MICROBIOLOGY PPT LECTURE NOTES | Karya Tulis Ilmiah
Chlamydiae
17/9/7
microbiology 8-year course
1
Biological Features
Structure and chemical composition
Developmental cycle
Staining properties
Antigens
Growth and metabolism
Characteristics of host-parasite relationship
Classification
17/9/7
microbiology 8-year
2
Structure and chemical composition
a nonreplicating, infect
ious particle called the
elementary body (EB)
an intracytoplasmic for
m called the reticulate
body (RB)
17/9/7
microbiology 8-year
3
Structure and chemical composition
17/9/7
microbiology 8-year
4
Structure and chemical composition
The elementary body, which is covered by a rigid cell wall, contains a DNA geno
me with a molecular weight of 66 X 107 (about 600 genes, one-quarter of the g
enetic information present in the DNA of Escherichia coli).
A cryptic DNA plasmid (7,498 base pairs) is also found. It contains an open read
ing frame for a gene involved in DNA replication.
the elementary body contains an RNA polymerase responsible for the transcripti
on of the DNA genome after entry into the host cell cytoplasm and the initiation
of the growth cycle.
Ribosomes and ribosomal subunits are present in the elementary bodies. Throu
ghout the developmental cycle, the DNA genome, proteins, and ribosomes are r
etained in the membrane-bound reticulate body.
17/9/7
microbiology 8-year
5
Developmental cycle
EBs attach to the microvilli of susceptive cells.
Penetration into the host cell via endocytosis or pinocytosis and for
ming phagosomes
Fusion of lysomes with the EB-containing phagosome are inhibited
EBs reorganize into the metabolically active RBs.
RBs synthesize their own DNA, RNA and protein but lack the necess
ary metabolic pathways to produce high-energy phosphate compou
nds.
Energy parasites.
RBs replicate by binary fission and inclusion forms.
RBs begin reorganizing into EBs.
Cell ruptures and releasesthe infective Ebs.
The developmental cycle takes 24 ～ 48 hours.
17/9/7
microbiology 8-year
6
Developmental cycle
17/9/7
microbiology 8-year
7
Staining properties
EBs stain purple with Giemsa stain—in contrast to the blue
of host cell cytoplasm.
RBs stain blue with Giemsa stain.
The Gram reaction of chlamydiae is negative or variable and
is not useful in identification.
Inclusions stain brightly by immunofluorescence ,with group-
specific,species-specific, or serovar-specific antibodies.
17/9/7
microbiology 8-year
8
Antigens
Group(fenus)-specific antigens:
– heat-stable LPS as an immunodominant component.
– Antibody to these antigens can be detected by CF an
d immunofluorescence
Species-specific or serovar-specific antigens
– Antigens are mainly outer membrane proteins(MOM
P).
– Specific antigens can best be detected by immunoflu
orescence,particularly using monoclonal antibodies.
17/9/7
microbiology 8-year
9
Growth and metabolism
Unable to synthesize ATP and depend on the host cell for energy requirement
s.
Grow in cultures of a variety of eukaryotic cell lines
– McCoy cells are used to isolate chlamydiae
– C pneumoniae grows better in HL or Hep-2 cells.
– All types of chlamydiae proliferate in embryonated eggs,particularly in th
e yolk sac.
The replication of chlamydiae can be inhibited by many antibacterial drugs.
– Cell wall inhibitors (penicillins) result in the production of morphologicall
y defective forms but are not effective in clinical diseases.
– Inhibitors of protein synthesis (tetracyclines,erythromycins)are effective
in most clinical infections.
– C trachomatis strains synthesize folates and are susceptible to inhibition
by sulfonamides.
17/9/7
microbiology 8-year
10
Classification
C trachomatis
– Biovar trachoma
– Biovar lymphogranuloma venereum
– Biovar mouse
C pneumoniae
C psittaci
C pecorum 兽类衣原体
17/9/7
microbiology 8-year
11
Transmission
17/9/7
microbiology 8-year
12
Pathogenicity
transmission
Who is at risk
Virulence factor
Clinical syndromes
Epidemiology
immunity
17/9/7
microbiology 8-year
13
Transmission
C. trachomatis
– Sexually transmitted;most frequent bacterial pathogen in
united states.
