Chlamydia

CHLAMYDIA
Dr. Suprakash Das
M.D (Microbiology)

Introduction
 Chlamydiae are obligate intracellular bacteria that
replicate within eukaryotic cells.
 C. trachomatis, like all other Chlamydia spp., has one of
the smallest bacterial genomes.
 Its 1.04 Mb genome encodes approximately 900 genes,
which is less than a fifth of the genes in Escherichia coli.
 The large majority of these genes (668) are shared among
all Chlamydia, representing a core set of genes necessary
for the intracellular chlamydial lifestyle.
 The small genome size is due to reductive evolution in
which C. trachomatis has lost enzymes and metabolic
pathways for nutrients that are readily available from
the host cell.

Taxonomy
 The Chlamydia spp. are members of the order
Chlamydiales and the family Chlamydiaceae.
 Members of the family Chlamydiaceae had been
regrouped by Everett et al. (1999) from one genus,
Chlamydia, into two genera, Chlamydia and
Chlamydophila, based on differences in phenotype, 16S
ribosomal ribonucleic acid (rRNA), and 23S rRNA.
 This classification was not universally accepted by the
Chlamydia scientific community, and recently it was
agreed that the family Chlamydiaceae contains a single
genus, Chlamydia.

Important Species
 The genus Chlamydia contains nine recognized species:
1. Chlamydia trachomatis,
2. C. psittaci (agent of psittacosis; many species of birds),
3. C. pneumoniae,
4. C. pecorum (ruminants and koalas),
5. C. muridarum (formerly the agent of mouse pneumonitis),
6. C. suis (an important pathogen of swine),
7. C. abortus (causes abortion in cattle and sheep; rarely causes
abortion in humans),
8. C. caviae (formerly C. psittaci, the guinea pig inclusion
conjunctivitis strain), and
9. C. felis (causes epidemic keratoconjunctivitis in cats).
 C. trachomatis and C. pneumoniae are the most significant
human pathogens, and C. psittaci is an important zoonosis.

History
 Chlamydia-like disease affecting the eyes of people was first described
in ancient Chinese and Egyptian manuscripts.
 A modern description of Chlamydia-like organisms was provided by
Halberstaedter and von Prowazek in 1907.
 Chlamydial isolates cultured in the yolk sacs of embryonating eggs
were obtained from a human pneumonitis outbreak in the late 1920s
and early 1930s, and
 by the mid-20th Century isolates had been obtained from dozens of
vertebrate species.
 The term Chlamydia (a cloak) appeared in the literature in 1945,
although other names continued to be used, including Bedsonia,
Miyagawanella, ornithosis-, TRIC (Trachoma and Inclusion
Conjunctivitis), and PLT (Psittacosis, Lymphogranuloma Venereum
and Trachoma) agents.

Stanislaus von Prowazek
Ludwig halberstaedter

Morphology and Characteristics
 Members of the order Chlamydiales are obligate intracellular
bacteria that were once regarded as viruses
 because, like viruses, the chlamydiae require biochemical
resources of eukaryotic host cells to fuel their metabolism for
growth and replication by providing high-energy compounds such
as adenosine triphosphate.
 Chlamydia spp. are similar to gram-negative bacilli in that they
have lipopolysaccharide (LPS) as a component of the cell wall.
The chlamydial LPS, however, has little endotoxic activity.
 The chlamydiae have a major outer membrane protein
(MOMP) that is very diverse. The variation in MOMP in
Chlamydia trachomatis is used to separate the species into 18
distinct serovars.

Morphology and Characteristics
Chlamydia aren’t viruses-
• The chlamydiae were once considered viruses because they are
small enough to pass through 0.45 μm filters and are obligate
intracellular parasites; however, the organisms have the following
properties of bacteria:
1. Possess inner and outer membranes similar to those of gram
negative bacteria.
2. Contain both deoxyribonucleic acid (DNA) and ribonucleic acid
(RNA).
3. Possess prokayotic ribosomes.
4. Synthesize their own proteins, nucleic acids, and lipids.
5. Suceptible to numerous antibacterial antibiotics.

