Textbook Of Gynecology. Dc Dutta’s

Chapter 12. Infections of the Individual Pelvic Organs


The vulval and perineal skin is usually resistant to common infection. But the defence is lost following constant irritation by the vaginal discharge or urine (urinary incontinence). Furthermore, there may be atrophy or degenerative changes either in disease or following menopause when the infection is more likely. The vulval infection can thus occur de novo or may be affected secondarily, the primary site may be elsewhere in the adjacent structures. In this section, only the lesions affecting primarily the vulva will be discussed.

It is indeed difficult to classify the vulval infection but the following etiological classification is of help.

I. Due to specific infection.

II. Due to sensitive reaction.

III. Due to vaginal discharge or urinary contamination.



● Pyogenic (non-gonococcal)

● Sexually transmitted diseases (p. 146)

Gonorrhea (p. 147)

Syphilis (p. 148)

Chancroid (p. 150)

Lymphogranuloma venereum (p. 151)

Granuloma inguinale (p. 151)

● Tubercular (p. 137)


► Condylomata accuminata (p. 157)

► Herpes genitalis (p. 152)

► Molluscum contagiosum (p. 157)

► Herpes zoster (p. 161)


 Moniliasis (p. 164)

 Ringworm (p. 161)


■ Pediculosis pubis (p. 157)

■ Scabies (p. 158)

■ Threadworm (p. 161).


Vulval cellulitis: The causative organism is predominantly Staphylococcus aureus. The vulva is swollen, red, and tender. There may be profuse exudation. The inflammation is limited, in majority, upto the labiocrural fold.

The patient complains of intense pain, itching and problem in micturition. There may be excoriation of the skin due to scratching and laceration.

Treatment is effective by systemic antibiotics, local hot compress and analgesics.

Furunculosis: The infection affects the hair follicles of the mons and labia majora → folliculitis → furunculitis. The offending organism is Staphylococcus aureus. If it is recurrent, glycosuria should be excluded. Treatment is effective with systemic and local antibiotics and local cleanliness.

Infection of sebaceous and apocrine glands: Infection of an apocrine or sebaceous gland looks and presents the features of a boil. If it recurs, excision is to be done in the quiescent state.

Impetigo: Impetigo is a pustular infection caused by Staphylococcus aureus or Streptococcus. It may be localized to vulva or spread to other parts of the body, face, or hands.

Blebs should be incised or the crusts be removed aseptically. Systemic and local antibiotics are to be prescribed.

Erysipelas: This rare spreading cellulitis is caused by invasion of the superficial lymphatics by b-haemolytic Streptococcus. There may be systemic constitutional symptoms. It responds well to systemic broad spectrum antibiotics.

Intertrigo: Intertrigo is due to irritation and infection of retained secretions in the skinfolds usually in an obese patient. It may also result from friction of the undergarments or sanitary towels.

Treatment with local hygiene and local antiseptic application is quite effective. At times, systemic antibiotics may have to be used.


Herpes zoster: The causative agent is varicella zoster virus (VZV). This is due to re-emergence of VZV from posterior nerve roots. It produces an inflammatory painful eruption of groups of vesicles distributed over the skin corresponding to the course of peripheral sensory nerves (dermatome). It is commonly unilateral but may extend to the thigh or buttock of the same side. The vesicles may rupture or become dry with scab formation. It resolves spontaneously in 3 weeks time.

Treatment is by analgesics to relieve pain and antibiotics to prevent secondary infection. Acyclovir 800 mg orally five times daily for 7 days is recommended. Acyclovir cream (5%) may be used locally for less severe infection.


Moniliasis: See p. 164.

Ringworm: The causative organism is Tinea cruris. The lesions look bright red and circumscribed. The fungus can be detected microscopically from scraping of the lesion.

Treatment is very effective with imidazole (clotrimazole or miconazole) cream. Some fungi (Trichophyton rubrum) respond well to griseofulvin 500 mg twice daily by mouth for 4 weeks.


Threadworm: The causative organism is Oxyuris vermicularis. It is common in children. Nocturnal perineal itching with evidences of perianal excoriation is observed. The parasite is detected in the stool. Anthelmintic drugs such as mebendazole and local application of gentian violet cures the condition.


Bartholin’s glands are the two pea sized (2 cm) glands, located in the groove between the hymen and the labia minora at 5 O’Clock and 7 O’Clock position (see p. 2) of the vagina.

Causative Organisms: Although Gonococcus is always in mind but more commonly other pyogenic organisms such as Escherichia coli, Staphylococcus, Streptococcus, or Chlamydia trachomatis or mixed types (polymicrobial) are involved.

Pathology: Both the gland and the duct are involved. The epithelium of the gland or the duct gets swollen. The lumen of the duct may be blocked or remains open through which exudates escape out.

Fate: The infection may resolute completely or an abscess is formed. In others, the infection subsides only to recur in future. In such cases, the gland becomes fibrotic. Too often, the duct lumen heals by fibrosis with closure of the orifice → pent up secretion of the gland → formation of bartholin cyst. Thus, the end results of acute Bartholinitis are:

(i) Complete resolution (ii) Recurrence (iii) Abscess (iv) Cyst formation.

Clinical Features: Initially, there is local pain and discomfort even to the extent of difficulty in walking or sitting. Examination reveals tenderness and induration of the posterior half of the labia when palpated between thumb outside and the index finger inside the vagina (see Fig. 9.6). The duct opening looks congested and secretion comes out through the opening when the gland is pressed by fingers. The secretion should be collected with a swab for bacteriological examination.

Treatment: Hot compress over the area and analgesics to relieve pain are instituted. Systemic antibiotic like ampicillin 500 mg orally 8 hourly is effective or else appropriate antibiotic according to the bacteriological sensitivity should be instituted.

