1 Vulvitis BartholinitisBartholins cyst 2 Vaginitis 3 Cervicitis

1. Vulvitis Bartholinitis/Bartholin’s cyst 2. Vaginitis 3. Cervicitis 4. Pelvic inflammatory disease (PID) Genital tuberculosis Sexually transmitted diseases (STD)

Vulvitis

Clinical Manifestation Vulvar pruritus Pain Burning sensation Congestion Swelling Eczema

Etiology Specific organisms or non-infective dermatitis • Irritation from vaginal discharge or menses • Lack of vulvar hygiene • Glycouria

Treatment • Keep the vulva clean and dry • Remove the cause • 1/5000 k. Mn. O 4 (potassium permanganate, PP) solution bath • Antibiotics ointment

Bartholinitis Infection of the major vestibular glands (Bartholin’s glands) Bartholin’s Cyst

Major vestibular glands (Bartholin’s glands)

Bartholinitis Etiology Staphylococcus, E. coli, streptococcus, enterococcus, gonococcus, and polymicrobial infection is common. Clinical manifestation Symptoms of a local infection Abscess of Bartholin gland: a painful red swelling Treatment Antibiotics (Ampicillin) in the early stage Drain the abscess (excision of an elliptical piece of skin)

Bartholin’s Cyst • Marsupialization for preservation of the gland function • Excision for recurrent cases

Vaginitis • Trichomonal vaginitis • Candidal Vulvovaginitis • Bacterial Vaginosis (BV) • Senile vaginitis • Infantile vulvovaginitis

Trichomonal Vaginitis (Trichomoniasis)

Etiology Trichomonad A flagellate protozoan Best living environment : Moist, anaerobic, p. H: 5. 2 -6. 6

Transmission 1. Sexual contact (70% male infection, asymptomatic carrier) 2. Nonsexual transmission (iatrogenic) Pathogenesis • The trichomonad lives on glycogen and iron of the host cell • Direct contact and damage of the target cell • Induction of immune reaction resulting in inflammation

Clinical Picture Latent period: 4 -28 days Asymptomatic: 25 -50% Symptoms： Main: Profuse vaginal discharge and pruritus Occasional: odor, pain, dyspareunia , dysuria, infertility

Characteristics of the vaginal discharge Copious, Purulent Gray to yellow color, Malodorous Frothy Strawberry cervix: Tiny, punctate hemorrhages grossly visible on the mucosa

Diagnosis 1. Microscopic (wet mount) identification of the trichomonad (60%-70%) 2. Precautions for the examination Avoid : intercourse 1 -2 days before examination washing and medication lubricant heat preservation 3. Culture for suspected cases 4. PCR (Polymerase chain reaction)

Treatment (1) 1. Systemic therapy (First choice) Oral metronidazole a) 2 g single dose b) 400 mg, twice or 3 times a day, for 7 days. 2. Topical application (≤ 50%) a) Effervescent tablets of metronidazole 200 mg/day, 7 -10 days b) Metronidazole gel c) Acidification of vagina with 1% lactic acid or 0. 5% acetic acid

Treatment (2) Criterion for cure: Negative finding in postmenstrual examination of the vaginal discharge for three times Failure rate: 5%-10% Poor compliance Repeated infection To avoid repeated infection: Sterilization of underwear, towels, etc Treatment of the sexual partner Metronidazole is still effective in recurrent cases.

Candidal Vulvovaginitis (Vulvovaginal Candidiasis)

Etiology 1. Very common a) About 1/3 of vaginitis cases are caused by fungal infection. b) About 75% of women develop candidiasis at least once in life. 2. The etiologic agent is Candida albicans is responsible for 80 -90% of vulvovaginal candidiasis.

3. Candida albicans is an opportunistic pathogen. 1) Suitable environment: acidic (＜ 4. 5), warm, and moist 2) Candida albicans can be isolated from 10 -20% nonpregnant and 30% pregnant asymptomatic women. Treatment is not indicated unless symptoms are present.

