Genital Infections




This chapter reviews female genital tract infections in the pediatric and adolescent age groups. An initial review of normal vaginal microenvironment in the prepubertal, pubertal, and postpubertal period is followed by a section on lower genital tract infection in the prepubertal, pubertal, and postpubertal period. This section addresses infections of the external genital area, including vulvovaginitis; infections of the clitoris, urethra, and Bartholin ducts and glands; vulvovaginal lesions; ulcerative and granulomatous disorders; and infections of the cervix. Upper genital tract infections are rare in the prepubertal age group; thus, discussion of pelvic inflammatory disease (PID), tubo-ovarian abscess, and oophoritis, which follows, is predominantly addressed for the postpubertal period. Additional information on the microbes and the specific detailed treatment recommendations can be found in the respective chapters on each pathogen. Genital infections associated with pregnancy are not addressed in this chapter.


General Approach to Evaluation of Prepubertal Child


When genital tract symptoms are present in young girls, the history should include information about the manner and circumstances surrounding the onset of the complaint, the characteristics of any discharge, the duration of symptoms, whether the problem is recurrent, and the nature of any recent treatments or medications. Information should be elicited regarding the use of bubble baths, enuresis, history of atopic dermatitis or allergies, anal pruritus (associated with pinworm infection), recent respiratory or skin infections in family members, and hygienic practices. The possibility that the child may have had or has a systemic disorder affecting the genitalia should be explored.


Sexual abuse also must be considered when a child has a genital infection, regardless of the nature of the infection or the socioeconomic status of the family. This concern is particularly relevant when the child has a sexually transmissible disease. Sexual abuse and infection may occur without penile penetration of the vagina. The history of vaginal or penile discharge in other family members should be ascertained. Behavioral changes, nightmares, fears, abdominal pain, headaches, and enuresis can be indicators of abuse or other psychosocial stressors. The possibility of nonsexual transmission of these diseases often is raised, particularly when a preliminary investigation cannot elicit a history of sexual abuse. Two or three interviews with abused children often are required to enable them to provide informative reports. Forensic interviews by experts in child abuse are essential in these cases.


A general physical examination should precede assessment of the genital tract. The gynecologic examination begins with abdominal inspection and palpation followed by external examination of the perineum and genitalia, including the vulva, urethral meatus, clitoris, hymen, and anus. The examination should be done with the child in the supine, frog-leg position. The labia can be retracted gently to visualize the anterior of the vagina. Speculum and bimanual examinations generally are inappropriate in prepubertal children. Note should be made of structural abnormalities, inflammation, sores and ulcerations, and excoriations. If complaints consist only of vulvitis, and findings on external examination are limited to a scanty mucoid discharge and an erythematous introitus, further examination generally is unnecessary.


If the vaginal discharge is purulent, persistent, or recurrent, a thorough gynecologic assessment is warranted. Visualization of the vagina and cervix without instrumentation is possible with the child in the prone knee-chest position. This method is useful in children older than 2 years. In this position, with labial traction, the vaginal muscles relax and stretch the hymenal membrane open. An otoscope head or a magnifying lens with a good wall light is used to visualize the cervix. Because the vagina of a prepubertal child is short, a foreign body or a lesion may be seen.


A rectal examination may be important when persistent discharge, bleeding, or pelvic or abdominal pain is present. The rectal examination may help express discharge from the vagina that previously was not recognized and can permit palpation of hard foreign bodies or abnormal masses.


Visualization with instrumentation (vaginoscopy) is required in some situations. General anesthesia may be required for girls who are small or unable to cooperate or who may experience significant anxiety or discomfort during the procedure. Conscious sedation for the procedure may be an option in some situations. When a purulent, persistent, or recurrent vaginal discharge is present, samples should be obtained for culture and Gram stain. Wet mount preparations may be useful if fungal infection (potassium hydroxide preparations) or pinworms are suspected. Saline wet mount may be indicated for trichomoniasis if sexual abuse is suspected. Urinalysis with microscopic examination should be performed. A complete blood cell count may be useful when pyogenic infection is suspected or bleeding has occurred.


When cultures are indicated, separate vulvar and vaginal specimens may be necessary. The type and duration of discharge and considerations of potential sexual abuse influence this decision. Vulvar specimens alone may be appropriate when etiologies such as group A streptococci are suspected. Exudates emanating from the vagina in prepubertal girls also are adequate specimens for evaluation for gonorrhea, such that vaginal swabs or aspirates are not required. Further information on types of specimens required for specific sexually transmitted infections (STIs) such as gonorrhea or Chlamydia trachomatis is provided in Chapters 89 (gonorrhea) and 194 ( C. trachomatis ).


Options for obtaining vaginal specimens in young girls, when needed, include use of (1) a nasopharyngeal Dacron swab moistened in nonbactericidal saline, inserted carefully through the hymenal opening; (2) a catheter-within-a-catheter technique ( Fig. 42.1 ) ; or (3) a sterile newborn suction catheter, with insertion 2 to 3 cm into the vagina. For the catheter-within-a-catheter technique, the distal 4 inches of a soft, size 12 bladder catheter and the proximal 4 inches of butterfly needle intravenous tubing are excised from their parent devices by sterile technique. The catheter-within-a-catheter is inserted into the vagina, and fluid is flushed in and out of the upper part of the vagina several times before final aspiration into the syringe and removal of the device.




FIG. 42.1


Assembled catheter-within-a-catheter for obtaining specimens from a prepubertal child.

(From Pokorny SF, Stormer J. A traumatic removal of secretions from the prepubertal vagina. Am J Obstet Gynecol . 1987;156:581.)




Normal Vaginal Flora


The lower female genital tract is colonized by nonpathogenic bacteria from birth. Throughout life, this colonization is dynamic and complex. Even in the pre-microbiome assessment era, a wide range of aerobic and anaerobic species were cultured from asymptomatic girls. The results of several modern but pre-microbiome studies of vaginal flora in childhood are summarized in Table 42.1 . The majority of recent vaginal microbiome data to date has come from studies of adults and older adolescents.



TABLE 42.1

Vaginal Organisms Isolated From Asymptomatic Girls Aged 2 Months to 16 Years








































































































































Organism % a
Coagulase-negative staphylococci 35–73
Diphtheroids 14–78
Streptococcus viridans 13–39
Enterococci 29–62
Group B streptococcus 5–11
Group D streptococcus
Staphylococcus epidermidis
Staphylococcus aureus
Streptococcus pneumoniae
Micrococcus spp.
Gaffkya (Aerococcus) spp.
Lactobacillus spp. 10–39 b
Escherichia coli 12–67
Klebsiella spp. 15–52
Enterobacter spp.
Proteus spp. 3–5
Pseudomonas aeruginosa 5–6.5
Citrobacter spp.
Haemophilus influenzae
Neisseria spp. other than gonococci
Moraxella (Branhamella) catarrhalis
Flavobacterium spp.
Alcaligenes spp.
Acinetobacter spp.
Mycoplasma hominis
Ureaplasma urealyticum
Gardnerella vaginalis c
Peptostreptococcus spp. 29–56
Peptococcus spp. 39–76
Veillonella spp.
Eubacterium spp.
Propionibacterium acnes
Bacteroides fragilis
Bacteroides melaninogenicus
Other Bacteroides spp.
Prevotella spp.
Bifidobacterium spp.
Clostridium perfringens
Other Clostridium spp.
Fusobacterium spp.
Candida spp. 3–18
Other yeasts
Actinomyces spp.

Data from references .

a Percentage range when the organism was isolated from patients in at least two studies. If no range is present, the organism was isolated from 3% to 33% of patients in a single study.


b In one series, 88% of girls were >11 years.


c Isolated in numerous cases without discharge.



The vagina and its microbial flora form an ecosystem that changes over time from infancy to childhood to adolescence and adulthood. The major forces that influence these changes are fluctuations in estrogen levels and the advent of sexual activity. Hygienic practices and medications, including oral contraceptives and antimicrobial agents, also affect the complex interactions among the various flora present in the vagina in terms of persistence, predominance, and overgrowth.