Recurrent Bartholinitis: Periodic painful attacks cause problems in 5-10 percent women. Excision of the gland with the duct may have to be done in the quiescent phase.


Bartholin’s abscess is the end result of acute bartholinitis. The duct gets blocked by fibrosis and the exudates pent up inside to produce abscess. If left uncared for, the abscess may burst through the lower vaginal wall. A sinus tract may remain with periodic discharge through it.

Clinical Features

The local pain and discomfort become intense. The patient cannot walk or even sit. Fever is often associated.

On examination, there is an unilateral tender swelling beneath the posterior half of the labium majus expanding medially to the posterior part of the labium minus. The overlying skin appears red and edematous.

Treatment: Rest is imposed. Pain is relieved by analgesics and daily sitz bath. Systemic antibiotic— ampicillin 500 mg orally 8 hourly or tetracycline in chlamydial infection is effective. Abscess should be drained at the earliest opportunity before it bursts spontaneously.

In case of recurrent Bartholin’s abscess, excision should be done in the quiescent phase after the infection is controlled.


There is closure of the duct or the opening of an acinus.The cause may be infection or trauma followed by fibrosis and occlusion of the lumen.

Pathology: It may develop in the duct (common) or in the gland. Commonly, it involves the duct; the gland is adherent to it posterolaterally. Cyst of the duct or gland can be differentiated by the lining epithelium. The content is glairy colorless fluid—secretion of the Bartholin’s gland.

Fig. 12.1: Bartholin's cyst (left)

Clinical Features: A small size often remains unnoticed to the patient or escapes attention to the physician even following internal examination. If it becomes large (size of hen’s egg), there is local discomfort and dyspareunia. Examination reveals an unilateral swelling on the posterior half of the labium majus which opens up at the posterior end of the labium minus. Its medial projection makes the vulval cleft ‘S’-shaped. The overlying skin is thin and shiny. The cyst is fluctuant and not tender (Fig. 12.1).

Treatment: Marsupialization is the gratifying surgery for Bartholin’s cyst. An incision is made on the inner aspect of the labium minus just outside the hymenal ring. The incision includes the vaginal wall and the cyst wall. The cut margins of the either side are to be trimmed off to make the opening an elliptical shape and of about 1 cm in diameter. The edges of the vaginal and cyst wall are sutured by interrupted catgut, thus leaving behind a clean circular opening.

The advantages of marsupialization over the traditional excision operation are: (i) Simple.

(ii) Can be done even under local anesthesia.

(iii) Shorter hospital stay (24 hours). (iv) Postoperative complication is almost nil. (v) Gland function (moisture) remains intact.


● Vulvovaginitis in childhood.

● Trichomoniasis.

● Moniliasis.

● Vaginitis due to Chlamydia trachomatis.

● Atrophic vaginitis.

● Non-specific vaginitis.

● Toxic shock syndrome.


Inflammatory conditions of the vulva and vagina are the commonest disorders during childhood. Due to lack of estrogen, the vaginal defence is lost and the infection occurs easily, once introduced inside the vagina.


► Non-specific vulvovaginitis.

► Presence of foreign body in the vagina.

► Associated intestinal infestations—threadworm being the commonest.

► Rarely, more specific infection caused by Candida albicans or Gonococcus may be implicated.

Clinical Features: The chief complaints are pruritus of varying degree and vaginal discharge. There may be painful micturition.

Inspection reveals soreness of the vulva. The labia minora may be swollen and red. If a foreign body is suspected, a vaginal examination with an aural or nasal speculum may help in diagnosis.

Investigations: The vaginal discharge is collected with a platinum loop and two smears are taken, one for direct examination and the other for Gram stain.

A small amount may be taken with a pipette for culture in Stuart’s media. To exclude intestinal infestation, stool examination is of help.

Vaginoscopy is needed to exclude foreign body or tumor in a case with recurrent infection.

Treatment: In most cases, the cause remains unknown. Simple perineal hygiene will relieve the symptoms. In cases of soreness or after removal of foreign body, estrogen cream is to be applied locally, every night for two weeks. When the specific organisms are detected, therapy should be directed to cure the condition.


Vaginal trichomoniasis is the most common and important cause of vaginitis in the childbearing period. Causative Organism: It is caused by Trichomonas vaginalis, a pear-shaped unicellular flagellate protozoa. It measures 20 p long and 10 p wide (larger than a WBC). It has got four anterior flagellae and a spear-like protrusion at the other end with an undulating membrane surrounding its anterior two- third. It is actively motile (Fig. 12.2).

Mode of Transmission

The organism is predominantly transmitted by sexual contact, the male harbors the infection in the urethra and prostate. The transmission may also be possible by the toilet articles from one woman to the other or through examining gloves. The incubation period is 3-28 days.

Fig. 12.2: Physical appearance of Trichomonas vaginalis

Pathology: In about 25 percent of women in the reproductive period, the parasites harbor in the vagina in asymptomatic state. When the local defence is impaired—during and after menstruation, after sexual stimulation, and following illness, the pH of the vagina is raised to 5.5-6.5. At this level of pH, the trichomonads thrive. The organisms usually lie in between the rugae and produce surface inflammatory reaction when the defence is lost. In about 75 percent cases, the organism can be isolated from the urethra, Skene’s tubules, or even from the Bartholin’s glands.

Clinical Features

(a) There is sudden profuse and offensive vaginal discharge often dating from the last menstruation.

(b) Irritation and itching of varying degrees within and around the introitus are common.

(c) There is presence of urinary symptoms such as dysuria and frequency of micturition.

