METHODICAL INSTRUCTIONS



MINISTRY OF PUBLIC HEALTH OF UKRAINE

National Pirogov Memorial Medical University, Vinnytsya

CHAIR OF OBSTETRICS and Gynecology №1

METHODICAL INSTRUCTIONS

for practical lesson

« Genital tract infections. Vaginal discharge and pelvic pain»

MODULE 4: Obstetrics and gynecology

Topic 9

Objectives: to learn how to diagnose and prescribe special therapy for women with inflammatory diseases of the female genitals.

Professional motivation: The rate of inflammatory diseases is over 60% of all gynecologic diseases and about 30%patients of women’s hospitals have the inflammatory processes of the genital organs. Especially the quantity of inflammatory diseases has enlarged because of an increased sexual activity at young age, permissive sexual attitude, prostitution. Those at the highest risk are young unmarried women with many sex partners. Primarily inflammatory diseases affect human fertility because of infections of the female upper genital tract and their consequences. Women with persistent viral infection are at particular risk for cervical dysplasia and intrauterine fetal death.

Basic level:

1. Normal vaginal microflora.

2. Vaginitis (colpitis).

3. Acute endometritis.

STUDENTS’ INDEPENDET STUDY PROGRAM

1. Objectives for Students’ Independent Studies

You should prepare for the practical class using the available textbooks and lectures. Special attention should be paid to the following:

1. Inflammatory diseases of the external female genitals

2. Classification of diseases of the external female genitals

3. Examination and urgency aid for a women with inflammatory processes

4. Bacterial vaginosis

5. Acute and chronic endometritis

6. Salpingoophoritis

7. Tuboovarian abscess

II. Aim:

A student must know:

1. Etiology and pathogenesis of acute and chronic female genitals diseases.

2. Clinic symptoms of inflammatory gynecologic diseases.

3. Peculiarities in the course of inflammatory gynecologic diseases in different age.

4. Diagnostics methods of inflammatory gynecologic diseases.

5. Differential diagnostics of inflammatory gynecologic diseases.

6. Treatment methods of inflammatory gynecologic diseases.

A student should be able:

1. To carry out an objective gynecologic examination of a patient.

2. To make up a plan of a patient’s examination.

3. To evaluate the results of patient’s examination and to make a diagnosis.

4. To write out a prescription of medicine.

III. Recommendations to the student

The rate of inflammatory diseases is over 60% of all gynecologic diseases and about 30% patients of female hospitals have the inflammatory processes of genital organs. Especially the quantity of the inflammatory diseases has enlarged because of the increased sexual activity at the young age, permissive sexual attitude, prostitution. Those at the highest risk are young unmarried women with multiple sex partners. Primarily inflammatory diseases affect human fertility because of infections of the female upper genital tract and their sequel. Women with persistent virus infection are at particular risk for cervical dysplasia and intrauterine fetal death.

Normal flora has a significant role in defense against infection by genital pathogens. The female genital tract, especially the vaginal secretions, contain from 108 to 109 bacteria per gram of fluid examined. Lactobacilli produce lactic acid from glucose keeping the vagina at an acidic pH (3,8-4,2). Glycogen is metabolized by vaginal epithelial cells to glucose, which then serves as a substrate for Lactobacillus.

Normal vaginal microflora contains: Lactobacillus (70-90%), Staphylococcus epidermalis (30-60%>), diphteroids (30-60%>), Hemolytic Streptococci (10-20%), nonhaemolytic streptococci (5-30%>), Escherichia coli (20-25%), Bacte-roides (5-15%), Peptococcus (10-60%), Peptostreptococcus (10-40%), Clostridium (5-15%).

Presence of pathogenic flora without inflammation isn't a sign of pathologic processes.

It is considered that normal vaginal flora is represented by Lactobacillus. But not only Lactobacillus acidophilus provide the self-cleaning of the vagina. The normal vaginal ecosystem of reproductive age women contains 7 kinds of Lactobacillus: L acidophilus (42,8%), L. Paracasei, L. Fermentum, L. Plantarum (10-18,6%)), L.cateforme, L.corineformis, L. Brevis (2,5-5,7%), H202 producing Lactobacillus may play an important role in acting as a natural microbicide within the vaginal ecosystem.

Variation in vaginal colonization by Lactobacillus and other organisms could relate to estrogen level metabolism products of vaginal microflora, vaginal pH, and the type of Lactobacillus initially colonizing the vagina. Many endogenic and exogenic factors may change the balance of the vaginal ecosystem. Some vaginal microorganisms may cause the inflammation in certain conditions. Both vaginal and cervical epithelial cells have the capacity to convert glycogen to glucose, which is further metabolized to lactic acid. Vaginal acidity depends on adequate levels of estrogens as well as the presence of lactic acid-producing bacteria such as Lactobacilli. Concentrations of lactobacilli are probably important determinants of vaginal pH as well. The increased concentration of lactic acid producing bacteria in the vaginal fluid may result in a lower pH which determines decreased susceptibility to infection. Estrogens have a direct effect on the number of organisms and composition of the bacterial flora. The mucosal surface provides protection from invading pathogens. Mucous may act to eliminate a variety of pathogens or antigens. Mucous also serves for attachment of immunoglobulin A, lysozyme, lactoferrin and other biologically active substances. Mucous in the female genital tract is under hormonal control. Any abnormalities with low estrogen secretion and decreasing of estrogen level with age may damage defense mechanisms of the female genital tract. Using of contraceptives, shower can effect into vaginal ecosystem by changing vaginal pH, altering the vaginal fluid by direct dilution.

Bartholinitis

Bartholinitis is an inflammation of Bartholin's gland (large gland of vaginal vestibule). It may be caused by Staphylococcus, E.coli and N. gonorrhea. Any type of the pathogen initiates ductal inflammation and obstruction that can lead to Bartholin's abscess. There can be serous, serous-purulent, or purulent inflammation.

Obstruction of the opening of the main duct into the vestibule leads to abscess formation. Infection of Bartholin's glands can lead to secondary infections, abscess or cyst formation (fig 85). When the gland becomes full and painful, incision and drainage is appropriate. Patients with abscess usually require abscess incision with insertion of the catheter in abscess cavity. Recurrent infection from vaginal flora and mucous cyst formation are common sequelae of bartholinitis. If the infection of gland is caused by N. gonorrhea specific antibacterial treatment is prescribed.

Vulvitis

Vulvitis is a vulvar inflammation. It may be primary and secondary. Primary vulvitis is caused by local irritants (including feminine hygiene sprays, deodorants, tight-fitting synthetic undergarments in women with obesity or diabetes mellitus. Secondary vulvitis are caused by accompanying discharge from vagina. Reduced estrogens levels in reproductive age women, and more frequent in girls and menopause women may lead to vulvitis.

Clinic. Erythema, edema of vulva and skin ulcers are all indices of the infection.

Patient's complains are itching or burning. Excoriation caused by the patient's scratching of the skin of vulva are often seen in vulvar irritation.

