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ABOUBAKR ELNASHAR
BENHA UNIVERSITY HOSPITAL, EGYPT
Prevalence of fungal infection:
37%.
dramatic decrease after menopause
ABOUBAKR ELNASHAR
There are 150 candida species
C albicans is by far the most common, it accounts for
80-90%
C glabrata is the second most c...
In recent years, there is significant increase in non-
albicans species, particularly C glabrata & C
tropicalis, especiall...
2.Eradication of C albicans causes a selection of
species (such as C glabrata) that are resistant to
commonly used drugs.
...
Candida is found in 2 different states:
1.Blastopores or spores are the phenotype for
extension, dissemination & transmiss...
1. Vagina: 35% of healthy females,2ndry opportunistic
pathogen
2. GIT: anogenital transfer
3. Husband: 25% STD.
VVC is not...
1. Compromised immunity:
broad spectrum antibiotic, other vag. Infection, trauma
(SI), allergen causing skin sensitization...
4. Drugs:
OCPs, corticosteroids, immunosuppressive,
antibiotics, antitrichomonal
5. Clothing: occlusive tights.
Pregnancy:...
OCP: containing high estrogen,the mechanism is
same as in pregnancy. No synergic action has ever
been shown for low estrog...
To be invasive, C follow 3 stage mechanism
1.Adhesion
2.Blastopore germination, mycelium or hyphae
development
3.Epitheliu...
Symptomatic vaginitis development
Transformation of vaginal colonization into vaginitis
is a critical step in the pathogen...
Vaginitis appear because of:
1.An increased number or an enhanced virulence
of C organisms.or
2. Decreased vaginal defense...
.
Vulval itch (cardinal symptom): increase with warmth
& at night
. Discharge: ranging from scanty, thick, whitish,
adhere...
ABOUBAKR ELNASHAR
PH of discharge:4-5
. Wet mount: saline
Koh 10%: can ifentify pseudohyphae & blastospores
in 70%
. Gram stain.
. Pap. Smea...
ABOUBAKR ELNASHAR
.Colonization
.Uncomplicated VVC:
1.Sporadic or infrequent VVC
2.Mild or moderate VVC
3.Likely to be C. albicans
4.Non-imm...
.Complicated VVC:
1.Recurrent VVC
2.Severe VVC: extensive vulvar erythema, oedema,
and excoriation, fissure formation. Sym...
1. other causes of vaginal discharge.
Infection with Herpes genitals, TV, bacterial vaginosis,
&
2. Vulval disease, especi...
1.Wiping from front to back
2.Avoiding tight underwear especially synthetics
3.Avoidance of excessive washing, use of bubb...
Asymptomatic female should not be
treated even if the culture is positive
Uncomplicated:
. Local (topical, intravaginal) a...
•Both azoles & nystatin are fungistatic rather than
fungicidal.
•Nystatin (Nysert, Mycostatin and Nystan) less
effective t...
2. Oral antifungal: more effective against non-albican
species.
. Ketoconazole (Nizoral ,200mg)
Dose: 1X2X5
. Itraconazole...
Oral or vaginal antifungal
(Cochrane libarary, 2001)
.No differences in effectiveness (mycological &
clinical cure ) for u...
Follow-up:
Patients should be instructed to return for follow-up
visits only if symptoms persist or recur within 2
months ...
Causes of clinical failure:
1.Vaginitis due to other causes.
2.Undiagnosed urogenital infection.
3.Chemical irritants: per...
Complicated VVC
Recurrent VVC
Define:
4 or more episodes/Y. Reappearance of C in the
vagina of a patient, who was cured, ...
Prevalence:
5% in family planning clinic & 10% in antenatal
clinic. No apparent predisposing or underlying
conditions in m...
Although iron deficiency anaemia has been
suggested as a cause of recurrent VVC, there is no
evidence to support this.
DM ...
Treatment:
.Vaginal culture should be obtained to confirm clinical
diagnosis & to identify unusual species, including
non-...