(d) There may be history of previous similar attacks.

Women with trichomoniasis should be evaluated for other STDs including N. gonorrheae, C. trachomatis, and HIV.

On Examination

(a) There is thin, greenish-yellow and frothy offensive discharge per vaginum.

(b) The vulva is inflamed with evidences of pruritus.

(c) Vaginal examination may be painful. The vaginal walls become red and inflamed with multiple punctate hemorrhagic spots. Similar spots are also found over the mucosa of the portio vaginalis part of the cervix on speculum examination giving the appearance of ‘strawberry’ (Fig. 12.3).


(a) Identification of the trichomonas is done by hanging drop preparation (p. 110). If found negative even on repeat examination, the confirmation may be done by culture.

(b) Culture of the discharge collected by swabs in Diamond’s TYM or Feinberg Whittington medium. In suspected cases, gonococcal or monilial infection should be excluded.

Fig. 12.3 : Punctate hemorrhagic spots and 'strawberry' appearance on cervix


The treatment is very much effective with metronidazole. Metronidazole 200 mg thrice daily by mouth is to be given for 1 week. A single dose regimen of 2 g is an alternative. Tinidazole single 2 gm dose PO is equally effective. The husband should be given the same treatment schedule for 1 week. Resistance to metronidazole is extremely rare. The husband should use condom during coitus irrespective of contraceptive practice until the wife is cured.


Causative Organism

Moniliasis is caused by Candida albicans, a grampositive yeast-like fungus (Fig. 12.4).


Fig. 12.4: Physical appearance of Candida albicans

Clinical Features

The patient complains of vaginal discharge with intense vulvovaginal pruritus. The pruritis is out of proportion to the discharge. There may be dyspareunia due to local soreness.

On examination:

(a) The discharge is thick, curdy white and in flakes, (cottage cheese type) often adherent to the vaginal wall (Fig. 12.5).

(b) Vulva may be red and swollen with evidences of pruritus.

(c) Vaginal examination may be tender. Removal of the white flakes reveals multiple oozing spots.

Fig. 12.5: Curdy white flakes adherent to the vaginal wall

Diagnosis: Wet Smear of vaginal discharge is prepared. KOH solution (10%) is added to lyse the other cells. Filamentous form of mycella, pseudohyphae can be seen under the microscope (Fig. 12.4). Culture in Nickerson’s or Sabouraud’s media— become positive in 24-72 hours (chapter 9).

Women with recurrent vulvovaginitis, vaginal boric acid capsule (600 mg gelatin capusles) is effective. Boric acid inhibits fungal cell wall growth.

Treatment: Corrections of the predisposing factors should be done, if possible. Local fungicidal preparations commonly used are of the polyene or azole group. Nystatin, clotrimazole, miconazole, econazole are used in the form of either vaginal cream or pessary.

One pessary is to be introduced high in the vagina at bedtime for consecutive 2 weeks. In severe cases, additional use of pessary in the morning is advocated. The treatment should be continued even during menstruation. Single dose oral therapy with fluconazole (150 mg) or itraconazole is also found effective.

Associated intestinal moniliasis should be treated by fluconazole 50 mg daily orally for 7 days. Husband should be treated with nystatin ointment locally for few days following each act of coitus. The use of condom is preferred.

Resistance to these drugs is not known. The systemic antifungal drugs fluconazole and itraconazole are effective in a single dose oral therapy.


Vaginitis in postmenopausal women is called atrophic vaginitis. The term is preferable to senile vaginitis.

There is atrophy of the vulvovaginal structures due to estrogen deficiency. The vaginal defence is lost. Vaginal mucosa is thin and is more susceptible to infection and trauma. There may be desquamation of the vaginal epithelium which may lead to formation of adhesions and bands between the walls.

TABLE 12.1





Bacterial vaginosis


Normal vaginal discharge


Greenish yellow

Curdy white

Gray white to green yellow white




Thin, frothy





Whiff test (see p. 148)



Positive (Fishy amine)




> 5

< 4.5

> 5

< 4.5

< 4.5





Diagnosis (Wet mount microscopy)

Motile Trichomonas (see p. 164)

Hyphae or spores (see p. 165)

Clue cells (> 20%) (see p. 152)

Chlamydia NAAT (see p. 150)


Metronidazole 2 gm single dose or 200 mg. TID x 7 days (see p. 164)

Imidazole Fluconazole 150 mg P.O. weekly for 6 weeks

Metronidazole 200 mg. TID x 7 days (see p. 152)

Azithromycin 1 gm orally single dose (see p. 150)

Clinical Features

(a) Yellowish or blood stained vaginal discharge.

(b) Discomfort, dryness, soreness in the vulva.

(c) Dyspareunia.

On examination

(a) Evidences of pruritus vulvae.

(b) Vaginal examination is often painful and the walls are found inflamed.

Diagnosis: Senile endometritis may co-exist and carcinoma body or the cervix should be excluded prior to therapy (p. 559).


Improvement of general health and treatment of infection if present should be done. Systemic estrogen therapy may be considered if there is no contraindication. This improves the vaginal epithelium, raises glycogen content, and lowers vaginal pH.

Intravaginal application of estrogen cream by an applicator is also effective. About one-third of the vaginal estrogen is systemically absorbed.


TSS is commonly seen in menstruating women between 15 and 30 years of age following the use of tampons (polyacrylate). Other condition associated with TSS is use of female barrier contraceptives (diaphragm). It is characterized by the following features of abrupt onset Fever >38.9°C.

● Diffuse macular rash, myalgia.

● Gastrointestinal : Vomiting, diarrhea.

● Cardiopulmonary : Hypotension, adult respiratory distress syndrome.