To relieve inflammation and itching the main suspected cause must be removed. The therapy includes local application of boric acid solution or KMn04 solution. Candidasis is treated with Gyno-paveril 150mg in suppositories — 3 days, or Orungal lOOmg twice a day during 6-7 days orally, and then one capsule per day every first day of menstrual cycle during 3-6 cycles. Treatment with local antibiotics and steroids is successful.

Vaginitis (colpitis)

Vaginitis (colpitis) is an inflammation of vagina. It is the most frequent cause of visits to gynecologists. It may be caused by Staphylococcus, Streptococcus, E.coli and other.

Excessive vaginal discharge is associated with an identifiable microbiologic cause in 80% to 90%of cases. Hormonal or chemical causes account for most of the remaining cases. Vaginitis may be acute, subacute and chronic. There are two forms of vulvitis: purulent and granulosa-diffusional.

The main symptom is the increased, gray-white or yellow discharge generally serous or purulent with rancid odour. The patients complain of dysuria, vulvar itching, burning and dyspareunia. Examination may reveal edema or erythema of vulva and vagina, petechia or patches in the upper vagina or on the cervix. In case of chronic vaginitis all these signs are not so expressed.The cultures from vagina, cervix,urethra, ductus of Bartholin's gland should be microscopically examined.

Treatment of nonspecific vaginitis is comlex:

* using of antiinflammatory medicines

* treatment of neuroendocrinologic and immunodificiency conditions

* treating of male sexual partner; patients should avoid sexual contacts while therapy

Local treatment includes using of syringing with antiseptic fluid (KMn04, furacilin, chlorhexidin) no more than 3-4 days. In case of acute or chronic vaginitis laser therapy may be used.

Metronidazol (vaginal suppositories), chlorhinaldin, terginan, betadin, gyno-paveril may be prescribed. For normalization of vaginal ecosystem solkotry-chovac, vagilak, Lactobacterin and Bifidumbacterin are used.

Bacterial Vaginosis

10-25% of all gynecologic patients have this disease. Among sexually transmitted diseases, bacterial vaginosis is diagnosed in 60-65%> of women. Bacterial vaginosis is a result of an overgrowth of both anaerobic bacteria and the aerobic bacteria Gardnerella vaginalis. Anaerobes and G. vaginalis are normal inhabitants of vagina, but these bacteria overgrowth dominant of the normal Lactobacillus flora results in the appearance of a thin, fishy odor, gray vaginal discharge that adheres to the vaginal walls.

A small amount of vaginal discharge may be normal (2ml) particularly at the midcycle. Bacterial vaginosis causes an increased vaginal discharge (15-20ml), vulvar irritation, pruritus, dysuria and foul odour.

The diagnosis of bacterial vaginosis is based on the presence of the following characteristics of the discharge:

* pH is higher than 4,5

* a homogeneous thin appearance

* a fishy amine odour produced by anaerobes when 10% KOH is added

presence of clue cells (vaginal epithelial cells to which organisms are attached).

Cultures aren't helpful because anaerobes and Gardnerella vaginalis can be recovered from normal flora of healthy women, but the concentration of both bacteria is higher in patients with bacterial vaginosis (fig. 86). Factors that lead to overgrowth of G.vaginalis and anaerobes have not been identified.

Treatment includes elimination of anaerobic agent of microflora, inducement of local and general immunity and then the normal microflora should be renewed.

Oral using of metronidazol (Flagyl) 500mg twice a day for 7 days or by intravaginal Metrogel 0,75% cream twice a day for 5 days, 2% Clindamycin cream (Cleocin) once daily for 7 days.

For normalization of vaginal microflora the local bifidumbacterin insertion or 2-3%) solution of Lactic acid is used. The treatment of the male parthner with Metronidazol can be advocated only when bacterial vaginosis recurs, but effectiveness is not proven.

Endocervicitis

Endocervicitis is the inflammation of mucosa layer of the endocervix. Bacteria cause infection of the columnar epithelium. Chlamidia trachomatis, Mycoplasma, Trichomonada vaginalis, N. Gonorrhoeae, viruses, Candida, E.coli, Staphylococci cause endocervicitis.

Cervix is constantly exposed to trauma during childbirth, abortion.The abundant mucus secretion of the endocervical glands both with the bacterial ascend from the vagina creates a situation that is advantaging to infection.

The inflammatory process is chiefly confined to the endocervical glands. The squamous epithelium of the exocervix may be involved into the process called acute exocervicitis. The extent of endocervical involvement as compared with exocervical one appears to have some relation to the infecting agent.

Chronic cervicitis manifestation is cervical erosion. Erosion indicates the presence around the cervical os a zone of infected tissue that has a granular appearance. It implies the loss of superficial layers of the stratified squamous epithelium of the cervix and overgrowth of infected endocervical tissues.

The inflammatory process stimulates a reparative attempt in the form of an upward growth of squamous epithelium, causing some of the ducts of the endocervical glands to be obstructed. Retention of mucus and other fluid within these glands results in the formation of Nabothian cycts. These cysts are endocervical glands filled with infected secretion. Their ducts become secondarily included into the inflammation and reparative processes.

The most important in the diagnosis of chronic cervitis is the exclusion of the malignant process. Before the begining of treatment, examination with colposcope should be carried out. The cervicitis may appear as a reddish granulation raised above the surrounding surface, giving the impression of being papillary.

A Papanicolaou smear should be obtained and suspicious areas should undergo biopsy.

Treatment Acute cervicitis is treated with appropriate antibiotics (it depends on bacterial agent). Local treatment of acute phase is a real danger of dissemination of infection. Laser therapy is used in treatment of acute and chronic cervicitis.

Electocautherization is the traditional treatment of chronic cervicitis, especially with erosion, cervical ulcers or ectropion. Nowadays cryosurgery or laser surgery has replaced electrocautherization.

Acute endometritis

Acute endometritis is an inflammation of endometrium (mucus layer of uterine). It may occur in such cases as: endometritis after uterine curettage or suction and puerperal endometritis. Endometritis is caused by bacterias, viruses, mycoplasmas. The most frequent the associations of 3-4 anaerobic bacteria and 1-2 aerobic are the main reason of endometritis.

Anaerobic bacteria compose apart of the normal cervicogenital flora. There are two known mechanisms which cause anaerobic infection: antibiotic selection that preferentially inhibits aerobic bacteria and tissual trauma that occurs after surgery which reduces the redox potencial. Anaerobes produce odorous metabolic products.

Uterus has endometrium factors of local immunity. There are T-lymphocytes and other factors of cellular imunity in endometrial stroma. Lymphocytes and :utrophiels normally appear in the endometrium in the second half of menstrual 'cle; their presence does not necessarily constitute endometritis. The appearing 'plasma cells represents immune response, usually to foreign bacterial antigen. The organism should be cultured before applying of antimicrobal therapy, s anaerobes compose a part of normal flora, deep tissual cultures not mtaminated by surface bacteria are required. Forty eight or more hours are quired for anaerobe recovery, and treatment usually is based on clinical signs, here are nonspecific and specific endometritis. Specific endometritis is caused у М. Tuberculosis, N. Gonorrhea, Chlamidia trachomatis, Actinomyces.