2. Maintenance (Suppressive) therapy for 6 months:
Clotrimazole (500-mg dose vaginal sup once weekly)
Ketoconazole (100 mg...
Treatment of the husband: controversial
Treatment of the predisposing factors:
Nitrofurantoin & nalidixic acid are recomme...
Side effects of oral azoles: are few
(Inman et al,1993)
1.Gastrointestinal symptoms
2.Headache
3.Interactions with other d...
Severe VVC:
Response to short course of topical or oral therapy is
poor
Topical azole 7-10 days or
Fluconazole in 2 sequen...
Non-albicans VVC
1.First line therapy: Longer duration therapy with a
non-fluconazole azole is recommended i.e; Nstatin
pe...
3.The final resort: Topical 4% flucytosine, the only
fungicidal agent, & amphotericin B (Fungizone)in
lubricating gjelly f...
Non-C. albicans-related disease is less likely to respond to
azole therapy (184).
Vaginal boric acid, administered in a ge...
Compromised host:
1.Correction of the condition
2.Prolonged conventional treatment course (7-10
days)
Pregnancy:
Only topi...
VVC During pregnancy
VVC is more common during pregnancy
Cochrane library,( 2002):
•There is no evidence that VVC is harmf...
•There is no evidence that any one azole is any more
effective than another.
•Oral antifungal is not known to be effective...
ABOUBAKR ELNASHAR
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Vulvovaginal candidiasis

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Vulvovaginal candidiasis

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Vulvovaginal candidiasis

  1. 1. ABOUBAKR ELNASHAR BENHA UNIVERSITY HOSPITAL, EGYPT
  2. 2. Prevalence of fungal infection: 37%. dramatic decrease after menopause ABOUBAKR ELNASHAR
  3. 3. There are 150 candida species C albicans is by far the most common, it accounts for 80-90% C glabrata is the second most common, it accounts for 5-15% C tropicalis (5%) Other species eg C krusei, C guilliermondi are rarely isolated ABOUBAKR ELNASHAR
  4. 4. In recent years, there is significant increase in non- albicans species, particularly C glabrata & C tropicalis, especially in recurrent cases. At present non candidal account for 20% of cases & 30% of recurrent cases. 1.Widespread & inappropriate use of antimycotic treatments (self medication, long term treatment, repeated treatments). Shorter courses of imidazole for c. albicans may lead to an overgrowth of c glabrata ABOUBAKR ELNASHAR
  5. 5. 2.Eradication of C albicans causes a selection of species (such as C glabrata) that are resistant to commonly used drugs. Eradication of intestinal C with medication is not successful ABOUBAKR ELNASHAR
  6. 6. Candida is found in 2 different states: 1.Blastopores or spores are the phenotype for extension, dissemination & transmission. They are also a resistance form of the fungus, that can be associated with a symptomless colonization. 2.Mycelia are germinative forms; this phenotype can invade tissues & cause symptoms. ABOUBAKR ELNASHAR
  7. 7. 1. Vagina: 35% of healthy females,2ndry opportunistic pathogen 2. GIT: anogenital transfer 3. Husband: 25% STD. VVC is not usually acquired through sexual intercourse ABOUBAKR ELNASHAR
  8. 8. 1. Compromised immunity: broad spectrum antibiotic, other vag. Infection, trauma (SI), allergen causing skin sensitization, late pregnancy, immuno-suppression. 2. Endocrine disorders: DM, thyroid, parathyroid & adrenal. 3. Menstrual cycle: late luteal phase ABOUBAKR ELNASHAR
  9. 9. 4. Drugs: OCPs, corticosteroids, immunosuppressive, antibiotics, antitrichomonal 5. Clothing: occlusive tights. Pregnancy: High estrogen levels cause an increased glycogen load in epithelium, which is a nutritional source for C growth & germination. Estrogen promotes fungal adhesion & germination, fungi are more capable to penetrate vaginal wall ABOUBAKR ELNASHAR