Most girls harbor several organisms in the vagina at any given time. Younger adolescents have a greater prevalence of anaerobic bacteria than do women. From puberty, aerobic colonization increases with age, onset of sexual activity, and parity. Vaginal specimens obtained for culture during anesthesia for elective surgery from 19 healthy girls aged 3 months to 5.7 years yielded a mean of 12 bacterial species. Anaerobes predominated, with a mean of 8.7 species versus 3.4 aerobic species. In a series of 25 asymptomatic girls aged 2 months to 15 years, a mean of 8.7 different species (approximately four aerobes and five anaerobes) per vaginal specimen were detected. Another series of adolescents and young adults aged 13 to 21 years in which only aerobic flora were evaluated noted a mean of approximately three organisms in non–sexually active subjects versus six in sexually active patients. These numbers of culture-detected species are certainly underestimates in most instances. This heterogeneity in vaginal microflora during childhood and adolescence is similar to that found in women.


Gram-negative enteric bacteria and enterococci commonly are encountered in infants and toddlers before completion of toilet training but less frequently thereafter. In children, lactobacilli are present more often in girls younger than 2 years than in older prepubertal girls. Lactobacilli are the predominant flora in most girls by the end of adolescence and may play a protective role in limiting the overgrowth of other flora. The vaginal flora of most healthy women is dominated by one or more Lactobacillus spp., but a substantial minority may harbor other predominant flora, including Atopobium vaginae, Bifidobacterium, Gardnerella, Prevotella, Pseudomonas, or Streptococcus, in the absence of lactobacilli.


Genital mycoplasmas were found in 17% of one series of young girls who were not suspected of having been sexually abused.


Among women of reproductive age, several patterns of vaginal flora have been identified, with variation noted by race/ethnicity. These include a predominance of L. crispatis, L. iners, L. jensenii, and L. vaginalis ; a predominance of L. gasseri and L. vaginalis ; and a predominance of A. vaginae and G. vaginalis with none or few lactobacilli, a more bacterial vaginosis-like pattern. In a study of the vaginal microbiome of 31 healthy premenarcheal girls aged 10 to 12 years, lactobacilli were dominant in most before menarche. G. vaginalis was found in one third of the girls. As observed in adults, the vaginal flora changed over time, including variations in the relative quantities of different lactobacillus species in the same subject. Vulvar microbiota of the premenarcheal girls mirrored their vaginal flora but typically had more bacterial taxa overall.


Microbes that usually behave as commensals sometimes are associated with vulvovaginitis. The difference between colonization and disease is at least partially a function of the magnitude of the replication and the quantity of a given bacterial species. For example, in women with bacterial vaginosis in which G. vaginalis is a predominant microbe, colony counts generally are greater than 10 7 colony-forming units (CFU)/g of vaginal fluid. Asymptomatic colonization with G. vaginalis usually is associated with colony counts of less than 10 5 CFU/g of vaginal fluid. Alteration in the vaginal microenvironment by factors such as poor hygiene, foreign bodies, or hormonal fluctuations results in loss of environmental constraints on bacterial replication and facilitates the overgrowth of one or more commensals.




Lower Genital Tract Infections


This section includes the following topics according to anatomic areas: vulvovaginitis; infections of the clitoris, urethra, and vulvar glands; genital lesions, ulcerations, and granulomatous infections; and cervicitis. Each topic addresses the prepubertal and postpubertal aspects of infections where relevant.


Vulvovaginitis


Prepubertal


Infections and inflammation of the vulva and vagina account for 85% to 90% of all genital problems in prepubertal girls. These conditions are encountered most commonly in children 2 to 7 years old. Infections of the vulva and vagina usually occur together and generally are considered one entity—vulvovaginitis. The various types of vulvovaginitis are differentiated by determining the presence or absence of specific microbial or other agents associated with the inflammation in a particular case. Vulvovaginitis accounts for greater than 80% of cases of recurrent vaginal discharge in prepubertal girls.


Genital discharge does not always indicate infection or inflammation. Most female infants have a grayish white, mucoid discharge from the vagina during the newborn period. This discharge consists of desquamated vaginal mucosa and cervical epithelium that has undergone hypertrophy because of prenatal stimulation by placental and maternal hormones. Microscopic examination of the material reveals masses of large, superficial vaginal epithelial cells ( Fig. 42.2 ). The condition may last for several weeks, is not pathogenic, and does not require treatment.




FIG. 42.2


Cytosmear from the vaginal discharge of a newborn.


Similarly, a pubertal girl nearing menarche may develop a copious viscous, transparent secretion that exudes from the vagina. This normal state sometimes raises concern about possible vaginal infection. The vulvar and vaginal tissues appear thick and moist, a sign of increased estrogen stimulation, without erythema. Microscopic examination of the vaginal fluid reveals masses of estrogenized superficial vaginal epithelial cells and few leukocytes ( Fig. 42.3 ).




FIG. 42.3


Cytosmear from the vaginal secretion of a pubertal girl. Masses of epithelial cells and few bacteria or leukocytes attest.


Genital discharge and perineal or vulvar discomfort are the most common symptoms of vulvovaginitis. The discomfort may range from minor pain or soreness to intense perineal burning or pruritus. Genital erythema is the most common sign in girls, and vulvovaginitis can be found in more than 80% of cases. Visible discharge is present in one third of cases. Infections of the vulva and vagina are more likely to be accompanied by moderate or severe inflammation and prominent discharge than is nonspecific vulvovaginitis. Infection can be present at times, however, with neither discomfort nor discharge.


The characteristics of the discharge frequently do not help identify a specific cause. At the onset of an infection, the discharge is often thick, purulent, and profuse. It may become scanty and seropurulent in later stages of infection. Discharges that are odorless and bloody or serosanguineous may result from noninfectious conditions, such as vulvar irritation, trauma, precocious puberty, urethral prolapse, and tumor. Vulvovaginitis caused by Shigella or group A streptococci also can cause bleeding, as can an eroding foreign body. Foul-smelling discharge suggests a foreign body but also may result from a necrotic tumor. Urinary leakage from an ectopic ureter opening into the genital tract may mimic a vaginal discharge. Specific diagnoses are made more often when symptoms have been present for less than 1 month.


In several series of 80 to 500 prepubertal and pubertal girls up to age 12 with vulvovaginitis and no suspicion of sexual abuse, the most common bacterial isolates were groups A and B streptococci, Staphylococcus aureus, and nontypable Haemophilus influenzae , Escherichia coli, P. mirabilis, and enterococci. Anaerobes were found in more than half of patients in one series. These bacteria, especially group A streptococci, causing vulvovaginitis may lead to more severe symptoms that result in care being sought soon after onset, whereas pathogenic bacteria generally are less likely to be found when girls initially are examined after several weeks of symptoms.


Postpubertal


Infections of the pubertal and postpubertal vulva and vagina produce a variety of overlapping symptoms, including vulvar pruritus, dysuria, and increased or altered vaginal discharge and spotting. As a result, distinguishing among various lower genital tract infections based solely on symptoms is difficult. The history, physical examination, and laboratory tests play an important role in assisting the clinician in differentiating urethritis, vaginitis, and cervicitis.


Nonspecific Vulvovaginitis


Nonspecific vulvovaginitis is a frequently encountered condition in prepubertal girls and is addressed in this section. Nonspecific vaginitis in postpubertal females is called bacterial vaginosis and is addressed in its respective section in this chapter.


Prepubertal.


Nonspecific vulvovaginitis is responsible for 25% to 75% of cases of vulvovaginitis diagnosed in the prepubertal age group in referral centers. In most cases, as noted in Box 42.1 , identifiable secondary factors contribute to nonspecific vulvovaginitis. The presence of specific genital tract bacterial or viral pathogens excludes this diagnosis.