Predisposing factors 1. Pregnancy 2. Diabetes mellitus 3. Immunosuppressants 4. Broad-spectrum antibiotics suppressing the vaginal normal flora (esp. lactobacillus) 5. Others: restrictive synthetic underwear, obesity, contraceptive medication

Transmission 1) Endogenous infection (most often) Vagina, oral cavity, intestinal tract 2) Sexual contact 3) Contacting fomites

Pathogenesis Two phases of candida albicans 1) Yeast spores Asymptomatic parasitism 2) Pseudohyphae Pathogenic 3) Mechanism: a) Candida at the pseudohypha phse penetrate vaginal epithelium for nutrients b) Growing candida albicans release proteolytic enzymes and toxins etc. resulting in inflammation reaction

Clinical Picture 1. Vulvovaginal pruritus (main) usually intense, coincident with menses or intercourse 2. Increased vaginal discharge The classic finding is white, thick, curd-like discharge forming patches adherent to the vaginal walls.

Diagnosis 1. Wet mount microscopic identification of candida albicans in the discharge Saline: 30 -50% 10% KOH: 70 -80% 2. Gram’s stain: 80% 3. Culture: higher sensitivity and drug test 4. Measurement of p. H value may be useful for discovering cases of complicated infection (4. 0 -4. 7). a p. H<4. 5 simple infection a p. H>4. 5 combined infection

Treatment 1. Elimination of predisposing factors 2. Topical application of antifungal agents Vaginal suppositories： 1) Miconazole a) 200 mg/day for 7 days b) 400 mg/day for 3 days 2) Clotrimazole a) 150 mg/day for 7 days b) 150 mg, twice a day for 3 days c) 500 mg single dose

3) Nystatin 100, 000 units/day for 10 -14 days 4) Methyl violet 0. 5 -1% , 3 -4 times/week for 2 weeks. 3. Systemic medication Oral agents are used only for cases that can not be treated with topical application of antifungal drugs. 1) Fluconazole 150 mg, single use. 2) Itraconazole a) 200 mg/day for 3 -5 days b) 400 mg for 1 day divided in two doses

3) Ketoconazole 200 mg, once or twice/day until culture result is negative Hepatotoxicity may occur. Points of note for treating VVC • Treatment should be followed-up with a premenstrual examination of the vaginal discharge. • Approximately 10% of cases will not respond to initial therapy. • Prolongation of treatment up to 14 days may cure some patients. • Identification and elimination of predisposing factors is important. • Recurrent VVC should be treated with oral therapy followed by prophylactic doses.

Treatment of sexual partner? No treatment for asymptomatics. 15% should be treated

Bacterial Vaginosis

Etiology 1. Imbalance of normal vaginal flora Diminution of Doderlein lactobacillus and increase in other bacteria, in particular, anaerobic bacteria. 2. Causative factors of the imbalance are unknown Gardnerella vaginalis

Clinical Picture Symptoms: 1. 10 -40% asymptomatic 2. Mild pruritus or burning sensation 3. Increased vaginal discharge and fishy odor Signs: Discharge: thin, greyish-white, homogenous, but not sticky No inflammation reaction (No epithelial edema or erythema)

Diagnosis Identification of clue cells *(wet mount in saline) together with 2 of the following 3 items 1. Vaginal discharge: homogenous, thin and white 2. p. H>4. 5: in virtually all cases, usu. 5. 0 -5. 5 3. Positive Whiff test (with 10% KOH) * Clue cells are desquamated epithelial cells covered with clumps of coccobacili esp. Gardnerella vaginalis which gives the cells a speckled appearance.

