Non-gonococcal Urethritis
(Chlamydia, Mycoplasma,
Ureaplasma, and others)
Chlamydia trachomatis
Microscopy and culture:
 Small round-to-ovoid bacteria.
 Obligatory intracellular parasite (depends on the
host cellular energy ATP, and NAD).
 Cultured in embryonated eggs or tissue culture.
 Rigid cell wall although it does not contain
peptidoglycan or muramic acid.
 Cannot be stained by gram stain.
 Inclusion bodies retain Iodine or safranin.
 Tow forms: elementary body (EB) and reticulate
body (RB).
Pathogenesis and life cycle:
Transmission: Sexual route.
Infectious form: The elementary body (E.B).
• The E.B enters by phagocytosis into columnar
epithelial cells of endocervix and macrophages
(E.B prevents phagosome lysosomes fusion).
• Inside the cells the E.B differentiates to the
metabolically active dividing reticulate body (RB)
(diagnostic stage; inclusion bodies).
• After 48 hours, infected cells will rupture to release
many elementary bodies resulting in host cell death,
and infection of other cells.
0 -5 hours
48 hours
24-30 hours
n
Chlamydia inclusions: Reticulate body.
Serotypes and Tissue Damage:
• Chlamydia trachomatis has several serovars: A-L.
Chlamydial infections:
 Eye infection (trachoma): serotypes A, B and C.
 Genital tract infections:
o Nongonococcal urethritis (discharge):
Caused by: serovars: D- K.
o Lymphogranuloma venereum:(LGV):
Caused by serovars: L1, L2, and L3.
more invasive infection.
Nongonococcal urethritis:
Discharge: More mucus fewer pus.
 In male:
o Urethritis, the infection may extend to
epididymitis and prostatitis but rarely to the testes
(orchitis).
o One-third of patients have Reiter syndrome
(HLA-B27; acute aseptic arthritis and urethritis).
 In Female:
o Cervicitis and pelvic inflammatory disease.
o Most of the cases are asymptomatic.
o Exposure to ineffective antibiotics or interferon-γ
may results in persistence infection.
o Infertility and ectopic pregnancy.
N
 Lymphogranuloma venereum (LGV):
• Invasive infection caused by serovars: L1, L2,
and L3.
• Clinical presentation:
o Papules and then herpetic-like ulcers are formed
on the external genitalia and persist for one to
two months (more invasive infection).
o Painful swelling of inguinal and perirectal lymph
nodes (bubo). Cervical adenopathy (oral sex)
o Lymphatic obstruction; elephantiasis of
genitalia.
DD of genital ulcers: chancer, chancroid, genital
herpes, trauma, drug sensitivity.
Clinical picture of Chlamydia trachomatis:
Urethral discharge :
(more mucoid with fewer pus cell).
Chlamydial Cervicitis.
LGV penile ulcer
Inguinal adenopathy
Diagnosis of Chlamydia trachomatis infection:
• Clinical specimens:
Urethral discharge, HVS, endocervical swab, urine
(scraping of the epithelial or squamocolumnar
junction)
• Direct microscopy:
A-Immunofluorescent microscopy.
B-Electron microscopy.
• Culture: cell culture or embryonated eggs culture.
• Detection of chlamydia genetic material by PCR.
• Serology: helpful only in LGV.
Treatment: Doxycycline, azithromycin, erythromycin
Electron microscopy
Immunofluorescent
staining of inclusion
body.
Immuno-electrone microscopy
Mycoplasma hominis,
Mycoplasma genitalium, and
Ureaplasma urealyticum
Mycoplasma& Ureaplasma
• The smallest prokaryotic microbe capable of
growth on cell-free media.
• Extremely small size (0.1-0.3 micrometer): pass
through sterilization filters. Small Ds DNA.
• Lack cell wall: No peptidoglycan.
o Elastic and pleomorphic (cannot be classified as
cocci or bacilli).
o Resistance to penicillin and cephalosporins.
• Cell membrane: lipid bilayer membrane containing
sterols (should add cholesterol to the culture media).
• M. hominis and U. urealyticum are UG tract flora.
n
Cultural characteristics and colony morphology:
o Facultative anaerobes, some species are strict
anaerobes.
o Can be grown in cell-free media.
o Fastidious: need cholesterol (serum).
o Colonies are visualized microscopically. And
show a characteristics fried egg appearance.
o Biochemical activities:
• M. hominis degrades arginine for energy.