C. trachomatis-
Biovars & Serotypes
 Strains of C. trachomatis are divided into three biovars and are
further subtyped by serovar.
 The trachoma biovar (serovars A–C) is the leading cause of non-
congenital blindness in developing nations, whereas
 The genital tract biovar (serovars D–K) is the most prevalent
sexually transmitted bacterium. In women, 70–80% of genital tract
infections with C. trachomatis are asymptomatic, but 15–40%
ascend to the upper genital tract, which can lead to serious sequelae,
including pelvic inflammatory disease, infertility and ectopic
pregnancy.
 The lympho granuloma venereum (LGV) biovar (serovars L1–
L3) causes invasive urogenital or anorectal infection.

Life cycle
 Chlamydiae have a unique developmental life cycle
reminiscent of parasites,
 with an intracellular, replicative form, the reticulate body
(RB), and an extracellular,
 Metabolically inert, infective form, the elementary body
(EB) (200-400 nm in diameter).
 The EB cannot survive outside of a host cell for an extended
period. After infection of a host cell, the EB differentiates into
an RB.
 The RB divides by binary fission within vacuoles. As the
numbers of RB increase, the vacuole expands, forming an
intracytoplasmic inclusion.

Life cycle
 The RB then revert to EB, and 48 to 72 hours
postinfection, the EB are released from the host cell.
 In addition to the replicative cycle associated with acute
chlamydial infections, there is evidence that Chlamydia
can persist in an aberrant form in vitro,
 depending on the amount of interferon-gamma (IFN-g)
and tryptophan in the host cell as well as function of the
tryptophan synthase encoded by the organism.
 Removal of IFN-g or increase in tryptophan will result
in differentiation of chlamydiae into an active EB
infection.

Immune Response
Immune response-
• Chlamydia survives and multiplies by-
 Controlling host cell survival and death
 Modulating the host cell cycle
 Modulation of innate immune response.
Virulence factors-
 Chlamydial polymorphic outer membrane proteins
 Chlamydial type iii secretion systems
 Chlamydial stress response proteins
 Chlamydial toxin
 Chlamydial lipopolysaccharide (lps) and other glycolipids

Diseases caused by- C. trachomatis-
1. Trachoma
 Trachoma is manifested by a chronic inflammation of the conjunctiva
and remains a major cause of preventable blindness worldwide.
 The organism is acquired as a result of contact with infected secretions
on towels or fingers or by flies.
 Early symptoms of infection include mild irritation and itching of the
eyes and eyelids. There may also be some discharge from the infected
eye.
 The infection progresses slowly with increasing eye pain, blurred
vision, and photophobia.
 Repeated infections result in scarring of the inner eyelid that may then
turn the eyelid in toward the eye (entropion).
 As the inner eyelid continues to turn in, the eyelashes follow
(trichiasis), resulting in rubbing and scratching of the cornea.
 The combined effects of the mechanical damage to the cornea and
inflammation result in ulceration, scarring, and loss of vision.

2. LGV
 Lymphogranuloma venereum (LGV) is a sexually transmitted disease
rarely identified in North America but relatively frequent in Africa, Asia,
and South America.
 It is reemerging in Europe, especially in homosexual males.
 C. trachomatis serovars L1, L2, L2b, and L3 are invasive, causing LGV,
which leave the mucosa to spread to the regional lymph nodes.
 The disease is characterized by a brief appearance of a primary genital
lesion at the initial infection site. This lesion is often small and may be
unrecognized, especially by female patients.
 The second stage, acute lymphadenitis, often involves the inguinal lymph
nodes, causing them to enlarge and become matted together, forming a
large area of groin swelling, or bubo.
 During this stage, infection may become systemic and cause fever or may
spread locally, causing granulomatous proctitis.
 In a few patients (more females than males), the disease progresses to a
chronic third stage, causing the development of genital hyperplasia, rectal
fistulas, rectal stricture, draining sinuses, and other manifestations.