Box 42.1

Etiologic Factors in Premenarcheal Vulvovaginitis


Bacterial Infections





  • Nonspecific mixed infections secondary to:




    • Poor perineal hygiene



    • Foreign body in vagina



    • Respiratory tract infections



    • Skin infections (impetigo)



    • Urinary tract infection




  • Specific nonvenereal infection:




    • Hemolytic streptococci (groups A, B, F)



    • Escherichia coli



    • Shigella flexneri, Shigella sonnei



    • Neisseria meningitidis, Neisseria sicca



    • Haemophilus influenzae type b, nontypeable strains



    • Streptococcus pneumoniae



    • Corynebacterium diphtheriae



    • Yersinia enterocolitica



    • Mycobacterium tuberculosis



    • Moraxella (Branhamella) catarrhalis



    • Staphylococcus aureus




  • Specific venereal infections:




    • Neisseria gonorrhoeae



    • Treponema pallidum



    • Chlamydia trachomatis



    • Chancroid ( Haemophilus ducreyi )



    • Granuloma inguinale




  • Bacterial vaginosis:




    • Gardnerella vaginalis



    • Mobiluncus species




Fungal Infections





  • Candida albicans



  • Other yeasts



  • Dermatophytes



Protozoan and Parasitic Infections





  • Trichomoniasis



  • Amebiasis



  • Enterobius vermicularis



  • Hirudiniasis



  • Schistosomiasis



  • Other parasitic infections (ascariasis, trichuriasis)



Viral Infections





  • Venereal:




    • Herpes simplex



    • Condyloma acuminatum (papillomavirus)



    • Molluscum contagiosum




  • Involvement as part of systemic infection:




    • Measles



    • Varicella



    • Mononucleosis (Epstein-Barr virus)



    • Coxsackievirus



    • Smallpox




Infestations





  • Pediculosis



  • Scabies



Contact Irritation or Allergic Reactions





  • Bubble bath preparations



  • Hair shampoos



  • Vulvar deodorant sprays



  • Soaps, laundry detergents



  • Other medications



Vulvar or Perineal Skin Diseases





  • Local:




    • Seborrhea



    • Lichen sclerosus et atrophicus



    • Lichen planus



    • Lichen simplex chronicus



    • Premalignant leukoplakia



    • Erythrasma ( Corynebacterium minutissimum )



    • Bartholinitis



    • Skenitis




  • Involvement as part of a systemic disorder:




    • Psoriasis



    • Bullous pemphigoid



    • Atopic dermatitis



    • Drug eruption



    • Generalized pruritus with excoriation



    • Chronic liver disease



    • Chronic renal disease



    • Metabolic errors



    • Psychosomatic



    • Crohn disease



    • Sjögren syndrome



    • Henoch-Schönlein purpura



    • Histiocytosis



    • Kawasaki disease



    • Stevens-Johnson syndrome



    • Typhoid



    • Zinc deficiency




Physical Factors





  • Sand (sandbox)



  • Chemical or thermal trauma



  • Physical trauma (accidents, abuse, masturbation)



  • Nylon, rayon underclothing



  • Tight garments (maceration in warm climates)



  • Anatomic abnormalities:




    • Neoplasms (sarcoma botryoides)



    • Polyps



    • Labial agglutination, adhesion



    • Prolapsed urethra



    • Ectopic ureter



    • Rectal fistula



    • Draining pelvic abscess via fistula




Data from references .


Poor hygiene with subsequent overgrowth of a mixed aerobic and anaerobic bacterial flora that are typically nonpathogenic on mucosal surfaces is the most common cause of premenarcheal vulvovaginitis. Contact irritation and allergic reactions induced by soaps, detergents, and medications are frequent causes of vulvovaginitis. Some systemic diseases and focal skin disorders may mimic vulvovaginitis or allow it to develop as a secondary process when these conditions involve the vulvar or perineal tissues. Chronic vulvitis in young girls is often associated with atopic dermatitis or psoriasis. Anatomic abnormalities also may be associated with vulvovaginitis. An increased incidence of vulvovaginitis and urinary tract infections has been reported in girls with high posterior commissures. Drainage from an ectopic ureter into the vagina can cause chronic vulvovaginitis and lead to the formation of a vaginal calculus. Labial adhesions were present in 7% of girls with vulvovaginitis in one series. Box 42.1 outlines the causes of vulvovaginitis in premenarcheal girls.


Several factors other than those listed in Box 42.1 contribute to the occurrence of vulvovaginal infections in young children. The developing immature labia minora and majora flare outward as a young girl squats or sits. As a result, they do not protect the vestibular and vulvar mucosae from contamination, as occurs later in life. The nonestrogenized, prepubertal vulvar and vaginal epithelium, which consists of only a few layers of cells, is traumatized easily and infected readily; however, no evidence suggests that estrogen deficiency is a causative factor in premenarcheal vulvovaginitis. The alkaline vaginal reaction during childhood also is not as resistant to infection as is the acidic vaginal secretion of postmenarchal girls and women.


Vulvovaginitis secondary to poor perineal hygiene.


A vulvovaginal infection is considered secondary to poor perineal hygiene when bacteria native to the lower gastrointestinal tract are found in properly obtained cultures from the vagina. In a large series of cases of vulvovaginitis subjected to culture, E. coli or other coliform organisms were found in 70% of patients in the series. Other studies also have found a higher prevalence of E. coli and other enteric organisms in vaginal cultures from girls with vulvovaginitis than in asymptomatic controls. Reappearance and disappearance of premenarcheal vulvovaginitis secondary to poor perineal hygiene are related directly to the appearance and disappearance of coliform organisms in vulvovaginal cultures. The primary role of vulvar and vaginal contamination with fecal material as a result of inadequate cleansing after defecation is supported by the observation that symptoms resolve in most cases when proper perineal hygiene is the only treatment recommended. In children, 15% to 20% have recurrences, usually 1 month or more after resolution of the initial episode. In most instances, recurrences can be attributed to poor perineal hygiene.


Children with nonspecific vulvovaginitis secondary to poor perineal hygiene do not have any uniform historical findings. On examination, the vulvar mucosa and outer third of the vagina usually are hyperemic with associated scant, light gray, mucoid discharge. Many children wipe themselves from back to front after defecation. In girls, this practice easily results in fecal contamination of the vulvar area. Fecal soiling around the anus or on the perineum or in undergarments can be a clue to the etiology.


Proper cleansing of the perineum and anus after defecation and sitz baths lead to the resolution of symptoms and infection in most cases. Sitz baths (warm water with or without colloidal oatmeal or baking soda) 10 to 15 minutes in duration should be taken 2 to 6 times per day, depending on the severity of the vulvovaginal inflammation. For intense inflammation, wet compresses with Burow solution (1 : 40) or plain water applied every 3 to 4 hours may be used instead of sitz baths. In mild cases, the vulva may be washed twice per day with water or a mild, unscented, nonmedicated soap. Witch hazel pads may be used for cleansing after defecating and to provide mild analgesia.


Loose-fitting clothing should be worn for several days to a few weeks after the symptoms resolve. Continued wearing of such clothing also may be helpful in preventing recurrences of vulvovaginitis, especially in warmer climates. Instructing parents on proper perineal and vulvar cleansing when girls are bathed decreases the likelihood that nonspecific vulvovaginitis will develop. Young girls should be taught proper hygiene and that they should wash their hands before and after urinating and defecating. Shampooing the hair while sitting in a bathtub and using harsh soaps, bubble baths, or other preparations that might lead to chemical irritation of the vulvar skin and vaginal mucosa should be avoided throughout the course of vulvovaginitis. The application of powders should be avoided, at least until the acute symptoms have resolved.


