UNIVERSITY OF PERPETUAL HELP SUBJECT: MICROBIOLOGY

DR. JOSE G. TAMAYO MEDICAL UNIVERSITY TOPIC: Sexually Transmitted Infections

COLLEGE OF MEDICINE DATE: November 2016

LECTUER: Dra. Amoranto

 Chlamydia: Life Cycle

SEXUALLY TRNASMITTED DISEASES

 STDs are diseases and infections which are capable of being spread
from person to person through:
 sexual intercourse
 oral-genital contact or in non-sexual ways
 IV drug use

 What are the symptoms? How would I know if I have been

infected?
 Sores (either painful or painless)
 Blood in urine
 Burning sensation when urinating A. Normal Cervix B. Chlamydia Cervicitis
 Rashes
 Itching
 Bumps
 Warts
 Unusual discharge

PELVIC INFLAMMATORY DISEASE

 10%-20% women with Gonococcal infection develop PID

 In Europe and North America, higher proportion of C. trachomatis
than N. gonorrhoeae in women with symptoms of PID
 CDC minimal criteria
 uterine adnexal tenderness
 cervical motion tenderness
 Other symptoms include
 endocervical discharge
 Fever
 lower abdominal pain C. Mucopurulent Cervicitis D. Bacteria: Chlamydia
 Complications:
 Infertility: 15%-24% with 1 episode PID secondary to GC or  Laboratory Tests for Chlamydia
chlamydia  Tissue culture has been the standard
 7X risk of ectopic pregnancy with 1 episode PID chronic  Specificity approaching 100%
pelvic pain in 18%  Sensitivity ranges from 60% to 90%
 Non-amplified tests
CHLAMYDIA  Enzyme Immunoassay (EIA), e.g. Chlamydiazyme
 Four million new cases occur each year  sensitivity and specificity of 85% and 97%
 SYMPTOMS: respectively
 Fever  useful for high volume screening
 weight loss for no reason  false positives
 swollen glands  Nucleic Acid Hybridization (NA Probe), e.g. Gen-Probe
 Fatigue Pace-2
 Diarrhea  sensitivities ranging from 75% to 100%;
 white spots on the mouth specificities greater than 95%
 FEMALE SYMPTOMS:  detects chlamydial ribosomal RNA
 Vaginal discharge (white or grey) or burning with urination  able to detect gonorrhea and chlamydia from one
 Lower abdominal pain swab
 Bleeding between menstrual periods  need for large amounts of sample DNA
 Low-grade fever (later symptom)  DNA amplification assays
 polymerase chain reaction (PCR)
 MALE SYMPTOMS:  ligase chain reaction (LCR)
 Discharge from the penis and/or burning when urinating  Sensitivities with PCR and LCR 95% and 85-98%
 Burning and itching around the opening of the penis respectively
 Pain and swelling in the testicles  specificity approaches 100%
 Low –grade fever (associated with epididymitis –  LCR ability to detect chlamydia in first void urine
inflammation of the testicles)
 NON-GONOCOCCAL UREHTRITIS  Each year approximately 650,000 people in the United States are
 Etiology: infected with gonorrhea
 20-40% C. trachomatis  People get gonorrhea from close sexual contact (anal sex, oral sex.,
 20-30% genital mycoplasmas (Ureaplasma urealyticum, and vaginal)
Mycoplasma genitalium)  Gonorrhea can also be spread from mother to child during birth.
 Occasional Trichomonas vaginalis, HSV  Gonorrhea infection can spread to other unlikely parts of the body
 Unknown in ~50% cases  Symptoms of Gonorrhea
 Symptoms  Appear 5-7 days or can take up to 30 days
 Mild dysuria  sore or red throat if you have gonorrhea in the throat from
 mucoid discharge oral sex
 Diagnosis  rectal pain
 Ure  blood and pus in bowel movements if you have gonorrhea in
 the rectum from anal sex
 Leukocyte esterase (+)  FEMALE SYMPTOMS - may show up 2-21 days after having sex
 May notice a yellow or white discharge from the vagina
NEISSERIA  May experience burning or pain when urinating
 General Characteristics of Neisseria spp.  Bleeding between periods
 Aerobic  Heavier and more painful periods
 Gram-negative cocci often arranged in pairs (diplococci) with  Cramps or pain in the lower abdomen, sometimes with
adjacent sides flattened (like coffee beans) nausea or fever
 Oxidase positive  MALE SYMPTOMS
 Most catalase positive  Yellow or white drip/discharge from
 Nonmotile  Burning or pain when urinating
 Acid from oxidation of carbohydrates, not from fermentation  Frequent urination
 Important Human Pathogens  Swollen testicles
 Neisseria gonorrhea  Clinical Manifestations
 Neisseria meningitidis  Urethritis - male
 Other species normally colonize mucosal surfaces of oropharynx  Incubation: 1-14 d (usually 2-5 d)
and nasopharynx and occasionally anogenital mucosal membranes  Sx: Dysuria and urethral discharge (5% asymptomatic)
 Neisseria Associated Diseases  Dx: Gram stain urethral smear (+) > 98% culture
 Urogenital infection - female
 Endocervical canal primary site
 70-90% also colonize urethra
 Incubation: unclear
 symptoms usually in 10 days
 Sx: majority asymptomatic; may have vaginal
discharge, dysuria, labial pain/swelling, abdominal pain
 Dx: Gram stain smear (+) 50-70% culture
 Epidemiology of Gonorrhea
 Seriously underreported sexually-transmitted disease
 350,000 reported cases in USA in 1998
NEISSERIA GONORRHEA  Down from 700,00 cases in 1990
 Found only in humans with strikingly different
 Readily transmitted by sexual contact epidemiological presentations for females and males
 Gram-negative diplococci flattened along the adjoining side  Asymptomatic carriage is major reservoir
 Fastidious and susceptible to cool temperatures, drying and fatty  Transmission primarily by sexual contact
acids  Lack of protective immunity and therefore reinfection is
 Requires complex media pre-warmed to 35-37C common, partly due to antigenic diversity of strains
 Soluble starch added to neutralize fatty acid toxicity  Higher risk of disseminated disease in patients with late
 Grow best in moist atmosphere supplemented with CO2 complement deficiencies
 Produce acid from glucose, but not from other sugars

