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.