Whiff test

Treatment (1) 1. Systemic therapy (oral) (80%) 1) Metronidazole 400 mg, 2 -3 times a day for 7 days 2) Clindamycin 300 mg, twice a day for 7 days 2. Topical therapy (80%) 1) Effervescent tablets of metronidazole 200 mg/day, for 7 -10 days 2) 2% Clindamycin cream, once a day for 7 days 3. Vaginal washing 1 -3% H 2 O 2 , 1% lactic acid, 0. 5% acetic acid

Treatment (2) 1. Systemic or topical treatment has the same cure rate (80%). 2. Patients who are asymptomatic, but scheduled to have a gynecologic surgical procedure should be treated. 3. Patients who are pregnant can be treated with oral metronidazole. 4. Follow-up examination should be given 1 -2 and 3 -4 weeks (postmenstrual) after the treatment. Criteria for cure: Absence of clue cells with at least 1 of the following items: a) Normal vaginal discharge b) p. H≤ 4. 5 c) Whiff test negative

Other forms of vulvovaginitis 1. Senile vaginitis Atrophic vaginitis 2. Infantile vulvovaginitis

Differential Diagnosis of vaginitis Bacterial Vaginosis Candidiasis Complaints discharge↑m ild pruritus Trichomoniasis severe pruritus discharge↑ burning mild pruritus white Vaginal discharge homogenous fishy white curd-like thin purulent frothy Vaginal normal epithelium edema erythema punctate hemorrhage ＜ 4. 5 ＞ 5 (5. 6 -6. 5) － － Candida WBC some Trichomonad WBC many Vaginal p. H Whiff test ＞ 4. 5 (4. 7 -5. 7) ＋ Microscopic Clue cells examination WBC rare

Inflammation of the Cervix 1. Common: 50% women of reproductive age 2. May lead to pelvic infection 3. Need to identify a venereal disease and differentiate from malignancies Cervicitis: Vaginal portion of the cervix (Ectocervix) Mucosa of the cervical canal (Endocervix)

Acute Cervicitis

Etiology 1. Neisseria gonorrhoeae Chlamydia trachomatis causing superficial infection of the cervical columnar mucosa 2. Staphylococcus streptococcus enterococcus causing infection after an abortion, puerperium, cervical injury, foreign bodies

Clinical Picture Symptoms 1. Asymptomatic 2. Mucopurulent vaginal discharge Vaginal irritation symptoms: pruritus, burning sensation Lumbosacral pain, Intermenstrual bleeding, postcoital bleeding Symptoms of the lower urinary tract Signs Inflammation of the cervix with mucopurulent discharge (MPC for mucopurulent cervicitis)

Diagnosis 1. Gram’s stain of the cervical discharge for leukocyte ≥ 30/HP or ≥ 10/× 1, 000 2. Tests for gonococcus and chlamydia 3. Wet mount microscopy for trichomonads

Management Systemic medication Choice of drugs depends on the pathogens. Examples: Gonorrhea infection：Third generation Cephalosporins Ceftriaxone Sodium Spectinomycin Chlamydia trachomatis Doxycycline Azithromycin Erythromycin Ofloxacin

Chronic Inflammation of the Cervix

Cervical Erosion Etiology 1. When the stratified epithelium which normally covers the vaginal portion of the cervix is replaced by columnar epithelium which is continuous with that of the cervical canal. 2. Most erosion are not infected, nor they are the result of inflammation. 3. Occurs in the newborns, pregnancy, oral contracepives

Clinical Features Symptoms The only symptom is a mucoid discharge. A slight postcoital bleeding (but malignancy should be excluded) Signs A red area is seen around the external os. Classification Depends on the depth and area of the lesion Types: simple, granular, papillary Grades: I (＜ 1/3), II (1/3 -2/3), III (＞ 2/3)

Treatment • Erosion found on routine examination should not be treated unless it is causing troublesome discharge. • A cervical smear is needed before the treatment, and if necessary, colposcopy and biopsy. • Cervical ectropion • Physical therapy Thermal cauterization, Cryotherapy, Laser therapy

Cervical Polyps Small pedunculated neoplasms of the cervix • Endocervical polyp: Originating from the endocervix • Ectocervical polyp: Originating from the vaginal portion

Pathology Gross appearance: Endocervical polyp: Red or pink, rounded or tongue-like Ectoervical polyp: Pale, flesh-colored, smooth, rounded with a broad pedicle Microscopic: Vascular connective tissue stroma covered with columnar or squamous epithelium or both. Congestion, edema or leukocytein filtration may be present.