Clinic. Fever is the characteristic feature in the diagnosis of endometritis, nd it may be accompanied by uterine tenderness. If the infection has spread to he parametrium and adnexa, tenderness may be present there as well. Temperature :levation is probably proportionate to the extention of the infection and when :onfmed to the decidua, the cases are mild and there is minimal fever. Chills nay accompany fever. Women usually complain of abdominal pain. There is enderaess on one or both sides of the abdomen and parametrial tenderness is ilicited upon bimanual examination. The uterus is lightly enlarged.

A leukocytosis and increased erythrocyte's sedimentation rate is revealed n patient' blood test. In some cases acute endometritis may become a chronic me;

Treatment Various choices of initial antibiotic therapy are used. Most of them are successful. Single-agent therapy has the benefit of easy administration; Cephalosporins such as Cefotetan and Cefoxitin are commonly used. A combination of Ampicillin and Aminoglycoside is also popular. The combination of Clindamycin with Gentamicin or Metronidasol with Unasyn (Ampicillin with Sulbuctam) and Gentamicin is applied. It is desirable to provide additional antibiotic coverage if there has been no responce within 48 to 72 hours. Intravenous antibiotic therapy is continued until the patient is asymptomatic and afebrile period lasts for at least 24 hours.

Local uterine douching with antiseptic solution of chlorhexidin or furacilin has a good effect. In some cases uterine curettage is performed after temperature normalization.

Chronic endometritis

Chronic endometritis is a sequale of untreated acute endometritis or nona-dequate treatment of postabortion or purperal endometritis. The chronic endometritis sometimes is associated with the use of intrauterine device (IUD). In some cases it may occur without acute stage.

Clinic. The chronic endometritis results from organisms that are normally in lower genital tract (Protei, E. Coli, Staphylococcus, Mycoplasma). Bacteria that can be recovered are usually of low pathogenicity, but more virulent intrauterine bacteria occasionally cause the serous purulent' discharge, abnormal uterine bleeding and moderate uterine tenderness. Diagnosis is based on anamnesis and clinical manifestation. It could not be diagnosed unless plasma cells are found in the endometrium. Ultrasonography can identify gas vesicules in uterine cavity, hyperechogenic places (local fibrosis, sclerosis) in basal layer of endometrium.

Treatment. A complex treatment is used. It includes a medicines for curing of accompaning deseases, desensibilisative medicines and additional general health measures, vitamines.

Physiotherapy has an important role. It improves pelvic hemodynamics. Diathermy on lower abdomen, electrophoresis with copper, zinc, ultrasound, inductothermy, laser radiation are used. If during physiotherapy the process becomes strained antibiotic therapy is recomended. While remission antibiotic using is not proved.

Physiotherapy promotes to activation of hormonal ovarian function. If effect is not enouph than a hormonal therapy is used (taking into account the patient's age, term of deseases, degree of ovarian hypofunction). Health resort treatment is effective (balneologic therapy, mudcure resort).

Salpingoophoritis

Salpingoophoritis is the inflammation of the uterine tubes and the ovaries. Salpingoophoritis is the most frequent among all pelvic inflammatory deseases. Most cases of oophoritis are secondary to salpingitis. The ovaries become infected by the purulent material that escapes from fallopian tube. If the tubal fimbriae are adherent to the ovary, the tube and ovary together may form a large retort-shaped tubo-ovarian abscess.

Most patients with salpingoophoritis have lower abdominal, adnexal tenderness (unilateral or bilateral) purulent cervical exudate or purulent vaginal discharge (fig. 88).

Clinic. There are four stages of salpingoophoritis. The first — salpingitis without irritation (inflammation), of the peritoneum, the second—with signs of peritonitis, the third with occlusion of uterine tubes and tuboovarian abscess and the fourth is the rupture of tuboovarian abscess. During bimanual examination adnexal inflammatory mass is revealed.

The diagnosis of salpingoophoritis is based on the history, physical examination and laboratory tests. Besides that additional ultrasonography and laparoscopy can be used.

Laparoscopy provides the most accurate way to diagnose the inflammatory process and its stage. It should be used in cases when the diagnosis is unclear, especially in patients with severe peritonitis, to exclude a ruptured abscess and appendicitis. Besides diagnostic laparoscopy is used to provide treatment procedures.

Ultrasound can be used to distinguish the presence of an abscess from an inflammatory mass within the adnexal mass. It may also be helpful in defining mass in the obuse patient or if the bimanual examination is unsatisfactory because of the excessive tenderness.

Treatment. All patients with acute salpingoophoritis should be hospitalized. Adequate therapy of salpingitis includes the assessment of severity, antibiotic treatment, additional general health measures.

Before the culture test performing the antibiotic therapy is provide with broad spectrum antibiotics. The most effective is the combination of Clindamicin with Chloramphenicol, Gentamicin andLincomicin, Doxycyclin, Clacid, Cefobid, Cyfran, Claforan, Dalacin С and Unasyn.

When anaerobic agents are suspected metronidazol should be used, in severe cases intravenously. After temperature normalization and cessation of peritonitis signs antibacterial therapy is continued for 5 days. Detoxycation is indicated and is provided by using of 5% glucose solution, polyglucin, reopolyglucin, solutions of proteins, correction of pH balance by using of 4% solution of Sodium bicarbo-nates. Among physical methods of treatment cold on the lower part of the abdomen is used. Appropriate antibacterial treatment is combined with laparoscopy active drainage.

The tuboovarial abscess is drained of pus by puncture and rinsed with bacteriostatic solution and local application of antibiotics. In subacute stage aloe, ultraviolet radiation, authohaemotherapy is used. They prevent the chronic processes.

Chronic salpingoophoritis. In most cases chronic salpingoophoritis is the sequale of non treated acute process. Chronic stage of the process is characterized by tubal occlusion with periovarial adhesions, tubal dysfunction (fig. 89).

Clinic. The main complains of the patient are: mild tenderness in lower part of abdomen that becomes severe during menstruation. Pelvic nerves have more painful sensitivity (pelvic plexitis, ganglionevritis due to chronic inflammation). In some cases menstrual dysfunctions such as oligomenorrhea, polymenorrhagia, algodismenorrhagia occur. Changing in uterine tubes and hypofunction of ovaries lead to infertility or miscarriage. Secretory dysfunction like vaginal discharge or cervical exudate may be observed as a clinical finding of colpitis or endocervitis. Some patients complain of low libido, painful coitus, dysfunction of urinary bladder, liver tenderness.

Menstrual dysfunction (menorrhagia or metrorrhagia) is the most frequent symptom of chronic salpingoophoritis as a sequel of disorders of neurohomoral regulation of menstrual function. Metrorrhagia often occurs after cessation of menstruation and then the differential diagnosis should be made in case of ectopic pregnancy.