GONORRHEA
  Prevention & Treatment
 Penicillin no longer drug of choice due to:
 Continuing rise in the MIC
 Plasmid-encoded beta-lactamase production
 Chromosomally-mediated resistance
 Uncomplicated infxn: ceftriaxone, cefixime or fluoroquinolone
 Combined with doxycycline or azithromycin for dual
infections with Chlamydia
 Chemoprophylaxis of newborns against opthalmia
neonatorum with 1% silver nitrate, 1% tetracycline, or 0.5%
erythromycin eye ointments
 Pathogenesis of Neisseria gonorrhea  Treatment of newborns with opthalmia neonatorum with
 Fimbriated cells attach to intact mucus membrane epithelium ceftriaxone
 Capacity to invade intact mucus membranes or skin with  Measures to limit epidemic include education, aggressive
abrasions detection, and follow-up screening of sexual partners, use of
 Adherence to mucosal epithelium condoms or spermicides with nonoxynol 9
 Penetration into and multiplication before passing  Analytic Performance of Different Laboratory Detection Methods
through mucosal epithelial cells for Nesseria gonorrhoeae
 Establish infection in the sub-epithelial layer
 Most common sites of inoculation:
 Cervix (cervicitis) or vagina in the female
 Urethra (urethritis) or penis in the male
 Gonococcal Virulence Factors
 Antiphagocytic capsule-like negative surface charge
 Only fimbriated (piliated) cells (formerly known as colony
types T1 & T2) are virulent
 Acquisition of iron mediated through Tbp 1 and Tbp 2
(transferrin-binding proteins), Lbp (lactoferrin binding protein)
& Hbp (hemoglobin-binding protein)
 Outer membrane proteins (formerly Proteins I, II, & III)
 Por (porin protein) prevents phagolysosome fusion
following phagocytosis and thereby promotes
intracellular survival
 Opa (opacity protein) mediates firm attachment to
epithelial cells and subsequent invasion into cells NOTE: Importance of Sensitivity vs. Specificity for any Diagnostic Test
 Rmp (reduction-modifiable protein) protects other
surface antigens from bactericidal antibodies
 Lipooligosaccharide (LOS) (Lipid A plus core polysaccharide
but no O-somatic antigen polysaccharide side chain) has
endotoxin activity
 IgA1 protease
 Acquisition in last two decades of two types of antibiotic
resistance: A. Gonorrhea gram stain B. Ophthalmia neonatorum
 Plasmid-encoded beta-lactamase production
 Chromosomally-mediated changes in cellular GENITAL ULCER DISEASES
permeability inhibit entry of penicillins, tetracycline,  Painful
erythromycin, aminoglycosides  Chancroid
 Laboratory Characterization  Genital herpes simplex
 Small, gram-negative diplococci in the presence of  Painless
polymorphonuclear leukocytes (PMN’s) seen microscopically  Syphilis
in purulent urethral discharge  Lymphogranuloma venereum
 Susceptible to drying and cooling  Granuloma inguinale
 pre-warmed selective (e.g., modified Thayer-Martin,
Martin-Lewis agars) SYPHILIS
 non-selective media (chocolate blood agar) with moist  The long range effects can be very serious, including death
atmosphere containing 5% carbon dioxide  In the United States, an estimated 70,000 new cases of syphilis in
 Some strains inhibited by vancomycin and toxic substances like adults
fatty acids and trace metals in protein hydrolysates and agar found  passed from person to person through direct contact with a syphilis
in nonselective media sore
 Five morphologically distinct colony types (formerly T1 through T5)  Sores mainly occur on the external genitalia, vagina, anus, or
that can undergo phase transition are no longer considered to be a rectum; it can also occur on the lips and in the mouth
useful distinction
 Transmission of the organism occurs during vaginal, anal, or oral sex
 There are more than 70,000 new cases of syphilis each year
 Syphilis, chronic and slowly progressive, is the third most common
sexually transmitted disease
SPIROCHETES
 Gram negative bacteria
 long, thin, helical and motile
 Axial filaments
