Bacterial vaginitis can be considered a pathologic entity separate from bacterial vaginosis, candidiasis, and trichomoniasis. It can originate from the introduction of a bacterium that overgrows the dominant bacterium of the vaginal ecosystem, or an alteration within the ecosystem that causes Lactobacillus to lose dominance. In addition, one or more of the endogenous pathogenic bacteria can gain dominance. It is possible that when a significant alteration in the vaginal ecosystem occurs, one or more of the endogenous bacteria can become dominant and produce symptoms that are recognized as vaginitis.
The patient with bacterial vaginitis, regardless of the offending bacterium, typically presents with a copious purulent vaginal discharge. There can also be an associated discomfort that is frequently described as ‘soreness’. The vaginal discharge has a pH of 5 or higher, and this is consistent with a decrease in Lactobacillus growth and favorable to the growth of pathogenic bacteria. The vaginal epithelium is erythematous and at times beefy red.
It is imperative that the physician rule out other causes of a purulent vaginal discharge, such as trichomoniasis and cervicitis, especially cervicitis caused by Chlamydia trachomatis and Neisseria gonorrhoeae. Leukorrhea commonly occurs in patients with acute salpingitis; therefore, a work-up for the presence of sexually transmitted agents is indicated in patients with purulent vaginal discharge whose behavior places them at risk for contracting a sexually transmitted disease.
Evaluation of a patient with purulent vaginal discharge begins with obtaining a detailed history with regard to medications, especially antimicrobial agents taken within the last 30 days. It should be determined whether the patient practices douching, and if so how often and which specific douching agent is used. The physician should also obtain a detailed sexual history, determining whether the patient and her partner practice cunnilingus and/or anal intercourse. The frequency of sexual intercourse can be significant because semen is alkaline and if the patient is having sexual intercourse with significant frequency, then it may be the ejaculate that is causing a significant change in the hydrogen ion concentration. Although some believe there is no such thing as too much sex, ‘too much of a good thing’ may have a negative impact on the vaginal ecosystem.
The evaluation of the lower and upper genital tract should be meticulous. The external genitalia should be examined for the presence of discharge, especially discharge originating from the glandular organs of the vestibule and discharge from the vagina. The normal amount of vaginal discharge is estimated to be approximately 4—6 ml per day. Discharge spilling out from the vagina, causing the patient to wear a pad on a daily basis, is abnormal. This increase in the amount of discharge may be because of a vaginal, uterine, or fallopian tube infection or an increase in estrogen production.
The labia majora, crural folds, and labia minora should be inspected for the presence of excoriations, fissures, ulcerations, and erythematous areas with the presence of central pustules. The urethra should be examined for the presence of purulent discharge. This should be done by visual inspection and then followed with gentle palpation to determine if there is any expressible discharge. Additionally, Skene’s and Bartholin’s glands should be inspected for the spontaneous presence of discharge and then gently palpated to determine if any discharge can be expressed. If discharge is emitted from any of these organs, specimens should be sent for both Gram’s stain and the detection of C. trachomatis, N. gononhoeae, and aerobic, facultative, and obligate anaerobic bacteria.
The vaginal examination begins by noting the discharge amount (does it appear excessive), color, and pH. A pH of 5 or higher is indicative of an altered vaginal microflora. A specimen of the vaginal discharge should then be examined microscopically. The maturity of squamous epithelial cells should be noted—that is, do they appear naviculated (well estrogenized) or are there numerous intermediate and parabasal cells present. The well-estrogenized squamous cell to basal cell ratio should exceed 10:1. This helps to determine whether or not the patient has sufficient endogenous estrogen or if atrophic vaginitis exists. The number of white blood cells (WBC) seen under 40x magnification should not be greater than 5 per hpf. The presence of more than five WBC/40x magnification is consistent with an inflammatory state.
The color of the vaginal epithelium should also be noted. In a healthy vaginal ecosystem the epithelium is pink, and if estrogen is present in sufficient concentration the wall is rugated. In the absence of estrogen, the epithelium can appear pale and smooth. In advanced stages of atrophic vaginitis the epithelium can be erythematous. The major difference between atrophic vaginitis and bacterial vaginitis is that when the former is present the number of basal cells far exceeds the number of naviculated squamous epithelial cells.