As the inflammation and exudate subside over 1 to 2 days, sitz baths may be reduced in frequency and alternated two to four times per day with the application of either calamine lotion or protective ointments, such as zinc oxide. If pruritus is a significant symptom, an oral agent such as hydroxyzine or diphenhydramine may be administered. Topical application of 1% hydrocortisone cream or triamcinolone acetonide cream may be used as the inflammation resolves but should be avoided in the acute phase.


Patients who do not improve after 2 to 3 days of hygienic measures should be reevaluated. Specimens taken from the vagina should be sent for aerobic and anaerobic bacterial cultures if these were not done initially. Intractable nonspecific vulvovaginal infections that are not caused by foreign bodies, intestinal parasites, or poor perineal hygiene are encountered occasionally. Reducing vaginal pH from an alkaline or neutral to an acid reaction often helps in these difficult cases and may be achieved by the local use of estrogen. Topical estrogens are not recommended for the treatment of routine cases of premenarcheal vulvovaginitis because the results do not seem to be superior to nonhormonal therapies in these cases, and prolonged administration may cause isosexual pseudoprecocity. After 7 to 10 days, the vulvar and vaginal tissues usually thicken, and a mucoid vaginal secretion may appear.


Oral or parenteral antibiotics may be indicated if symptoms persist for 2 to 3 weeks or if a specific pathogen that requires antibiotic treatment is isolated. When possible, selection of antibiotic agents and the route of administration should be based on susceptibility testing of organisms isolated from vaginal cultures. Nonspecific vulvovaginal infections generally are benign, superficial, localized mucosal inflammations that usually respond to less potent chemotherapeutic agents when these are needed.


Vulvovaginitis secondary to intestinal parasites.


Pinworms (Enterobius vermicularis) are the causative factor in many cases of recurrent or intractable nonspecific vulvovaginitis in children. Infection occurs when the worms in the lower bowel crawl out of the anus onto the perineum and migrate into the vagina, where they deposit ova. The pinworms may carry E. coli and other coliform bacteria into the vagina, which may lead to vulvovaginitis.


Pinworm ova may be deposited in playground soil, on toys or books, and on the hands of infected individuals. Infection frequently is asymptomatic. A child with a pinworm infection and vulvovaginitis usually has a history of a chronic vaginal discharge that has recurred despite repeated attempts to eradicate it. Parents may note worms on the perineum of the child and that she awakens at night because of perineal itching.


Examination reveals a low-grade inflammation of the vulva and vagina. Excoriations from scratching may be seen on the perineum. Vaginoscopy (if indicated) shows an inflammatory reaction extending to, but not including, the cervix. Vaginal cultures produce a mixed growth of nonpathogenic bacteria, with E. coli and other coliform bacteria generally predominating.


The diagnosis depends on finding pinworm ova on smears from the perineum or in the vaginal discharge or a report from parents that worms are visible on the child’s perianal skin. A perineal smear is most likely to show the presence of pinworms, but pinworm ova of E. vermicularis may be detected in a wet smear of vaginal secretions (pinworms, Fig. 42.4 ).




FIG. 42.4


Pinworm ova discovered in a vaginal smear from a child with intractable vulvovaginitis.


The adhesive tape test can be performed in the office or the parent asked to collect three specimens at night. The parent is given a wooden tongue blade or paddle with adhesive tape and a glass microscopic slide ( Fig. 42.5 ). The adhesive side is applied firmly to several areas around the anus. It is removed and applied, adhesive side down, to the glass slide, which is sent to the laboratory for examination.




FIG. 42.5


Technique for obtaining a perianal smear for detection of pinworm ova, using adhesive tape and a tongue depressor.


Treatment consists of eradicating the pinworms. All members of the family are presumed to be infected and should be treated. Recommended treatment regimens are mebendazole 100 mg orally; albendazole 400 mg orally; or pyrantel pamoate 11 mg/kg base, not to exceed 1 g. Each is given in a single dose and repeated in 2 weeks. The vulvovaginitis caused by coliform organisms carried on pinworms is treated the same as in other cases of nonspecific vulvovaginitis caused by poor perineal hygiene (see earlier discussion).


Vulvovaginitis secondary to vaginal foreign bodies.


Foreign bodies account for approximately 4% of cases of vaginal discharge in premenarcheal girls. When a foreign body remains in the vagina for some time, it inevitably causes nonspecific vulvovaginitis. Many types of vaginal foreign bodies, including safety pins, glass beads, coins, beans, bits of crayon, and parts of toys, have been reported. The most common objects are bits of toilet paper or shreds of cloth from nightclothes or bedding ( Fig. 42.6 ).




FIG. 42.6


Bits of paper or cloth are the vaginal foreign bodies most frequently found in children.


The history does not contribute to the diagnosis unless the child is known to have previously put objects in her vagina. The child usually is brought to a physician because of a profuse, foul-smelling, sometimes blood-tinged discharge. The presence of such a discharge is almost pathognomonic for the presence of a foreign body. Even without a profuse discharge or bleeding, a foul odor from the vagina suggests a foreign body. In addition a foreign body should be suspected when a recurrent discharge is reported.


Examination reveals inflammation of the vulvar and vaginal mucosa. Soft foreign bodies, such as toilet paper, can be flushed out of the vaginal canal. Although foreign material may be seen when the labia are separated, a vaginoscopy may also be necessary to explore the full length of the vagina. A topic anesthetic agent such as xylocaine jelly can be helpful in such situations. Rarely a metallic object that has been in the vagina for some time erodes the mucosa and becomes hidden in granulation tissue. When such a condition is suspected, a radiograph should be obtained. Most foreign bodies, such as glass, plastics, paper, or cloth, are not radiopaque, however, and radiographic examination fails to detect the foreign material. An examination under anesthesia may also be necessary when a larger foreign body has to be extracted.


The nonspecific vulvovaginitis caused by a foreign body disappears gradually after removal. Recovery can be hastened by using the hygienic treatments previously described. Repeat episodes are common.


Specific Non–Sexually Transmitted Vulvovaginitis


Vulvovaginitis secondary to respiratory pathogens


Streptococcus pyogenes (group A Streptococcus ) vulvovaginitis.


Streptococcus pyogenes is a frequent cause of vulvovaginitis in premenarcheal girls and accounted for 9% to 20% of cases in several series. Most cases occur in girls aged 2 to 7 years, but cases in infants and teenagers have been reported. Group B and group F streptococci also have been isolated from girls with acute vulvovaginitis. A marked seasonal variation in incidence in some geographic regions, with peak rates occurring in late fall and winter, may explain the low number of cases of vulvovaginitis caused by S. pyogenes in some series. The nasopharynx seems to be the primary reservoir for S. pyogenes in these girls. Infection may occur from self-inoculation by hand to nose to the vulvovaginal area. The skin also may serve as the source of S. pyogenes vulvovaginitis. Preceding or concurrent symptoms of upper respiratory tract infection are uncommon findings, but many girls with vulvovaginitis have throat cultures positive for S. pyogenes . Perineal symptoms have preceded pharyngeal symptoms in some patients. S. pyogenes vulvovaginitis may occur during the course of scarlet fever.


The signs and symptoms of S. pyogenes vulvovaginitis often overlap those caused by other bacterial infections, but symptoms usually are abrupt in onset. Most patients seek medical care within 1 week of onset. Vaginal discharge and dysuria are the most common complaints. These girls usually are afebrile. Localized tenderness and an intense, fiery red erythema of the vulvar tissues are frequent findings, but some cases have only mild erythema. Pruritus and excoriation may be present. The discharge usually is seropurulent but may be serosanguineous. The color may be white or green. Petechiae may be present on the vaginal mucosa, and regional papular or scarlatiniform rashes can occur. Acute poststreptococcal glomerulonephritis has been reported in association with S. pyogenes . Labial abscesses caused by S. pyogenes have been noted rarely in prepubertal girls.


