Vulvovaginal candidiasis (VVC) is probably the most commonly perceived abnormal condition affecting a woman’s lower genital tract. There is no doubt that this perception has been fueled by the availability of over-the-counter antifungal products for the treatment of vulvovaginal candidiasis. Almost every time a woman experiences itching, burning, discomfort, or abnormal discharge of the lower genital tract she will diagnose herself with a ‘yeast infection’. While approximately 75% of women will experience at least one episode of yeast vulvovaginitis in their lifetime, about 50% will experience more than one episode and 5% will have recurrent episodes. The problem with vulvovaginal candidiasis is that in a symptomatic patient it is difficult to know if it is an infection or an overgrowth of the endogenous yeast present as part of the endogenous vaginal microflora. Approximately 15 — 20% of women in the reproductive age group are colonized by yeast; this is referred to as asymptomatic endogenous carriage.
Typically, acute symptomatic episodes of vulvovaginal candidiasis are responsive to one of the many antifungal agents available. However, these infected women usually do not have predisposing factors that can be linked to their recurrent episodes of VVC. For a patient who complains of vulvovaginal pruritus and burning, has erythema, and has a vaginal pH less than 4.5 but no yeast identified on microscopic examination with potassium hydroxide (KOH), some physicians recommend that a specimen be obtained for culture and identification of yeast. A positive yeast culture is interpreted as the cause of her symptoms. However, this may not be a valid interpretation of the culture results since 15 — 20% of women are asymptomatic carriers of Candida. Perhaps the culture results should be viewed as any other result obtained from an area where numerous microorganisms reside; the quantity of yeast recovered should be the determining factor. If the culture returns with scant versus heavy yeast growth, this may not be the cause of her symptoms. If the patient with scant growth of yeast is treated with an antifungal agent and her symptoms resolve, the diagnosis is definite. If she then returns with her symptoms and the subsequent culture is positive, the diagnosis is recurrent vulvovaginal candidiasis and she is treated again, and again, and again. I believe that this scenario characterizes the problem. Can we determine which patient is an asymptomatic carrier of Candida, and which patient may have a normal background of Candida and symptoms suggestive of candidiasis, but Candida is not the cause of her symptoms?
The genera Candida, Torulopsis, and Rhodotorula are all yeast that do not have a sexual stage (do not form ascospores). The principal genus is Candida, which is comprised of approximately 81 species that all produce pseudohyphae. If Torulopsisglabrata is included in the genus Candida (C. glabrata), then this is an exception as this species only produces budding forms without the development of pseudohyphae. Rhodotorula produces a carotenoid pigment.
C. albicans produces B vitamins that stimulate growth of Lactobacillus in vitro, while Lactobacillus has been shown to enhance, as well as inhibit, the growth of C. albicans.C. albicans also has been demonstrated to stimulate the growth of Staphylococcus in vitro Members of the Enterobacteriaceae, such as Escherichiacoli, have been shown to have an inhibitory, although weak, effect on the growth of C. albicans,. Additionally, C. albicans has been shown to produce a factor that can inhibit the growth of Neisseria gonorrhoeae in vitro. Thus, it appears that when colonizing the lower genital tract Candida is able to compete in this environment, especially at the more acidic pH, by producing inhibitor compounds that affect the growth of the bacteria found in this ecosystem.
Candida is able to grow over a wide pH range of 3 to 8. The typical pH of the vagina in a healthy state is 3.8 — 4.5, while if the microflora is skewed the pH can range from 4.5 to 6. Therefore, it is not surprising to find Candida in a variety of situations, for example in the presence of bacterial vaginosis or vaginitis (BV) or trichomoniasis, an inflammatory vaginitis. Candida reproduces when buds develop from blastospores. The blastospore can be ovoid, elongated, or spherical. C. albicans is pleomorphic; that is, it can grow as a budding yeast, can produce pseudohyphae, and when grown in serum can produce true hyphae. The cell wall of Candida serves three important functions: it serves as the outer containment of the cell maintaining its shape; it undergoes metabolic turnover during growth and reproduction; and it serves as the point of contact between the organism and the host during infection.
