FEMININE HYGIENETREA TMENTS (2)
The human female vagina (“sheath”) is a tubular, elastic, fibromuscular organ measuring approximately eight to ten centimeters (three to four inches) in length. Lined internally with a mucus membrane, it lies between the bladder and the rectum. It is directed superiorly and posteriorly, extending from the cervix of the uterus to the vestibule, a space surrounded by the female external genitalia. Often called the birth canal, the vagina provides a passageway for delivery of a fetus and for menstrual flow. As the female organ of copulation, the vagina receives the male penis and semen during sexual intercourse. The vaginal mucosal lining contains no glands, but it is lubricated by secretions from the cervical mucus glands. The cervical mucus glands release copious amounts of glycogen (a complex carbohydrate), which is subsequently anaerobically metabolized to organic acids (e.g., lactic acid) by resident vaginal bacteria. Thus, because of the presence of organic acids, the vagina possesses an acidic pH, which allows for a healthy vaginal environment by prohibiting the growth of various pathogens.
An inflammation of the vaginal canal, known as vaginitis, is often the result of vaginal colonization by fungi, bacteria, or parasites. Vaginal dis- charge, odor, irritation, and burning and/or itching generally characterize this condition. Vaginal yeast infection (also called vulvovaginal candidiasis) is a common cause of vaginal irritation. While frequent symptoms of yeast infection in women are itching, burning, and irritation of the vagina and vulva (external genitalia), painful urination and/or sexual inter- course are common as well. In addition, mostly odorless watery to thick curdy vaginal discharge of whitish-gray coloration (typically described as cottage cheese-like in nature) can be present. Adverse symptoms only ap- pear with yeast overgrowth, as yeasts are typically present in the vagina in small quantities. Because the acidic environment of the vagina prohibits yeast overgrowth, biological factors that lead to acidic imbalance within the vagina typically allow for the formation of vaginal infection. Such factors include menstruation, pregnancy, diabetes mellitus, compromised immune function, specific antibiotics, birth control pills, and steroids. Moisture, per- spiration, and irritation caused by the use of particular over-the-counter feminine hygiene products, or by wearing tight, poorly ventilated clothing and undergarments, may also promote vaginal yeast colonization.
A yeastlike fungus called Candida albicans causes vaginal yeast infec- tions. As a normal inhabitant of humans that normally causes no ill ef- fect, this fungus is commonly found in the mouth, intestinal tract, and vagina. Although C. albicans is the pathogen often identified in women with vulvovaginal candidiasis, other possible pathogens include Candida tropicalis and Candida glabrata. As unicellular fungi inhabiting a variety of natural habitats, yeasts typically multiply as single cells that divide by budding or direct division, or they may grow as simple irregular fila- ments (mycelium). In sexual reproduction, most yeasts form asci, which contain up to eight haploid ascospores. These ascospores may fuse with adjoining nuclei and multiply through vegetative division; in some yeasts, they fuse with other ascospores.
Various over-the-counter antifungus medications, in the form of creams, tablets, or suppositories, are available to treat vaginal yeast infections. These agents are typically inserted into the vagina with a plunger- type applicator and massaged into the vulva for one to seven days de- pending on the formulation. Such products usually contain one of three active antifungus ingredients: butoconazole nitrate, miconazole nitrate, or tioconazole. Approved as over-the-counter drugs by the Food and Drug Administration in the 1980s and 1990s, these drugs are characterized as within the same antifungus chemical family (imidazoles) and function similarly in destroying the Candida organism. As azole derivatives, imi- dazoles inhibit cytochrome P450 and lanosterol 14cx-demethylase en- zyme activity within fungi. With respect to antifungus activity, this action then prevents hydroxylation of the 14cx-methyl group of lanosterol, thus decreasing the conversion of 14cx-methylsterols to ergosterol, an important membrane lipid component of fungi. Failure of ergosterol synthesis, and additional accumulation of 14cx-methylsterols, causes altered membrane permeability, leading to loss of the ability to maintain a normal cellular environment and subsequent growth arrest. In addition, the azole antifungals inhibit morphogenetic transformation of yeast blastospores into the invasive mycelium form in C. albicans.
Clotrimazole, an imidazole antifungus drug, may also be included as an active ingredient in over-the-counter treatments for vaginal candidiasis. This agent is related to other azoles but elicits a different mechanism of action in destroying invasive fungi, such that it acts on fungal cell membranes and interferes with essential amino acid transport into the organism.
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