Concomitant streptococcal proctitis and perianal skin infections have been reported. Perianal pruritus, erythema, and tenderness are common findings. The diagnosis of S. pyogenes infection may be missed if vaginal secretions are not plated onto sheep blood agar or other media that readily support the growth of streptococci. The vulvovaginitis caused by group A streptococci usually shows initial response to oral antimicrobial therapy within 24 hours. A 10-day course of oral penicillin or amoxicillin is sufficient. A cephalosporin can be prescribed when a child has a nonanaphylactic penicillin allergy. For type 1 hypersensitivity, clindamycin 30 mg/kg per day in three divided doses for 10 days can be administered. Alternative medications are erythromycin or azithromycin. A second course sometimes is necessary when perianal disease is present. Adjunctive use of the hygienic measures discussed for nonspecific vulvovaginitis hastens clinical improvement.


Vulvovaginitis secondary to other nasopharyngeal bacteria.


Often a history of an upper respiratory tract infection precedes the onset of vulvovaginitis by a few days. Suspicion that the two conditions are related is strengthened when vaginal cultures yield organisms that commonly colonize the nasopharynx. Vulvovaginitis is assumed to result from autoinoculation of microbes from the nasopharynx to the genitalia. The onset of vulvovaginal symptoms in these infections tends to be acute, the inflammation and discomfort marked, and the discharge less profuse and less purulent than in nonspecific vulvovaginitis.


H. influenzae and S. aureus are the species isolated most frequently from cultures. Streptococcus pneumoniae and Neisseria meningitidis are seen occasionally, and Moraxella catarrhalis has been isolated as well. Labial abscesses caused by S. aureus have been described in prepubertal girls. However, vulvovaginitis caused by S. aureus in prepubertal girls has not been reported in connection with toxic shock syndrome. H. influenzae was the organism isolated most frequently in a series of 200 girls with vulvovaginitis. Acute and chronic cases of H. influenzae vulvovaginitis do occur, and the discharge usually is mucoid or mucopurulent, yellow, and odorless. Vulvovaginitis can be caused by H. influenzae serotypes a, b, and c and by nontypeable strains. Concurrent otitis media or urinary tract infection may be present. All three of these species occasionally are found in vaginal cultures from asymptomatic children. Their isolation in pure culture from symptomatic girls is what leads to the clinical conclusion of cause and effect. One Kenyan study in toddlers has shown no change in the prevalence of H. influenzae in the nasopharynx after H. influenzae vaccine, thus indicating that this organism should continue to be suspected as a cause of vulvovaginitis. Vulvovaginitis caused by S. aureus in prepubertal girls has not been reported in connection with toxic shock syndrome. Labial abscesses caused by S. aureus have been described in prepubertal girls.


Neisseria meningitidis is an uncommon cause of vulvovaginitis, but the last reports were in the early 1970s. These gram-negative intracellular and extracellular diplococci resemble Neisseria gonorrhoeae on stained smears. Moraxella catarrhalis also is identical on Gram stain. Gram-negative diplococci should be speciated completely by the microbiology laboratory to avoid misidentifying nongonococcal diplococci as gonococci and vice versa. Especially for pediatric patients, misidentification can result in serious medicolegal consequences for the family when unwarranted intervention is initiated, or it can result in failure to protect the child’s welfare when appropriate measures are deemed unnecessary.


Diphtheritic vulvovaginitis can be the primary site of infection, but most reported cases have been secondary to nasopharyngeal infection. Although diphtheria seldom occurs today, sporadic cases occasionally appear in areas where immunization coverage is inadequate. The vulva is the most common genital site involved in diphtheria, but diphtheritic lesions may occur in the vagina without vulvar involvement. The diagnosis is suspected when a child has the severe systemic symptoms produced by upper respiratory tract diphtheria and a local ulceration covered by a gray adherent membrane; it is confirmed by finding Corynebacterium diphtheriae in discharge from the lesion.


Vulvovaginitis caused by H. influenzae, S. aureus, and other nasopharyngeal organisms often resolves with hygiene measures alone (as described earlier for nonspecific vulvovaginitis secondary to poor perineal hygiene). Systemic antibiotics may be required for persistent cases or may be helpful early in severely symptomatic cases. The choice of agent depends on the anticipated or known antimicrobial susceptibilities of the specific organism.


Treatment of N. meningitidis vulvovaginitis, once the organism is isolated, is the same as for N. gonorrhoeae. The organism may not be resistant to penicillin, but decreased susceptibility has been reported. Although data are unavailable, a single dose of ceftriaxone probably should be as effective as it is for gonorrhea, pending cultures. Chemoprophylaxis, generally with rifampin, should be considered for family members and other contacts in cases of meningococcal vulvovaginitis.


Treatment of diphtheria is the same regardless of the site of the infection and is discussed in Chapter 90 .


Vulvovaginitis secondary to specific enteric pathogens.


Shigella spp., mainly Shigella flexneri and Shigella sonnei, seem to account for most of these cases. Vaginal discharge without pain, pruritus, or dysuria is the most frequent manifestation of Shigella vulvovaginitis. The course can be acute, but discharge that persists for 4 weeks to several months before the diagnosis is made is common. Bloody discharge has been observed in approximately half the cases reported from developed countries, but it was not seen in any of 27 girls with Shigella vulvovaginitis in Rwanda between 1988 and 1991. The discharge may be purulent and heavy; occasionally it is absent. The vulvar tissues usually appear inflamed.


In most instances, Shigella vulvovaginitis is not associated with current or recent diarrhea. Local application of triple-sulfa cream (Sultrin) may clear the infection in some cases. Refractory cases have been described, however, and systemic treatment with an antibiotic to which the Shigella isolate is susceptible is recommended. Trimethoprim-sulfamethoxazole and cefixime are reasonable choices for susceptible isolates; however, most Shigella isolates are resistant to ampicillin and trimethoprim-sulfamethoxazole. Ciprofloxacin and ceftriaxone are also effective treatment options. As with other causes of vulvovaginitis, adjunctive use of hygienic measures may help resolve the process and prevent recurrence.


One case of vulvovaginitis with Yersinia enterocolitica isolated as the predominant organism was reported in a 4-year-old girl who also had a positive stool culture and associated fever and abdominal pain but no diarrhea. In other members of the community in which she lived diarrhea developed with cultures positive for Y. enterocolitica. The outbreak was linked to contaminated food. Infections with this organism may be missed because special culture techniques are required for isolation.


Rarely ulcerative vulvovaginitis caused by Entamoeba histolytica or related to typhoid fever has been reported. Generally specific genital infections with pathogenic organisms usually found in the gastrointestinal tract are the result of fecal contamination of the vulva and vagina. Treatment of infections caused by E. histolytica is described in Chapter 210 .


Vulvovaginitis secondary to skin infections.


Similar to a child with an upper respiratory tract infection, a child with impetigo or an infected superficial wound may transmit bacteria from the wound to the genitalia by hand contamination. Cultures in such cases usually yield hemolytic streptococci or S. aureus . Treatment is the same as that described for nonspecific vulvovaginitis secondary to respiratory tract infections.


Mycotic (fungal) vulvovaginitis


Prepubertal.


The role of Candida spp. as a causative agent of vulvovaginitis in healthy prepubertal children has been controversial. While diaper dermatitis with Candida spp. colonization or secondary infection is common in infants, co-occurrence with vulvovaginitis is unusual.


Candida vulvovaginitis is rare in prepubertal children and is more likely to occur in girls starting with pubertal development.


Risk factors for developing recurrent and persistent fungal vulvovaginitis in prepubertal children include a history of recent antibiotic use, uncontrolled diabetes mellitus, or immunosuppression. Mycotic infections are not considered STIs.


A study in Turkey among children 8 to 12 years of age with type 1 diabetes mellitus Candida spp. was reported in 50% of vaginal specimens; C. albicans in 50%, C. glabrata in 37%, and other Candida spp. in 13% ( C. dubliniensis, C. krusei ). A higher prevalence rate of Candida spp. was reported in postpubertal versus prepubertal children; 30% versus 6%.