The endogenous microflora in patients with bacterial vaginitis and atrophic vaginitis will be altered. In both conditions the pH is at or above S, Lactobacillus is no longer the dominant bacterium, and there are numerous WBC. The discharge can be purulent in both conditions. In atrophic vaginitis a single bacterium can be dominant, as is the case with bacterial vaginitis. The potential pathogenic bacteria outgrow Lactobacillus when the pH is 5 or more. If no pathogen, such as T. vaginalis or Candida, is identified, specimens of the vaginal discharge should be sent for culture. The specimen should be sent for the culture and identification of aerobic, facultative, and obligate anaerobic bacteria.
Interestingly, the streptococci are commonly found as commensal bacteria in the vagina. It is not uncommon to isolate a and streptococci, as well as group B hemolytic Streptococcus. In fact the latter can be found to colonize the vagina in up to 25—30% of women who are asymptomatic.
Patients with group B streptococcal (GBS) vaginitis (Streptococcus agalactiae) typically present with erythema and maceration of the vaginal introitus and perianal area. They also have a copious, odorless, watery discharge that is yellow to white. The vaginal epithelium is erythematous. Since the year 2001, the author has treated ten patients with a diagnosis of GBS vaginitis (unpublished). The patients’ symptoms ranged from copious discharge alone to copious discharge associated with vaginal soreness. The diagnosis was based on the following:
(1) copious white to yellow to greenish, odorless discharge;
(2) erythema of the vaginal epithelium;
(3) vaginal pH of greater than 5; and
(4) microscopic examination of the vaginal discharge revealed:
a. well-estrogenized squamous epithelium;
b. absence of intermediate and parabasal cells;
c. ratio of squamous:parabasal epithelial cells was usually above 10:1;
d. Lactobacillus was noticeably absent; and
e. cocci, typically in chains, were the dominant bacterial morphotype.
Patients are usually treated with oral penicillin, ampicillin, or amoxicillin. However, if the outcome is successful it is usually shortlived and recurrence is frequent. Improved success has been achieved by combining orally administered penicillin, ampicillin, or amoxicillin with the intravaginal administration of a vaginal acidifying agent such as boric acid, 600 mg suppositories twice a day for 14 days, or Aci jel , one applicator-full twice a day for 3-4 weeks. Honig and co-workers treated their two patients with clindamycin and co-trimoxazole several times. These investigators found that during asymptomatic periods, GBS could not be recovered from the vagina; however, when the symptoms returned the bacterium could easily be recovered from the vagina. They also found that after repeated courses of clindamycin therapy the organism became resistant to clindamycin. These investigators prescribed chlorhexidine 5% intravaginal gel but this treatment did not prove to be any more efficacious than the previous treatments.
In our unpublished study, vaginal cultures obtained from each patient revealed a single bacterial dominance and this was reported as a heavy growth of group ( -hemolytic streptococci by commercial laboratories. Patients were treated with benzathine penicillin, 2.4 million units intramuscularly and there was initial resolution but then relapse. Neither the oral administration of ampicillin or amoxicillin was particularly efficacious. One patient responded to two courses of doxycyline, 100 mg twice a day for 10 days.
Thus, individual antibiotic regimens must be tried as treatment for patients with group B streptococcal vaginitis. No one regimen appears to be effective in the treatment of all cases of GBS vaginitis.
Staphjlococcus can be isolated from the vagina but it is relatively uncommon. Investigators have reported that Staphjlococcus aureus was isolated from the vagina of S—15% of women with a healthy vaginal ecosystem. However, S. aureus colonization of the skin is common. Aly and co-workers reported that 67% of asymptomatic women were found to harbor S. aureus on their vulva. This is an interesting finding because while S. aureus is commonly found to colonize the vulvar skin it is unusual to find it in the vagina. This finding implies that there is some mechanism in the vagina that inhibits the colonization and growth of S. aureus.
S. aureus did cause a significant problem in the 1980s when numerous toxic shock syndrome cases were reported. Shands and co-workers reported that toxic shock syndrome occurred in menstruating women who were using tampons and had vaginal colonization of S. aureus. This was later found to be caused by specific rare strains capable of producing the exotoxin that caused this disease.