Diagnosis. Correct history taking (reveal of inflammation after abortion, delivery or dilatation and curettage) makes it possible to suspect the chronic inflammatory process. Primary chronic salpingoophoritis is found in more than 60% of cases. Some information gives physical examination and laboratory tests. Bimanual examination gives nonspecific information. Enlargement, consistency and degree of adnexa mobility should be examined. Sometimes because of peritubal and periovarian adhesions the sizes and mobility of adnexa are changed.

Additionally, ultrasound and laparoscopy, hysteroscopy should be held. Tomography or endoscopy may be used. Laparoscopy is the most informative diagnostic method to differentiate salpingoophoritis, external endometriosis, uterine myoma with inflammatory changes, cysts. Disorders of adjacent organs (bladder, intestine) while serous inflammation is present without structural changes. But women with disorders of urinary tract, gastro-intestinal tract must be additionally examined (urography, irrigoscopy).

Treatment of chronic salpingoophoritis is provided with minding of pathogenesis and clinic. Antibiotics are indicated in acute period, when there are signs of inflammation.

Nonsteroidal antiinflammatory drugs (Voltaren, Butadion) are prescribed. To stimulate immune system immunomodulators are used: (Decaris, T-activin). FIBS, aloe, autohaemotherapy are also used. Analgesia both by medicines and by reflextherapy is of great importance. Physiotherapy is conducted in hospital while in case of acute process and remission it can be used in ambulatory conditions. Ultrasound has analgetic and fibrinolityc influence and is prescribed in sinusoid and modulate of high frequency. Laserotherapy is also used. To escape chronic salpingoophoritis the acute salpingoophoritis must be treated in proper way and the quantity of abortion should be reduced.

Parametritis

Parametritis is an inflammation of parametrium. Inflammation of the whole pelvic cellular is called pelviocellullitis. According to international statistics these diseases are classified as acute parametritis or pelvic phlegmona.

Infection agents may be staphyloccocus, streptoccocus, E.coli, etc. It can be caused by one microbic agent or microbe association. It occurs after pathologic delivery, abortion, operation on genitals. The main way of infection spreading is lymphogenic. Morphologically parametritis is characterized by all signs of inflammation: dilation of blood and lymphatic vessels, peripheral edema, exudation. There are 3 stages in course of parametritis (infiltration, exudation, firming). Exudation may be serous, and very rarely it is purulent. Sometimes it undergo resorbtion and dissolves, sometimes a fibrose connective tissue grows and leads to uterine dislocation to the side of previous inflammatory process.

Clinic. Moderate tenderness in lower parts of abdomen, in back, high body temperature (38-39°C), tachicardia are found. Signs of peritoneal irritation and diminished or absent bowel sounds, especially associated with ileus, indicate more serious infection, including the possibility of abscess formation. Fever is a characteristic feature in the diagnosis of metritis and it is accompanied by uterine tenderness. Bimanually before or behind on left or right side of the uterus infiltration may be palpated. It is firm and immovable. Infiltration is classified into anterior, posterior and lateral.

Treatment begins from using antibiotic of broad coverage against a variety of common microorganisms and is usually prescribed without cultures.

Various choices of initial antibiotic therapy are used. Most of them are successful. Cephalosporins such as Cefotetan and Cefoxitin are commonly used. A combination of Ampicillin and Aminoglucoside and also the combination of Clindamycin with Gentamicin are used.

A bottle with ice on the lower part of abdomen is used in case of infiltrative stage of disease. Bio stimulators should be prescribed. Management of a persistent pelvic abscess includes drainage by colpotomy, or laparotomy. Intraabdominal rupture of pelvic abscess is a surgical emergency. Sepsis may occur in association with pelvic infection, with or without frank abscess formation. Phisiotheraputic precedures are used for rehabilitation.

Tuboovarian abscess

Tuboovarian abscess (TOA) may occur as a complication of salpingoopho-ritis. It begins from acute purulent salpingitis when all layers of uterine tubes are involved into the process. The tubes characteristically become swollen and redde is the muscularis and serosa are inflamed. If exudate drips from the fimbriated mds of the tubes a pelvic peritonitis is produced then it can give rise to peritoneal idhesions. The swollen and congested fimbriaes may adhere to one another and produce tubal occlusion. The fimbriae may occlude tubes producing permanent ubal infertility. The swollen and congested fimbriae may adhere to ovary, trapping he exudate in the tube and giving rise to pyosalpinx or if the ovary becomes nfected, a tuboovarian abscess (fig. 90). The mucosal folds may adhere to one mother forming gland-like spaces that are filled with exudate. If the infection subsides after agglutination of the fimbria and closure of the peripheral end of he tube, secretion accumulates and distends the tube, forming pyosalpinx. Each •ecidive of chronic salpingoophoritis has more clinical manifestation and is treated vith difficulty. TOA is associated with IUD, microbe association, chronic salpingoophoritis.

Intoxication in case of TOA leads to liver disorders. Decreasing of albumin-globulin index is observed while the level of general proteins is normal for a ong time. The degree of these disorders depends on the time of duration of the process.

Clinic. Clinic of TOA depends on the volume of purulent damage of adnexa, duration of the process, disorders of adjacent organs. There are some syndromes vhich are divided into local syndrome (pain, purulent discharge, peritoneal symptoms and palpation of tuboovarian mass).

Inflammatory-intoxicative syndrome includes fever, tachycardia, nausea, vomiting. Luecocytosis, decreasing of albumin-globulin index, C-reactive protein are observed in blood. Immune syndrome (decreasing of lymphocytes and mono-cytis in blood) is found.

Syndrome of adjacent organs disorders (dysuria, urinary frequency, menstrual disorders) is also possible.

Severe lower abdominal pain occurs, pelvic peritonitis may be present. Pain can irradiate to back, pelvic bottom, in the chest. In such cases the examinations should be performed to exclude pneumonia, pancreatitis, cholecystitis. Musclar defance which prevents abdominal palpation in the lower quadrants, adnexa are tender to various degrees and cervix movement may cause pain in case of bimanual examination. The adnexa often are either adherent to the posterior aspect of the uterine or prolapsed in cul-de-sac, which may pull the uterine into a retroverted position. TOA is characterized by pain and tenderness, fever or chills, temperature rises up 39°C, blood pressure decreases. Abdomen takes part in breathing, and it is painful in lower parts. In blood analysis elevated white blood count (9-10x107 1) erythrocytes' sedimentation rate more than 30mm/hour, positive C-reactive protein, decreasing of albumin-globulin index till 0,8 are observed.

Sometimes there can be urinary syndrome with proteinuria, leucocyturia. There may be disorders of filtrative kidney' function, even unuria. Changing of albumin-globulin index and hypofybrinogenemia characterizes the liver dysfunction.

Diagnosis is based on clinic, bimanual examination, laboratory analyses and additional methods of investigation (ultrasound, laparoscopy).

Treatment Tuboovarian abscess is treated by antibiotics, desensibilisative and nonsteroidal antiinflammatory medicines, detoxication and immunostim-mulation. Best of all one should combine taking of penicillin with tetracyclins. When anaerobic infection is suspected metronidazole is used. Daily punctions of tuboovarian abscesses are indicated to remove purulent containts.