Mycotic vulvovaginitis in prepubertal children, when it does occur, usually causes severe persistent and/or recurrent episodes of vulvar and vaginal itching. When a discharge is present it is white, thick, and curdled and has a yeasty sour odor. The patient may have pain during and after voiding or external dysuria as a result of urine coming in contact with excoriated areas on the urethra and vulva ( Fig. 42.7 ).




FIG. 42.7


Mycotic vulvovaginitis. The child had diabetes.


Postpubertal.


Prevalence studies of Candida spp. in asymptomatic and symptomatic postpubertal adolescent females are few. In 198 adolescents 15 to 19 years of age at a sexually transmitted disease clinic in the northwestern United States, 30% were positive for C. albicans . In another study of 200 sexually active adolescents (mean age, 19 years) at an adolescent health center in Sweden, a history of vulvovaginal candidiasis was reported at least once by 60% and recurrent candidiasis (at least three or more episodes) by 22%. C. albicans was isolated by culture in 43% and C. glabrata in 3 adolescents; 15% of adolescents with culture positive for Candida spp. were asymptomatic. Several factors play roles in causing the increased incidence of vaginal candidiasis after menarche: menstruation, oral-genital sex, fecal contamination of the vulva, wearing tight-fitting underclothes, widespread use of antibiotics, and the use of oral contraceptives. Other predisposing factors include pregnancy, obesity, uncontrolled diabetes mellitus, immunosuppressive therapy, and illicit drug addiction. Candida vulvovaginitis can occur concomitantly in sexually active adolescents.


Mycotic vulvovaginitis in the postpubertal period causes severe vulvar and vaginal itching and external dysuria. The discharge is white, thick, and curdled and has a sour odor. Sexually active adolescents can report painful sexual intercourse. Examination in the acute stage reveals intense inflammation of the vulva and vagina with shiny and beefy red mucosa with linear excoriations and edema. Long-standing infection can cause lichenification and hyperpigmentation of the perineal skin. Vaginal pH usually is less than 4.5.


Diagnosis.


The diagnosis in all age groups is frequently based on clinical findings. It can be established by finding hyphae and buds of the fungus in vaginal fluid by a vaginal saline wet preparation under microscopy ( Fig. 42.8 ). If debris and cellular material render identifying the fungus difficult, a smear using 10% potassium hydroxide solution is helpful. The potassium hydroxide solution dissolves other extraneous material without affecting the fungus. Even with an experienced microscopist, this method yields a sensitivity range of 40% to 86% in symptomatic girls; however, the yield may be only 40%. Further confirmation can be obtained by identifying fungus by culture of material from the vagina or vulva on Sabouraud or Nickerson media and is helpful in recurrent candida vulvovaginitis. Culture remains the gold standard. Nucleic acid amplification tests for Candida spp. have not been cleared by the U.S. Food and Drug Administration (FDA). In sexually active adolescents, testing for Chlamydia and gonorrhea infection should be considered.




FIG. 42.8


Hyphae of Candida albicans discovered on a wet smear of vaginal discharge.


Treatment.


Antifungal creams have no place in the initial treatment of vulvovaginitis in prepubertal females unless budding hyphae are seen on microscopy of vaginal fluid. Numerous antifungal creams are available, and the topical azole creams including miconazole, clotrimazole, or terconazole are more effective than nystatin. The creams should be applied as prescribed to the affected area after cleansing.


Curing fungal infections often is difficult in prepubertal children who receive repeated courses of antibiotic therapy or with systemic risk factors for Candida vulvovaginitis. Fluconazole (Diflucan) can be administered as a one-time oral dose.


In adolescents a variety of azoles are available as over-the-counter vaginal creams, tablets, and coated tampons. A short course of a single-dose or 3-day regimen is appropriate for an uncomplicated vaginitis. Intravaginal creams or suppositories and oral tablets (prescription) are equally effective. Over-the-counter intravaginal creams include clotrimazole (1% daily for 7 days or 2% daily for 3 days) or miconazole (2% daily for 7 days or 4% daily for 3 days) or terconazole (0.4% daily for 7 days or 0.8% daily for 3 days) or ticonazole (6.5% single application). Over-the-counter intravaginal suppositories include terconazole 80 mg daily for 3 days, miconazole 100 mg daily for 7 days, 200 mg daily for 3 days, or 1200 mg one suppository for 1 day. The cure rate with intravaginal treatment is up to 90%. Oral fluconazole 150 mg as a single dose is an effective preparation for the treatment of uncomplicated vulvovaginal candidiasis. If recurrent unexplainable or resistant infection occurs in children and adolescents, diabetes mellitus should be suspected.




Specific Sexually Transmitted Vulvovaginitis


Specific sexually transmitted vulvovaginitis in this section includes discussion of gonorrhea and chlamydia in prepubertal girls and trichomoniasis and bacterial vaginosis in prepubertal and postpubertal females. Gonorrhea and Chlamydia infections in postpubertal period females cause cervicitis instead of vulvovaginitis and are addressed under the discussion of cervicitis.


Gonorrhea


Prepubertal


Gonococcal infections of the prepubertal genital tract are manifested as vulvovaginitis. The alkaline environment of the unestrogenized vaginal tissues of young girls apparently limits spread of infection to the upper genital tract. Gonorrhea is found less commonly in children now than in the past but must be considered whenever a girl has vulvovaginitis.


In infants, perinatal nonsexual transmission is considered the most likely cause of gonococcal infection. In 1965, Branch and Paxton reported that, in 1- to 11-month-old infants, all the mothers were found to have gonococcal infection and no history of sexual contact could be elicited. The authors concluded that transmission of the infection was perinatal from freshly contaminated hands or through fomites. They also reported that 93% of children aged 1 to 9 years with gonorrhea had sexual contact with relatives in the household.


N. gonorrhoeae has been shown to survive for 20 to 24 hours in infected secretions on towels and handkerchiefs. Although N. gonorrhoeae has survived on toilet seats for 2 hours, no gonococci were recovered from toilet seats in public restrooms or in a clinic for STIs. Nonsexual transmission to adults is rare.


Prepubertal children with gonococcal infection frequently are found to have a history of sexual contact. The rate of eliciting a history of sexual contact in prepubertal children with gonorrhea ranges from 36% to 93%. Ingram and colleagues found that 35% of 1- to 4-year-old children and 100% of children older than 4 years with gonorrhea reported having sexual contact with an older male family member. Folland and coworkers elicited a history of sexual contact from 34% of children with gonococcal urethritis and vaginitis.


Testing of household members in an infected child’s environment can detect infected adults at a rate of 18% to 29%. In a retrospective study of 14 Native Alaskan children with gonococcal infection, 3 reported having sexual contact. Seven children slept with their parents, one or both of whom had gonorrhea; the authors assumed that these children acquired the infection by nonsexual means. Nonsexual transmission conceivably occurs in children who sleep and bathe with their parents.


N. gonorrhoeae was the most common cause of vulvovaginal discharge among prepubertal girls in Rwanda in the late 1980s. Sexual contact was considered likely in all cases because of a cultural belief that a man with a purulent urethral discharge could be cured by rubbing his penis on the external genitalia of a prepubertal girl. In a prospective study of girls 12 months to 12 years of age in the mid-1990s in Cincinnati, Ohio, who had vaginal discharge and no suspicion of sexual abuse, 4 of 43 had positive cultures for N. gonorrhoeae . Such cases should lead to investigation for probable sexual abuse.


In summary, sexual transmission is the more common and most likely mode of transmission, and the presence of gonorrhea should be considered diagnostic of sexual abuse. Thus an investigation for sexual abuse must be pursued in a child with gonorrhea by reporting the case to the appropriate legal authority.