– Infected patients , who may be asymptomatic.
– Inoculation through break in skin or membranes.
– Passage to new born at birth.
– Trachoma spread to eye by means of contaminated hand,d
roplets,clothing, and flies.
17/9/7
microbiology 8-year
14
Transmission
C. pneumoniae
– Person-to-person spread by inhalation of infecti
ous aerosols.
– No animal reservoir
C. psittaci
– Infection acquired by contact with infected bir
d or animal(may appear healthy).
– Person-to-person infection very uncommon.
17/9/7
microbiology 8-year
15
Who is at risk?
C. trachomatis
– People with multiple sexual partners.
– Homosexuals,who are more at risk for LGV.
– Newborns born of infected mothers.
– Reiter’s syndrome: young white men.
– Trachoma:children,particularly those in crow
ded living conditions where sanitation and hygi
ene are poor.
17/9/7
microbiology 8-year
16
Who is at risk?
C. pneumoniae
– High prevalence of infections throughout life;m
ost infections asymptomatic.
– Diease most common in adults.
C. psittaci
– Disease most common in adults.
– Occupations at increased risk include veterinari
ans,zookeepers,pet shop workers,and employee
s in poultry processing plants
17/9/7
microbiology 8-year
17
Virulence factors
C. trachomatis
– Intracellular replication,
– prevention of phagolysosomal 吞噬溶酶体 fusi
on,
– survival of infectious EBs as a result of cross-li
nkage of membrane proteins.
17/9/7
microbiology 8-year
18
Virulence factors
C. pneumoniae
– Intracellular replication;
– prevention of phagolysosome 吞噬溶酶体 fusi
on;
– ability to infect and destroy ciliated epithelial c
ells of respiratory tract,smooth muscle cells,end
othelial cells,and macrophages;
– extracellular survival of infectious EBs.
17/9/7
microbiology 8-year
19
Virulence factors
C. psittaci
– Intracellular parasite,
– prevention of phagolysosomal fusion,
– survival of infectious EBs as result of cross-link
age of membrane proteins.
17/9/7
microbiology 8-year
20
Clinical syndromes
C. trachomatis
– Trachoma
– Adult inclusion conjunctivitis
– Neonatal conjunctivitis
– Infant pneumonia
– Ocular lymphogranuloma
venereum
– Urogenital infections
– Reiter’s syndrome
– Lymphogranuloma venereum
17/9/7
microbiology 8-year
21
Clinical syndromes
C. pneumoniae
– Bronchitis
– Pneumonia
– Sinusitis 鼻窦炎
– Pharyngitis
– atherosclerosis 动脉粥样硬化
17/9/7
microbiology 8-year
22
Clinical syndromes
C. psittaci
– psittacosis
17/9/7
microbiology 8-year
23
Epidemiology
Trachoma
– Trachoma is still prevalent in Africa and Asia, and sporadic cases o
ccur all over the world.
– The disease flourishes in hot, dry areas where there is a shortage of
water and where standards of hygiene are low.
– The agent is spread to the eyes by flies, dirty towels, fingers, or co
smetic eye pencils.
– The initial infection usually occurs in childhood, and the active dis
ease eventually appears (mostly by 10 to 15 years of age). Tracho
ma may leave a residuum of permanent lesions that can lead to bli
ndness.
– Chlamydia trachomatis also resides in the genital tract, cervix, and
urethra of adults, and genital infection is spread sexually.
17/9/7
microbiology 8-year
24
Epidemiology
Lymphogranuloma venereum
– Lymphogranuloma venereum persists in the genital tract of infecte
d persons.
– LGV is a chronic sexually transmitted disease caused by serotype
L1,L2,and L3.
– Because C trachomatis is able to infect both the eyes and the urog
enital tract, antitrachoma campaigns involving only ocular treatme
nts are futile.