The cell wall is a multi -layered polymer of glucan and mannan polysaccharides containing chitin, protein, and lipid. Although the cell wall is a multi-layered structure it is flexible, allowing the organism to appear as ovoid, budding yeast, pseudohypae, and hyphae. This polymorphic appearance can lead to confusion when viewing the patient’s vaginal discharge through a microscope. If the organism is present in its ovoid form, it may be overlooked or not recognized as yeast. Therefore, a culture should be obtained for patients with symptoms suggestive of vulvovaginal candidiasis.
The polymorphism of C. albicans is of interest to mycologists and clinician researchers because it is believed that this capability to change morphology is related to the organism’s pathogenicity (Table Definition of morphologic forms of Candida albicans).
Table Definition of morphologic forms of Candida albicans
|Blastospore – unicellular form, reproduces by mitotic division referred to as budding. There is a specific site on the mother cell that produces new growth, the bud, which grows over time to accept the new nucleus that migrates into the daughter cell. A septum forms between the mother and daughter cells. The cells separate lo form two blastospores|
|Hyphae – long tube-like structures that are divided by cross-walls (septa) and branches containing all cellular elements. The hyphae grow and branch repeatedly forming a mycelium|
|Pseudohyphae – resemble true hyphae but are distinguished from the hyphae by their development. A single cell or bud gives rise to new cells but they remain attached. The buds elongate forming an aggregate of elongated blastospores with constrictions and not septa at the junction between daughter cellsYeast hardy organisms that can survive in a variety of environmental conditions. They are opportunistic pathogens with regard to causing systemic disease but appear lo be good competitors in the vaginal environment. Although C. albicans is susceptible to a variety of antifungal agents, when the organism is present in the vagina its susceptibility to antifungals is impaired|
Yeast are ubiquitous and found in almost all habitats. In the human body, yeast make up part of the microbial ecology of the gastrointestinal and lower genital tracts. Although the microbial ecology is complex, bacteria typically outnumber yeast. Yeast can also be found in the oral cavity of up to 20% of healthy individuals. Colonization of the rectum occurs in up to 25% of healthy individuals. Colonization of the oral cavity and rectum has important implications in women with recurrent or chronic vulvovaginal candidiasis. Candida has been isolated from the vagina in up to 37% of healthy, asymptomatic non-pregnant women- Asymptomatic carriage of yeast can be a significant problem, since large numbers of yeast can be isolated from the vaginas of healthy women: for example, concentrations of yeast cells as high as 10 and 10 yeast cells per ml of vaginal fluid have been isolated from approximately 15% of asymptomatic women. There are well over 80 species of yeast; however, only nine species have been isolated from humans (Table Candida species isolated from humans).
Table Candida species isolated from humans
|C. albicans||C. kruse’s||C. lusitaniae|
|C. brigtis||C. limbica||C parapstlosis|
|C. giabrata||C. lipoiytica||C. tropicafis|
Candida vulvovaginitis is a common problem and the exact incidence is unknown; however, it is believed that 75% of all women will experience one episode of vulvovaginitis caused by Candida. As previously mentioned, it is estimated that 50% of individuals who have one yeast infection will experience at least one additional episode, and approximately 5% will have recurrent infections. C. albicans continues to be the most common cause of vulvovaginitis. There is concern that non-albicans species, specifically C. giabrata, are increasing in frequency as a cause of vulvovaginal candidiasis. Approximately SO — 55% of college women will be treated for confirmed vulvovaginal candidiasis by the time they are 20 years old, and 75% will have had one confirmed episode in their lifetime.