The acute stage of gonorrheal vulvovaginitis is characterized by inflammation and a purulent discharge. The child may complain of vulvar discomfort, dysuria, frequent urination, and pain on walking. The child usually is well otherwise. Asymptomatic vaginal infection is rare. On examination, the vulvar tissues are edematous, hyperemic, and covered by a profuse, thick, yellowish discharge that exudes from the vagina. The entire vaginal mucosa is inflamed.


The urethra, paraurethral glands, and major vestibular (Bartholin) glands rarely are involved in a premenarcheal gonorrheal infection. Vulvovaginal infections, including gonorrhea, in prepubertal children rarely if ever affect the upper genitalia (uterus, uterine tubes, ovaries, or pelvic peritoneum). Symptoms suggestive of pelvic peritonitis have been reported in premenarcheal children who had gonorrheal vulvovaginitis; all the patients recovered promptly after the administration of penicillin.


Diagnosis


The diagnosis of gonorrheal vulvovaginitis and its differentiation from other types of vulvovaginitis are established by vaginal cultures. Gram stain of a vaginal specimen is not an appropriate diagnostic test. Specimens from the pharynx and rectum to test for N. gonorrhoeae also should be obtained. Cervical specimens are not recommended from prepubertal girls. Because of the potential medicolegal use of the test results for N. gonorrhoeae among children, standard culture systems should be used for the diagnosis of N. gonorrhoeae in children. Nucleic amplification testing for gonorrhea using urine and vaginal swabs was conducted in 485 premenarcheal girls with alleged sexual abuse from four cities in the United States. The sensitivity of urine nucleic acid amplification testing (NAAT) for gonorrhea relative to vaginal swabs was 100%. The Centers for Disease Control and Prevention (CDC) states that consultation with an expert is necessary prior to obtaining a NAAT test to minimize cross-reactivity with other Neisseria spp. and to assure correct interpretation of positive results.


Treatment


The presence of gram-negative intracellular diplococci in vaginal smears from a child with a history of exposure or with typical clinical findings is sufficient reason to start treatment, but it does not establish a definitive diagnosis. Further details on treatment are addressed in Chapter 89 .


Chlamydia


Prepubertal


Although C. trachomatis appears to be an uncommon cause of vaginitis in prepubertal girls, vaginal infection with C. trachomatis can occur in children. In contrast to prepubertal gonorrhea infections, chlamydial vaginitis in children often seems to be asymptomatic. Although coinfection with C. trachomatis has not been studied well in prepubertal children, experience from adult populations has shown that it should be suspected in children with N. gonorrhoeae infection. In one study in prepubertal girls, 30% with N. gonorrhoeae also tested positive for C. trachomatis.


Perinatally acquired genital Chlamydia infection is a strong possibility in children younger than 1 year. C. trachomatis has been isolated from the conjunctiva, nasopharynx, vagina, and rectum of infants born to infected mothers. Subclinical infections have been reported in 14% of infants of mothers with active C. trachomatis infection. However, perinatal transmission is possible in children up to 3 years of age. This may be due to persistence of perinatal infection. Infants infected with C. trachomatis at birth have remained infected for up to 372 days in the vagina; 383 days in the rectum; and 866 days in the conjunctiva, nasopharynx, and oropharynx. Thus persistent chlamydial infection of the pharynx in infants can persist for 2 years. Persistence of perinatal infection for 18 months and for 6 years has been reported in other studies as well.


Studies of C. trachomatis infection in prepubertal girls have involved mostly children being evaluated for sexual abuse or vulvovaginal symptoms, or both, and some have included a control group in an attempt to control for either a history of sexual abuse or vaginal symptoms.


The variation in rates among studies may reflect differences in the prevalence of C. trachomatis in different communities. The highest rates of C. trachomatis infection were seen in a Los Angeles study, in which 47 prepubertal girls were examined for alleged sexual abuse and 17% had vaginal C. trachomatis . In other studies evaluating children suspected of being sexually abused, rates of recovery (pharyngeal and rectal infection included) tend to be higher (6–8%) than those seen in children with vaginitis or controls (0–2%). Initial evaluations of children presenting with vaginitis or in the control groups may not elicit a history of sexual abuse, but further questioning or testing of all orifices (pharyngeal and rectal) may elicit suspicion or a history of sexual abuse. For example, a history of sexual abuse was discovered in two control children only after C. trachomatis was identified. Initially, 2% of children with a history of sexual abuse versus 4% of healthy controls had positive vaginal cultures for C. trachomatis . On further questioning, however, the two children in the control group with C. trachomatis were siblings who were sexually abused 3 years earlier, increasing the rate of C. trachomatis vaginal infection in the sexual abuse group to 6% and decreasing the rate in the control group to zero. This report illustrates the importance of thoroughly investigating the possibility of sexual abuse whenever a sexually transmitted pathogen is isolated in a young child.


In studies evaluating premenarcheal children presenting with vulvovaginitis, recovery of C. trachomatis has been low in children with symptoms and healthy control groups. In one study, none of the 35 children with symptoms had C. trachomatis, whereas 1 of 35 without symptoms had C. trachomatis isolated. In another study conducted in a pediatric gynecology clinic, 4 of 29 (14%) premenarcheal girls were found to have C. trachomatis. All four had a homogeneous white discharge, and one had a bloody discharge. Sexual abuse occurred in two of the children and was considered possible in another. In a Cincinnati study evaluating vaginitis in girls younger than 12 years in whom sexual abuse was not suspected, none of the 87 children had a positive culture for C. trachomatis. Similarly, in a smaller study of 11 girls with vaginitis, none was found to have C. trachomatis.


In summary, although persistence of perinatal infection can occur, when C. trachomatis is identified in vaginal specimens, sexual abuse as a potential mode of transmission of C. trachomatis infection should be considered in children older than 1 year. There are no data demonstrating survival of C. trachomatis on fomites or its coexistence in family members of infected children. Thus an investigation for sexual abuse must be pursued in a child with Chlamydia infection by reporting the case to the appropriate legal authority.


Diagnosis


Numerous diagnostic methods for Chlamydia are available. Direct tissue culture isolation of C. trachomatis remains the gold standard and is the only test that should be used in prepubertal children or in cases in which sexual abuse is under consideration. Culturing for Chlamydia requires isolation of the organism in tissue culture and confirmation of the characteristic intracytoplasmic inclusions by fluorescent monoclonal antibody staining. Although the specificity of tissue culture approaches 100%, tissue culture is only 70% to 85% sensitive in contrast to DNA amplification techniques. The low recovery rate in studies of prepubertal children may be due to the low sensitivity of tissue culture or the use of vaginal cultures in young children. Isolation rates from the vagina usually are lower than rates of recovery from the endocervix.


Nonculture tests for Chlamydia, including enzyme immunoassays, direct fluorescent antibody tests, DNA hybridization, and DNA amplification tests, have not been field tested for large numbers of vaginal specimens or rectal or pharyngeal specimens from premenarcheal girls. False-positive results have been reported in vaginal specimens for some of these tests in children, and these tests should not be used in premenarcheal children. False-positive results probably are caused by cross-reactivity with common anogenital organisms, such as group A and B streptococci , N. gonorrhoeae, G. vaginalis, E. coli, and Proteus, Acinetobacter, and Staphylococcus spp.


However, more recently, NAAT for C. trachomatis using urine and vaginal swabs was conducted in 485 premenarcheal girls with alleged sexual abuse from four cities in the United States. The sensitivity of urine NAAT for Chlamydia relative to vaginal swabs was 100%. The CDC states that consultation with an expert is necessary prior to obtaining a NAAT test to assure correct interpretation of a positive result.


Treatment


Treatment for Chlamydia infection is addressed in Chapter 194 .


Trichomoniasis


Trichomonas vaginalis is a triflagellated protozoan ( Fig. 42.9 ). The organism, which is larger than a polymorphonuclear leukocyte, has a distinctive vibrating or whiplike movement when seen microscopically in fresh wet smears taken from the vagina. It quickly succumbs to reduction of the pH, drying, cooling, and changing the osmotic pressure of the fluid surrounding it. Most infections are encountered in sexually active adolescents and young adult women. Chapter 215 addresses trichomoniasis, including epidemiology, in more detail.