The vaginal microflora can become altered and then one of the coliform bacteria might gain dominance. Probably the most common coliform is Escherichia coli. Because of the close proximity of the rectum, these bacteria can colonize the perineum, the vestibule, and the vagina. Although this bacterium is commonly isolated from the anatomical sites adjacent to the vagina and is a common cause of urinary tract infection, it is not a common vaginal isolate. It has been reported to be present in the vaginas of 12% of women with a healthy vaginal ecosystem. Obtaining a specimen for culture can be of assistance when examining and evaluating a patient for vaginitis once all common causes have been ruled out. A report indicating that the vagina is colonized and dominated by one particular bacterium can be significant. However, if the report states that there are several bacteria present and the growth of each is light, then the growth is not significant. A pH 5 is also significant, but if the vaginal pH is 4.5 it is not worth culturing for bacteria. A yeast culture might prove more rewarding.
For patients with a variety of coliforms the existence of a recto vaginal fistula should be considered. The patient should also be investigated for the possible existence of diverticulitis and ulcerative colitis, since these conditions can result in occult fistula formation and cause constant seeding of the vagina with bacteria from the sigmoid and rectosigmoid colon. Wiseniewski and co-workers described a case of sigmoid colon vaginal fistula in which the patient has significant vaginitis caused by contamination with a variety of coliforms originating from the colon.
Although a variety of vaginitis causes have been described, including Shigella vaginitis, Entamoeba histolytica vaginitis, Schistosoma haematobium vaginitis, these are uncommon and not frequently seen in the United States.
In 1982 Cibley and Cibley described a vaginitis that was characterized by an overgrowth of normal lactobacilli with a profuse vaginal discharge that tends to be thick or pasty, and a pH less than 4.5. The characteristics of cytolytic vaginosis were initially described as Doderlein cytolysis and were reported by Bibbo in Papanicolaou smears. The diagnosis of cytolytic vaginosis is based on the following:
(l) the absence of a pathogen; (2)the absence of bacterial vaginosis;
(3) the absence of bacterial vaginitis;
(4) the presence of an apparent overgrowth of Lactohacillus;
(5) a vaginal pH of < 4.5;
(6) a relative absence of WBC;
(7) profuse desquamation of squamous epithelial cells;
(8) disruptive squamous cells;
(9) naked nuclei;
a. a great deal of cellular debris; and
b . intermediate squamous cells.
(10) vulvar burning and itching;
(11) vaginal burning;
(12) dyspareunia; and
(13) increased symptoms in the luteal phase.
The etiology of this condition is also unknown. While there appears to be an overgrowth of Lactohacillus, whether or not the Lactohacillus present is a beneficial species is not known. It may be that the species of Lactohacillus that gained dominance adapted to acidic conditions and is not affected by the lactocin produced by the Lactohacillus species that can maintain a healthy vaginal ecosystem. It is interesting to note that when viewing the vaginal discharge of a patient with cytolytic vaginosis microscopically, the absence of other bacteria is noticeable and the large number of lactobacilli is impressive.
At this time, antibiotics do not have a place in the treatment of cytolytic vaginosis. This is not an infection and the relative absence of WBC indicates that this is not an inflammatory disease. Since this condition is associated with an acid environment, Cibley and Cibley recommended sodium bicarbonate douches (30—60 g of sodium bicarbonate in a liter of warm water) two to three times a week. When the patient notes improvement, douching should be tapered off to once a week and eventually as needed.
Individuals presenting with complaints of vaginitis, like vaginal burning, soreness, itching, or a combination of symptoms and a copious purulent discharge, should be evaluated in a systematic manner. Localization of the disease must be established at the vulva, the vestibule and glands of the vestibule, the vagina, the cervix, and the uterus. The existence of a common pathogen like Trichomonas or Candida, infection of the cervix, and the presence of vaginal warts, must be ruled out. The microscopic examination of the vaginal discharge should reveal the presence of a dominant bacterium other than Lactobacillus. If one sees predominantly small rods or coccal forms, then a vaginal culture could prove beneficial. Treatment should be directed at the bacterium identified and broadspectrum antibiotics should not be used. An attempt to correct the vaginal alteration can be put forth with the use of acidifying agents such as boric acid vaginal suppositories, 600 mg each, administered twice a day for 14 days.
Selections from the book: “Vaginitis: Differential Diagnosis and Management” (2003)