Indications to surgical removal of tuboovarian abscess are:

* abscence of efficiency of complex treatment with usage of punctions during 2-3 days

* suspicion on tuboovarian abscess perforation; volume of surgical intervention depends on process' spreading, woman's age and extragenital pathology

Peritonitis

Pelvioperitonitis is an inflammation of pelvic peritoneum.The polymicrobial infection such as Escherichia coli and other aerobic, enteric, gramnegative rods, group of p-hemolytic staphylococci, anaerobic, streptococci, Bacteroides species, aphylococci, mycoplasms cause the process. Pelvioperitonitis occurs secon-ary. Primary process is in uterine tubes, ovaries, uterus and parametrium. In lost cases purulent damage of uterine adnexa lasts with pelvioperitonitis. lfection can be spread by limphogenic or blood vessels, and from uterine tubes l case of salpingitis, especially gonococcial infection.

Clinic characterizes the acute inflammation. High temperature, severe lower bdominal pain, fever or chills, tachycardia are common. There can be nausea nd sometimes vomiting. Muscular defence and rebound tenderness are the ymptoms of peritoneal irritation. Anterior abdomen wall takes part in breathing ct.Tender adnexa are present at bimanual examination. Cervical motion causes ain. Posterior fornix is painfull.

Laboratory tests reveal increasing of white blood cell count and erythrocyte edimentation rate. C-reactive protein levels may appear. Generall blood test hould be done 4-5 times per day to diagnose transformation of pelvioperitonitis о peritonitis.

Treatment All the patients should be hospitalized. Ideally, the antibiotic hould be selected according to the organism present in the fallopian tube or items, but in most cases empiric therapy must be used. Treatment includes intravenous doxycycline and either cefoxitin or cefotetan or intravenous clindamycin ind gentamicin for at least 4 days followed by oral clindamicin or tetracyclin for [0-14 days. Hospitalized patients who have peritonitis but do not have adnexal ibscess usually respond rapidly to the regimens. In the presence of an adnexal ibscess, even if the systemic manifestations are mild, antibiotics which eliminate 3.fragilis should be selected because most pelvic abscesses contain this organism. Clindamycin, Metronidazol, Cefoxitin, or Impinem should be used to treat pelvic ibscess. If there is an intrauterine device it should be removed as soon as therapy s started. Surgery is indicated in the case of ruptured pyosalpinx or ovarian ibscess. Colpotomy drainage usually is preferable when unruptured midline cul-de-sac abscess is present. Laparotomy is required for such problems as unresolved abscess or adnexal mass that does not subside, surgery should be limited to the most conservative procedures that will be effective. Unilateral abscess respond to unilateral salpingoophorectomy.

Septic shock

Septic shock is associated with infection caused gram-negative aerobic coliform organisms those are producing endotoxins. In gynecological practice it may occur in case of septic abortion, localized or spreading peritonitis, thrombophlebitis. Septic shock is a special organism reaction that is expressed in development of severe systemic disorders. It may be caused by using of broad spectrum antibiotic in high doses, that results in releasing of great amount of endotoxin.

Endotoxin, a complex cell wall-associated lipopolysaccharide, is released into the circulation at the time of bacterial death, resulting in multiple hemodynamic effects. The subsequent activation of lymphocytic T-cells and mass cells results in histamine and kinin activation as well as the activation of kallikrenin and decrease in kallikreinogen and kallikrein inhibitor. These changes result in the release of bradykinin, a potent arterial dilator. Early septic shock is a classic example of distributive shock, related to a systemic maldistribution of relatively normal or even increased cardiac output. Clinical findings include hypotension, fever and chills. Initial hemodynamic findings include decreased systemic vascular resistance and high normal or elevated cardiac output. The continued maldistribution of cardiac output leads to local tissue hypoxia and to the development of lactic acidosis and organ dysfunction. This decrease in systemic vascular resistance is caused by the release of vasoactive substances, as well as by vascular endothelial cell injury, which promotes capillary plugging secondary to complement induced leukocyte aggregation. These factors lead to increased arteriovenous shunting.

If the process continues a second hemodynamic phase of septic shock is developed. The primary importance in this late phase is the development and progression of myocardial dysfunction leading to ventricular failure. Studies assessing stroke work index and ventricular ejection fraction have demonstrated depressed intrinsic ventricular function even in the early stage of septic shock. Pulmonary hypertension, another important hemodynamic alteration is often associated with septic shock, may have additional profound hemodynamic consequences. As the sequalae of renal kidneys filtration disorders — the shock kidney is formed and acute renal insufficiency is developed. Signs of liver disorders are hyperbilirubinemia, lipid metabolism abnormalities.

Patients who recover from the initial hemodynamic instability of septic shock may suffer prolonged morbidity secondary to endotoxin-mediated pulmonary capillary injury and noncardiogenic pulmonary edema. Such lung failure is a major cause of death in patients whose hypotension was prolonged and may experience acute tubular necrosis. Endotoxin mediated endothelial cell injury and associated thromboplastine-like activity as well as prolonged shock from any other cause may also lead to activation of the coagulation cascade and a clinical picture of disseminated intravascular clotting syndrome (DIC).

Clinic and diagnosis. The clinical manifestation develops just after surgical operation on infected organs. The body temperature rises till 39-40°C and is high during 1-3 days. Then the temperature decreases, chills is a characteristic feature of the septic shock.

Among clinical findings there are hypotension without bleeding or nonade-quete to it, tachycardia, 120-140 per minute. Decreasing of blood circulative volume leads to rising of shock index till 1,5 (normally 0,5). Skin is pale and wet because of perspiration, later akrocyanosis can appear. Breath disorders, like tachypnoe till 30-60 per minute, is the sign of shock lungs. Skin may be colored in yellow, there may be blood vomiting.

The most dangerous complication of septic shock is kidney insufficiency. Clinical manifestation at the beginning is oligouria — less than 30 ml per hour. Later anuria is developed. All these changes in organism appear in very short time in 6-8 or sometimes 10-12 hours.

Diagnosis is based on the following signs:

* septic organ

* low blood pressure, nonadequate to blood loss

* nervoues system disorders

* pain of different parts of body

* decreasing of diuresis

* rash on the skin

The blood temperature should be taken every 3 hours, blood pressure is measured every 30 minutes, urine quantity must be measured. Bacterial culture from infected organ, blood analysis, coagulogram and biochemical tests are performed.

Treatment of septic shock. The treatment of septic shock involves optimising preload relative intravascular volume with crystalloid infusion as well as treating of the underlying infection. Although some authorities advocate the use of colloid solutions for volume replacement, there is noconvincing evidence that using of such solutions decreases the incidence of pulmonary edema or adult respiratory distress syndrome. In most cases the infection is polymicrobial and broad spectrum coverage for gram-negative and gram-positive aerobic and anaerobic organisms is most appropriate. If an abscess is involved, promt surgical drainage after initial resuscitation is mandatory. Patients in septic shock should be treated with dopamine hydrochloride. This agent in doses of less than 5mg/kg/minute improves renal blood flow by means of dopaminergic mesenteric vasodilatation; in doses of 5 to 30 mg/kg/minute, a positive inotropic effect is also seen. The hemodynamic manipulation of patients whose hypotension fails to respond rapidly to volume infusion may be assisted by pulmonary artery catheterization, allowing the clinician to achieve optimal preload before the institution of inotropic or vasoconstrictive therapy. High-dose corticosteroids are advocated (60-120 mg of prednizolone or 8-16 mg of dexamethazone). To renew Ph balance lactosol or bicarbonate natrii are indicated.