  10. 10. OCP: containing high estrogen,the mechanism is same as in pregnancy. No synergic action has ever been shown for low estrogen OCP regarding C growth IUCD: is associated with recurrence because the thread acts as a C reservoir DM: Metabolic disturbance predispose to clinical vaginitis Antibiotics: suppress lactobacilli flora, C are free to grow, adhere & germinate. However several studies failed to show this ABOUBAKR ELNASHAR
  11. 11. To be invasive, C follow 3 stage mechanism 1.Adhesion 2.Blastopore germination, mycelium or hyphae development 3.Epithelium invasion Defense factors against C in the vagina: 1. Lactobacilli 2. Humoral immunity, antibodies 3. Cellular immunity ABOUBAKR ELNASHAR
  12. 12. Symptomatic vaginitis development Transformation of vaginal colonization into vaginitis is a critical step in the pathogenic mechanism of C vaginitis. During colonization stage, C are present basically in blastopore forms, & their number is not very high. There is a balance between C organisms & vaginal defense factors controlling & limiting fungal growth. ABOUBAKR ELNASHAR
  13. 13. Vaginitis appear because of: 1.An increased number or an enhanced virulence of C organisms.or 2. Decreased vaginal defense mechanisms. When this occurs, blastopores adhere to vaginal epithelium & germinate; mycelium develops & finally invades mucous membrane producing vaginitis. ABOUBAKR ELNASHAR
  14. 14. . Vulval itch (cardinal symptom): increase with warmth & at night . Discharge: ranging from scanty, thick, whitish, adherent to vagina to a thin watery liquid,pH:4-5. . Burning: Vulval & vaginaL is not dominant, but gets worse with micturition or coitus . dysparunia , dysuria. ABOUBAKR ELNASHAR
  15. 15. ABOUBAKR ELNASHAR
  16. 16. PH of discharge:4-5 . Wet mount: saline Koh 10%: can ifentify pseudohyphae & blastospores in 70% . Gram stain. . Pap. Smear: 50%. It is not performed for this condition . Culture: Nickerson, Sabourad, Only when microscopy is not diagnostic . Kits: slide agglutination test is rapid diagnostic test. ABOUBAKR ELNASHAR
  17. 17. ABOUBAKR ELNASHAR
  18. 18. .Colonization .Uncomplicated VVC: 1.Sporadic or infrequent VVC 2.Mild or moderate VVC 3.Likely to be C. albicans 4.Non-immunocompromized . ABOUBAKR ELNASHAR
  19. 19. .Complicated VVC: 1.Recurrent VVC 2.Severe VVC: extensive vulvar erythema, oedema, and excoriation, fissure formation. Symptoms are correlated with the amount of yeast in the vagina (Odds,1988) 3.Non-albicans VVC 4.Women with uncontrolled , DM, debilitation, immunosuppression or those who are pregnant ABOUBAKR ELNASHAR
  20. 20. 1. other causes of vaginal discharge. Infection with Herpes genitals, TV, bacterial vaginosis, & 2. Vulval disease, especially vulval eczema, dermatitis, lichen sclerosis & vulval vestibulitis. Ask the patient to identify the itchy area. If there are symptoms of dysparunia, the Q-tip test for the vulval vestibulitis syndrome should be performed ABOUBAKR ELNASHAR
  21. 21. 1.Wiping from front to back 2.Avoiding tight underwear especially synthetics 3.Avoidance of excessive washing, use of bubble baths & perfumed soaps ABOUBAKR ELNASHAR
  22. 22. Asymptomatic female should not be treated even if the culture is positive Uncomplicated: . Local (topical, intravaginal) antifungal: Polyene: nystatin. Azoles: clotrimazole, miconazole, econazole, butoconazole, ticonazole, terconazole. ABOUBAKR ELNASHAR
  23. 23. •Both azoles & nystatin are fungistatic rather than fungicidal. •Nystatin (Nysert, Mycostatin and Nystan) less effective than azole treatment. It needs to be given for 14 days, but is indicated if there is a possibility of non-albicans yeast infection. •Azoles resulted in higher rates of clinical & mycologic cure (80-95%) than nystatin (&0-90%) in non pregnant acute VVC. •Short course (single dose & regimens of 1-3 days)effectively treat uncomplicated VVC. ABOUBAKR ELNASHAR