Some investigators consider vulvovaginal candidiasis to be a sexually transmitted disease. Indeed there is no doubt that, in some patients with chronic recurrent vulvovaginitis, treating the sexual partner does result in resolution of recurrent disease. Candida has been isolated from the male sexual partners of women with vulvovaginal candidiasis. The frequencyof vulvovaginal candidiasis does increase with the onset of sexual activity; there also appears to be an association between vulvovaginal candidiasis and the practice of orogenital sex
There has been a great deal of theorizing regarding risks that predispose the patient to vulvovaginal yeast infections. Other than diabetes, immunosuppression, and pregnancy, sufficient data to establish cause and effect relationships between suspected risk factors do not exist. The truth of the matter is, perfectly healthy women develop vulvovaginal yeast infections. The basic problem is determining who has a true yeast ‘infection’ and who has developed an alteration in their vaginal ecosystem, permitting the endogenous yeast to grow and become symptomatic. Remember, Candida, especially C. albicans, can be grown from the lower genital tract of healthy asymptomatic women. The precise proportion of healthy women who harbor yeast and are asymptomatic is unknown, but studies indicate the figure may be up to 30%. This creates a problem for the clinician making a diagnosis and determining treatment.
Clinical Presentation And Diagnosis
The patient with symptoms attributed to candidiasis can have any one of a variety of conditions that mimic vulvovaginal candidiasis. It is important that when evaluating the patient suspected of having vulvovaginal candidiasis consideration be given to other possible etiologies, especially when yeast are not observed in the patient’s vaginal discharge. The physician should not automatically come to the diagnosis of vulvovaginal candidiasis but should establish the diagnosis by documenting the presence of yeast in the vagina and vulva.
The patient with VVC presents with vulvovaginal burning and itching. There is an increase in these symptoms, especially burning, with or shortly after sexual intercourse. The labia become erythematous and swollen. Frequently excoriations are present and the diabetic patient is at risk of the development of cellulitis, which can progress to necrotizing fasciitis. Therefore if the labia are markedly swollen and there is an advancing erythema extending beyond the labia, secondary bacterial infection should be suspected. The patient should be discouraged from trying to diagnose herself with a yeast infection. In a study of 365 women previously diagnosed with vulvovaginal candidiasis, only 35% were able to correctly diagnose recurrent vulvovaginal candidiasis.
The vaginal discharge should be evaluated as follows:
(l) The pH should be determined. Although yeast prefer a more acidic pH, they can be found at any pH. A pH of 4.5 or less rules out bacterial vaginosis and bacterial vaginitis, but a pH of 5 or more does not rule out the possible existence of yeast.
(2) An aliquot of the vaginal discharge should be obtained by wiping the lateral vaginal wall with a cotton- or Dacron-tipped applicator. The applicator should be immersed in 2 ml normal saline and vigorously agitated. The applicator should then be touched to a glass slide so one or two drops of the diluted vaginal discharge is present on the slide. Two slides should be prepared and concentrated KOH should be added to the diluted vaginal discharge. The KOH will dissolve all non-chitinous material, leaving the yeast intact. The specimens should be covered with a glass cover slip.
(3) The specimens of vaginal discharge should be viewed under 40x magnification. If budding yeasts cells or hyphal elements are observed, the diagnosis of vulvovaginal candidiasis is established.
(4) A specimen should also be obtained for culture and identification of yeast. This is important because if the patient does not respond to treatment, knowing that she is colonized by a non-albicans species will help in directing further antifungal treatment. Although cultures are now being touted as the gold standard, they should not be used indiscriminately. Following treatment, if the patient is asymptomatic and no yeast are observed on microscopic examination of the vaginal discharge, a specimen of the vaginal discharge should not be cultured (a test of cure culture). It is important to remember that approximately 37% of healthy asymptomatic women can have yeast as part of their normal endogenous vaginal microflora.
Patients with recurrent or chronic persistent vulvovaginal candidiasis should have documentation that they are infected, and a culture should only be obtained to determine if they are infected with a non-albicans species. As mentioned, recurrent vulvovaginal candidiasis affects approximately 5% of patients and is defined as four or more infections occurring annually. The majority of patients who experience recurrent vulvovaginal candidiasis are typically healthy and have no obvious or recognizable predisposing factors. Studies trying to determine the relationship between recurrent vulvovaginal candidiasis and the strain of Candida revealed that individuals with early recurrent episodes — less than 6 months — were likely to have the same strain as the previous infection. Infections recurring more than 6 months apart were likely to have a different strain.
