chlamydia trachomatis
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Transcript chlamydia trachomatis
Infection by Chlamydia,Gardenella
and Ureaplasma.
Dr. Mohammad Shakeeb, MD
Specialist in clinical
pathology/Microbiology and
immunology
CHLAMYDIAL INFECTIONS
• Chlamydiae that infect humans are divided into
three species,
Chlamydia trachomatis.
Chlamydia (Chlamydophila) pneumoniae.
Chlamydia (Chlamydophila) psittaci.
• All Chlamydiae exhibit similar morphologic
features, share a common group antigen, and
multiply in the cytoplasm of their host cells by a
distinctive developmental cycle.
• lack mechanisms for the production of metabolic
energy and cannot synthesize adenosine
triphosphate (ATP).
• Chlamydiae are obligate intracellular parasites.
• Chlamydiae possess a heat-stable, family-specific
antigen that is an essential component of the cell
membrane lipopolysaccharide.
• Species and type-specific protein antigens also
exist.
• Chlamydiae have a unique developmental life cycle,
with an intracellular growth, or replicative form, the
reticulate body (RB), and an extracellular,
metabolically inert, infective form, the elementary
body (EB).
• Structurally, the chlamydial EB closely resembles a
gram-negative bacillus; however, its cell wall lacks a
peptidoglycan layer.
• Chlamydiae possess shared group (genus)–
specific antigens.
• Species-specific or serovar-specific antigens
are mainly outer membrane proteins.
• There are different serovars of C trachomatis;
these include A, B, Ba, C–K, and L1–L3.
• CHLAMYDIA TRACHOMATIS
• Is the most common cause of sexually transmitted disease in
the United States, and in trachoma-endemic regions of the
Middle East, sub-Saharan Africa, and Asia, it is the primary
infectious cause of blindness.
• The disorder is endemic in more than 50 countries.
• Estimates indicate that more than 3 million people are
affected, with over a third having progressed to blindness
• TRACHOMA
• CHLAMYDIA TRACHOMATIS GENITAL
INFECTIONS AND INCLUSION CONJUNCTIVITIS
• CHLAMYDIA TRACHOMATIS AND NEONATAL
PNEUMONIA
• LYMPHOGRANULOMA VENEREUM
TRACHOMA
• It is a chronic keratoconjunctivitis that begins
with acute inflammatory changes in the
conjunctiva and cornea and progresses to
scarring and blindness.
• The C trachomatis serovars A, B, Ba, and C are
associated with clinical trachoma.
• Clinical Findings
• Classic trachoma is an important cause of blindness in areas
where public sanitation is inadequate and personal hygiene
poor.
• The disease is due to repeated infections of the conjunctiva,
resulting in a pathologic sequence over time.
follicular conjunctivitis
Subepithelial scarring
contraction of the scar resulting in turning inward of the
eyelid (entropion).
Rubbing of the eyelashes on the cornea (trichiasis) with
subsequent corneal injury, and corneal scarring with
opacification and reduced vision.
• Typically, acute infection is transmitted among children via
fingers, fomites, and probably flies
• Most children become chronically infected within a few years
of birth.
• Conjunctival scarring usually becomes evident by the second
or third decade of life, and blindness can occur anywhere
from 10–40 years after the first infection.
CHLAMYDIA TRACHOMATIS GENITAL INFECTIONS
AND INCLUSION CONJUNCTIVITIS.
• C trachomatis serovars D–K cause sexually transmitted
diseases, especially in developed countries, and may also
produce infection of the eye (inclusion conjunctivitis).
• In sexually active men, C trachomatis causes nongonococcal
urethritis and, occasionally, epididymitis.
• In women, C trachomatis causes urethritis, cervicitis, and
pelvic inflammatory disease, which can lead to sterility and
predispose to ectopic pregnancy.
• Proctitis and proctocolitis may occur in men and women,
although these infections appear to be most common in men
who have sex with men.
• Up to 50% of nongonococcal urethritis (men) or the urethral
syndrome (women) is attributed to chlamydiae and produces
dysuria, nonpurulent discharge, and frequency of urination.
• Genital secretions of infected adults can be self-inoculated
into the conjunctiva, resulting in inclusion conjunctivitis, an
ocular infection that closely resembles acute trachoma.
• The newborn acquires the infection during passage through
an infected birth canal.
• Probably 20–60% of infants of infected mothers acquire the
infection.