● Platelets : ≤ 100,000/mm3.

● Renal : ↑ BUN (≥ twice normal).

● Hepatic : Bilirubin, SGOT, SGPT rise twice the normal level.

● Mucous membrane (vaginal, oropharyngeal) : Hyperemia.

The pathological features are due to liberation of exotoxin by Staphylococcus aureus. It may lead to multiorgan system failure. Blood cultures are negative.

Treatment is supportive. Correction of hypovolemia and hypotension with intravenous fluids and dopamine infusion is done in an intensive care unit. Parenteral corticosteroids may be used. Blood coagulation parameters and serum electrolytes are checked and corrected. Infection is controlled by b-lactamase resistant antistaphylococcal penicillin (cloxacillin, clindamycin and oxacillin) for 10-14 days. The tampon should be removed. Cotton tampons are the safest. Mortality following TSS is 6-10 percent.


The term cervicitis is reserved to infection of the endocervix including the glands and the stroma. The infection may be acute or chronic.


The endocervical infection usually follows childbirth, abortion, or any operation on cervix. The responsible organisms are pyogenic (p. 127). Other common pathogens are : Gonococcus, Chlamydia trachomatis, Trichamonas bacterial vaginosis, Mycoplasma and HPV, the first one being less common nowadays.

The organisms gain entry into the glands of the endocervix and produce acute inflammatory changes. The infection may be localised or spread upwards to involve the tube or sidewards involving the parametrium.

Clinical Features: The vaginal examination is painful. The cervix is tender on touch or movements. Cervix looks edematous and congested. Mucopurulent discharge is seen escaping out through the external os. Prognosis: (a) It may resolve completely. (b)The infection may spread to involve the adjacent structures or even beyond that. (c) Becomes chronic.

Treatment: High vaginal and endocervical swabs are taken for bacteriological identification and drug sensitivity test. Appropriate antibiotics should be prescribed. General measures are to be taken as outlined in acute pelvic infection (ch. 10).


Chronic cervicitis is the commonest lesion found in women attending gynecologic outpatient. It may follow an acute attack or usually chronic from the beginning. The endocervix is a potential reservior for N. gonorrhoeae, Chlamydia, HPV, mycoplasma and bacterial vaginosis.

Pathology: The mucosa and the deeper tissues are congested, fibrosed, and infiltrated with leukocytes and plasma cells. The glands are also hypertrophied with increased secretory activity. Some of the gland mouths are closed by fibrosis or plugs of desquamated epithelial cells to cause retention cyst— nabothian follicles (Fig. 18.4)Thus, in fact, it should be called chronic endocervicitis as the ectocervix is protected by the overlying stratified squamous epithelium. There is associated lacerated and everted endocervix, the so-called eversion or ectropion.

Clinical Features: There may not be any symptom as it may be accidentally discovered during examination. Excessive mucoid discharge, at times mucopurulent, is the predominant symptom. History of contact bleeding may be present.

On examination: (a) The cervix may be tender to touch or on movement. (b) Speculum examination reveals—mucoid or mucopurulent discharge escaping out through the cervical os. There may be enlargement, congestion, or ectropion of the cervix. Associated ectopy may be present (Fig. 12.6).

Fig. 12.6: Ectropion with unilateral tear of the cervix


Cervical scrape cytology to exclude malignancy is mandatory prior to any therapy.

(i) There is no place of antimicrobial therapy except in gonococcal or proved cases of chlamydial infection or bacterial vaginosis.

(ii) The diseased tissue may be destroyed by electro or diathermy cauterization or laser or cryosurgery. The ectropion is corrected by deep linear burns and the coincidental ectopy may be coagulated (See p. 591).


During childbearing period, infection hardly occurs in the endometrium except in septic abortion or puerperal sepsis and acute gonococcal infection.

Endometrium is protected from infection due to vaginal and cervical defence and also due to periodic shedding of endometrium.


It almost always occurs after abortion or childbirth. The details of such infection has been dealt on page 133. For details see author’s Textbook of Obstetrics Chapter 29. Treatment of acute endometritis is similar to acute salpingitis (p. 172) for 14 days.


It is indeed rare for chronic endometritis to occur during reproductive period even following acute PID and endometritis. This is because of cyclic shedding of endometrium.

The infection can gain foothold, however, when there is persistent source of infection in the uterine cavity. Such conditions are IUCD, infected polyp, retained products, uterine malignancy, and endometrial burns due to radium. Tubercular endometritis is chronic from the beginning and has been described in p. 138.

Women often presents with purulent or seropurulent vaginal discharge. Diagnosis is made by cervical smear, culture of the discharge, transvaginal ultrasonography and histology, of the endometriumTreatment: The offending cause is to be removed or eradicated. Levofloxacin 500 mg PO daily for 14 days with Metronidazole 400 mg PO twice daily for 14 days are given.


Following menopause, due to deficiency of estrogen, the defense of the uterocervicovaginal canal is lost. There is no periodic shedding of the endometrium. As a result, organisms of low virulence can ascend up to infect the atrophic endometrium. There is intense infiltration of the endometrium with polymorphonuclear leukocytes and plasma cells. The endometrium becomes ulcerated at places and is replaced by granulation tissues. The purulent discharge either escapes out of the uterine cavity or may be pent up inside producing pyometra.

Clinical Features: The postmenopausal women complain of vaginal discharge, at times offensive or even blood-stained. Pelvic examination reveals features of atrophic vaginitis. Purulent discharge may be seen escaping out through the cervix. In presence of pyometra, the uterus is enlarged; feels soft and tender.