• U. urealyticum hydrolyses urea to ammonia
which destroys the epithelial cells.
Mycoplasma and Ureaplasma infections:
 In female:
•
M. hominis cause PID, postpartum and post abortion
fever.
• U. urealyticum and M. genitalium are associated with
cases of PID; endometritis and bacterial vaginosis.
 In male:
• Ureaplasma urealyticum and Mycoplasma
genitalium: Urethritis.
 The infection can disseminate to other tissues in
immunocompromised patients.
Treatment:
• U. urealyticum and M. genitalium: sensitive to
azithromycin.
• M. hominis: Erythromycin and azithromycin resistance.
nd
2
Lecture
Bacterial vaginosis:
• The most common vaginal infection worldwide.
• Disruption of vaginal normal flora
(Lactobacillus).
• Causative agents:
o Gardnerella vaginalis: gram-variablestaining facultative anaerobic coccobacilli.
o Mycoplasma species and other bacterium.
• Other causes of vaginal infection (vaginitis):
- Candidiasis.
- Protozoan infection: Trichomonas vaginalis.
Normal Vagina
Bacterial vaginosis
Vaginal Candidiasis
• Thin-walled, yeasts reproduce mainly by
budding.
• Candida spp. are members of the normal flora.
• Candidiasis is the most common opportunistic
mycoses worldwide (cellular immunity protects
against mucocutaneous candidiasis, neutrophils
protect against invasive candidiasis)
• More than 150 species of candida but only few
species cause disease in humans.
• The species of most medical significance are:
o Candida albicans.
o Candida tropicalis.
Clinical presentation of Candida albicans:
Candida albicans causes most of the cases of
oropharyngeal candidiasis and vulvovaginal
candidiasis.
• In female:
Vaginal candidiasis:
• Itching and burning pain of the vagina.
• Thick or thin white discharge (cheesy).
• In male: Urethritis.
Morphology and cultural characteristics:
o Microscopically: Candida albicans is a dimorphic
fungi, reproduce mainly by budding, but can produce
pseudohyphae and true hyphae.
o Culture: after 24 hours at 37 C or room temperature,
white, creamy, rounded colonies with feet projection
or regular margin appears.
Asexual germination of candida occurs by production
of blastopores or chlamydiospores.
o Germ tube test: To differentiate C. albicans from
other spp.
C. albicans produce germ tube (true hyphae) when
incubated with serum at 37ᴼ C for 90 minutes.
Asexual germination: blastopores & chlamydiospores
Germ tube
Trichomoniasis:
Trichomonas vaginalis.
o Classification: Protozoa: class Mastigophora.
o Morphology: oval or pyriform in shape, with short
undulating membrane, axostyle & four free flagella
o Reproduce by binary fission.
Transmission: sexual and contaminated clothes.
Pathology and clinical picture:
Urethritis: in male and female.
Vaginitis: itching, copious- yellowish offensive
discharge.
Prostatitis and seminal vesiculitis in male.
Diagnosis: Detection of the trophozoite in vaginal
or urethral discharge.
Congenital and Perinatal infections:
Congenital (intrauterine or prenatal) infections are
those transmitted transplacentally.
The causative agents are:
- Cytomegalovirus.
- Herpes simplex virus.
- HIV.
- Parvovirus B19.
- Rubella virus.
- Treponema pallidum.
- Toxoplasma gondii.
The effect of intrauterine infections on the
fetus:
 Abnormal organogenesis:
rubella: structural abnormalities in tissue and
organs; defects in retina, pulmonary artery stenosis.
 Inflammatory response results in tissue
damage:
CMV and T.gondii: cause cerebritis
(encephalitis); so cerebral atrophy and intracranial
calcification.
 Placental insufficiency:
low birth weight, premature birth, fetal death.
N
Perinatal infections:
acquired at birth or during the first four weeks after
birth from maternal or non-maternal sources.
Causative agents:
- E.coli and other Enterobacteriaceae.
- Group B Streptococci and Listeria monocytogenes.
- Gonococci and Chlamydia.
- Viruses.
- Candida.
Effects:
Bacterial sepsis: Mortality rate is 10-40%.
Meningitis: neurological damage: in 20-50% of survivors.