• with 15–20% of infected infants manifesting eye symptoms
and 10–40% manifesting respiratory tract involvement.
• Inclusion conjunctivitis of the newborn begins as a
mucopurulent conjunctivitis 7–12 days after delivery.
• It tends to subside with erythromycin or tetracycline
treatment or spontaneously after weeks or months.
• It is essential that chlamydial infections be treated
simultaneously in both sex partners and in offspring to
prevent reinfection.
• Tetracyclines (eg, doxycycline) are commonly used in nongonococcal urethritis and in non-pregnant infected women.
• Azithromycin is effective and can be given to pregnant
women.
• Systemic therapy should be used for inclusion conjunctivitis
because topical therapy may not cure the eye infections or
prevent respiratory disease.
CHLAMYDIA
PNEUMONIA
TRACHOMATIS
AND
NEONATAL
• Of newborns infected by the mother, 10–20% may develop
pneumonia 2–12 weeks after birth.
• Affected newborns have striking tachypnea, a characteristic
paroxysmal staccato cough, an absence of fever, and
eosinophilia.
• Consolidation of lungs and hyperinflation can be seen on
radiographs.
• The diagnosis should be suspected if pneumonitis develops in
a newborn who has inclusion conjunctivitis and can be
established by isolation of C trachomatis from respiratory
secretions.
• In such neonatal pneumonia, an immunoglobulin M (IgM)
antibody titer to C trachomatis of 1:32 or more is considered
diagnostic.
• Oral erythromycin for 14 days is recommended; systemic
erythromycin is effective treatment in severe cases.
LYMPHOGRANULOMA VENEREUM
• Lymphogranuloma venereum is a sexually transmitted disease
caused by C trachomatis and is characterized by suppurative
inguinal adenitis.
• It is most common in tropical climates
• C trachomatis serovars L1–L3.
• Several days to several weeks after exposure, a small,
evanescent papule or vesicle develops on any part of the
external genitalia, anus, rectum, or elsewhere.
• The lesion may ulcerate, but usually it remains unnoticed and
heals in a few days.
• The regional lymph nodes enlarge and tend to become
matted and painful.
• In men, inguinal nodes are most commonly involved
• The overlying skin often turns purplish as the nodes
suppurate and eventually discharge pus through multiple
sinus tracts.
• In women and in homosexual men, the perirectal nodes are
prominently involved.
• proctitis and a bloody mucopurulent anal discharge
• During the stage of active lymphadenitis, there are often
marked systemic symptoms.
• Unless effective antimicrobial drug treatment is given at that
stage, the chronic inflammatory process progresses to
fibrosis, lymphatic obstruction, and rectal strictures.
• The lymphatic obstruction may lead to elephantiasis of the
penis, scrotum, or vulva.
• The chronic proctitis of women or homosexual men may lead
to progressive rectal strictures, rectosigmoid obstruction, and
fistula formation.
• LABORATORY DIAGNOSIS
• Specimens for detection of C. trachomatis are determined by
the type of disease suspected
• Screening women at risk for genital C. trachomatis infection
has been shown to decrease the rate of pelvic inflammatory
disease, thus preventing subsequent reproductive sequelae.
• Demonstration of C trachomatis by smear or culture requires
the collection of epithelial (not inflammatory) cells from the
site of infection (conjunctiva, urethra, cervix).
• Culture is carried out in specially treated cells in which
chlamydial inclusions are detected by immunofluorescence.
• Results require incubation for 3 to 7 days.
• Direct fluorescent antibody (DFA) and immunoassay methods
have also been developed.
• All these methods have now been replaced by the newest
generation of nucleic acid amplification (NAA) tests.
• They are rapid, sensitive, specific for genital infections.
• Urine is a suitable specimen although less sensitive than
direct genital samples.
• Culture or DFA are now reserved for pharyngeal and rectal
specimens which for NAA tests might generate false positives.
• Nucleic acid amplification methods for genital Chlamydia
infection are now combined with parallel tests for N
gonorrhoeae.
• Serodiagnostic methods have limited use.
• difficulty of distinguishing current from previous infection
• detection of IgM antibodies against C trachomatis is helpful in
cases of infant pneumonitis.
• Chlamydial serology is also useful in the diagnosis of LGV,
where a single high complement fixation antibody titer
(higher than 1:32) or a fourfold rise supports a presumptive
diagnosis.
• The most satisfactory method for diagnosis of LGV is isolation
of an LGV strain of C trachomatis from aspirated lymph nodes
or tissue biopsies.