Clinical Features Some are asymptomatic. Slight postcoital bleeding Treatment Cervical polyp should be treated. • Malignant change (<1%) • Polypoid cervical cancer Twisting off a polyp without an anesthetic and cauterizing the base. Recurrent cases are treated with canal dilation and cauterization of the stalk.

Chronic Endocervicitis (Infection) Etiology Pathogens: Normal cervical and vaginal flora Pathology • Thickened endocervix that produces a whitish pus • A cervical os surrounded by a reddish area • Hypertrophy of the lacerated cervix

Clinical Features 1. Persistent leukohrrea usu. mucopurulent 2. Slight postcoital staining 3. Pains lower abdominal discomfort, lumbosacral backache, dysmenorrhea, dyspareunia 4. Infertility 5. Urinary symptoms frequency, urgency, dysuria due to subvesical lymphangitis not to cystitis

Diagnosis • The characteristic discharge from external os of the cervix. • Cytologic and colposcopic studies are helpful, but only biopsy is definitive. • Cultures are not so helpful.

Treatment Even if chronic endocervicitis is asymptomatic, it should be treated. 1. Medical treatment Systemic rather than topical Based on culture and sensitivity test 2. Surgical treatment A note of caution: postoperative bleeding, infection, stricture formation, infertility. Methods: thermal therapy, cryotherapy, laser therapy conization, hysterectomy.

Nabothian Cysts Retention cysts of the cervical glands caused by obstruction of the gland orifices by the growth of squamous epithelium. The cysts may be infected and contain pus. Cervical Hypertrophy

Cervical Hypertrophy

Pelvic Inflammatory Disease (PID) Infection of the upper genital tract Terms: Endometritis (子宫内膜炎) Salpingitis (输卵管炎) Oophoritis (卵巢炎) Myometritis (子宫肌炎) Pyosalpinx (输卵管积脓) Hydrosalpinx (输卵管积水) Peritonitis (腹膜炎) Tubal ovarian abscess (TOA) (输卵管卵巢脓肿)

Epidemiology Sexual activity A disease of sexually active, menstruating women. Acute PID occurs in 1 -2% of young sexually active women annually. Age The peak incidence occurs in their late teens and early twenties. The most common serious infection in women of 16 -25 years of age

Contraceptive practices Contraceptive methods No. of PID/woman-years Sexually active, using no contraception: 3. 42 Oral contraceptives: 0. 91 Barrier methods 1. 39 Intrauterine devices (IUD) 5. 21

Financial cost In USA, $3. 5 billion annually in 1990 s Medical sequelae Ectopic pregnancy: 6 -10 fold increase PID accounts for 50% Chronic pain: 4 fold increase Infertility: acute PID account for 5 -60% of cases Tubal obstruction: 11. 4%, 23. 1%, 54. 3% from 1, 2, 3 episodes of infection Mortality: septic shock and death

Etiology Pathogens that are sexually transmitted 1) Neisseria gonorrhoeae: in USA, 40 -50% cases of PID 2) Chlamydia trachomatis: in USA, 10 -40% cases of PID The two pathogens may account for 2/3 of the PID 3) Mycoplasma (支原体) Recovered from the pus in 2 -20% cases of salpingitis Endogenous bacteria 1) Aerobic: streptococci, staphylococci, Escherichia coli 2) Anaerobic: Bacteroides fragilis (脆弱类杆菌), peptococcus (消化球菌) ， peptostreptococcus (消化链球菌)

Spreading Route of Infection 1. Ascending along the reproductive tract For non-pregnant and non-puerperal women Gonococcus, C. trachomatis, staphylococcus 2. Lymphatic vessels In puerperal infection, post-abortion infection and IUD associated infection Streptococcus, E. coli, anaerobic bacteria 3. Blood vessels Tuberculosis 4. Direct spreading Infection from other visceral organs.

