Vaginitis Medication

  • Author: Hetal B Gor, MD, FACOG; Chief Editor: Michel E Rivlin, MD   more...
 
Updated: Oct 27, 2011
 

Medication Summary

The goals of pharmacotherapy in vaginitis are to reduce morbidity, prevent complications, and eradicate the infection. Drugs used for infectious causes of vaginitis may be applied topically or may require oral or parenteral administration.

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Antiprotozoal agents

Class Summary

Metronidazole is the antimicrobial agent of choice for treating Trichomonas vaginalis infections and bacterial vaginosis.

Metronidazole (Flagyl)

 

Metronidazole causes a chemical reduction reaction within anaerobic bacteria and sensitive protozoa. It is readily absorbed and permeates all tissues, including cerebrospinal fluid (CSF), breast milk, and alveolar bone. It is metabolized and excreted in the liver and kidneys. Treatment of partners increases cure rates.

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Antifungals

Class Summary

The antifungal agents used to treat vaginitis are imidazole derivatives that exert a fungicidal effect by altering permeability of the fungal cell membrane. The mechanism of action also may involve alteration of RNA and DNA metabolism or an intracellular accumulation of peroxides toxic to fungal cell.

Intravaginal and topical therapy with a variety of antifungals (eg, clotrimazole, miconazole, terconazole, tioconazole) is highly effective. Many of these preparations are now available over the counter. Various 1-, 3-, and 7-day regimens may be used. Cure rates of 90% are reported with longer courses.

Miconazole vaginal (Monistat-7, Monistat-1)

 

Miconazole damages the fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out, which results in fungal cell death. Metabolism occurs in the liver. Recurrent infections usually are treated with intravaginal regimens for 10-14 days, followed by maintenance oral treatment for 6 months. Dual Pak is not for use in children.

Clotrimazole (Gyne-Lotrimin-3, Gyne-Lotrimin-7)

 

Clotrimazole is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing the death of fungal cells. The recommended duration of intravaginal therapy is generally 3-7 days.

Terconazole (Terazol 7, Terazol 3)

 

Terconazole damages the fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out, which results in fungal cell death.

Tioconazole (Vagistat 1, 1-Day)

 

Tioconazole is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing the death of fungal cells.

Butoconazole (Gynazole-1)

 

Butoconazole is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing the death of fungal cells. It is effective only for vaginitis caused by candidal organisms.

Nystatin vaginal tablet

 

Nystatin is a fungicidal and fungistatic antibiotic obtained from Streptomyces noursei. It is effective against various yeasts and yeastlike fungi. It changes the permeability of the fungal cell membrane after binding to cell membrane sterols, causing cellular contents to leak.

Fluconazole (Diflucan)

 

Fluconazole is a synthetic PO antifungal agent (a broad-spectrum bistriazole) that selectively inhibits fungal cytochrome P-450 and sterol C-14 alpha-demethylation. Whereas ease of use should be considered, direct cost may be a limiting factor. PO antifungals should not be recommended in pregnancy. Current recommendations are for a 7-day course of antifungal topical therapy.

Ketoconazole (Nizoral)

 

Ketoconazole is an imidazole broad-spectrum antifungal agent. It inhibits synthesis of ergosterol, causing cellular components to leak, which results in fungal cell death. Ketoconazole is generally used as maintenance therapy for recurrent vulvovaginal candidiasis

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Antibiotics

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

The use of antibiotic combinations usually is recommended for the treatment of serious gram-negative bacillary infections. This approach ensures coverage for a broad range of organisms and polymicrobial infections, prevents emergence of bacterial subpopulations that may be resistant to one of the antibiotic components, and provides additive or synergistic effects. Once organisms and sensitivities are known, however, antibiotic monotherapy is recommended.

Clindamycin (Cleocin)

 

Clindamycin is a lincosamide used to treat serious skin and soft tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). Clindamycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It is widely distributed in the body without penetrating the central nervous system (CNS). It is protein-bound and is excreted by the liver and kidneys.

Clindamycin has been used as an alternative to metronidazole in pregnancy; however, intravaginal use is not recommended for pregnant women, because it has been associated with an increased risk of preterm delivery. Treatment of bacterial vaginosis with oral clindamycin during the second and third trimesters of pregnancy has been shown to reduce the occurrence of preterm birth.

For recurrent infections, administer a trial of alternative regimens.

Ceftriaxone (Rocephin)

 

Ceftriaxone is a third-generation cephalosporin that has a broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. It arrests bacterial cell wall synthesis and inhibits bacterial growth by binding to 1 or more of the penicillin-binding proteins.