 form of flagella
 locomotory organelles
 found between the peptidoglycan layer and outer membrane
and running parallel to them
 Treponema pallidum
CONGENITAL SYPHILIS
 Symptoms - Stage 1
 Symptoms usually appear 10-90 days after contact
 An infected person gets a sore (chancre), which may be
painful at the point of contact (mouth, anus, rectum, throat
or the sex organ)
 chancre is usually firm, round, small, and painless
 appears at the spot where the bacterium entered the
body
 lasts 1-5 weeks and heals on its own
 disappear on its own, but may last 4-6 weeks
 In the female, the chancre is often internal and cant be seen
 Secondary Syphilis - Clinical Manifestation
 Represents hematogenous dissemination of spirochetes
 Usually 2-8 weeks after chancre appears
 Findings:
 rash - whole body (includes palms/soles)
 mucous patches
 condylomata lata - HIGHLY INFECTIOUS
 constitutional symptoms
 After the chancre comes a copper-colored skin rash which
may appear on the palms of the hands, soles of the feet, or in
more severe cases covers the entire body
 The rash may be accompanied by fever, headaches,
indigestion, loss of appetite, or loss of hair in spots over the
scalp
 Sn/Sx resolve in 2-10 weeks
 Third Stage - Latent Period
 All symptoms disappear so that the victim thinks he/she is
cured
 If no treatment was given
 bacterium remains in the body
 begins to damage the internal organs including the
brain, nerves, eyes, heart, blood vessels, liver, bones,
and joints
 Fourth Stage - Tertiary
 The results of the internal damage from the 3rd stage shows
up many years later
 Ten, twenty, even thirty years after the initial infection
 sudden heart attack
 failure of vision
 loss of motor coordination
 mental disturbances
 Diagnosis(1)
 organisms are often present in sufficient numbers in exudates
detected by dark field microscopy
 actively motile organisms appears brightly lit against the dark
backdrop
 The FTA-ABS is often used
 Diagnosis(2)
 Serological methods are usually used to detect syphilis
 Screening methods are based on detecting serum antibodies
to cardiolipin in patients
 VDRL and RPR are also widely used
 Therapy
 No vaccine exists
 antibiotic therapy (usually penicillin G) is highly effective
HERPESVIRIDAE
 double stranded DNA viruses with envelope
 ubiquitous, world-wide distribution
 8 human herpesviruses recognized; species specific
 Latency
 “once infected, always infected”
 site varies with virus type:
 HSV 1 & 2, VZV - sensory nerve ganglia
 CMV, EBV, HHV6, HHV7 – lymphocytes
 Replication occurs in the nucleus of infected cell
 Viral DNA remains episomal (i.e. not integrated into host cell DNA)
 Transmission
 do not survive for prolonged periods in the environment
 requires inoculation of fresh virus-containing body fluid of
infected person into susceptible tissue of uninfected person
 may be transmitted during primary or reactivation infections;
often the person shedding virus is asymptomatic
 HERPES SIMPLEX VIRUS (HSV)
Antibody
0 7d 14d 21d 28d 2m 3m 6m 12m 2yr 3yr
Time
 Spread via contact with infected secretions:
 transmission both during lesions or from asymptomatic
carrier
 1-15% of adults excrete HSV-1 or HSV-2 at any given time
 efficiency of transmission of HSV-2 is lower than HSV-1
 Clinical Disease: Primary vs Recurrent
 HERPES
 Symptoms usually show 2-20 days after contact.
 May be extremely painful or very mild.
 “outbreaks” of blisters and ulcers.
 Once infected with HSV, people remain infected for life.
 Stress, bruising, chaffing, or a woman’s period may cause an
onset of the disease.
 FEMALE SYMPTOMS
 Blisters in or around the vagina, fever and headaches
 MALE SYMPTOMS
 Small sore or cluster of blisters on the penis
 GENITAL HERPES SIMPLEX
 Direct contact – may be with asymptomatic shedding
 Primary infection commonly asymptomatic; symptomatic
cases sometimes severe, prolonged, systemic manifestations
 