3. Nongonococcal and Postgonococcal Urethritis
 Nongonococcal urethritis (NGU) is a diagnosis of exclusion that is applied to
men with symptoms and/or signs of urethritis who do not have gonorrhea.
 Postgonococcal urethritis (PGU) refers to NGU developing in men 2–3 weeks
after treatment of gonococcal urethritis with single doses of agents such as
penicillins or cephalosporins that lack antimicrobial activity against
chlamydiae.
 Since current treatment regimens for gonorrhea include tetracycline,
doxycycline, or azithromycin for possible concomitant chlamydial infection,
both the incidence of PGU and the causative role of chlamydiae in this
syndrome have declined.
 C. trachomatis causes 20–40% of cases of NGU in heterosexual men but is less
commonly isolated from homosexual men with this syndrome.
 The cause of most of the remaining cases of NGU is uncertain; considerable
evidence suggests that
 Ureaplasma urealyticum and
 Mycoplasma genitalium cause many cases of NGU, whereas
 Trichomonas vaginalis and
 herpes simplex virus (HSV) cause some cases.

 NGU is diagnosed by documentation of a leukocytic
urethral exudate and by exclusion of gonorrhea by Gram’s
staining or culture.
 C. trachomatis urethritis is generally less severe than
gonococcal urethritis, although in an individual patient, these
two forms of urethritis cannotbe reliably differentiated solely
on clinical grounds.
 Symptoms include urethral discharge (often whitish and
mucoid rather than frankly purulent), dysuria, and
urethral itching.
 Physical examination may reveal meatal erythema and
tenderness and a urethral exudate that is often demonstrable
only by stripping of the urethra.

 Such patients generally have first-glass pyuria (≥15 leukocytes per
400× microscopic field in the sediment of first-void urine),
 a positive leukocyte esterase test, or an increased number of
leukocytes on a Gram stained smear prepared from a urogenital
swab inserted 1–2 cm into the anterior urethra.
 For the enumeration of leukocytes, the smear is first scanned at
low power to identify areas of the slide containing the highest
concentration of leukocytes.
 These areas are then examined under oil immersion (1000×).
 An average of four or more leukocytes in at least three of five
1000× oil-immersion fields is indicative of urethritis and correlates
with the recovery of C. trachomatis.

4. Epididymitis
 C. trachomatis is the foremost cause of epididymitis in sexually
active heterosexual men <35 years of age, accounting for ∼70% of
cases.
 N. gonorrhoeae causes most of the remaining cases, and some men
have simultaneous infections with both pathogens, usually
accompanied by asymptomatic urethritis.
 Men with chlamydial epididymitis typically present with
 unilateral scrotal pain,
 fever, and
 epididymal tenderness or
 swelling on examination.
 The illness may be mild enough to treat with oral antibiotics on an
outpatient basis or severe enough to require hospitalization and
parenteral therapy.

5. Reiter’s Syndrome
 Reiter’s syndrome consists of-
 conjunctivitis,
 urethritis (or, in female patients, cervicitis),
 arthritis, and
 characteristic mucocutaneous lesions.
 C. trachomatis has been recovered from the urethra of up to
70% of men with untreated nondiarrheal Reiter’s syndrome
and associated urethritis.
 In the absence of overt urethritis, it is important to exclude
subclinical urethritis in the men in whom this diagnosis is
suspected.
 More than 80% of affected patients have the HLA-B27
phenotype.

5. Reiter’s Syndrome
 Chlamydial infection is thought to initiate an aberrant and
hyperactive immune response that produces inflammation at the
involved target organs in these genetically predisposed individuals.
 Evidence of exaggerated cell-mediated and humoral immune
responses to chlamydial antigens in Reiter’s syndrome supports
this hypothesis.
 The presumptive demonstration of chlamydial EBs and chlamydial
DNA in the joint fluid and synovial tissue of patients with Reiter’s
syndrome suggests that chlamydiae may actually spread from
genital to joint tissues in these patients, perhaps in macrophages.

6. Proctitis
 C. trachomatis strains of either the genital immunotypes D through K or
the LGV immunotypes cause proctitis in homosexual men who
practice receptive anorectal intercourse.
 These infections may develop in heterosexual women as well. Patients
present with mild rectal pain,mucous discharge, tenesmus, and
(occasionally) bleeding.
 Nearly all have neutrophils in Gram-stained rectal samples. Anoscopy in
these non-LGV cases of chlamydial proctitis reveals mild, patchy
mucosal friability and mucopurulent discharge, and the disease
process is limited to the distal rectum.
 LGV strains produce more severe ulcerative proctitis or proctocolitis that
can be confused clinically with HSV proctitis (severe rectal pain, rectal
bleeding, discharge, and tenesmus) and that histologically resembles
Crohn’s disease in that giant cell formation and granulomas can be seen.
 In the United States, these cases of LGV proctitis occur almost
exclusively in homosexual men, many of whom are positive for HIV.

