STDs and PID...Obstetrics and gynaecology

Sexually transmitted infections

1. STDs and PID
Dr Bellington Vwalika
Obstetrician and Gynaecologist-UTH
Honorary Lecturer -UNZA

2. STDs are very common
5 of the top 10 most frequently reported
diseases are STD
STD accounted for 87% of all cases
reported among the top ten most
frequently reported diseases in 2000
More than 12 million Americans (including
3 million adolescents) are infected each
year

3. Who Gets STDs?
Anyone who is having sex...regardless of
their age, gender, race and socioeconomic
status
Inner city, low income communities have
higher incidence:
women,
teens and young adults,
substance users
Anyone who is having unprotected sex is at
risk

4. STD are important because:
They are common and cause significant
morbidity; incurable viral STD increasing
They are preventable
Chlamydia has major adverse upper
genital tract sequelae
Both ulcerative and non-ulcerative STD
facilitate HIV transmission
MOST PEOPLE WITH STD ARE SEEN
OUTSIDE OF STD CLINICS!

5. STD-attributable Morbidity
Cancer (HPV, HBV, HCV, HSV8)
Immunodeficiency (HIV)
Infertility (Chlamydia, Gonorrhea, PID)
Ectopic Pregnancy (CT,GC,PID)
Chronic Liver disease (HBV, HCV)
Perinatal (pre-term; LBW; stillbirth;
occular, respiratory, and systemic disease)

6. “Silent” STD are the Majority
Most chlamydiain women, many in men
Most gonorrhea in women
Most genital herpes (HSV)
Almost all human papillomavirus(HPV)
HIV for most of its clinical course

7. STD: Largely Asymptomatic
75% of Chlamydia in women
33-50% of Hepatitis B in adults
75% of Hepatitis C in adults
Almost all carcinogenic HPV types
Two-thirds HSV-2 infected adults have
no recollection of an episode of genital
herpes
Latency for infertility, cancer, and chronic
liver disease mask the associations

8. HIV-STD Interactions
Concurrent STD-HIV replication and viral
load
Concurrent STD -HIV shedding
STD increases risk of HIV acquisition due
to disrupted epithelial integrity, recruitment
of target cells
Community-wide control of STDs can
reduce HIV transmission/acquisition

9. STDs Increase Risk of HIV
Acquisition
Chlamydia risk 3-5 times
Genital HSV risk 3-6 times
Gonorrhea risk 3-5 times
Syphilis risk 3-4 times
Trichomonas risk 2-4 times
Other GUDs risk 4-6 times

10. PRINCIPLES IN MANAGEMENT
OF STDs
Screen for concurrent disease
Treat and screen regular partner for other
infections
Contact tracing –identification and
contacting recent sexual contacts for
screening and treatment
Confidentiality
Health education
Barrier methods of contraception

11. Chlamydia
Organism: intracellular bacteria
Transmission: penile, vaginal, anal,
perinatal
Sites infected: urethra, cervix, rectum
(eyes, resptract-neonates/infants)
Incubation: approx 1-3 weeks though most
cases are asymptomatic ( F>M)
Symptoms: Men-dysuria, clear or cloudy
urethral discharge, rectal pain and or
bleeding

12. Chlamydia
Symptoms: women-vaginal discharge,
dysuria, deep dyspareunia, spotting or
postcoitalhemorrhage, lower abdominal pain
Diagnosis: endocervicalswabs for MCS,
antigen detection, DNA amplification tests
Treatment: azithro, doxy, oflox, erythro,
amox
Prevention: barriers -abstinence -
monogamy high re-infection rate.

15. Gonorrhea
Organism: bacteria
Transmission: penile, vaginal, anal,
pharyngeal, perinatal
Sites infected: urethra, cervix, rectum,
pharynx (eyes-neonates/infants)
Incubation: approx 2-10 days though most
non-urethral infections are asymptomatic (
F>M)
Symptoms: Men-dysuria, purulent urethral
discharge usually green, rectal discharge,
pain and or bleeding

16. Gonorrhea
Symptoms: women-vaginal discharge,
dysuria, deep dyspareunia, spotting or
postcoitalhemorrhage, lower abdominal pain
Diagnosis: Gram stain, culture, antigen
detection, DNA amplification tests
Treatment: cefitaxime, cephtriaxone,
ciprofloxacin
Prevention: barriers -abstinence -
monogamy high re-infection rate

19. Syphilis
Organism: bacteria
Transmission: direct contact with an infected
site, perinatal
Sites infected: sex organs, blood, body tissue,
all organ systems
Incubation: approx 10-90 with average of 21d.
Symptoms: primary-chancre often painless
secondary-rash, mucus patch, alopecia
tertiary/latent-with no obvious symptoms for 5-
20+yearsdestructive lesions targeting bones,
heart, CNS etc

20. Syphilis
Diagnosis: physical exam, darkfield
microscopy, CSF and serology tests
Treatment: penicillin (benzathine, procaine)
Prevention: barriers -abstinence -monogamy
Serious outcome: increased risk of HIV
infection, severe organ damage, severe illness
or death in newborns.