– It occurs sporadically in North America ,Australia ,and Europe but
is highly prevalent in Africa, Asia and South America.
– Male homosexuals are the major reservoir of disease.
– Acute LGV is seen more frequently in men,primarily because sym
ptomatic infection is less common in women.
17/9/7
microbiology 8-year
25
Epidemiology
Chlamydia pneumoniae
– Chlamydia pneumoniae spreads in human populations
by respiratory tract infections.
– It is the agent of atypical pneumonia in hospitalized pat
ients as well as in young individuals with an acute respi
ratory disease.
– It has caused epidemics in Scandinavia.
– Studies of the prevalence of antibodies to C pneumonia
e in humans around the world showed that it also prevai
ls in Japan, Panama, and North America.
17/9/7
microbiology 8-year
26
Epidemiology
Chlamydia psittaci
– the cause of psittacosis in birds and occasionall
y in humans,
– it is carried by wild and domestic birds, includi
ng poultry.
– The severity of psittacosis in humans has been
considerably reduced by the susceptibility of C
psittaci to antibiotics.
17/9/7
microbiology 8-year
27
Immunity
C. trachomatis
– Untreated infections tend to be chronic with per
sistence of the agent for many years.
– Little is known about active immunity.
– The coexistence of latent infection,antibodies,a
nd cell-mediated reactions is typical of many ch
lamydial infections.
17/9/7
microbiology 8-year
28
Immunity
C. pneumoniae
– Little is known about active or potentially prote
ctive immunity.
– Prolonged infections can occur with C. pneumo
niae, and asymptomatic carriage may be comm
on.
17/9/7
microbiology 8-year
29
Immunity
C. psittacosis
– Immunity in animals and humans is incomplete.
– A carrier state in humans can persist for 10
years after recovery.
– During this period, the agent may continue to
be excreted in the sputum.
– Live or inactivated vaccines induce only partial
resistance in animals.
– They have not been used in humans.
17/9/7
microbiology 8-year
30
Diagnosis
Most diseases caused by the chlamydiae are
diagnosed on the basis of their clinical ma
nifestations.
Eye damage caused by C trachomatis is typ
ical, as are the vesicles in the infected uroge
nital tract.
Diagnosis of pneumonitis requires laborator
y testing
17/9/7
microbiology 8-year
31
Diagnosis
Chlamydia trachomatis can be identified microscopically i
n scrapings from the eyes or the urogenital tract. Inclusion
bodies in scraped tissue cells are identified by iodine staini
ng of glycogen present in the cytoplasmic vacuoles in infe
cted cells.
To isolate the agent, cell homogenates that contain the chla
mydial elementary bodies are centrifuged onto the cultured
cells (e.g., irradiated McCoy cells).
After incubation, typical cytoplasmic inclusions are seen in
the cells stained with Giemsa stain or iodine.
17/9/7
microbiology 8-year
32
Diagnosis
Staining with iodine can distinguish between inclusion bod
ies of C trachomatis and C psittaci, as only the former cont
ain glycogen.
Each chlamydial agent can also be identified by using spe
cific immunofluorescent antibodies prepared against either
C trachomatis or C psittaci.
Homogenates or exudates of infected tissues also have bee
n used to isolate the agent in the yolk sac of embryonated e
ggs.
17/9/7
microbiology 8-year
33
Diagnosis
Sera and tears from infected humans are use
d to detect anti-Chlamydia antibodies by the
complement fixation or microimmunofluore
scence tests.
The latter is useful for identifying specific s
erotypes of C trachomatis.
Fluorescent monoclonal antibodies are used
to stain C trachomatis elementary bodies in
urethral and cervical exudates.
17/9/7
microbiology 8-year
34
Diagnosis
It is possible to diagnose C trachomatis in tissue biopsy sp
ecimens by in situ DNA hybridization with cloned C trach
omatis DNA probes.
DNA from C trachomatis isolates can be examined by rest
riction endonuclease analysis.
The DNA cleavage pattern of C trachomatis isolates differ
s greatly from that of DNA from C psittaci isolates.