  24. 24. 2. Oral antifungal: more effective against non-albican species. . Ketoconazole (Nizoral ,200mg) Dose: 1X2X5 . Itraconazole (Sporanox, 100 mg ) Dose: 2X2X1 . Fluconazole (Diflucan, Alkanazol,150 mg) Dose : 1 tab single dose • ABOUBAKR ELNASHAR
  25. 25. Oral or vaginal antifungal (Cochrane libarary, 2001) .No differences in effectiveness (mycological & clinical cure ) for uncomplicated candidiasis. (Both routes had clinical cure 80%) .The oral route is the preferred route by the patient. The decision to prescribe oral or vaginal depends on safety, cost, effectiveness, & patient preference. Oral preparation is more expensive & associated with more systemic side effects than vaginal route. Vaginal route is first line of therapy (Reef, 1993) ABOUBAKR ELNASHAR
  26. 26. Follow-up: Patients should be instructed to return for follow-up visits only if symptoms persist or recur within 2 months of onset of initial symptoms T.T of the husband with oral antifungal did not influence either cure rate or recurrence rate (Shihadeh & Nawafleh,2000) ABOUBAKR ELNASHAR
  27. 27. Causes of clinical failure: 1.Vaginitis due to other causes. 2.Undiagnosed urogenital infection. 3.Chemical irritants: perfumed products, detergents 4.Physical damage: sexual intercourse, tampons Causes of therapeutic failure: 1.Resistance to the antifungal 2.Presence of species out side the spectrum of the antifungal. Non albicans C are associated with vaginitis & are more resistant to conventional antifungal therapy. These is evidence that C glabrata & C Krusei are resistant to fluconazole & itraconazole (Rex,2000)ABOUBAKR ELNASHAR
  28. 28. Complicated VVC Recurrent VVC Define: 4 or more episodes/Y. Reappearance of C in the vagina of a patient, who was cured, & may be either Relapse, (due to re-growth of a previously undetected residual population of C.) or Re-infection (the vagina is re-inoculated from some extravaginal source). ABOUBAKR ELNASHAR
  29. 29. Prevalence: 5% in family planning clinic & 10% in antenatal clinic. No apparent predisposing or underlying conditions in most cases. Pathogenesis: Non-albicans are found in 30% of cases Source: 1.Vaginal inoculation: most common Intestinal reservoir theory Sexual transmission 2.Vaginal recurrence ABOUBAKR ELNASHAR
  30. 30. Although iron deficiency anaemia has been suggested as a cause of recurrent VVC, there is no evidence to support this. DM is rarely newly diagnosed. Allergic rhinitis/hayfever may be immunologically linked with RVVC. Mechanisms: 1.Increased C virulence 2.Host factors Decreased secretory local immunity IgE mediated hypersensitivity reaction Loss of lactobacilli protective effect ABOUBAKR ELNASHAR
  31. 31. Treatment: .Vaginal culture should be obtained to confirm clinical diagnosis & to identify unusual species, including non-albicans species, particularly C glabrata (not form hyphae). 1. Longer duration of initial therapy a.7-14 days of topical therapy or b. 150-mg, oral dose of fluconazole repeated 3 days later to achieve mycologic remission before initiating a maintenance therapy. In contrast to severe VVC, increasing the length of therapy by up to 1 week, for example by adding a second dose of fluconazole, does not improve response (Sobel et al, 2001) ABOUBAKR ELNASHAR
  32. 32. 2. Maintenance (Suppressive) therapy for 6 months: Clotrimazole (500-mg dose vaginal sup once weekly) Ketoconazole (100 mg once daily) Fluconazole (100-150 mg once weekly) Itraconazole (400 mg once monthly or 100 mg once daily) The frequency of therapy depend on frequency of attacks (White & Vanthuyne,2002): > 1/month: weekly doses, 1/month: monthly doses. Twice-monthly doses are usually adequate: D8 & D 18 of the cycle just before the hormonal peaks ABOUBAKR ELNASHAR