The source of Candida has not been established. It was believed that the rectum served as the reservoir; however, treatment with oral nystatin has not been effective in reducing recurrences, and recurrent vulvovaginal candidiasis occurs in the absence of rectal colonization. The difficulty in managing a patient with recurrent vulvovaginitis is determining if she is experiencing an exacerbation of an existing colonization or has developed reinfection. Odds demonstrated that to obtain a positive culture from a vaginal specimen, the concentration of yeast must be at least 10 yeast cells per ml of vaginal fluid in order to develop one colony on agar medium. Therefore, when a patient who has been treated subsequently becomes asymptomatic, if microscopic examination does not reveal the presence of hyphal forms and the culture is negative, she will be considered cured. If she should experience another yeast infection in the following 30 — 60 days this will be considered a reinfection. The difficulty in this case is establishing if this is an exacerbation of pre-existing candidiasis, if there was a change in the vaginal ecosystem that stimulated overgrowth of endogenous Candida, or if there is a new infection.
Attempts have been made to establish risk factors that predispose an individual to recurrent vulvovaginal candidiasis (Table Factors associated with recurrent vulvovaginal candidiasis). The vaginal environment that favors the growth of yeast is acidic, with a sufficient concentration of glucose.
Table Factors associated with recurrent vulvovaginal candidiasis
Again, the problem associated with recurrent and chronic persistent vulvovaginal candidiasis is that these conditions are frequently found in women who are healthy. Their vaginal ecosystems are not in a state of significant imbalance because even though they are colonized with Candida and are often symptomatic, there is normal colonization by Lactobacillus. This latter fact alone indicates that the vaginal ecosystem is not imbalanced because in order to support significant growth of Lactobacillus, the ecosystem must be in balance.
Most likely, the patient with recurrent vulvovaginal candidiasis is not being re-infected since most of these women do not have exogenous risk factors, e.g. douching (especially with compounds that can alter the vaginal ecosystem like Betadine ), multiple sexual partners, or a diet that may contribute to an increased vaginal glucose concentration. One theory that persists is that women with recurrent and/or chronic vulvovaginal candidiasis have significant rectal colonization. This rectal colonization provides a source for repeated vaginal colonization. Odds and Abbott found that the oral cavities and rectums of women with vulvovaginal candidiasis were colonized by the same yeast, which was determined by typing. Some investigators also found 100% of patients with vulvovaginal candidiasis had rectal colonization; however, this has not been substantiated by other investigators. Treatment regimens that include either oral nystatin or ketoconazole have not been shown to eliminate rectal colonization.
Antibiotic therapy has been associated with vaginal colonization by Candida. It is believed that antibiotics reduce the vaginal bacterial flora and allow the growth of Candida. The possibility exists that when bacteria like Lactobacillus crispatus or other hydrogen peroxide- and lactocin-producing lactobacilli are the dominant organisms in the vagina, Candida is suppressed. One study demonstrated that ingesting yogurt, which contains L. acidophilus, daily for 6 months could decrease Candida vaginal and rectal colonization and vaginal infection. However, this was a small study and should be repeated with a large number of patients before this can be recommended as part of the therapeutic regimen for treatment of recurrent vulvovaginal candidiasis. Two clinical studies demonstrated an increase in vaginal yeast colonization from 10 to 30% following 2 — 3 weeks of tetracycline use- Animal studies, specifically in the rat, demonstrated that two organisms, Lactobacillus and Candida, exist in a commensal relationship within the gastrointestinal tract, each colonizing specific sites. Lactobacillus colonizes the stratified squamous epithelium and Candida colonizes, and attaches to, the secretory mucosal cells. When the animals received tetracycline, the lactobacilli were significantly reduced in number to levels below detection and the yeast increased in number to colonize the entire mucosal surface. Following the discontinuation of tetracycline and administration of lactobacilli, the original microflora of the stomach was re-established.