The diagnosis is confused with carcinoma of the endometrium which must be excluded prior to treatment (see p. 356). In fact, pyometra may be present both in atrophic endometritis and endometrial carcinoma. Ultrasonography (TVS) is helpful to the diagnosis. Diagnostic curettage should be done and the endometrium is subjected to histological examination.

If however, pyometra is present, drainage of pus by simple dilatation should be done first. After 1-2 weeks, diagnostic curettage is to be done under cover of antibiotics.

Treatment: In women with recurrent attacks, hysterectomy should be done and the specimen should be subjected to histological examination.


Collection of pus in the uterine cavity is called pyometra. The prerequisites for pyometra formation are :

• Occlusion of the cervical canal.

• Enough sources of pus formation inside the uterine cavity.

• Presence of low grade infection.

Treatment: Once malignancy is excluded, the pyometra is drained by simple dilatation of the cervix.

Even in non-malignant cases or in cases of recurrence, hysterectomy may be indicated. Definite surgery for malignancy is to be done following drainage of pus.



• Obstetrical—The only condition is following infection of lochiometra.

• Gynecological—The conditions which are associated with pyometra are: (a) Carcinoma in the lower part of the body of uterus (b) Endocervical carcinoma (c) Senile endometritis (d) Infected hematometra following amputation, conization or deep cauterization of cervix (e) Tubercular endometritis.

Pathology: There is abundant secretion of pus from the offending sites. The cervical canal gets blocked due to senile narrowing by fibrosis or due to debris. The accumulated pus distends the uterine cavity. The postmenopausal atrophic myometrium fails to expel the collected pus. Thus, the uterus gets enlarged more and more with thinning of its wall. The lining epithelium is lost at places and replaced by granulation tissue.

The organisms responsible are coliforms, streptococci or staphylococci. Rarely, it may be tubercular. Except in tubercular (caseous), the fluid is thin, offensive, at times purulent or blood stained. The pus may be sterile on culture or the offending organism can be detected.

Clinical Features: The patient complains of intermittent blood stained purulent offensive discharge per vaginam. There may be occasional pain in lower abdomen. Systemic manifestation is usually absent. Per abdomen: An uniform suprapubic swelling may be felt of varying size. It is cystic with well-defined margins but lower pole is not felt. It may be tender.

Internal examination reveals: The swelling is uterine in origin. The offensive discharge is seen escaping out through the cervix. Pelvic ultrasonography reveals distended uterine cavity with accumulation of fluid within.

Diagnosis is confirmed by dilatation of the cervix when pus escapes. In every case, all types of investigations are to be made to exclude malignancy of the body of the uterus and endocervix. Diagnostic curettage should be withheld for about 7-14 days following dilatation and drainage of pus. This will minimize such complications such as perforation of the uterus and spreading peritonitis. During the interval period, antibiotics should be prescribed.

Infection of the fallopian tube is called salpingitis. The details of salpingitis has already been described in the chapter of pelvic infection (ch. 10). The pathogenesis of salpingitis (acute and chronic) will be described in this section. The following facts are to be borne in mind while dealing with salpingitis.

● The infection is usually polymicrobial in nature (Table 12.2).

● Both the tubes are usually affected.

● Ovaries are usually involved in the inflammatory process and as such, the terminology of salpingo- oophoritis is preferred.

● Tubal infection almost always affects adversely the future reproductive function.


I. Ascending infection from the uterus, cervix and vagina

Pyogenic organisms (see Table 12.2).

Sexually transmitted infections (STIs) (see Table 11.1).

II. Direct spread from the adjacent infection

One or both the tubes are affected in appendicitis, diverticulitis, or following pelvic peritonitis. The organisms are usually E. coli or Streptococcus fecalis. Bacteroides fragilis is too often involved whenever abscess is formed.

III. Tubercular (see p. 137, 138)

Modes of Spread to the Tubes (see p. 127).


Pathology: • Pyogenic • Gonococcal


The pathological changes in the tubes depend on the virulence of the organisms and the resistance of the host.

There is intense hyperemia with dilated vessels visible under the peritoneal coat. The enlargement of the tube is greater than gonococcal infection because of interstitial involvement. The wall is enormously thickened and edematous. The mucopurulent or purulent exudate can be expressed out through the abdominal ostium.

Microscopically, the epithelium looks normal or the mucosa slightly edematous. The muscularis shows marked edema and acute inflammatory reaction. As the outer coat is involved, adhesions are likely and are dense.

If the infection is very severe, the endosalpinx is destroyed in part or whole and pus is formed. If the fimbrial end is open, the pus escapes out to cause pelvic peritonitis and abscess. The organisms may be present for even a year and as such chances of repeated infections are more.

Acute gonococcal: Like pyogenic infection, there is hyperemia and the tube is swollen and edematous. As the pathology is principally endosalpingitis, adhesions are less and flimsy.

The purulent exudate may escape in the peritoneal cavity and produces pelvic peritonitis and pelvic abscess. The ovaries may be involved in the process.

More often, the fimbriae get edematous, phymotic with closure of the abdominal ostium. The uterine opening is closed by congestion. The exudate is pent up inside the lumen producing pyosalpinx. The pus becomes sterile by 6 weeks and become hydrosalpinx.


(i) Pelvic or generalized peritonitis (ii) Pelvis cellulitis

(iii) Pelvic thrombophlebitis (iv) Pelvic abscess (v) Tubo-ovarian abscess.


Complete resolution: Provided the tissue destruction is not appreciable, the tube returns to its normal structure and function.

But endosalpingitis too often produces loss of cilia which is responsible for infertility or delay in transport of the fertilized ovum, resulting in ectopic pregnancy (10%).

Chronic: The infection may be chronic due to reinfection or flaring up of the infection at the site.