7. Mucopurulent Cervicitis
 Although many women with C. trachomatis infection of the cervix
have no symptoms or signs, a careful speculum examination reveals
evidence of MPC in 30–50% of cases.
 MPC is associated with yellow mucopurulent endocervical
discharge and with ≥20 neutrophils per 1000× microscopic field
within strands of cervical mucus on a thinly smeared, Gram-stained
preparation of endocervical exudate.
 Other characteristic findings include edema of the zone of cervical
ectopy and a propensity of the mucosa to bleed on minor
trauma—e.g., when specimens are collected with a swab.
 A Pap smear shows increased numbers of neutrophils as well as a
characteristic pattern of mononuclear inflammatory cells, including
plasma cells, transformed lymphocytes, and histiocytes.
 Cervical biopsy shows a predominantly mononuclear cell infiltrate
of the sub-epithelial stroma, often with follicular cervicitis.

8. Pelvic Inflammatory Disease
 In the United States,C. trachomatis has been identified in the fallopian tubes or
endometrium of up to 50% of women with pelvic inflammatory disease (PID),
and its role as an important etiologic agent in this syndrome is well accepted.
 PID occurs via ascending intraluminal spread of C. trachomatis from the lower
genital tract.
 MPC is thus followed by endometritis, endosalpingitis, and finally pelvic
peritonitis.
 Chlamydial salpingitis produces milder symptoms than does gonococcal
salpingitis and may be associated with less marked adnexal tenderness.
 Thus mild adnexal or uterine tenderness in sexually active women with cervicitis
suggests PID.
 Infertility associated with fallopian-tube scarring has been strongly linked to
antecedent C. trachomatis infection in serologic studies.
 Since many infertile women with tubal scarring and antichlamydial antibody
have no history of PID, it appears that subclinical tubal infection (“silent
salpingitis”) may produce scarring.

9. Urethral Syndrome in Women
 In the absence of infection with uropathogens
such as coliforms or Staphylococcus
saprophyticus, C. trachomatis is the pathogen
most commonly isolated from college women
with dysuria, frequency, and pyuria.
 This organism can also be isolated from the
urethra of women without symptoms of urethritis,
and up to 25% of female STD clinic patients with
chlamydial urogenital infection have cultures
positive for C. trachomatis from the urethra only.

10. Infection in Pregnancy and the Neonatal Period
 Studies in the United States have demonstrated that 5–25% of pregnant
women have C. trachomatis infections of the cervix. approximately
one-half to two thirds of children exposed during birth have acquired C.
trachomatis infection.
 Roughly half of the infected infants (25% of the group exposed) have
developed clinical evidence of inclusion conjunctivitis.
 Pneumonia develops in 10% of children infected perinatally, and otitis
media may in some cases result from perinatally acquired chlamydial
infection.
 Neonatal chlamydial conjunctivitis has an acute onset 5–14 days after
birth and often produces a profuse mucopurulent discharge.

Neonatal chlamydial conjunctivitis

Diseases caused by- C. psittaci-
 Psittacosis is primarily an infectious disease of birds and mammals
that is caused by C. psittaci.
 Transmission of infection from birds to humans results in a febrile
illness characterized by pneumonitis and systemic manifestations.
Inapparent infections or mild influenza-like illnesses may also
occur.
 The term ornithosis is sometimes applied to infections contracted
from birds other than parrots or parakeets, but psittacosis is the
preferred generic term for all forms of the disease.
 C. psittaci is an endemic pathogen of all bird species.
 Psittacine birds (e.g., parrots, parakeets) are a major reservoir for
human disease, but outbreaks have occurred among turkey
processing workers and pigeon aficionados.