  33. 33. Treatment of the husband: controversial Treatment of the predisposing factors: Nitrofurantoin & nalidixic acid are recommended for UTI since they give low tissue levels. Psychosexual problems are common in RVVC, use of vaginal lubricants is important Relapse: 40% of women, the cycle of suppressive therapy can be continued indefinitely (Sobel et al,1992) ABOUBAKR ELNASHAR
  34. 34. Side effects of oral azoles: are few (Inman et al,1993) 1.Gastrointestinal symptoms 2.Headache 3.Interactions with other drugs: astemizole, calcium channel antagonists, cisapride, coumadin, cyclosporin A, oral hypoglycemic agents, phenytoin, theophylline, rifampicin. .If there is poor response: typing to exclude C glabrata: Itraconazol 200 mg daily for a month combined with Nystatin 500 iu qds orally & nystatin pessaries one bd for 3-4 months (Emens, 1998). Monitoring of liver function is mandatory ABOUBAKR ELNASHAR
  35. 35. Severe VVC: Response to short course of topical or oral therapy is poor Topical azole 7-10 days or Fluconazole in 2 sequential doses (second dose 72 hrs after initial dose) ABOUBAKR ELNASHAR
  36. 36. Non-albicans VVC 1.First line therapy: Longer duration therapy with a non-fluconazole azole is recommended i.e; Nstatin pessaries once or twice nightly for 14 days. 2.2nd line treatment (If recurrence occurs) 600 mg of boric acid in gelatin capsule vaginally once daily for 2 weeks. ABOUBAKR ELNASHAR
  37. 37. 3.The final resort: Topical 4% flucytosine, the only fungicidal agent, & amphotericin B (Fungizone)in lubricating gjelly for 14 nights 4.If non-albicans VVC continues to recur, a maintenance regimen of 100,000 units of nstatin delivered vaginally. 5. Intravaginal painting with gentian violet & oral progesterone ( little information is available) ABOUBAKR ELNASHAR
  38. 38. Non-C. albicans-related disease is less likely to respond to azole therapy (184). Vaginal boric acid, administered in a gelatin capsule at a dosage of 600 mg daily for 14 days, cures up to 70% of C. glabrata infections (238). Treatment with AmB suppositories (50 mg nightly for 14 days) is another option with minimal side effects that has shown to be successful in 70% of women with non-C. albicans VVC, mostly due to C. glabrata, that did not respond to azole treatment (197). Other alternatives include topical 17% flucytosine cream alone or in combination with 3% AmB cream administered daily for 14 days,albeit at considerable expense due to the high cost of flucytosine (189). Of note is that all the treatment options for non-C. albicans VVC need to be compounded. ABOUBAKR ELNASHAR
  39. 39. Compromised host: 1.Correction of the condition 2.Prolonged conventional treatment course (7-10 days) Pregnancy: Only topical azole therapies applied for 7 days are recommended (CDC, 2002) ABOUBAKR ELNASHAR
  40. 40. VVC During pregnancy VVC is more common during pregnancy Cochrane library,( 2002): •There is no evidence that VVC is harmful to the baby •Azole drugs are more effective than nystatin. •Treatment for 7 days is necessary. Treatment for > 1w confer no extra benefit. 4-day course will cure half of infections & 7 day course cures over 90%. ABOUBAKR ELNASHAR
  41. 41. •There is no evidence that any one azole is any more effective than another. •Oral antifungal is not known to be effective or safe in pregnancy. •Benjamin et al (2000) reported that •itraconazole is safe during pregnancy. It is teratogenic in rat through affecting the adrenal gland. These adrenal effects do not occur in human being. ABOUBAKR ELNASHAR
  42. 42. ABOUBAKR ELNASHAR

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