Acute PID

Predisposing Factors 1. Intrauterine manipulation e. g. artificial abortion , IUD, etc. 2. Infection in the lower reproductive tract, esp. STD 3. Sexual activity 4. Bad hygiene 4. Direct spreading from adjacent viscera 6. Acute onset of a chronic PID

Pathology 1. Acute endometritis and myometritis 2. Acute salpingitis, pyosalpinx and tubo-ovarian abscess (TOA) 3. Acute pelvic peritonitis 4. Acute inflammation of the peritoneal connective tissue (parametritis)(宫旁结缔组织炎) 5. Septicemia (败血症) and pyemia (脓毒血症) 6. Fitz-Hugh-Curtis syndrome

Fitz-Hugh-Curtis syndrome • Perihepatitis: inflammation of Glisson’s capsule without involvement of the liver parenchyma. Suppurative (脓性) and fibrous exudation of the capsule occurs causing adhesion between the capsule and the anterior peritoneum. • It happens in 5 -10% cases of salpingitis. • It is caused by gonococcus or Chlamydia trachomatis. • Edema and adhesion of the capsule may lead to pain in the upper abdominal region.

Clinical Features Symptoms Vary depending on severity and extent of the infection and types of pathogens Most common: lower abdominal pain, fever, increase in vaginal discharge. Gonorrhea/Chlamydia Trichomatis Signs Variable Typical: Bimanual examination:

Diagnosis Criteria for the diagnosis of PID Minimum: 1) Pain on compression of uterine body or the adnexal region 2) Tenderness of the cervix Specific: 1) Biopsy of the endometrium showing endometritis 2) Ultrasound/MRI identification of liquid-filled enlarged oviducts or TOA 3) Laparoscopic examination Additional:

Differential Diagnosis Appendicitis Rupture or abortion of tubal pregnancy Torsion or rupture of an ovarian tumor

Treatment (1) 1. Systemic medication (Ideal) Based on drug sensitivity test (Empirical) Combination use of drugs Patient’s condition and possible pathogens 1) Oral: Ofloxacin (氧氟沙星) Metronidazole for 14 days 2) Intravenous: Penicillin or Erythromycin (红霉素) Gentamycin (庆大霉素) or Amikacin (阿米卡星/丁胺卡那霉素) Metronidazole for endogenous bacteria 3) Cefuroxime sodium (头孢呋辛钠/西力欣) for gonococcus 4) Doxycycline (多西环素/强力霉素) or Azithromycin (阿奇霉素) for chlamydia or mycoplasma 5) Clindamycin (克林/氯林/氯洁霉素) for anaerobic bacteria

Treatment (2) 2. Surgical treatment for TOA or peritoneal abscesses that can not be controlled by drugs (2 -3 days) Indications: 1) Failure of drug therapy 2) Persistent existence of abscesses (2 -3 weeks) 3) Rupture of the abscess 3. Traditional Chinese medicine

Chronic PID

Etiology 1. Incomplete treatment of the acute PID 2. Infection from certain pathogens such as Chlamydia trachomatis 3. Residual lesions from previous acute PID Characteristics of chronic PID: 1. Persistence of the condition 2. Difficult to identify the pathogens

Pathology 1. Chronic endometritis 2. Chronic salpingitis and hydrosalpinx 3. Salpingo-oophoritis and tubo-ovarian cyst 4. Chronic inflammation of pelvic connective tissue

Clinical Features 1. Chronic pelvic pain 2. Infertility (20 -30%) and ectopic pregnancy 3. Abnormal menstrual cycle 4. Systemic symptoms 5. Signs

Diagnosis Based on history of acute PID, symptoms and signs Differential diagnosis Pelvic congestion or varicosity (静脉曲张) Endometriosis Tumors Ultrasound and laparoscopic examination is helpful

Treatment According to place of the lesion and the patient’s complaint Usu. comprehensive treatment is required. 1. Physical 2. Traditional Chinese medicine (赤丹丸) 3. Antibiotics (抗炎II号栓) 4. Drugs that dissolve and absorb inflammatory lesions 5. Surgical treatment