Diseases caused by- C. psittaci-
 The birds may show diarrheal illness or may be
asymptomatic.
 Humans acquire the disease by inhalation of aerosols.
 The organisms are deposited in the alveoli; some are
ingested by alveolar macrophages and then carried to
regional lymph nodes.
 From there they are disseminated systemically, growing
within cells of the reticuloendothelial system.
 Human-to human transmission is rare, thus obviating
the need for isolating patients if admitted to the
hospital.

Psittacosis-
Clinical Manifestations
 The clinical manifestations and course of psittacosis are
extremely variable.
 After an incubation period of 7–14 days or longer, the
disease may start abruptly with shaking chills and fever,
with temperatures ranging as high as 40.5°C (105°F);
 however, the onset is often gradual, with fever increasing
over 3–4 days.
 Headache is almost always prominent, is usually diffuse and
excruciating, and is often the chief complaint.
 Many patients present with a dry hacking cough that is
usually nonproductive, but small amounts of mucoid or
bloody sputum may be raised as the disease progresses.

Psittacosis-
 Cough may begin early in the course of the disease or
as late as 5 days after the onset of fever.
 Chest pain, pleurisy with effusion, or a friction rub may
all occur but are rare.
 Pericarditis and myocarditis have been reported.
 Most patients have a normal or slightly increased
respiratory rate;
 marked dyspnea with cyanosis occurs only in severe
psittacosis with extensive pulmonary involvement.
 In psittacosis, as in mycoplasmal pneumonias, the
physical signs of pneumonitis tend to be less prominent
than symptoms and x-ray findings would suggest.

Psittacosis-
 Patients often report generalized myalgia, and spasm
and stiffness of the muscles of the back and neck may
lead to an erroneous diagnosis of meningitis.
 Lethargy, mental depression, agitation, insomnia, and
disorientation have been prominent features of the
illness in some epidemics but not in others;
 delirium and stupor develop near the end of the first
week in severe cases.
 Occasional patients are comatose when first seen; the
diagnosis of psittacosis may be elusive in these cases.

Psittacosis-
 Gastrointestinal manifestations such as abdominal
pain, nausea, vomiting, or diarrhea are noted in
some cases;
 constipation and abdominal distention sometimes
occur as late complications.
 Icterus, the result of severe hepatic involvement,
is a rare and ominous finding.
 A faint macular rash (Horder’s spots) resembling
the rose spots of typhoid fever has been described.

Diseases caused by-
C. pneumoniae-
 The clinical spectrum of C. pneumoniae infection includes acute
pharyngitis, sinusitis, bronchitis, and pneumonitis, primarily in
young adults.
 The pneumonitis resembles that of Mycoplasma pneumonia in that
leukocytosis is frequently lacking and patients often have
prominent antecedent upper respiratory tract symptoms, fever,
nonproductive cough, mild to moderate illness,
 minimal findings on chest auscultation, and small segmental
infiltrates on chest x-ray.
 In elderly patients, pneumonia due to C. pneumoniae can be
especially severe and may necessitate hospitalization and
respiratory support.
 It causes 5% to 10% of cases of community-acquired pneumonia.

Laboratory Diagnosis-
C.trachomatis
Specimen Collection and Transport-
 The organism can be recovered from or detected in infected cells of the
urethra, cervix, conjunctiva, nasopharynx, rectum, and material aspirated
from the fallopian tubes and epididymis.
 The endocervix is the preferred anatomic site to collect screening
specimens from female patients.
 The specimen for C. trachomatis culture should be obtained after
collection of all other specimens (e.g., those for Gramstained smear,
Neisseria gonorrhoeae culture, or Papanicolaou [Pap] smear).
 A large swab should first be used to remove all secretions from the
cervix.
 The appropriate swab (for nonculture tests, use the swab supplied or
specified by the manufacturer) or endocervical brush is inserted 1 to 2 cm
into the endocervical canal, rotated against the wall for 10 to 30 seconds,
 withdrawn without touching any vaginal surfaces, and then placed in the
appropriate transport medium or applied to a slide prepared for direct
fluorescent antibody (DFA) testing.

