone Sodium
Spectinomycin
Chlamydia trachoma
Azithromycin
Erythromycin
Ofloxacin
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58. Part II Chronic Cervicitis
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59. General consideration
lymphocytes in cervical stroma
Almost in all parous women
Five types of pathology
Cervical erosion
Cervical polyps
Endocervicitis
Cervical Hypertrophy
Nabothian cysts
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60. Cervical erosion Histopathology
The stratified epithelium (normally covers the vaginal portion of the cervix) is replaced by columnar epithelium (continuous with the cervical canal)
Physiological erosion
Columnar epithelium extrophy—Influenced by estrogen
Occurs in the newborns, pregnancy, oral contracepives
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61. Cervical erosion Clinical findings Symptoms Signs: red area is seen
Mucoid discharge
Slight postcoital bleeding
Signs: red area is seen
around the external os
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62. Cervical erosion Classification
Depends on the depth and area of the lesion
Types: simple, granular, papillary
Degree
I (＜1/3)
II (1/3-2/3)
III (＞2/3)
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63. Treatment No treatment if there is no symptom
A cervical smear is needed before treatment
Physical therapy
Thermal cauterization
Cryotherapy
Laser therapy
Microwave therapy
Medical therapy: result is not satisfactory
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64. Cervical polyps Histopathology
Small pedunculated neoplasms of the cervix
Originate from the endocervix or vaginal portion
Microscopic
Vascular connective tissue stroma covered with columnar or squamous epithelium
Congestion, edema or leukocyte infiltration may be present.
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65. Clinical findings Signs Symptoms Red or pink Rounded or tongue-like
Some are asymptomatic
Intermenstrual or postcoital bleeding
Leukorrhea and hypermenorrhea
Signs
Red or pink
Rounded or tongue-like
Smooth with a pedicle
Too soft
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66. Treatment Malignant change (<1%)
Twist off a polyp without anesthesia and cauterize the base.
Recurrent cases: dilate the canal and cauterize the stalk
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67. Endocervicitis Histopathology
Thickened endocervix produces a whitish pus
Cervical os surrounded by a reddish area
The cervix may become hypertrophy
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68. Clinical findings Symptoms
Persistent leukohrrea usually mucopurulent
Slight postcoital staining
Pains: lower abdominal discomfort; lumbosacral pain; dysmenorrhea or dyspareunia
Infertility
Urinary symptoms: subvesical lymphangitis
Signs: cervical os surrounded by a reddish area
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69. Treatment Medical treatment Surgical treatment
Systemic rather than topical
Based on culture and sensitivity test
Surgical treatment
Thermal therapy
Cryotherapy
Laser therapy
Conization
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70. Hypertrophy
Histopathology: Cervical hyperplasia stimulated by infections
Clinical findings
Often no symptom
Signs
Cervix is harder
>3cm in diameter
No treatment if no complications
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71. Nabothian Cysts
Histopathology: Retention cysts of the cervical glands caused by obstruction of the gland orifices by growth of squamous epithelium
Clinical findings
Often no symptoms
Cyst extrude surface
Treatment
No symptom: no treatment
Cysts become larger: Thermal therapy, cryotherapy, laser therapy, conization
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