Recurrent acute PID is observed in about 25% cases.



■ Hydrosalpinx.

■ Pyosalpinx.

■ Chronic interstitial salpingitis.

■ Salpingitis isthmica nodosa.


Collection of mucus secretion into the fallopian tube is called hydrosalpinx.

Fig. 12.7: Hydrosalpinx. Note the retort shape of the tube. Depending on tubal diameter hydrosalpinx may be mild <15 mm; moderate 15-30 mm; severe > 30 mm

Pathogenesis: It is usually due to the end result of repeated attacks of mild endosalpingitis by pyogenic organisms of low virulence but highly irritant. The organisms involved are Staphylococcus, E. coli, Gonococcus, Chlamydia trachomatis, etc.

During initial infection, the fimbriae are edematous and indrawn with the serous surface, adhering together to produce closure of the abdominal ostium.

The uterine ostium gets closed by congestion. The secretion is pent up to make the tube distended. The distension is marked on the ampullary region than the more rigid isthmus. As the mesosalpinx is fixed, the resultant distension makes the tube curled and looks ‘retort’-shaped. The wall is smooth and shiny containing clear fluid inside, which is usually sterile (Figs. 12.7 and 37.55).

The uterine ostium is not closed anatomically, thus favors repeated infection. At times, there is intermittent discharge of the fluid into the uterine cavity (intermittent hydrosalpinx or hydrops tubal profluens).

Hydrosalpinx is also considered as the end stage of pyosalpinx when the pus becomes liquefied to make the fluid clear.

Ultrasound and Color Doppler (TVS)

Sausage-shaped complex cystic structure with reduced resistance index (RI) in the adnexal region is suggestive of the diagnosis (Fig. 12.8).


The following may happen : (i) Formation of tubo- ovarian cyst (ii) Torsion (iii) Infection from the gut (iv) Rupture.

Pyosalpinx: The pyogenic organisms, if become virulent, produce intense inflammatory reaction with secretion of pus. The tube becomes closed at both ends; the abdominal ostium by adhesions of the fimbriae and the uterine end by exudate. Because of intense inflammatory reaction and/or escape of pus into the peritoneal cavity, there is dense adhesions with the surrounding structures like ovaries, intestines, omentum, and pelvic peritoneum. Thus, a tubo- ovarian mass is formed. The inner wall of the tube is replaced in part by granulation tissue (Figs 12.9 and 12.11).

Chronic Interstitial Salpingitis

The tube enlarges mainly due to great thickness of the wall. The distension of the tube by the exudate is unusual. The abdominal ostium may be closed or partially open. The adjacent organs are adherent to the tube. Microscopically, there is extensive infiltration of plasma cells and histiocytes in all the layers. The epithelium is usually intact. There is intense fibrosis of the muscle coat along with inflammatory changes.

Fig. 12.9: Bilateral pyosalpinx

This hinders the tubal motility and favors ectopic pregnancy.

Salpingitis Isthmica Nodosa

Pathogenesis: The exact nature still remains unclear.

The following are the probabilities:

(i) It is related to tubercular infection, although it may be the residue of any form of chronic interstitial salpingitis.

(ii) There is infiltration of the tubal mucosa directly into the muscularis resembling adenomyosis of the uterus.

(iii) It is one form of endometriosis of the tube. Absence of endometrial stroma, however, points against it.

Naked eye examination reveals one or two nodules in the isthmus of the tube, often involving the uterine cornu. The nodule is small but may be as large as 2 cm.

Microscopically, there is thickening of the muscularis in which the tubal epithelium lined spaces are scattered, giving an adenomatous picture. There may be inconsistent mild inflammatory reaction (Fig. 12.10).

The clinical features and investigations of salpingitis have already been described in the p. 170 (Table 12.3).



• Outpatient therapy: (i) Ofloxacin 400 mg PO twice daily for 14 days plus metronidazole 500 mg PO twice daily for 14 days (see Table 10.4) are given. Patient is admitted for inpatient therapy if there is no response by 72 hours.

• Inpatient therapy (Temp >39°C, toxic look, lower abdominal guarding, and rebound tenderness). Clindamycin 900 mg IV 8 hourly, plus gentamicin 2 mg/kg IV, then 1.5 mg/kg IV every 8 hours are given. This is followed by doxycycline 100 mg twice daily orally for 14 days. IV fluids to correct dehydration and nasogastric suction in the presence of abdominal distension or ileus are maintained. Laparotomy is done if there is clinical suggestion of abscess rupture.

Fig. 12.10: Histology of salpingitis isthmica nodosa. Note: the tubal epithelial lined spaces inside the muscularis

Fig. 12.11: Bilateral tubo-ovarian mass (TO mass)


With early diagnosis and therapy with potent antibiotics, the immediate risk is markedly reduced. With effective therapy, the prospect of future reproductive function of the tube is not so gloomy. But once the cilia is damaged, commonly with gonococcal infection or pyogenic infection (repeated), the prospect of future fertility is very much poor even with reconstructive surgery. Even if pregnancy occurs, chances of ectopic is more (10-15%).


Isolated infection to the ovaries is a rarity. The ovaries are almost always affected during salpingitis and as such the nomenclature of salpingo-oophoritis is preferred. The affection of the ovary from tubal infection occurs by the following routes:

● Directly from the exudates contaminating the ovarian surface producing perioophoritis.

● Through lymphatics of the mesosalpinx and mesovarium producing interstitial oophoritis.

● Blood borne—mumps.

● Through the rent of the ovulation producing interstitial oophoritis.