C.trachomatis
 Urethral specimens should not be collected until 2 hours after the patient
has voided.
 A urogenital swab (or one provided or specified by the manufacturer) is
gently inserted into the urethra (females, 1-2 cm; males, 2-4 cm), rotated at
least once for 5 seconds, and then withdrawn.
 Again, swabs should be placed into the appropriate transport medium or
onto a slide prepared for DFA testing.
 Screening of rectal or pharyngeal specimens for C. trachomatis by nucleic
acid tests has proven useful in homosexual male patients.
 Because chlamydiae are relatively labile, viability can be maintained by
keeping specimens cold and minimizing transport time to the laboratory.
 For successful culture, specimens should be submitted in a chlamydial
transport medium such as 2SP (0.2 M sucrose-phosphate transport medium
with antibiotics.
 Specimens should be refrigerated upon receipt, and if they cannot be
processed for culture within 24 hours, they should be frozen at –70°C.

C.trachomatis
Culture-
 Several different cell lines have been used to isolate C. trachomatis
in cell culture, including McCoy, HeLa, and monkey kidney cells;
cycloheximide-treated McCoy cells are commonly used.
 After shaking the clinical specimens with 5-mm glass beads,
centrifugation of the specimen onto the cell monolayer (usually
growing on a coverslip in the bottom of a vial, commonly called a
“shell vial”) facilitates adherence of elementary bodies.
 After 48 to 72 hours of incubation, monolayers are stained with a
fluorescein labeled monoclonal antibody that is either species
specific, targeting the MOMP of C. trachomatis, or genus specific,
targeting the LPS.
 The monolayers are examined microscopically for inclusion.

C.trachomatis
 Although its specificity approaches 100%, the sensitivity of culture
has been estimated at between 70% and 90% in experienced
laboratories.
 Limitations of Chlamydia culture contributing to the lack of
sensitivity include prerequisites to maintain viability of patient
specimens by either rapid or frozen transport and
 to ensure the quality of the specimen submitted for testing (i.e.,
endocervical specimens devoid of mucus and containing
endocervical epithelial or metaplastic cells or urethral epithelial
cells).
 In addition, successful culture requires a sensitive cell culture
system and a minimum of at least 2 days turnaround time between
specimen receipt and the availability of results. Despite these
limitations, culture is still recommended as the test of choice in
some situations

C.trachomatis
Direct Detection Methods-
Cytological Examination
 Cytologic examination of cell scrapings from the
conjunctiva of newborns or persons with ocular
trachoma can be used to detect C. trachomatis
inclusions, usually after Giemsa staining.
 Cytology has also been used to evaluate
endocervical and urethral scrapings, including
those obtained for Pap smears.
 However, this method is insensitive compared
with culture or other methods

C.trachomatis
Antigen Detection and Nucleic Acid Hybridization-
 The sensitivity and specificity of DFA are similar to those of
culture. Chlamydial antigen can also be detected by enzyme
immunoassays (EIA).
 Numerous U.S. Food and Drug Administration (FDA)–
approved kits are commercially available.
 These assays use polyclonal or monoclonal antibodies that
detect chlamydial LPS. These tests are not species-specific for
C. trachomatis and may cross react with LPS of other bacterial
species present in the vagina or urinary tract and thereby
produce a false-positive result.

Epithelial cells of conjunctiva containing intra-cytoplasmic inclusions "draped"
around nucleus

C.trachomatis
 Nucleic acid hybridization tests for Chlamydia were first
available for the clinical microbiology laboratory in the late
1980s.
 The Digene Hybrid Capture II assay uses a ribonucleic acid
(RNA) probe to detect chlamydial deoxyribonucleic acid
(DNA) in a sample.
 The DNA/RNA hybrids are captured using monoclonal
antibodies imbedded on the side of the well that recognize
the unique structure produced by the DNA/RNA hybrid.
 A second enzyme labeled anti-DNA/ RNA hybrid antibody
binds to captured hybrids, and enzyme activity is measured
by chemiluminescence. The assay is species specific for the
detection of C. trachomatis.