• TREATMENT
• Strains of C trachomatis are sensitive to tetracyclines,
macrolides
and
related
compounds,
and
some
fluoroquinolones.
• Azithromycin is the first-line therapy because it is given as a
single oral dose for non-LGV C trachomatis infection.
• Doxycycline is also a first-line drug and preferred for LGV.
• Erythromycin and fluoroquinolones are alternatives.
• For trachoma, a single dose of azithromycin is the treatment
of choice.
Gardnerella
• Gardnerella vaginalis is a thin, gram-variable rod or
coccobacillus
• Over the years, this organism, in its association with bacterial
vaginosis.
• Catalase is not produced, and cells are nonmotile.
• Growth is best observed after 48 hours of incubation in a 5%
CO2-enriched atmosphere.
• Colonies are small and exhibit β-hemolysis on media
containing rabbit or human blood.
• Clinical Manifestations and Pathogenesis
• This organism is associated with bacterial vaginosis but is not
the cause.
• It has been found in the blood of patients with postpartum
fever and can cause infection in newborns.
• G. vaginalis is a part of the anorectal flora of healthy adults of
both sexes, as well as of children.
• It is part of the endogenous vaginal flora of women of
reproductive age.
• Laboratory Diagnosis
• Diagnosis of bacterial vaginosis does not require culture.
• The diagnosis is made by:
Direct examination of vaginal secretions for the presence of
clue cells (epithelial cells covered with bacteria on the cell
margins) and
Small gram-negative rods and coccobacilli.
The absence of lactobacilli (gram positive thin rods).
a pH greater than 4.5.
Fishy amine odor after addition of 10% potassium hydroxide
(KOH) to the secretions.
• Antimicrobial Susceptibility
• Metronidazole is the drug of choice for bacterial vaginosis.
• Systemic infection due to G. vaginalis may be treated with
ampicillin because this organism has not been found to
produce β-lactamase.
GENITAL MYCOPLASMAS
• Mycoplasmas are the smallest free-living organisms.
• They are pleomorphic, ranging from spherical cells 0.2 μm in
diameter to filaments 0.1 μm wide by 1–2 μm long.
• Most are facultative anaerobes that replicate by binary
fission.
• Mycoplasmas are unique among bacteria because they have
no cell wall.
• They are unable to synthesize cell wall precursors, and they
require cholesterol and related sterols for membrane
synthesis
• The potential pathogens, M. pneumoniae and the genital
mycoplasmas
(Mycoplasma
hominis,
Mycoplasma
genitalium, Ureaplasma urealyticum, and Ureaplasma
parvum),
• Other mycoplasmas are part of the normal human flora,
primarily of the respiratory and genitourinary tracts.
• Epidemiology
• Ureaplasma species can be found colonizing the
vagina and cervix in 40%–80% of adult women.
• M. hominis can be found in 21%–53% of women.
• The frequency in males appears to be lower.
• Prevalence studies for M. genitalium are infrequent in
the literature, but it appears to be less common as a
colonizer in asymptomatic individuals and is found
with a frequency of around 1%.
• Colonization of infants with genital
mycoplasmas can occur during passage
through the birth canal, but colonization
appears to be temporary in many cases,
and a lower rate of colonization has been
noted in children.
• The
increase
in
colonization
by
mycoplasmas after puberty indicates an
association with sexual activity
• Neonates can acquire infections due to
Ureaplasma
spp.
and
M.
hominis
hematogenously through the placenta or
through an ascending infection, resulting in
seeding of amniotic fluid.
• Clinical Manifestations
• the presence of mycoplasma in the placental
membranes or amniotic fluid is consistently
associated with :
chorioamnionitis,
preterm birth.
adverse perinatal outcomes associated with several
neonatal disorders, including perinatal pneumonia
and sepsis in preterm infants
Both Ureaplasma spp. and M. hominis are
associated with postpartum fever.
• Ureaplasma spp. can cause urinary calculi and
are a cause of nongonococcal urethritis (NGU)
• M. hominis has been related to both pelvic
inflammatory disease (PID) and pyelonephritis
and may have an association with bacterial
vaginosis .
• M. genitalium has been linked to NGU in
males only relatively recently, but it is now
firmly established as a significant cause of the
disorder and is the etiologic agent in
approximately 25% of cases.
• Among women, M. genitalium has shown
an association with cervicitis, endometritis,
PID, and tubal infertility.