Erythromycin (E.E.S., Erythrocin, Ery-Tab)

 

Erythromycin is indicated for the treatment of infections caused by susceptible strains, including Staphylococcus aureus. It is an alternative for the treatment of chlamydial infection in pregnancy.

Metronidazole (Flagyl, MetroGel-Vaginal, Vandazole)

 

Metronidazole is active against various anaerobic bacteria and protozoa. It appears to be absorbed into the cells; the intermediate metabolized compounds that are formed bind DNA and inhibit protein synthesis, causing cell death.

Metronidazole is indicated for the treatment of bacterial vaginosis (formerly referred to as Haemophilus vaginitis, Gardnerella vaginitis, nonspecific vaginitis, Corynebacterium vaginitis, or anaerobic vaginosis). Treatment of bacterial vaginosis with oral metronidazole during the second and third trimester of pregnancy does not reduce the occurrence of preterm delivery.

Metronidazole is highly effective in treating trichomoniasis with 1 dose. Topical metronidazole is not effective therapy for trichomoniasis. The numbers of T vaginalis cases with metronidazole resistance are increasing.

Cefixime (Suprax)

 

Cefixime is an oral third-generation cephalosporin indicated for management of infections caused by susceptible gram-positive cocci and gram-negative rods. It is used to treat gonorrhea, tonsillitis, and pharyngitis.

Doxycycline (Doryx, Monodox, Vibramycin)

 

Doxycycline inhibits protein synthesis and thus bacterial growth by binding with the 30S and, possibly, 50S ribosomal subunits of susceptible bacteria.

Azithromycin (Zithromax, Zmax)

 

Azithromycin is used to treat mild-to-moderate infections caused by susceptible strains of microorganisms. It is indicated for chlamydial infections of the genital tract.

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Hormones

Class Summary

Hormones are indicated for management of atrophic vaginitis resulting from diminished levels of circulating estrogens. A relative lack of estrogen also predisposes the vagina and vulva to infection.

Estrogen (Premarin)

 

Estrogen is indicated for the treatment of atrophic vaginitis and atrophic urethritis associated with menopause. It should be reserved for women experiencing vaginal changes secondary to a deficiency of estrogen.

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Anti-Infectives, Topical

Class Summary

Boric acid can be used in the treatment of refractory, recurrent vaginal candidiasis.

Boric acid

 

Boric acid is soothing to chafed skin, abrasions, burns, and other skin irritations. For recurrent infection, maintain the treatment frequency at every other day initially, then decrease it to twice weekly.

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Contributor Information and Disclosures
Author

Hetal B Gor, MD, FACOG  Obstetrician/Gynecologist, Private Practice

Hetal B Gor, MD, FACOG is a member of the following medical societies: American College of Obstetricians and Gynecologists and Society of Laparoendoscopic Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Michel E Rivlin, MD  Professor, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine

Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh

Disclosure: Nothing to disclose.

Additional Contributors

Ann S Botash, MD Director, Child Abuse Referral and Evaluation Program, Professor and Vice Chair for Educational Affairs, Department of Pediatrics, State University of New York Upstate Medical University

Ann S Botash, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, American Pediatric Society, Helfer Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Susanne Ching, MD Staff Physician, Department of Obstetrics and Gynecology, Santa Clara Valley Medical Center

Susanne Ching, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists

Disclosure: Nothing to disclose.

Pamela L Dyne, MD Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center

Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David S Howes, MD Professor of Medicine and Pediatrics, Section Chief and Emergency Medicine Residency Program Director, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

David S Howes, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Bruce A Meyer, MD, MBA Executive Vice President for Health System Affairs, Chief Clinical Officer, Interim CEO, University Hospitals; Professor, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical School

Bruce A Meyer, MD, MBA is a member of the following medical societies: American College of Obstetricians and Gynecologists, American College of Physician Executives, American Institute of Ultrasound in Medicine, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Medical Group Management Association, and Society for Maternal-Fetal Medicine

Disclosure: Nothing to disclose.