 Recurrence a potential
 Diagnosis:
 Culture
 Serology (Western blot)
 PCR
 Epidemiology of Genital Herpes
 One of the 3 most common STDs, increased 30% from
late 70s to early 90s
 25% of US population by age 35
 HSV-2: 80-90%, HSV-1: 10-20% (majority of infections in
some regions)
 Most cases subclinical
 Transmission primarily from subclinical infection
 Complications: neonatal transmission, enhanced HIV
transmission, psychosocial issues
 Epidemiology of HSV Infections
 Only 10-15% of HSV-2 primary infections are symptomatic
 4 out of every 5 people with genital herpes have not been
diagnosed; three out of five people have symptoms that are
unrecognized as genital herpes
 Recurrent disease can be either symptomatic or
asymptomatic
 Herpes Simplex Virus - Clinical Manifestations
 Recurrent Infection is common with both HSV-1 and HSV-2:
due to reactivation of endogenous virus despite antibodies
 recurrent lip or perioral lesions in 20 - 40 %
 recurrent genital lesions in 60 - 90%
 frequency depends on sex, HSV type, titre of
neutralizing antibody
 precipitating factors include: sunlight, fever, local
trauma, menstruation, emotional stress
 Herpes labialis (“cold sore”) - pain, burning, itching
 vesicles to ulcer/crust in 48 hrs; healing within 8 - 10
days
 Genital lesions
 pain, itching, burning for several hours before vesicles
appear; healing within 6 - 10 days
 HSV -CONGENITAL/PERINATAL
 Intrauterine infection: rare; follows 10 infection
 Perinatal infection:
 75% are due to HSV 2; acquired during delivery
 many women unaware they are infected; 60 - 80% have
no signs or symptoms of genital herpes at time of labor
(asymptomatic shedders)
 HSV-1 acquired from maternal genital, oral or breast
lesions, paternal or other family member, or nosocomial
infection from other infected babies
 pregnancy is associated with state of
immunosuppression: increase shedding,increase
reactivation, increase recurrences
 subclinical infection in neonates is uncommon
 not all infants of infected mothers will become infected;
depends on 10 (30 – 50% risk) vs recurrent disease
(1 – 3% risk)
 Clinical manifestations of perinatal infection:
 disseminated ± CNS disease (49%)
- liver, lungs, eyes, CNS; 80 - 85% mortality
 localized to CNS, skin, eyes, oral cavity (50%)
- 10 - 40% mortality
asymptomatic infection (1%)
 Treatment:
 Mother - acyclovir contraindicated during pregnancy
 Neonate - acyclovir if mother has active lesions or prolonged
membrane rupture
 Prevention:
 maternal history, surveillance
 if with active lesions at time of delivery then C-section
indicated
 Diagnosis
 History and physical examination
 Vesicle fluid: culture, EM, immunofluorescence, molecular
(e.g. PCR)
 Serology
 difficult to distinguish HSV-1 and HSV-2; no reliable IgM
test
 seroprevalence
 cannot distinguish 1° infection from recurrent disease
 ? Value of type-specific serology
 Immunoglobulin response in HSV infections
 IgM Arrives approximately 7 days before IgG
 IgM can reappear during recurrences
 HSV Serology
 Patients with Primary Infection
 18% -30% with both IgG and IgM antibodies
 Patients with Recurrent HSV Infection
 65% only IgG
 35% both IgG and IgM
 When should we test for HSV 2?
 Symptomatic patients: Use to supplement virus detection
tests when:
 Lesions are negative or not sampled for virus
 Recurring symptoms suggest atypical or undiagnosed
herpes
 Lesions appear herpetic but may have other etiology
 High risk patients but not symptomatic:
 Patient has history of symptoms
 Patient’s partner has genital herpes
 Patient has a history of other STDs
 Patient is at risk of HIV infection
 Pregnancy:
 To screen for HSV-2 unrecognized infection
 To determine risk of acquiring infection
 To determine partner’s status for treatment and
counselling
 Herpes Simplex Virus - Prevention and Treatment
 Supportive
 education, psychological support, analgesics, keep area
clean and dry
 Antiviral (Acyclovir / Famciclovir / Valacyclovir)
 topical, oral, intravenous
 all effective in 1° genital herpes -
 minimal effect on recurrent attacks
 pattern and natural history not affected
 suppressive (oral) therapy for severe and/or frequent
attacks; once stopped, episodes may recur
 No vaccine
HUMAN PAPILLOMA VIRUS
 HPV is the virus that causes warts.
 More than 100 different kinds, 30-some of this cause genital HPV.
 Spread by sexual contact or from mother to baby.
 Genital warts appear 6 weeks to 8 months after contact with an
HPV infected person.
 The most common sexually transmitted disease worldwide.
 Certain types of HPV are linked with cervical cancer.
 Divided into 2 subcategories: Genital Warts and Cervical Dysplasia.
 Most people do not know they have it.
 There are high risk and low risk types of it.
 History
 The papillomaviruses are part of the PAPOVAVIRIDAE family
of DNA tumor viruses.
 First discovered in the early 40’s.
 Gained notoriety in the early 80’s when it was discovered that
some types of HPV caused cervical cancer.
 Morphology
 Papilloma virus genome is circular covalently closed double
stranded DNA of about 8 kbp.
 All PV genes are coded in one of the 2 DNA strands utilizing
the alternative splicing for the individual expression of each
gene.
 Papillomavirus expression is characterized by a large array of
mRNAs cells coding for different genes.
 55 nm in diameter.
 Mechanism of Infection
 All PV exhibit extreme specificity for infection on epithelial
cells.
 The papillomavirus epitheliotrophy resides in the interaction
of specific transmission factors with the viral regulatory
region .
 The infection normally results in hyperproliferation of the
host cell and may lead to transformation and immortalization.
 Genital warts
 Sometimes called condylomata acuminata.
 Are soft, moist or flesh colored, and appear in the genital area
within weeks or months after infection.
 Sometimes appear in clusters and are either raised or flat,
small or large.
 Women: appear in the vulva, cervix, vagina and anus.
 Men: Can appear on the scrotum or penis.
 Genital warts/Venereal warts
 Growths that appear on the vagina or penis, near the anus,
and sometimes in the throat.
 They are caused by viruses and spread through sexual
contact.
 The virus that causes genital warts is spread by vaginal or anal
intercourse and by oral sex.
 Warts may appear within several weeks after sex with a
person who has HPV; or they may take months or years to
appear; or they may never appear.
 HPV & CERVICAL CANCER
 Infection is generally indicated by the detection of HPV DNA
 HPV infection is causally associated with cervical cancer and
probably other anogenital squamous cell cancers (e.g. anal,
penile, vulvar, vaginal)
 Over 99% of cervical cancers have HPV DNA detected within
the tumor
 Routine Pap smear screening ensures early detection (and
treatment) of pre-cancerous lesions
 Estimates for HPV-Associated Cancers
Cervical cancer:
 In the U.S., an estimated 14,000 cases and 5,000 deaths