This is an extremely interesting area since the vagina is a complex ecosystem containing numerous microorganisms living together in a variety of relationships. When a condition of the vagina requires treatment with antimicrobial agents it is important to remember that these agents can have far-reaching effects. There is little doubt that the non-specific effects of the antimicrobial agents can influence the status of the microecology, thus giving rise to additional problems. Therefore, when prescribing antimicrobial agents the physician should administer a narrow-spectrum antimicrobial that will have the least scatter effect, thereby reducing the possible disturbance to the associated microorganism in the ecosystem.
Another potential area that has received significant attention is the role of sexual behavior related to recurrent vulvovaginal candidiasis. Several studies have shown that the penis is asymptomatically colonized in 5 — 25% of the male sexual partners of women with symptomatic vulvovaginal candidiasis. Penile colonization with yeast is four times more prevalent among these males than among those whose sexual partners do not have vulvovaginal candidiasis. However the male is often asymptomatic. Sober reported that in 100 women with vulvovaginal candidiasis, three male partners developed Candida balanoposthitis. Additionally, 20% of the male partners developed an acute hypersensitivity reaction, which is a severe itch and redness shortly after intercourse that disappears without treatment within 24 hours. However, these findings do not explain the male who develops erythema of the head and coronal sulcus of the penis associated with persistent chronic itching. While these individuals report significant burning shortly following intercourse, they do not develop balanoposthitis but require treatment. There is no doubt that the male penis can become colonized with yeast when exposed to a vagina colonized by a significant number of yeast. Whether or not the penis becomes colonized and re-inoculates the female most likely depends upon the inoculum size.
The local immunity of the lower genital tract may play a vital role in the pathogenesis of vulvovaginal candidiasis, especially in patients with recurrent disease. In one study of women with recurrent vulvovaginal candidiasis, immunoglobulin A (IgA) and the secretory component of IgA were found to be absent from the patients’ cervicovaginal secretions. These investigators found that IgG was present in the cervicovaginal secretions of 94% and IgA in 73% of the controls, and in women with vulvovaginal candidiasis IgG was found in 36% and IgA in 32% (p < 0.001). The secretory component of IgA was found in cervicovaginal secretions of 13% of women with infection and 79% of uninfected women (p < 0.001). Witkin postulated that women who experience recurrent vulvovaginal candidiasis developed a transient and local inhibition of cell-mediated immunity. vulvovaginal candidiasis is more frequently found in patients with diabetes mellitus, individuals on steroid therapy, individuals taking broad-spectrum antibiotics, pregnant patients, and individuals with immunologic dysfunction. All individuals with one or more of these risk factors suffer from impairment of their cellmediated immunity. Patients with insulin-dependent diabetes have a defect in interlukin-2 (IL-2) synthesis, while patients taking broad-spectrum antibiotics can experience suppression of phagocytic function, and pregnant women often have selective inhibition of their cellular immune responses. Therefore, all of these patients may be at an increased risk of developing recurrent vulvovaginal candidiasis. Hobbs and coworkers demonstrated in vitro a reduced lymphocyte proliferative response to Candida antigens in 65% of 23 women with recurrent vulvovaginal candidiasis. Witkin and co-workers also showed a decreased lymphocyte proliferative response in patients with recurrent vulvovaginal candidiasis. These investigators also demonstrated that serum from patients with recurrent vulvovaginal candidiasis inhibited the pr oliferative response to Candida of lymphocytes obtained from women without vulvovaginal candidiasis. Witkin and colleagues confirmed this lack of proliferative response in lymphocytes in 73% of 65 women with recurrent vulvovaginal candidiasis. These women did not have predisposing factors and possessed lymphocytes that did not have the inherent cellular ability to proliferate in vitro in response to Candida antigen stimulation.