SPECIFIC INFLAMMATORY DISEASES

(Sexually transmitted diseases)

To specific inflammatory diseases of the female reproductive organs belong tuberculosis and sexually transmitted diseases. According to the WHO's classification, there are 21 such diseases. Their frequency has been risen for the last years.

SEXUALLY TRANSMITTED DISEASES

(the WHO's classification)

Classic venereal diseases

|Nosology |Microorganism |

|1. Syphilis |Treponema pallidum |

|2. Gonorrhea |Neisseria gonorrhoeae |

|3. Chancroid |Hemophilus ducrei |

|4. Lymphogranuloma venereum |Chlamydia trachomatis |

|5. Donovanosis, or granuloma inguinale |Callimmantobacteriumgranulomatis |

3,4,5 are mostly in tropic countries

Other sexually transmitted infections

|Nosology |Microorganism |

|A — that affect mostly genital tract |

|1. Syphilis |Treponema pallidum |

|1. Urogenital chlamydiasis |Chlamydia trachomatis |

|2. Urogenital trichomoniasis |Trichomonas vaginalis |

|3. Urogenital mycoplasmosis |Mykoplasma hominis |

|4. Candidosis vulvovaginitis |Candida albicans |

|5. Genital herpes |Herpes simplex virus |

|6. Genital warts |Papillomavirus hominis |

|7. Molluscum contagiosum |Molluscoviras hominis |

|8. Bacterial vaginosis |Gardnerella vaginalis та mini збудники |

|9. Urogenital shigellosis of homosexualists |Shigella species |

|10. Pediculosis pubis |Phthyrus pubis |

|11. Scabies |Sarcoptes scabiei |

|В — With mostly affection of other organs |

|1. Infection, caused by HIV |Human immunodeficiency virus |

|2. Hepatitis В |Hepatitis В virus |

|3. Cytomegalovirus infection |Cytomegalovirus hominis |

|4. Amebiasis |Entamoeba hystolytica |

|5. Lambliosis |Giardia lamblia |

Gonorrhea

Gonorrhea is a contagious disease caused by Neisseria gonorrhoeae. Among the specific inflammatory diseases of the female genital tract gonorrhea takes the second place and is in 5-25% of cases of all STDs.

Etiology and pathogenesis. Gonorrhea is caused by Neisseria gonorrhea (fig. 92). The causative agent was found in 1879 by A. Neisser. Gram-negative N. gonorrhea is not stable in the outer surrounding and dies quickly at the influence of antiseptic solutions, boiling, drying, but it is rather stabile in human organism. In uncomfortable conditions they transform into L-forms, which can transform into the usual form in the favourable conditions. In case of chronic gonorrhea, N. gonorrhoeae are situated mostly in leukocytes and out of the cells, in case of the acutening of the process they are found in the leukocytes.

Fig. 92. An agent of gonorrhea — gonococus

N. gonorrhea affects mostly those parts of urogenital tract, that are covered with cylindric epithelium: mucosa of urethra, cervical canal, Bartholin's glands ducts, mucosa of uterine cavity, uterine tubes, ovarian epithelium, peritoneum. During the pregnancy, childhood and menopausal period there can be gonorrheal vaginitis.

The source of infection is a person with gonorrhea.

Ways of infecting:

* the disease is sexually transmitted

* homosexual contacts, orogenital contacts

* very rarely through sponges, towels, underwear

* during labour from mother (infected eyes, vagina in girls)

Incubational period lasts for 3-7 days, sometimes for 2-3 weeks.

According to the stage of spreading the process the gonorrhea of lowei part of genital organs (gonorrheal urethritis, endocervicitis, Bartholinitis, vulvovaginitis) and gonorrhea of upper parts — gonorrhea ascendens (endometritis, salpingitis, pelvioperitonitis) is classified.

According to duration there are such forms of gonorrhea:

* fresh gonorrheal infection with acute, subacute, torpid passing, which lasts less than two months

* chronic gonorrheal infection, lasting more than two months

* latent gonorrheal infection

In women the clinic of gonorrhea depends on the localization of the process, virulency of causative agent, age of woman, organism's reactivity, stage of the disease (chronic, acute).

Fresh gonorrhea in acute forms has expressed clinical manifestations. Subacute form is characterized by subfebrile condition, sometimes by expressed clinical symptoms, which appeared two weeks before. Torpid gonorrhea in acute form has mild clinical manifestations or is asymptomatic, but N. gonorrhoeae are found in the patient. Latent form is diagnosed when there is no bacteriologic and bacterioscopic confirment, no symptoms, but person is a source of infection. Chronic gonorrhea lasts for more than 2 months, or without establishing of the beginning.

Gonococcal urethritis. Clinical manifestation appears within 3-5 days after infection and is characterized by dysuria. Variable degrees of edema and erythema of the urethral meatus, purulent or mucopurulent discharge are present.

Gonococcal Bartholinitis. It may occur when N. gonorrhea with vaginal discharge infects the Bartholin's gland. It is manifested by edema, erythema around the duct's os. When the occlusion occurs, pseudoabscess or Bartholin's abscess which are accompanied by purulent process symptoms can develop.

Gonococcal endocervicitis. Inflammatory process develops in mucosal layer of the cervical canal. Examination reveals edema and erythema of vagina and part of the cervix. There is a red crown around the cervical os and a mucopurulent cervical discharge.

Gonococcal proctitis occurs very rarely. Rectum is involved into the process in the result of contamination with the infected genital discharge. Clinic includes tenesmus and rectal pain.

Gonococcal endometritis is the first stage of the ascendant gonorrhea with infection of basal and functional layer of endometrium. It is manifested by lower abdominal pain, high body temperature, sometimes nausea, vomiting. Pain often has spasmatic character. Discharge is sanguine-purulent or mucopurulent. Uterus is painful at palpation. Chronic endometritis is characterized by menstrual disorders.

Gonococcal salpingitis is the infection of the fallopian tubes, mostly bilateral. In acute stage the pain in lower part of abdomen is common. It becomes stronger, motion, nausea, vomiting. Menstrual disorders can occur.

Smears must be taken on the 2-4th day of the menstrual cycle and after provocation in 24, 48, 72 hours, that allows to reveal N. gonorrhea.

Treatment is provided in special clinic. Sometimes the patient is treated by the venerologist in ambulatory.

To reveal another sexually transmitted diseases clinical and laboratory examination must be performed. While prescribing medicines the clinical form, complications and severity of the process should be taken into consideration.