If the organisms are severe, an abscess is formed and a tubo-ovarian abscess results. In others, the ovaries may be adherent to the tubes, intestine, omentum, and pelvic peritoneum producing tubo-ovarian mass (TO mass). Such a mass is usually bilateral (Fig. 12.11).

Direct affection of the ovaries without tubal involvement may be due to mumps or influenza. In mumps, there is no sterilizing effect on the ovaries unlike testes. This is because the capsule of the ovary is elastic and as such, ischemic injury to the graafian follicles is not likely. Even if some follicles are damaged, many are left behind to carry on the reproductive function.

The symptomatology and treatment are like those of salpingitis.


Inflammation of the pelvic cellular tissue is called parametritis.

Etiology—(Source of Infection)

► Delivery and abortion through placental site or from lacerations of the cervix, vaginal vault, or lower uterine segment.

► Acute infections of the cervix, uterus, and tubes.

► Cesarean section or hysterectomy-abdominal or vaginal (cuff cellulitis).

► Secondary to pelvic peritonitis.

► Carcinoma cervix or radium introduction.


The causative organisms are anerobic Streptococcus, Staphylococcus, E. coli, bacteroides species (fragilis, fusobacteria) etc. There is intense hyperemia with exudation of serous fluid, lymph, and polymorphonuclear leukocytes. The exudate may resolute completely or an abscess is formed. The purulent exudate may be localized or may have extrapelvic extension along the tract of blood vessels and ureter. The abscess thus points towards the perinephric region along the ureter, to the buttock along the gluteal vessels, to the thigh along the external iliac vessels and to the groin above the inguinal ligament.

Rarely, the abscess may burst into the pelvic organs, or into the peritoneal cavity. There may be associated pelvic thrombophlebitis with chance of ‘white leg’ and pyemia.

Clinical features: ■ Acute ■ Chronic

Acute: The onset is usually insidious and appears about 7-10 days following initial infection.

The temperature rises to about 102°F. Pain is not a prominent feature, may be dull aching deep in the pelvis.

On examination, the pulse rate is raised proportionate to the temperature. There is generalized deep tenderness on lower abdomen. Rigidity is absent because the lesion is extraperitoneal. Pelvic examination reveals hot and tender vagina. There is an indurated tender mass usually unilateral, which extends to the lateral pelvic wall and to which the uterus is firmly fixed. The uterus is pushed to the contralateral side (Fig. 12.12).

Rectal examination confirms the indurated tender mass or horse shoe-shaped induration of the uterosacral ligaments surrounding the rectum.

An abscess formation is featured by spiky rise of temperature, toxic look, and fluctuant swelling in the regions mentioned earlier.

Chronic: The clinical features vary, as it is often associated with chronic salpingo-oophoritis and as such, the symptoms and signs are overshadowed by the latter condition.

The chief complaint is chronic deep seated pelvic pain, may be localized to one side. There is deep dyspareunia.

Fig. 12.12: Acute parametritis pushing the uterus to contralateral side

Pelvic examination reveals the uterus fixed to an indurated and tender mass. The uterus is also drawn to the affected side because of scarring. Movement of the cervix produces pain. Ultrasonograhy can localize the abscess with its site and extent.


Acute: The outline of management protocol is the same like that of acute salpingitis of pyogenic origin.

Only when an abscess is pointing and easily accessible that it should be drained surgically.

Chronic: The treatment is the same as for chronic salpingo-oophoritis. Deep pelvic short wave diathermy may be tried to relieve pain and dyspareunia. Too often, all the measures fail, hysterectomy decision may have to be considered even at an early age specially in women whose family is completed.


Encysted pus in the pouch of Douglas is called pelvic abscess.


Pelvic causes (common)

► Postabortal and puerperal sepsis.

► Acute salpingitis.

► Perforation of an infected uterus such as attempted uterine curettage in septic abortion or pyometra.

► Infection of pelvic hematocele usually following disturbed tubal pregnancy.

► Postoperative pelvic peritonitis following abdominal or vaginal operation.

► Irritant peritonitis following contamination of urine, bile, vernix caseosa, meconium (spilled during cesarean section), iodine containing dye used in hysterosalpingography or contents of ruptured ovarian cyst (sebum in dermoid cyst), etc.

Extrapelvic causes (rare)

Appendicitis, diverticulitis, ruptured gallbladder, perforated peptic ulcer usually produce generalized peritonitis. The condition may ultimately settle to the dependent pouch of Douglas and produces pelvic abscess.

Clinical features: Patient is ill from any of the causative factors mentioned earlier. But the localization of pus in the pouch of Douglas is evidenced by:


 Spiky rise of high temperature with chills and rigor.

 Rectal tenesmus—frequent passage of loose mucoid stool.

 Pain lower abdomen—variable degrees.

 Urinary symptoms—difficulty or even retention of urine.


General: The face is flushed with anxious look. Pulse rate is raised out of proportion to temperature.

Per abdomen:

● Tenderness and rigidity in lower abdomen.

● A mass may be felt in the suprapubic region— tender, irregular, soft, and resonant on percussion.

Per vaginam:

 The vagina is hot and tender.

● The uterus is pushed anteriorly; the movement of the cervix is painful.

 A boggy, fluctuant, and tender mass is felt in the pouch of Douglas.

 A separate mass may be felt through the lateral fornix.

Rectal examination defines precisely the mass in the pouch of Douglas.


Blood: There is high leukocytosis with increased polymorphs.

Bacteriological study: Swabs are taken from high vagina, endocervical canal and from the pus. Culture is done for both aerobic and anaerobic microorganisms. Sensitivity of the microorganisms to antibiotics is also to be detected.