29. Contrasting Most Common Types of VaginitisDiagnosis Normal BV VVC Trich
pH <4.7 >4.5 <4.5 >4.5
Discharge White, clearThin, homo-
geneous, gray,
adherent
White,
curdy
Yellow,
green,
frothy
Amine odor
(KOH)
None + None +/-
Micro Lactos Clue cells, no
lactos, other
bacteria, no
WBC
Yeast on
KOH
Trich, WBC
>10/hpf
Patient c/o None (?) Discharge, odorDischarge
pruritis,
rash,
fissures
Discharge,
pruritis, odor

30. Trichomonas
Organism: protozoa -Trichomonasvaginalis
Transmission: direct contact with an infected
site, sex toys and douching equipment.
Sites infected: vagina, male and female urethra
Incubation: 4-20 days with average 7 days
Symptoms: vulvaritching, odorous greenish-
yellow vaginal discharge, dysuriaand milky
urethral discharge in men.
Most men and some women are
asymptomatic and unaware.

31. Trichomonas
Diagnosis: microscopic evaluation of
discharge, culture (performs better
in women)
Treatment: metronidazole
Prevention: note: asymptomatic transmitters-
male partners should always be treated
barriers -abstinence -monogamy
Serious outcome: increased risk of HIV
infection, due to disruption of mucus
membrane (cervical inflammation)

35. Definition of BV
Gram stain findings (Nugent scale): based on
number of lactobacilli and other bacterial
morphotypes
Clinical findings (Amselcriteria): 3 of the
following must be present:
homogeneous discharge
pH >4.5
clue cells (>20%) on microscopy
amine odor on addition of KOH (+Whiff test)

36. BV Complications in Non-
Pregnant Women
PID:
Post-abortalPID
Post-hysterectomy infection

37. BV and Adverse Outcomes in
Pregnancy
Data support role for BV in promoting:
Post-abortalinfections
Preterm labor and delivery*
premature rupture of membranes
intramnioticinfection
histological chorioamnionitis
postpartum endometritis
spontaneous abortion in second trimester
(IVF)
*infection implicated in up to 40% of cases

38. BV: Wet Prep

39. BV: Gram Stain

40. Vulvovaginal Candidiasis
(VVC)
Vulvarcomponent often dominates picture
KOH prep + in 70-80% of symptomatic;
saline + in 30-50%
Albicansstill dominant (90%); glabratanext
Distinguish between two syndromes:
uncomplicated: sporadic; mild-mod sx, usually
albicans; nml(non-pregnant) host
complicated: recurrent; severe sx; non-albicans;
altered host (DM, preg, immune)

44. Human Papilloma Virus
Organism: Human Papilloma Virus (HPV)
Transmission: direct contact with an infected
site,low rate of perinatal/neonatal trans.
Sites infected: on or around the genitals, anal
area, rectum, cervix, urethra, oral, skin
Incubation: 30days -22 months
Symptoms: painless warts on infected area,
most people are asymptomatic and unaware.

45. Human Papilloma Virus
Diagnosis: physical exam, biopsy, DNA base
tests role of PAP
Treatment: no known cure, treatment vscontrol
(L-nitrogen, pod, aldara, condy, surgery)
Prevention: note asymptomatic shedding
avoid sexual contact during flare-ups
barriers -abstinence -monogamy
Serious outcome: strong association between
HPV (16,18) and cervical, vulvar, rectal, penile
cancer

46. Genital HPV Infection
Over 100 HPV types identified; > 30
genital types
Low-risk types (6,11)
genital warts and early Pap smear
changes (atypia, LSIL)
Higher-risk types (16,18,31,33,35,others)
“flat lesions” (SIL) and both early/late
Pap smear changes
All types cause subclinical infection

47. HPV and Anogenital
Cancer
Genital HPV
found in 95% of cervical cancers (and
majority of anal, vulvar, vaginal, penile
cancers)
In vitro studies
interaction between “high-risk” HPV
proteins and cellular oncogenes

48. Viral HepatitisAgentModes IncubationSerologic
tests
Chronic
infection
Vaccine
A Fecal-oral2-6 wks anti HAV
-total
-IgM
No Inactivated
whole HAV
B Parenteral
Sexual
2-6 mos HBsAg
anti-HBs
anti-HBc
-total
-IgM
HBeAg
anti-HBe
Yes Recomb
HbsAg
C Parenteral
Sexual (?)
2-24 weeksanti-HCV
-EIA
-RIBA
Yes None
DeltaParenteral
Sexual
Varies
2-10 weeks
anti-HDVYes None
G
Parenteral??? research
settings
??? None

49. Risk Factors for Sexual
Transmission of HAV
MSM
Multiple anonymous partners
Oral-or digital stimulation of anorectum
IDU