 Worldwide, an estimated 450,000 cases and 200,000
deaths
 HPV Types
 Numbered in order of discovery.
 30 HPV types primarily infect the squamous epithelium of the
lower anogenital tracts of both males and females.
 HPV types 6, 11, 42, 43, or 44 present as papillary condylomas,
may also present as flat lesions that may or may not be visible
to the unaided eye are part of the “low-risk” HPV types.
 Types 16, 18, 31, 33, 35, 45, 51, 52, and 56 are considered
“high-risk” types because they have been found in cervical
and other lower genital tract cancers.
 How HPV Causes Cancer
 HPV DNA integrates into the host genome.
 The proteins E6 and E7 are produced from the resultant DNA.
 E6 binds and degrades p53 (a tumor suppressor gene).
 If the DNA is altered, the cell keeps replicating. The mutation
rate of the cell increases.
 E7 binds and degrades retinoblastoma (another tumor
suppressor gene).
  Retinoblastoma normally keeps the cell from growing too fast
or responding to growth stimulators. This inhibitory factor is
now lost.
 without these two mechanisms to slow down cell growth and
prevent mutation. . .
 Malignant Transformation Occurs.
 Symptoms
 Usually the warts look like tiny cauliflowers, but sometimes
they are flat.
 The warts may cause itching, burning and some pain, but
often don’t cause any pain at all.
 Warts may be inside the vagina or on the cervix, or in the
rectum or throat, so you might not notice them.
 They might also be so small that you cannot see them.  The parasites multiply by longitudinal binary fission.
 HPV Treatment  Species of Trichomonas are found in man, monkeys, cattle,
 Genital warts can be treated by a doctor and by different rodents and fowls.
methods.  Three species of Genus Trichomonas occuring in man:
 Podofilox gel: A patient-applied treatment for external genital
warts.  Trichomonas tenax: the mouth.
 Imiquimod cream: A patient-applied treatment.  Trichomonas hominis: the intestine.
 Chemical treatments (including trichloracetic acid and  Trichomonas vaginalis: the urogenital tract.
podophyllin), which must be applied by a trained health care  Trichomonas vaginalis is the only pathogenic one
provider to destroy warts.
 Cryotherapy: Uses liquid nitrogen to freeze off the warts.  Trichomoniasis
 Laser therapy: Uses a laser beam or intense lights to destroy  An estimated 5 million new cases occur each year in women
the warts. and men.
 Electrosurgery: Uses and electric current to burn off the  Occurs in vagina of women so may be sexually transmitted to
warts. men using infected washcloths and towels.
 Surgery: Can cut away the wart in one office visit .  It is transmitted to the baby during delivery.
 Interferon: an antiviral drug, which can be injected directly  It also can occur in the urethra (carries urine to penis) in men,
into warts. doesn’t have symptoms usually.
 Cure/Prevention  Method of Infection
 There is currently no cure for human papillomavirus.  Sexual intercourse: main method of transmission since the
 Once an individual is infected, he or she carries the virus for organism cannot survive long periods outside the body.
life even if genital warts are removed.  Contaminated underwear, toilet seats and towels.
 Vaccines are now available.  Infants may be infected from their mothers during birth.
 Cervarix (2 valent)  Life cycle
 Gardasil (4 Valent)
- Can be given to males
 If left untreated, some genital warts regress on their own.