Confirmation of Diagnosis

The diagnosis is easy in most of the cases but at times confusion arises between pelvic hematocele and pelvic abscess. Pelvic ultrasonography reveals accumulation of fluid in the pouch of Douglas. Examination under anesthesia (EUA) and puncture of pouch of Douglas (culdocentesis) give the correct diagnosis. Old blood comes out in the former and pus in the latter.


General: Systemic antibiotics should cover anaerobic as well as aerobic microorganisms (broad spectrum): Cefoxitin 1-2 gm IV every 6-8 hours and gentamicin 2 mg/kg IV per 24 hours and metronidazole 500 mg IV 8 hourly are started. Antibiotic regimen may have to be changed depending upon the sensitivity report.

Surgery: Posterior colpotomy is the definitive surgery to drain the pus through posterior fornix. The loculi should be broken with finger.

Laparotomy is done when the patient’s condition deteriorates despite aggressive management. In patients with recurrent infection and with loss of reproductive function total abdominal hysterectomy with bilateral salpingo-oophorectomy is the preferred treatment.

The pus should be sent for culture and drug sensitivity test.


Principle: Treatment of STDs should be initiated at the patient’s first visit to a clinic. At the same time, the couple is counseled about the importance of condom use and prevention of STD transmission.

Syndromic managements are based on epidemiological studies all over the world. Syndromic diagnosis and laboratory assisted diagnosis have been found similar in terms of accuracy.

Method: Management is done by criteria for syndromic diagnosis of PID. These include detection of vaginal discharge (p. 166), abdominal pain, cervical motion tenderness, bilateral adnexal tenderness, and negative pregnancy test. Healthcare providers are trained up to follow a standardized protocol (flowcharts) to treat such a patient. This is particularly suitable in a healthcare setting of developing countries.


● It avoids delay of treatment, where laboratory facilities are limited.

● It avoids loss of patient follow up, where referral system is not well-structured.

● Continued transmission of infection is prevented.

● It is a simple, inexpensive, and rapid management for STDs.


> In recurrent vulvitis due to fungal infection, diabetes is to be excluded.

> Bartholin's cyst usually develops in the duct. The gratifying treatment is marsupialization under local anesthesia. A normal Bartholin's gland cannot be palpated.

Excision of Bartholin's duct and gland is indicated for persistent and/or recurrent infections specially when it occurs beyond the age of 40.

> During childbearing period, vaginal trichomoniasis is the commonest STD caused by Trichomonas vaginalis — a flagellated parasite. Hanging drop preparation with identification of trichomonas is diagnostic. Treatment is specific with metronidazole to both partners. The husband is to use condom during treatment. Vaginitis may be due to other causes also (p. 164).

> A vaginal discharge with pH >5.0 indicates atrophic vaginitis, bacterial vaginosis, or trichomonas infection whereas a vaginal discharge with pH <4.5 may be either physiologic or due to fungal infection. Vaginal discharge needs to be differentiated before treatment (Table 12.1)

> Moniliasis is caused by Candida albicans—a Gram-positive fungus. The infection is more likely related to diabetes, pregnancy, or amongst 'pill' users (p. 164). Diagnosis is by identification of the mycelia by direct smear and stained by methylene blue or culture in Sabouraud's media.

> Toxic shock syndrome is due to improper use of vaginal tampon. The causative organism is Staphylococcus aureus. Dysfunction of multiple organ system is due to the bacterial exotoxin (p. 166). Treatment is supportive. b-lactamase resistant anti-staphylococcal penicillin (cloxacillin, methicillin) should be the choice.

> The feature of senile endometritis may simulate endometrial carcinoma which should be ruled out prior to treatment. Common causes of pyometra are endometrial carcinoma, endocervical carcinoma, senile endometritis, infected hematometra, and tubercular endometritis.

> Pyogenic non-gonococcal organisms affect the tubes by producing perisalpingitis; gonococcal produces endosalpingitis and tubercular infection produces interstitial salpingitis.

> The organisms producing hydrosalpinx are Staphylococcus, Streptococcus, E. coli, Gonococcus, Cl. trachomatis, etc. Hydrosalpinx is the end result of repeated attacks of mild endosalpingitis. It may also be the end stage of pyosalpinx when the pus becomes liquefied. Prognosis of salpingitis in terms of reproductive function depends on the type of infection, severity, and number of episodes. When the cilia is damaged and or motility is impaired (adhesion), prospect is very poor.

Salpingitis isthmica nodosa may be one variety of endometriosis or related to tubercular infection. Tube is nodular and thickened. There is proliferation of tubal epithelium within the muscle layer (myosalpinx).

> Pelvic abscess is the encysted pus in the pouch of Douglas. The common causes are following acute salpingitis, postabortal sepsis, infected pelvic hematocele and postoperative pelvic peritonitis, etc.

Confirmation of diagnosis is by culdocentesis and the definitive surgery is drainage of pus through posterior colpotomy.

> Endocervix is the major reservoir of pathogenic organisms. Most common site of Chlamydia infection in the female genital tract is the columnar cells of the endocervix.

> Mode of spread of infection to the tubes are : Pyogenic infection spreads through veins and lymphatics causing perisalpingitis and endosalpingitis. Cornual block following postabortal or puerperal sepsis may occur.

Gonococcal infection ascends through continuity and contiguity causing endosalpingitis.

Tubercular infection spreads through bloodstream (hematogenous) causing interstitial salpingitis.

> Clinical diagnostic criteria for acute salpingitis include : Abdominal tenderness, cervical or uterine motion tenderness, adnexal tenderness plus one or more other features (see p. 170).

Indication of surgery for PID are restricted to life-threatening infection, not responding to medical therapy (e.g. tubo-ovarian abscess, pelvic abscess, or any clinical suspicion of abscess rupture).

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