Download 1-STD,gonorrheanimer-mansour (1)

Sexually
Transmitted
Diseases
(STDs)
Epidemiology:
USA:
• More than 110 million are living with STD. 20
million will become infected every year.
• 50% of the new cases are teenagers.
WHO:
• More than 1 million people acquire a sexually
transmitted infection (STI) every day.
• The majority of STIs are present without
symptoms.
• Some STIs can increase the risk of HIV
acquisition three-fold or more.
Currently, more than 30 diseases are known to
spread through sexual activity:
o Bacterial: gonorrhea, syphilis, chlamydial
infection, chancroid, bacterial vaginosis.
o Viral: Genital herpes, warts, HIV.
o Parasitic: Trichomoniasis.
o Fungal: Candidiasis.
Entry, Spread, Damage and Complications:
Entry:
Most of the STD-causing agents enter the body through
the mucosal or squamous epithelial layers of the urethra,
vagina, cervix, rectum or oral pharynx. *
Some agents may spread by blood products,
transplacental,………
Reservoir: Asymptomatic human carriers.
Damage:
Acute manifestations of STDs are classified into:
• Mucopurulent discharge (urethritis and cervicitis):
Example: Gonorrhea and chlamydial infection.
• Genital ulcer disease:
Example: Syphilis, chancroid and genital herpes.
N
Consequences of STDs include:
Most complications are experienced by
women:
• Pelvic inflammatory disease (PID).
• Infertility, ectopic pregnancy, spontaneous
abortion and premature delivery.
• Congenital and neonatal infections.
• Increased risk of acquiring HIV.
• Anogenital or cervical cancer.
• Tertiary syphilis &recurrent herpes
infection (chronicity).
Gonorrhea
Gonorrhea is an infection that involves mucous
membranes, and epithelial layers of the urethra and
the cervix, resulting in a copious- purulent discharge.
• Causative agent: Neisseria gonorrhoeae. Gram
negative diplococci.
• Reservoir:
• Humans are the only reservoir.
• Asymptomatic carriage is greater among
women.
Pathogenesis and tissue damage:
•
After introduction to the urethra and the vagina
gonococci attach via its pili to the non-ciliated
columnar cells of:
o male urethra.
o Adult female endocervix.
o Adolescent female has larger zone of ectopy of
columnar epithelial cells in the ectocervix.
o Young girls vagina.
N
Factors of multiplication and inflammation:
• IgA Protease: Escape humoral response.
• Phase variation: Turning on /off genes of surface
adherence components: escape neutrophil killing
and antibodies protection.
• The microbial lipooligosaccharide (LOS):
o Polyclonal B lymphocyte activator.
o Death of ciliated-epithelia: TNF-α production
from the macrophages.
• The result is urethritis in males and cervicitis in
females and vulvovaginitis in adolescent females.
Summary
o Attachment to non ciliated cells by the pili.
o Evade immune response by IgA protease and phase
variation mechanism.
o Multiply within the non ciliated cells.
o Death of ciliated cells by the LOS and TNFα.
o Outcome:
• Copious purulent discharge (pus) in most male
and some female patients.
• Subclinical infection in 30% of females.
• Pelvic inflammatory disease.
• Systemic dissemination.
Gonorrhoeae
(PMN rich
pus)
Infected cervix (Inflammation with
exudate discharge)
Normal cervix
N
Neisseria gonorrhoeae, other pathogens and vaginal
flora can ascend to female upper reproductive tract
due to:
- Loss of endocervix mucus production.
- End of menses (menstrual cycle; loss of mucus).
The ascending infection results in pelvic
inflammatory disease (PID):
 Endometritis: Endometrium infection (columnar).
 Salpingitis : Fallopian tubes infection.
 Ovaritis (oophoritis).
 DGI: septic arthritis, tenosynovitis, skin pustules,
bacteremia (rare) and endocarditis (rare).
N
Other causative agents of STDs and PID:
- Chlamydia trachomatis.
- Mycoplasma hominis.
- Mycoplasma genitalium.
- Ureaplasma urealyticum.
- Endogenous E. coli.
Late complications: infertility, ectopic pregnancy,
chronic pelvic pain.
N
Neisseria gonorrhoeae infection in male:
Urethritis:
•
Dysuria, redness, pain, and thick copious(greenish- yellow) discharge of pus.
•
The infection could be disseminated to the
epididymis (epididymitis), prostate gland
(prostatitis), testicular tissue (orchitis).
•
DGI.
Diagnosis of Neisseria gonorrhoeae infection:
Clinical specimens:
Urethral discharge, cervical swab, rectal swab,
vaginal discharge, pharyngeal swab.
Laboratory tests: microscopic examination,
culture, PCR .
Microscopic examination: (gram stain):
Intracellular gram negative diplococci (inside the
polymorphnuclear leukocytes).
N
• Culture:
Neisseria gonorrhoeae is a fastidious bacteria it
needs:
• NADP and Hematin (X and V factor): so the
bacteria grow best on: Chocolate agar or the
selective medium: Thayer-Martin agar which
contains antibiotics (vancomycin, colistin, and
nystatin).
• 5-10% CO2 for primary isolation.
• All species are oxidase positive.
• Sugar fermentation to differentiae it from other
neisseriae: N. gonorrhoeae ferments only glucose.
N
PCR:
Detection of microbial genetic material in the
clinical specimen.
Antibiotic sensitivity test:
• More than 20% of current isolates are resistant to
penicillin due to Beta-Lactamase plasmids.
• Penicillinase producing N. gonorrhoeae (PPNG)
strains are sensitive to third generation
cephalosporin.
• Add antichlamydial antibiotic (co-infection is
very common)
• Treat the partner.