Trichomonas vaginaiis

 Morphology of genus Trichomonas

 The trichomonads possess a trophic stage only. The cystic
stage is absent.
 The trophozoites have a single vesicular nucleus, four free
flagella and the fifth flagellum runs along the outer margin of
an undulating membrane, which is supported at its base by
the costa.
 A prominent axostyle which is a stout median rod is also
present
 Anteriorly there is a cleft like opening, the cytostome, which
lies opposite the undulating membrane.
 SYMPTOMS:
 Appear within 5 to 28 days of exposure
 Women usually have a vaginal discharge that
 FEMALE SYMPTOMS:
 Itching and burning at the outside of the opening of the
vagina and vulva.
 Painful and frequent urination
 Heavy, unpleasant smelling greenish, yellow discharge
 MALE SYMPTOMS:  None of these symptoms or signs is specific for the
 Usually nothing, or discomfort in urethra, inflamed head of  As many as 50% of women diagnosed based on these clinical
the penis. features alone do not have candidiasis
 Diagnosis  Differential Diagnosis of Vaginitis
 In females:  Infectious
 identification of parasites by microscopic examination of  BV 40-50%
sedimented urine and vaginal secretion.  VVC 20-25%
 Vaginal smear from the vaginal fornices. (if the wet  Trichomonal 15-20%
smear can’t be examined immediately, the sample  Less Common
should be air dried, fixed and stained with giemsa ).  Atrophic vaginitis w/ 2° bacterial infection
 Culture of the organism.  Foreign body w/ 2° bacterial infection
 Streptococcal vaginitis
 In males:  Ulcerative vaginitis
 The parasite can be present in the sedimented urine or  HIV
prostatic secretions following massage of the gland.  Noninfectious Chemical/irritant
 Treatment  Allergic, contact dermatitis (lichen simplex)
 Metronidazole (flagyl)  Traumatic
 oral tablets: 250 mg TID for 7 days  Atrophic vaginitis
 vaginal suppositories: 250 mg for 7 days  Postpuerperal atrophic vaginitis
 Toxicity: nausea, vomiting, rashes, metallic taste in the  Desquamative inflammatory vaginitis
mouth  Erosive lichen planus
 Contraindications: Pregnancy and alcohol intake.  Collagen vascular disease e.g. Behcets, Pemphigus
 Tinidazole (fasigyn)  The most common cause of culture negative vulvovaginitis is
 2 g (4 tablets) once contact dermatitis.
 Toxicity: Occasional metallic taste, vomiting and rash.  Etiologies: soaps, deodorants, underwear, detergents,
 Since imidazole compounds are contraindicated during pads, spermicides, douche solution, and vaginal
pregnancy, clotrimazole can be given in the form of vaginal lubricants, azole antifungals
suppositories.  Vulvovaginal Candidiasis - Diagnosis
 Clotrimazole  pH 4-4.5
 vaginal suppositories: 100 mg for 7 days.  Wet mount
 N.B.: Both sexual partners should be treated.  10% KOH
 In general, both oral and local vaginal treatment are  Culture
indicated, and correction of vaginal pH by acidic
douches should be done.