A healthy endogenous vaginal microflora is probably the most important defense against an overgrowth of Candida. Lactobacillus apparently plays a pivotal role in suppressing or inhibiting Candida overgrowth. Like other microorganisms, Candida produces substances that can inhibit the growth of other microbes. When vulvovaginal candidiasis is present, there is a reduction in the number of lactobacilli present in the colonized vagina. The prevention of Candida adhering to vaginal squamous epithelial cells was observed when the vaginal squamous cells were preincubated with lactobacilli in vitro.
Typically vulvovaginal candidiasis does not occur in association with other abnormal conditions or infections. However, there are exceptions because vulvovaginal candidiasis has been observed with BV, trichomoniasis, C. trachomatis, and N. gonorrhoeae. In fact, the presence of an increased number of white blood cells (WBC) in the vaginal discharge should alert the physician to look for an infection, such as trichomoniasis or cervicitis.
The following characteristics can be identified in a patient with vulvovaginal candidiasis:
(1) Vulvar erythema
(2) Vulvar edema
(3) Vulvar excoriations
(4) White patsy to liquid discharge present on the vulva
(5) Vaginal epithelium is erythematous
(6) Vaginal discharge
Patients complaining of vulvovaginal itching and/or burning, and who have a white to slate-gray discharge with a pH of less than 4.5 but no evidence of yeast, i.e. no hyphal forms or budding yeast on microscopic examination of the vaginal discharge, should have a specimen of the vaginal discharge cultured for the isolation and identification of yeast. There are times when the wet prep contains only small, elliptical, individual yeast cells that go unnoticed by the examiner but the culture returns positive. An additional benefit of the culture, if positive, is the identification of the species. If the isolated yeast is a species other than C. albicans, then it may be resistant to the typical antifungals used for treatment. The physician can then institute therapy with Butoconazole 2%, Terazol , Tioconazole , or boric acid vaginal suppositories or capsules (Table Available antifungal agents).
Table Available antifungal agents
|Fluconazole (Diflucan) 150 mg oral tablet administered once a week|
|Clotrimazole 1 % cream (Femzol-7) 7-day therapy|
|Clotrimazole 1% cream (Gyne-Lotrimin) 7-day therapy|
|Clotrimazole 100 mg vaginal tablets (Gyne-Lotrimin) 7-day therapy|
|Clotrimazole 200 mg vaginal tablets (Gyne-Lotrimin) 3-day therapy|
|Butoconazole 2% cream (Femstat-3) 3-day therapy|
|Butoconazole 2% emulsion (Gynazol-1) single-dose intravaginal therapy|
|Miconazole 2% cream (Femzol-M) 7-day therapy|
|Miconazole 2% cream (Monistat-7) 7-day therapy|
|Miconazole 200 mg vaginal tablet (Monistat-3) 3-day therapy|
|Miconazole 100 mg vaginal tablet (Monistat-7) 7-day therapy|
|Terconazole 0.8% cream (Terazole-3) 3-day therapy|
|Terconazole 80 mg vaginal suppositories (Terazole-3) 3-day therapy|
|Tioconazole (Vagistat-1, Monstat-1) ointment, single-dose treatment|
The presence of WBC and yeast may indicate the presence of an additional condition, such as cervicitis. Again, the physician should look for a cervical infection. If the patient has risk factors, then cervical specimens should be obtained f or C. trachomatis and N. gonorrhoeae, and if the Pap smear is abnormal then a specimen should be obtained for human Papillomavirus (HPV). If the vaginal pH is 5 or more, then T. vaginalis should be considered.