FIG. 42.9


Trichomonas vaginalis is a triflagellated protozoan that, when motile, is identified easily in wet smears of vaginal discharge.


Prepubertal


Vaginal trichomoniasis is reported infrequently in prepubertal children. This low prevalence may be accurate or could be due to lack of appropriate testing or limitations of the diagnostic techniques used in studies in prepubertal children.


Trichomoniasis in newborns has been described in several case reports through the acquisition of T. vaginalis from the mother’s vagina during delivery, with recovery of T. vaginalis from urine, vaginal, and respiratory tract specimens. The prevalence of T. vaginalis in healthy, vaginally delivered infants of mothers with T. vaginalis is unknown. In one study of 868 infants, T. vaginalis could not be identified in any of the 14 female infants of mothers in whom T. vaginalis was diagnosed. The overall prevalence of T. vaginalis was 4%, but the denominator of mothers of female infants was not described. In another study of 984 female infants, direct smear or culture (or both) of infant vaginal specimens identified three infants with T. vaginalis, a prevalence of 0.3%. Of the three infants, two had a vaginal discharge. The overall prevalence of infection in the mothers of the 984 infants was not reported. Of the three infants with T. vaginalis, one mother had a history of vaginal discharge and a negative direct smear for T. vaginalis, and the other two mothers had no history of T. vaginalis. In conclusion, transmission of T. vaginalis in infants aged 1 year probably is perinatal.


The mode of transmission in children older than 1 year is controversial. Numerous reports confirm the occurrence of T. vaginalis in prepubertal girls evaluated for vaginitis but no history of sexual abuse with prevalence rates ranging from 0% to 4%. In studies with a healthy control population, T. vaginalis was not identified in any of the children in the asymptomatic control group.


A case report in 1985 described T. vaginalis in two sexually abused children with vaginal discharge ; however, in studies systematically evaluating children for sexual abuse regardless of symptoms, T. vaginalis has not been recovered. In an Australian study evaluating 160 children younger than 10 years and 95 healthy age-matched controls, none of the children had T. vaginalis isolated from vaginal cultures. Similarly, none of the 119 prepubertal girls evaluated for sexual abuse in a Cincinnati, Ohio, study had T. vaginalis identified by urinalysis or wet mount of vaginal secretions. Without additional studies using culture techniques and conducted in diverse populations of prepubertal girls, determining the true prevalence of T. vaginalis in prepubertal girls who have vaginitis, with or without a history of sexual abuse, is difficult.


Nonsexual transmission within a family without sexual abuse or contact can conceivably occur. In a case report, T. vaginalis was diagnosed in the mother, and her three prepubertal daughters were symptomatic with a vaginal discharge. Two of the three girls had T. vaginalis identified on wet-mount evaluation of their vaginal specimens. They had no history or evidence of sexual abuse, the father was asymptomatic, and microscopy of an early morning urine specimen was negative for T. vaginalis.


A study from Poland found one case of T. vaginalis infection in children aged 2 to 7 years and a significantly higher number of cases in 8- to 10-year-old girls. The numbers increased even further for children older than 10 years, suggesting a strong association between T. vaginalis and the presence of an estrogenic environment, which promotes glycogen production and decreases vaginal pH.


The Polish investigation tested families of women infected with T. vaginalis and found that almost a third of their sexual partners and 8% of the children (mostly girls) had T. vaginalis. When families of men infected with T. vaginalis were tested, 91% of their sexual partners and 13% of the children had T. vaginalis. When families of children (mostly girls) infected with T. vaginalis were tested, 72% of the mothers and 43% of the fathers had the infection. The investigators considered that the infection in the latter group originated from mothers and that the primary mode of transmission was nonsexual (beds, sponges, towels, overcrowding). Information regarding sharing of potentially infected fomites, sexual abuse, or physically intimate behavior between parents and children was not gathered in these cases.


Although T. vaginalis has been known to survive on fomites in controlled experiments, its ability to spread by these means is unknown. No cases of adults being infected by fomites have been documented. T. vaginalis has been found to survive for 6 hours on droplets of discharge and enameled surfaces of wood blocks. It has been isolated from droplets of water splashed from toilets containing the urine of an infected individual. T. vaginalis also has been found to survive in mud baths, bathing waters, and warm mineral waters and on moist bathing implements. In rural India, a survey found that young girls who bathed in tanks or rivers had a significantly higher risk for acquiring T. vaginalis than did girls who used piped or well water.


In summary, the likelihood of perinatal transmission of T. vaginalis is high in infants younger than 1 year. In a child older than 1 year, T. vaginalis infection may have resulted from transmission within a family without sexual abuse; however, the probability of sexual abuse must be considered highly suspicious, and the case must be investigated and reported for possible sexual abuse. Perinatal transmission and transmission through fomites should not be assumed without an investigation for sexual abuse. Additionally if T. vaginalis is recovered from a child, the child should be evaluated for other STIs, including syphilis, N. gonorrhoeae, C. trachomatis, hepatitis B, and HIV infection.


Postpubertal


Trichomoniasis is common and frequently is asymptomatic in sexually active adolescents (see Chapter 215 ). When it is symptomatic, patients complain of a profuse, irritating discharge. The discharge and the pruritus tend to be more severe just before and immediately after a menstrual period. Patients occasionally report dysuria and abdominal pain. Recurrent exacerbations of the infection occur commonly.


Examination reveals diffuse vulvitis with erythema and excoriations and copious leukorrhea that covers the vulvar tissues. The discharge typically is frothy or bubbly, grayish yellow, and watery or mucopurulent. It has a pH of 5.0 to 7.0 and an acrid or musty odor. A “strawberry” or punctate vaginal eruption with hemorrhagic spots has been described as being typical of trichomoniasis. Such eruptions frequently are not present, however, even in severe cases. More often, diffuse inflammation causes the vaginal mucosa to be brilliant red.


Diagnosis


There are numerous diagnostic methods available to diagnose trichomoniasis. The diagnosis of trichomoniasis usually is confirmed clinically by finding trichomonads in a wet saline smear of vaginal fluid. It is important that the slide be viewed under the microscope (dry high power) promptly because the organisms do not remain viable for long outside the vagina and are difficult to detect when they cease to be motile. The observer sees numerous ovoid-shaped, motile organisms (see Fig. 42.9 ). The sensitivity of this test with immediate evaluation is 60% to 70%. A Papanicolaou (Pap) smear to detect trichomoniasis is not recommended because of the high rate of error in identifying trichomonads in stained smears. Other methods used to diagnose trichomoniasis include isolation by special culture medium, direct fluorescent immunoassay, NAAT, rapid antigen test, and nucleic acid probe. The choice of test is often based on availability. The NAATs are highly sensitive and specific and have become the gold standard for diagnosing trichomoniasis. Culture also has high sensitivity and specificity, but it is not routinely available. The NAAT is available in some clinical settings (point-of-care test); however, a false-positive result may occur in low-prevalence populations.


Treatment


Treatment for trichomoniasis is addressed in Chapter 215 .


Bacterial Vaginosis


Bacterial vaginosis is caused by a change in the relative proportions of bacteria in the vaginal flora: an overgrowth of anaerobes, especially Bacteroides and Mobiluncus spp., G. vaginalis, and M. hominis; and a decrease in hydrogen peroxide–producing lactobacilli.


The clinical criteria used for establishing the diagnosis of bacterial vaginosis in adolescents and adults are the presence of three of four findings: a grayish homogeneous discharge, the presence of clue cells on a wet-mount evaluation ( Fig. 42.10 ), a pH greater than 4.5, and a positive amine test result (amine or fishy odor when vaginal secretions are mixed with 10% potassium hydroxide).


Mar 9, 2019 | Posted by in PEDIATRICS | Comments Off on Genital Infections

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