The main medicines in gonorrhea treatment are antibiotics. Gonococcal infection very often is accompanied with trichomoniasis, chlamidiasis, candidiasis, mycoplasmosis.

Antibiotics that have influence on the following agents such as: Ciprofloxacin, Doxycyclin, Trobicyn, Sumamed, Cephtriaxon, Afloxacin in combination with Metronidazol, Tiberal, Naxogyn should be prescribed. The dose of antibiotics is taken according to the methodical instructions of the Ukraine МНР and annotation of medicines.

Gonovaccine is used after ineffective antibiotic treatment and relapse in the latent fresh torpid and chronic form of the disease (200-300 mln. of microbe bodies, in 2-3 days intramuscularly). During pregnancy immunotherapy and antibiotics with negative influence on a fetus are not used.

For toilet of external genital organs 0,002% solution of Chlorhexidine, Re-cutan, Baliz-2 are prescribed. Local treatment of chronic gonorrhea is conducted after disappearing of the signs of acute inflammation. In chronic and subacute stages physiotherapeutic methods are used: laser radiation, paraffinotherapy, mud-cure, diathermy, inductothermy, U.H.F-therapy.

The control of the results of treatment: disappearing of subjective signs and microbe agents in all the infected organs and discharge. On the 7-10th day after medical therapy the bacterioscopic and bacteriologic methods are used to confirm the results of treatment. If there is no N. gonorrhea in the material, then the combined provocation is conducted: injection of Gonovaccine (500 mln. of microbe bodies), instillation of 1% Lugol's solution in urethra, 0,5% solution of Argentum Nitrate into cervical canal. Discharge from this organ should be examined during 3 days. Smears are taken during menstruation and then after provocation in 24, 48, 72 hours. Such examinations are provided during 2-3 menstrual cycles. Women which have contacts or work with children are not allowed to work.

Prophylaxis. Using of condom is the most effective prevention method. If the sexual intercourse has happened without it, then the external genital organs should be washed with water and soap, and after urination syringing with 0,05% Chlorhexidin solution should be performed.

Urogenital trichomoniasis

Urogenital trichomoniasis is caused by Trichomonas vaginalis and is a result f their invasion into the lower part of genital tract and urethra.

Ethiology. Trichomonas vaginalis is a flagellate protozoan (fig. 93, 94) and t is transmitted by sexual intercourse. It is not stable in outer environment, dies n few seconds under the influence of antiseptic solutions, in water it dies during 5-45 minutes, and also when they wash hands with soap, it is sensitive to drying, n human organism Trichomonas vaginalis can exist in 3 forms: common one pear-shape form), amebiform with the expressed phagocytosis action (it can ihagocytise mycoplasmas, N. gonorrhea and other bacteria that caused the recur-ence of mycoplasmas or gonorrhea. This is the most spread disease among all he sexually transmitted ones. Its frequency rate reaches 50-70% of sexually ictive women. According to the WHO statistics, 10% of world population suffer rom trichomoniasis. Non-sexual transmission is very seldom: when they use ;ponges, underwear, towels.

Incubation period lasts for 5-15 days, the main places of trichomonas >arasitizing are mucose membranes of vagina, cervical canal, uterus cavity, uterine ubes, Bartholin gland's duct, urethra, urinary bladder.

Inflammatory process develops in the infected mucous membrane: edema, lyperemia, exudation, desquamation affects epithelial cells.

[pic]

Fig. 93. An agent of trichomoniasis — vaginal trichomonas

Clinical manifestations. Vaginitis, urethritis, endocervicitis, proctitis are he most common manifestations, ascendant infection meets rarely.

bodies. Practically they don't cause the infection. Microscopy allows to identify both kinds of bodies. Chlamidia has a complicated antigenic structure. It is very sensitive to disinfectant substances. At 35-37°C during 24-26 hours outcellular Chlamidia become nonvirulent, at temperature 95-1000C they die during 5-10 minutes. In cotton material they can survive up to 2 days at temperature 19-20°C.

The source of infection is the ill person.

Ways of transmission:

* sexual

* intrapartum (passing through the infected birth canal)

* nonsexual way (polluted hands, instruments, underwear, toilet, etc.)

Besides infection of urogenital organs, Chlamidia trachomatis can cause pharyngitis, conjunctivitis, perihepatitis, otitis, pneumonia, other diseases (Rei-ter's syndrome).

Clinical manifestations. Incubational period lasts from 5 to 30 days. The main primary form of chlamidial infection is endocervicitis with mild symptoms or without any. In acute stage purulent or mucopurulent discharge from the cervix, edema and erythema of the vaginal part of the cervix are observed. In chronic stage there is the mucopurulent discharge and pseudoerosion of the cervix.

Chlamidial urethritis can be asymptomatic or it manifests itself by dysuria. There are no specific symptoms for clinical diagnostics of chlamidiasis.

Salpingitis, caused by Chlamidia trachomatis, is characterized by the same symptoms like the process caused by other bacteria.

The sequale of chlamidial salpingitis is infertility.

Diagnosis is based on the history (both partners are ill, there is the infertility). Residual diagnosis is established after revealing chlamidias in the scrap from the cervix and vagina. The most exact are immuno-enzyme and immuno-fluorescent methods.

Treatment. It is necessary to cure the woman and her sexual partner. The woman should avoid sexual intercourses, alcohol, psychical and physical overload.

Medicines from the tetracyclin group are prescribed (Doxycyclin, Rondo-micyn, Morphocyclin), Sumamed, Tarivid, Macrolids (Clacid, Erythromycin).

To prevent candidosis Diflucanum in dose 150 mg is used, Nistatin or Levorin (2.000.000 IU per day during treatment) are prescribed. Fromilid (Clarythro-mycin), an acid-resistant antibiotic from macrolid group is recommended. An important property of this drug is its possibility to cell penetration, that's why Fromilid is 8 times more active, than Erythromycin. It doesn't suppress immune system, activates phagocyto-macrophagal system and some enzymes, that take part in destroying of pathogenic bacterias. The dose of fromilid is 500 mg twice a day during 7-14 days in case of fresh incomplicated chlamidiosis. In chronic forms the treatment course must be elongated till 3-4 weeks.

At urogenital chlamidial infection medicines from ftorchinolon group, Ciprofloxacin (Ciprinol) are used. Ciprinol is prescribed in the dose of 0,5g orally or 0,2g intravenously each 12 hours during 10-14 days. During treatment the ultraviolet irradiation including sun radiation are contraindicated.

Treatment of chlamidiasis demands from the doctor and patient accurate fulfilling of all the indications (dose and duration of the therapy), especially at chronic, long-lasting forms of disease. At the same time accompanying urogenital diseases should be treated. To reduce side effects of antibiotics hepatoprotectors, antioxydants, polivitamins are used.

Urogenital mycoplasmosis

Ethiology. Microbal agents are Mycoplasma hominis, Mycoplasma genita-loum, Ureaplasma urealiticum.