 Vulvovaginal Candidiasis
 More than 50% of women age 25 yr will have
 had at least one episode of physician
 diagnosed VVC
 An estimated 75% of all women will develop a
 yeast vaginitis sometime during their lifetime
 40-50% will have a 2nd infection
 5% of women will have recurrent VVC
 Candida Culture – Differentiation
 Candida Infection of the Vaginal Mucosa/Vaginitis
 CANDIDA
 Vaginitis accounts for more than 10 million physician office visits annually
 tropicalis – steel blue
 Vaginitis is most common reason for patient visit to OB-Gyn.
 krusei – rose, fuzzy
 First OTC antifungal 1991 - clotrimazole
 albicans - green
 OTC antifungal therapies rank among top 10 selling products
 glabrata - pink, small, smooth
 OTC antifungal therapies bring in more than
 Clinical Features
 Symptoms Signs
 Vulvar itching Erythema
 Vulvar soreness Fissuring
CHROM AGAR
 Vaginal discharge Discharge
 External dysuria Edema
 Superficial dyspareunia
 Signs
 Erythema
 Fissuring
 Discharge
 Edema
 VVC Treatment
 Uncomplicated VVC
 The differences among antimycotics are not clinically
relevant

 Complicated VVC
 In complicated VVC, yeast or host factors exist that have
an adverse impact on the cure rate
 All topical and oral azole therapies give an 80-95% clinical and
mycological cure rate.
 *Nystatin preparations give a 70-90% cure rate
 Host:
 Uncontrolled diabetes
 Immunocompromised
 Ongoing antibiotics
 Severe inflammation
 Recurrent VVC
 Yeast: Non-albicans
 The complicated category = more prolonged therapy e.g.
Fluconazole 150 mg po day 1 and day 4.
 Single dose = therapeutic concentrations for 72-96 h,
 Two doses – 1 week
 VVC Treatment and Pregnancy
 Currently no oral regimens are approved for use in pregnancy
 Fluconazole is category C
 Azoles are teratogenic – demonstrated in both animals and
humans
 Topical miconazole nitrate is absorbed less than other
through the mucous membranes and may be used
 Longer courses may be necessary.
 Recurrent Vulvovaginal Candidiasis 250 million dollars/year in US alone
 Definition = 4 or more episodes per year
 Affects less than 5% of women
 Pathogenesis is most often inapparent
 The first step in management is to make sure the patient
actually has Candida VV
 Most common causes of chronic vaginal symptoms include:
 recurrent vaginal candidiasis
 Vulvar vestibulitis syndrome
 Irritant dermatitis
 Often related to topical antifungals
 The most common reason patients fail to respond to

 Suppressive Antifungal Regimens

 Oral Agent
 Ketoconazole - 100 mg/d 100 mg/d
 Fluconazole - 100 mg/week 100 mg/week
 Itraconazole - 200 mg/month
400 mg/month
 Topical agent
 Clotrimazole - 500 mg supp/week
200 mg supp 2x/week
 Terconazole - 5 g 1x/week
 Boric acid - 600 mg/d – 5d during menstrual period for
4-6 months
 On maintenance - more than 90% will not experience a
relapse
 Up to 50% of women will relapse after therapy is
discontinued 200 mg supp 2x/week
200 mg/month
400 mg/month antifungal therapy is i