50. Public Health Service Guidelines
for Counseling Anti-HCV-Positive
Persons
Anti-HCV-positive persons should:
•Be considered potentially infectious
•Keep cuts and skin lesions covered
•Be informed of the potential for sexual
transmission
•Be informed of the potential for perinatal
transmission
–no evidence to advise against pregnancy or
breastfeeding
Anti-HCV-positive persons should not:
•Donate blood, organs, tissue, or semen
•Share household articles (e.g., toothbrushes,
razors)

51. Arguments for HCV as an
STD
History of sex with person at risk for
HCV in about 10% of cases
High risk sexual history associated with
seropositivity
Ulcerative STD and HIV associated with
seropositivity
More female partners of infected men
are seropositive than are male partners
of infected women
Association with duration of partnership

52. Arguments against HCV as an
STD
High risk sexual practices associated
with concomitant percutaneous
exposures
Convincing evidence of transmission
difficult to demonstrate
Divergent isolates in some co-infected
partnerships
In MSM, risk correlates more with
percutaneous than sexual risk
behaviors
Cohort effects in cross-sectional

53. Perinatal Transmission of HCV
Most studies suggest that it occurs
only rarely (e.g., <5%)
Risk associated with plasma RNA
load 1,000,000 copies/mL
Observed transmission in setting of
maternal HIV: 18%

54. AIDS
Organism: Human Immunodeficiency Virus
Transmission: vag, rectal, and oral secretions,
blood,breast milk, perinatal/neonatal
Sites infected: blood borne systemic infection
Incubation: weeks-years before symptoms
occur.
Symptoms:flu like symptoms in early stages,
weight loss, diarrhea, fatigue, swollen glands,
other oral and skin manifestations

55. AIDS
Diagnosis: antibody test, HIV viral RNA by
PCR
Treatment: no known curable, treatment vs
suppression vs immunization
(antiretroviral therapies)
Prevention: note viral load and CD4 count
barriers -abstinence -monogamy
Serious outcome: fatal disease,

56. Herpes simplex virus
HSV type 2 causes 70% of herpetic
genital-tract infections
Fetus has no intrinsic immunity and no
passive immunity during primary infection
Risk of fetal infection is 40% after primary
and 3% if recurrent infection

57. Suggested policy in management
Primary infection with active genital
lesions
Delivery by C/S if labouroccurs and if
membranes intact,orwithin 4 hours of rupture
If more than 4 hours since rupture allow
vaginal delivery
In both take swabs from baby and treat with
acyclovirif positive

58. Secondary infection with active genital
lesions
Although perceived risk of neonatal infection
is much less the extent is not fully known
Consider-diagnosis of neonatal infection if
infant unexpectedly becomes ill in the first
week of life even in the absence of risk factors
for HSV infection
Let mother make informed choice on C/S

59. Pelvic inflammatory disease
Primary-an infection ascends from lower
genital tract due to :
STDs
E coli and other gut organisms
BV
Iatrogenic-15% of cases e.gD&C,HSG,TOP,
insertion of IUCD
After delivery or miscarriage

60. Secondary –less than 1% of all cases
An infection is caused by direct spread from
nearby organs eg appendix
A minority of women with PID are HIV positive

61. Clinical features of acute PID
Lower abdominal pain
(usually bilateral) is
commonest, may be
accompanied by:
Abnormal PVD
Irregular PVB
Dysuria
Dyspareunia
Nausea and/or
vomitting
Fever
General malaise

62. Differentials
Acute appendicitis
Endometriosis
Ectopic pregnancy
Corpus luteum hemorrhage
Ovarian cysts
Inflammatory conditions of other organs
Lower abdominal and adnexal tenderness ,and
pain on moving the cervix (cervical excitation)
are found in >90% of women with proven PID

63. Diagnosis
Consider in any woman of reproductive age with
acute pelvic pain
Endocervical( not high vaginal !) swabs for
chlamydiaand gonorrhoea
Laparoscopy is gold standard:
Erythemaof fallopian tubes
Oedemaand swelling of tubes
Seropurulentexudateon the surface of the tube from
fimbriatedend
Swabs may be taken for culture at laparoscopy

64. Treatment of acute PID
Most women can be treated as outpatients
In patient treatment may be needed as in ;
Failure to respond to or tolerate treatment as out
patient, no follow up in 72 hours
Severe disease
Suspected pelvic abscess
Uncertain diagnosis/ other acute abdomen
Adolescent
Multiple regimen
Role of surgery after rupture of tubo-ovarian
abscess or to drain pyosalpinx

65. Sequelae
Chronic pelvic pain-20%
Subfertilitydue to tubal damage and occlusion
10% after single episode
20% after 2 episodes
40% after 3 or more episodes
Ectopic pregnacy-PID increases risk by 7-10 times
Tubo-ovarian abscesses
Curtis-Fitz-Hugh syndrome (Perihepatitis)
Septicemia
Recurrent PID –patient C/O
Heavy and irregular menses due to endometritis
Dysmenorrhoea
Dyspareunia
Chronic pelvic pain
Infertility