In the etiology of the inflammatory diseases of female genital organs the associaton of mycoplasmosis with trichomoniasis, N. gonorrhea, Chlamidia trachomatis, anaerobes is of great importance.

Mycoplasmas are transmitted sexually and they are highly spread among the population.

Clinic. Mycoplasmas infection can occur in acute and chronic form, and has no symptoms, which are specific for this agent. It is often found in healthy women. Mycoplasmosis is characterized by torpid course, sometimes the latent forms of the reproductive system inflammation are observed. The agents may be activated under the influence of menstruation, oral contraceptives, pregnancy, delivery. Ureaplasma is identified in the patients with vaginitis, cervicitis, urethritis, in association with other bacteria the symptoms are typically and described in the part "Nonspecific inflammatory diseases of the female genital organs".

Diagnosis. To reveal ureaplasmas the bacteriological method is used. Material is taken from the purulent discharge of Bartholin's glands, from uterine tubes at salpingitis, tuboovatian tumors at pelvic inflammatory disease. Test on the urease is done (colour index). It is based on the property of ureaplasms to product urease, that changes the pH and the colour of indicator. Serological diagnosis is also used. Immunogram in diagnosis of mycoplasmosis and other infection (Chlamidia, gonorrhea, trochomoniases, herpes simplex virus) is indicated.

Treatment. Using of antimicrobal medicines from macrolid group (Erythromycin, Sumamed, Roxitromycin), Tetracyclin group (Tetracyclin, Doxycyclin), Fluorochinolones (Ciprofloxacin) is etiotropic treatment. They are prescribed for not less than 10-14 days with the following laboratory control. Another course of treatment is immunity stimulation (Immunoglobulin, Levamizol, T-activin, Ginseng Tincture).

Prophylaxis. Examination of the risk group (prostitutes, women with infertility, inflammatory processes of genital organs), and keeping to the same measures for preventing sexually transmitted diseases are used.

Candidiasis vulvovaginitis (Monilia vaginitis)

Candidiasis is a polyorganic disease, caused by yeast fungi (Candida albicans, C. glabrata, С tropicalis) (fig. 95). It can be transmitted sexually. The most frequent localization is in vagina, vulva, but there can be candidiasis endocervi-citis, endometritis, salpingitis.

Predisposing factors:

[pic]

Fig. 95. An agent of candidiasis — Candida albicans

* endogenous long lasting diseases, such as diabetes mellitus, avitaminosis

* exogenous factors, that predispose fungal colonization and decrease the general reactivity of the organism (long treatment with antibiotics) and local immunity in vaginal mucosa high virulency of Candidas.

There are such kinds ofcandididas vulvovaginitis:

* primary

* antibiotics-induced (as a result of antibiotic treatment)

* as a sequale of changes in different systems of the organism (diabetes, pregnancy, using of estrogens)

On the suppressed immunity of the organism fungi, that were previously saprophites, become pathogenic. They adher to vaginal epithelial cells, causing superficial inflammation and desquamation of vaginal cells. Genital candidiasis mostly doesn't cause a deep damage of mucosa and spreading of the process, but if the agent has high virulence, it can penetrate into intra- and subepithelium parts. In some cases there can be dissemination of candidiasis.

Clinical manifestations: Candidiasis vulvovaginitis is characterized by vulvar itching, pruritus, cottage-cheese-like discharge.

Examination reveals edema and erythema of genital mucos with whitish adherent discharge, that include pseudomicelium of fungi, exfoliated epithelial cells and leukocytes.

Diagnosis. Diagnosis is based on the clinical manifestations, vaginal examination, colposcopy, bacterioscopic and bacteriological methods.

Treatment. Acute form is treated by Orungal 200 mg twice a day during 3 days; at chronic form they use 100 mg twice a day during 6-7 days, then during 3-6 menstrual cycles 1 capsule on the first day of menstrual cycle is taken. High effectiveness is observed while using Diflucan in dose 150 mg per 1 reception, and Gyno-pevaril — one suppository (150 mg) during 3 days. In case of relapse one suppository (50 mg) twice a day for 7 days and application of Gyno-pevaril creme on glans penis during 10 days is recommended. The next step of treatment is normalization of vaginal ecosystem.

Prophylaxis: rational antibiotic treatment with keeping to optional doses and duration of the therapy course, in-time using of antimycotic medicines with the preventive aim. Avoiding of premarriage and extramarital relationships, condom using for preventing fungal colonization of the female genital tract.

Syphilis

Syphilis is an infective disease, that is transmitted sexually.

Etiology. The pathogene is Treponema pallidum. In microscopic examination it has spiral shape and is movable. Optional temperature for reproduction of Treponema is 37°C. It is very sensitive to different external conditions. It dies during boiling, drying, under the influence of different chemical agents and 90% ethanol. While working with the infected persons hands are cleaned with ethanol. It prevents from infection at contact with syphilitic rash having Treponema pallidum on its surface. At 40°C (temperature for keeping blood for transfusion in refrigerator) Treponema pallidum dies in 24 hours.

The source of infection is the infected person.

Ways of transmission:

* sexual perversion (oro-genital, homosexual contacts)

* transplacental — congenital syphilis, when a child is infected by transplacental transmission

* professional — while examining the ill person with wet surfaced rash

* transfusion (very rarely) — as a sequale of blood transfusion from the ill person

Clinical manifestations. 3-4 weeks pass from the moment of agent penetration into organism and till the first manifestations of the disease. This is the so-caled incubational period. The microbe is already in human organism, but there are no complications and signs of the disease.

After finishing of incubational period the first signs appear only in the area of agent inoculation. This is the so-called primary lesion (ulcerated shancre) (fig. 96). It appears as a painless indurated papula on skin or mucos with erosion or necrosis of the surface. Is a hard-based, well-

Fig. 96. Ulcerated shancre of labia major

circumscribed lesion. There is no inflammation around it and it has smooth surface with serous discharge. Its

[pic]

[pic]

size is from several mm to few cm, and it can be coated with whitish discharge like old fat. On mucos of genital organs or anus it is like fissure. Sometimes shancre can gangrenize. Indurative edema belongs to the atypical forms of shancres. Labia major enlarges in size, they are firm and painless. Chancre on pubis, thighs and cervix can occur rarely.

If the shancre is situated on the genital organs, then after nearly 7 days the inguinal lymphatic nodes enlarge on one side (scleradenitis, bubo), rarely on both sides. They are firm, movable, painless. They are not connected with skin and have no suppuration. This is the primary syphilis, that lasts for 6-8 weeks from the appearing of the shancre (the first 3-4 weeks is primary seronegative period, when Wassermann reaction is negative, and next 3-4 weeks, when Wassermann test is positive). Diagnosis in this period is based on the history taking (sexual contact, incubation period, examination of sexual partner, revealing of Treponema pallidum on shancre surface, positive serological reactions (Wasser-mann's, immunofluorescence).

Without identification of the agent or positive serological reactions diagnosis of syphilis is not proved.

After 6-8 weeks of shancre development, the body temperature may rise, there is the night headache, bone pain can appear. This is the so-called/?ro ................
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