Phuong H Nguyen, MD Clinical Associate Professor of Obstetrics and Gynecology, Stanford University School of Medicine; Chief of Gynecology, Department of Obstetrics and Gynecology, Santa Clara Valley Medical Center

Phuong H Nguyen, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Obstetricians and Gynecologists, American Medical Association, American Medical Women’s Assocation, and California Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Mark Zwanger, MD, MBA Assistant Professor, Department of Emergency Medicine, Thomas Jefferson University

Mark Zwanger, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Ann S Botash, MD Director, Child Abuse Referral and Evaluation Program, Professor and Vice Chair for Educational Affairs, Department of Pediatrics, State University of New York Upstate Medical University

Ann S Botash, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, American Pediatric Society, Helfer Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Susanne Ching, MD Staff Physician, Department of Obstetrics and Gynecology, Santa Clara Valley Medical Center

Susanne Ching, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists

Disclosure: Nothing to disclose.

Pamela L Dyne, MD Professor of Clinical Medicine/Emergency Medicine, David Geffen School of Medicine at UCLA; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center

Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David S Howes, MD Professor of Medicine and Pediatrics, Section Chief and Emergency Medicine Residency Program Director, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

David S Howes, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Bruce A Meyer, MD, MBA Executive Vice President for Health System Affairs, Chief Clinical Officer, Interim CEO, University Hospitals; Professor, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical School

Bruce A Meyer, MD, MBA is a member of the following medical societies: American College of Obstetricians and Gynecologists, American College of Physician Executives, American Institute of Ultrasound in Medicine, Association of Professors of Gynecology and Obstetrics, Massachusetts Medical Society, Medical Group Management Association, and Society for Maternal-Fetal Medicine

Disclosure: Nothing to disclose.

Phuong H Nguyen, MD Clinical Associate Professor of Obstetrics and Gynecology, Stanford University School of Medicine; Chief of Gynecology, Department of Obstetrics and Gynecology, Santa Clara Valley Medical Center

Phuong H Nguyen, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Obstetricians and Gynecologists, American Medical Association, American Medical Women’s Assocation, and California Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Mark Zwanger, MD, MBA Assistant Professor, Department of Emergency Medicine, Thomas Jefferson University

Mark Zwanger, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association

Disclosure: Nothing to disclose.

References
  1. Vaginitis. NHIOnDemand. Available at http://content.nhiondemand.com/psv/HC2.asp?objID=100638&cType=hc. Accessed 12/8/08.

  2. CDC. Tracking the Hidden Epidemics 2000: Trends in STDs in the United States. Centers for Disease Control and Prevention, Sexually Transmitted Diseases. Available at http://www.cdc.gov/std/Trends2000/trichomoniasis.htm. Accessed 12/8/2008.

  3. Donati L, Di Vico A, Nucci M, et al. Vaginal microbial flora and outcome of pregnancy. Arch Gynecol Obstet. Apr 2010;281(4):589-600. [Medline].

  4. Islam A, Safdar A, Malik A. Bacterial vaginosis. J Pak Med Assoc. Sep 2009;59(9):601-4. [Medline].

  5. [Best Evidence] Black CM, Driebe EM, Howard LA, et al. Multicenter study of nucleic acid amplification tests for detection of Chlamydia trachomatis and Neisseria gonorrhoeae in children being evaluated for sexual abuse. Pediatr Infect Dis J. Jul 2009;28(7):608-13. [Medline].

  6. Fredricks DN, Fiedler TL, Thomas KK, Oakley BB, Marrazzo JM. Targeted PCR for detection of vaginal bacteria associated with bacterial vaginosis. J Clin Microbiol. Oct 2007;45(10):3270-6. [Medline]. [Full Text].

  7. Angotti LB, Lambert LC, Soper DE. Vaginitis: making sense of over-the-counter treatment options. Infect Dis Obstet Gynecol. 2007;2007:97424. [Medline]. [Full Text].

  8. Sobel JD, Chaim W, Nagappan V, Leaman D. Treatment of vaginitis caused by Candida glabrata: use of topical boric acid and flucytosine. Am J Obstet Gynecol. Nov 2003;189(5):1297-300. [Medline].

  9. Van Kessel K, Assefi N, Marrazzo J, Eckert L. Common complementary and alternative therapies for yeast vaginitis and bacterial vaginosis: a systematic review. Obstet Gynecol Surv. May 2003;58(5):351-8. [Medline].

  10. American College of Obstetricians and Gynecologists (ACOG). Vaginitis. Washington (DC): American College of Obstetricians and Gynecologists (ACOG); May 2006:12 p. (ACOG practice bulletin; no. 72). [Full Text].

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(A) Two trophozoites of Trichomonas vaginalis obtained from in vitro culture, stained with Giemsa. (B) Trophozoite of T vaginalis in vaginal smear, stained with Giemsa. Images courtesy of Centers for Disease Control and Prevention.
 
 
 
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