C.trachomatis
 FDA-approved nucleic acid amplification tests
(NAATs) for the laboratory diagnosis of C.
trachomatis infection use three different formats:
polymerase chain reaction (PCR),
strand displacement amplification (SDA), and
transcription-mediated amplification (TMA).
 The first two assay formats amplify DNA
sequences present in the cryptic plasmid that is
present in 7 to 10 copies in the chlamydial EB,

C.trachomatis
 whereas the last format amplifies 23S ribosomal RNA
(rRNA) sequences.
 Studies clearly indicate that NAATs are more sensitive
than culture and other non–nucleic acid amplification
assays.
 Because of the increased sensitivity of detection, first-
voided urine specimens from symptomatic and
asymptomatic males and females are acceptable
specimens to detect C. trachomatis, thereby affording a
noninvasive means of chlamydia testing.
 NAATs are the preferred methodology for detecting C.
trachomatis in most clinical stuations.

Psittacosis-
Laboratory Diagnosis
 Diagnosis of psittacosis is almost always by serologic means.
 Because of hazards associated with working with the agent, only
laboratories with Biosafety Level 3 biohazard containment facilities can
culture C. psittaci safely.
 State health departments take an active role in consulting with clinicians
about possible cases.
 Complement fixation and indirect micro-immunofluorescence have been
used to detect anti–C. psittaci antibodies in patients with suspected
psittacosis infections.
 Either a fourfold rise in titer between acute and convalescent serum
samples or a single IgM titer of 1:32 or greater in a patient with an
appropriate illness is considered diagnostic of an infection.
 Finally, amplification of rRNA sequences using a PCR assay followed by
restriction fragment length polymorphism (RFLP) analysis was able to
identify and distinguish all nine chlamydial species, including C. psittaci.

C. pneumoniae-
 In the laboratory, C. pneumoniae infections are diagnosed by cell culture,
serology, or NAATs.
 Direct Detection Methods To date, assays to directly detect C. pneumoniae
antigens have poor sensitivity.
 A variety of NAAT, including conventional and real-time PCR assays, have
been developed to detect C. pneumoniae nucleic acid sequences in clinical
specimens.
 Several of these amplification assays are commercially available. Using
these methods, the organism has been detected in throat swabs and other
specimens, such as nasopharyngeal, bronchoalveolar lavage fluids, and
sputum.

C. pneumoniae-
Cultivation
 Specimens for isolation are usually swabs of the
oropharynx;
 techniques for isolation of the organism from sputum are
unsatisfactory.
 Swabs should be placed into chlamydial transport media,
 transported on ice, and stored at 4°C;
 organisms are rapidly inactivated at room temperature or by
rapid freezing or thawing.
 A cell culture procedure similar to that used for C.
trachomatis but using the more sensitive HL or Hep-2 cell
lines must be substituted for McCoy cells.

Treatment-
C. trachomatis
 A 2-week course is recommended for complicated chlamydial infections
(e.g., PID, epididymitis) and at least a 3-week course of doxycycline (100
mg orally bid) or erythromycin base (500 mg orally qid) for LGV.
 C. trachomatis is eradicated from the urethra in nearly all cases by
treatment with tetracycline hydrochloride (500 mg qid for 7 days) or
doxycycline (100 mg by mouth bid for 7 days).
 Azithromycin (a single oral 1-g dose) is the regimen of choice for pregnant
women with C. trachomatis infection.
 However, amoxicillin (500 mg tid for 7 days) can also be given to pregnant
women.
 Tetracycline hydrochloride (500 mg qid) or doxycycline (100 mg bid) for
14 days produces clinical and microbiologic cure of epididymitis and PID
associated with C. trachomatis infection, but in this situation a tetracycline
should always be used together with a drug that is highly effective against
gonorrhea.
 Inclusion Conjuctivitis-azithromycin-(a 1-g single oral dose) or
doxycycline (100 mg bid for 7 days).

Treatment-
C. psittaci
 The tetracyclines are consistently effective in the
treatment of psittacosis.
 Defervescence and alleviation of symptoms
usually take place within 24–48 h after the
institution of therapy with 2 g daily in four
divided doses.
 To avoid relapse, treatment should probably be
continued for at least 7–14 days after
defervescence. Doxycycline (100 mg by mouth
bid) can also be used.

Treatment-
C. pneumoniae
Recommended therapy consists of 2 g/d of
either tetracycline or erythromycin for 10–14
days.
Other macrolides (e.g., azithromycin) and
some fluoroquinolones (e.g., levofloxacin and
gatifloxacin) also appear to be effective.

Chlamydia

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