The patient may also present with vaginal burning shortly after sexual intercourse, which may persist for 24 hours. This could be followed by a mild vulvar pruritus that lasts 1 — 2 days. The patient’s sexual partner may also complain of penile burning shortly after intercourse that lasts for a day or two. These patients should be examined and a specimen for culture and identification of yeast should be obtained. There is little doubt of the value of a vaginal culture, especially in the patient with signs and symptoms of vulvovaginal candidiasis but without fungal elements detected in the vaginal discharge. Several investigators have demonstrated the value of a vaginal culture when evaluating a patient with suspect vaginitis. Handa and Stice cultured 40 women with cyclic vulvitis and found 61.5% to be positive for yeast. These investigators found that 54% of the isolated yeast were C. albicans, while the remaining isolates were C. glabrata, C. tropicalis, C. krusei, C. parapsilosis, and Saccharomyces cerevisiae. These patients frequently have Candida and should be treated vigorously because they often will manifest symptoms consistent with vulvovaginal candidiasis. In addition, their partners may serve as a source of reinfection. Therefore, their partners should be treated with a topical agent such as Mycostatin® cream. In a study of 4228 women with symptomatic lower genital tract infection, candidiasis was detected in 3351 cases (79%): C. albicans was identified in 1431 (43%) of these cases, and non-albicans species were found in 1920 (57%). These investigators also found that among the non-albicans species the most frequently isolated were C. glabiata (63%), C. tropicalis (21%), and C. husei (15%). Additionally, these investigators found that C. albicans was most frequently isolated in patients using oral contraceptive hormones while women previously treated with topical antimicrobial agents were more frequently infected with non-albicans species. However, these associations were not statistically significant. C. albicans was also isolated more frequently in women whose partners reported symptoms consistent with the presence of penile candidiasis.
In summary, the diagnosis and management of vulvovaginal candidiasis can be approached as follows:
(1) Obtain a detailed history regarding the start of symptoms and factors that aggravate the conditions;
(2) Determine if the patient has been treated with oral antibiotics within the last 14 days;
(3) Determine if the patient has recently used intravaginal medications, home remedies, or has been douching and if so determine what agent was used;
(4) Determine the anatomic location of her symptoms;
(5) Describe the physical findings and location of all abnormal findings;
(6) Obtain a specimen from the vulva for culture and microscopic examination (differential diagnosis, Table Differential diagnosis of vaginitis);
Table Differential diagnosis of vaginitis
|One dominant microorganism?||yes||yes||no||no||yes||yes||no|
(7) Obtain a specimen from the vagina for culture and microscopic examination;
(8) Determine the vaginal pH. A pH 5 indicates that the vaginal microflora is altered. If yeast are also found, this suggests that two conditions are present;
(9) The presence of WBC in a patient with a cervix can indicate the presence of cervicitis; and
(10) If no yeast are present, a specimen for culture should be obtained.
Interpreting the vaginal discharge with microscopic examination:
(1) Squamous cells should be estrogenized. More basal cells than well-estrogenized squamous cells, or the appearance of a large number of basal cells and intermediately mature estrogenized squamous cells instead of well-estrogenized squamous cells suggests an estrogen deficiency, for example developing or established atrophic vaginitis.
(2) A pH 5 S indicates an alteration in the endogenous vaginal microflora. The absence of WBC indicates that Lactobacillus may no longer be the dominant bacterium. If there are numerous morphologic bacteria present, look for clue cells. The presence of clue cells and the absence of a dominant bacterial morphotype indicates BV.
(3) Numerous WBC, i.e. > 5 WBC/high-power field at 40x magnification, indicate the presence of either an infection or hypersensitivity reaction. First, search for the presence of T. vaginahs, if this is not found consider obtaining a specimen for T. vaginahs culture. Also examine the cervix for signs of cervicitis and obtain specimens for the detection of C. trachomatis and N. gonorrhoeae. If the patient’s Pap smear is abnormal, obtain a specimen for HPV.
(4) Fungal elements will present as either individual elliptical cells, budding cells, elliptical cells with a short germ tube, or hyphal elements. The presence of any of these elements in a patient with vulvovaginal erythema, itching, and/or burning establishes a diagnosis of VVC.
Treatment should be initiated if fungal elements are found on the microscopic examination of the vaginal discharge. Treatment should also be initiated in the patient who has symptoms consistent with vulvovaginal candidiasis, but whose microscopic examination does not confirm the presence of fungal elements.