DNAs of the agents of trachoma and lymphogranuloma ve
nereum differ in their cleavage patterns, and this allows ide
ntification of the biovars
17/9/7
microbiology 8-year
35
Diagnosis
Chlamydia pneumoniae DNA has 10 percent homology
with C trachomatis or C psittaci;
C pneumoniae isolates have 100 percent homology. Chl
amydia pneumoniae isolates can be diagnosed by hybrid
ization with a specific DNA probe that does not hybridi
ze to other chlamydiae.
Two additional serologic tests are in use:
the microimmunofluorescence test with C pneumoniaespecific elementary body antigen, and the complement f
ixation test, which measures Chlamydia antibodies.
17/9/7
microbiology 8-year
36
Prevention and control
C. trachomatis
– It is difficult to prevent C. trachomatis infection
s because the population with endemic disease f
requently has limited access to medical care.
– It is difficult to eradicate the disease within a po
pulation and to prevent reinfections.
– Chlamydia conjunctivitis and genital infections
are prevented through the use of safe sexual pra
ctices and the prompt treatment of symptomatic
patients and their sexual partners.
17/9/7
microbiology 8-year
37
Prevention and control
C. pneumoniae
– Treatment is with tetracycline or erythromycin.
– Failures are common.
– Retreament maybe required.
17/9/7
microbiology 8-year
38
Prevention and control
C. psittaci
– Tetracycline or erythromycin is used for treatm
ent.
– Infections should be controlled in domestic and
imported pet birds using chlortetracycline.
17/9/7
microbiology 8-year
39
Treatment
C. trachomatis
– Ocular,genital & respiratory infections
– In endemic areas,sulfonamides,erythromycins,and tetracyclines have b
een used to suppress chlamydiae and bacteria that cause eye infections.
– Genital infections & inclusion conjunctivitis
– It is essential that chlamydial infections be treated simultaneously in bo
th sex partners and in offspring to prevent reinfection.
– tetracyclines are commonly used in non pregnant in fected females.
– Erythromycin is given to pregnant women.
– LGV
– The sulfonamides and tetracyclines have been used with food results es
pecially in the early stages.
– Little is known about active immunity.
17/9/7
microbiology 8-year
40
Treatment
C. pneumoniae
– It is susceptible to the macrolides and tetracyclines and
to some fluoroquinolones.
– Treatment with doxycycline, azithromycin,or clarithro
mycin appears to benefit patients with the infection.
– The symptoms may continue after routine courses of th
erapy with erythromycin,doxycyclinbe, or tetracycline.
– These drugs should be given for 10- to 14-day courses.
17/9/7
microbiology 8-year
41
Treatment
C. psittacosis
– tetracyclines. Are the drugs of choice and shoul
d be continued for 10 days.
– It may not free the patient from the agent.
– Intensive antiviotic treament may also delay the
normal course of antibody development.
– Strains may become drug-resistant.
– With antibiotic therapy the mortality rate is 2﹪
or less.
17/9/7
microbiology 8-year
42
17/9/7
microbiology 8-year course
1
Biological Features
Structure and chemical composition
Developmental cycle
Staining properties
Antigens
Growth and metabolism
Characteristics of host-parasite relationship
Classification
17/9/7
microbiology 8-year
2
Structure and chemical composition
a nonreplicating, infect
ious particle called the
elementary body (EB)
an intracytoplasmic for
m called the reticulate
body (RB)
17/9/7
microbiology 8-year
3
Structure and chemical composition
17/9/7
microbiology 8-year
4
Structure and chemical composition
The elementary body, which is covered by a rigid cell wall, contains a DNA geno
me with a molecular weight of 66 X 107 (about 600 genes, one-quarter of the g
enetic information present in the DNA of Escherichia coli).
A cryptic DNA plasmid (7,498 base pairs) is also found. It contains an open read
ing frame for a gene involved in DNA replication.
the elementary body contains an RNA polymerase responsible for the transcripti
on of the DNA genome after entry into the host cell cytoplasm and the initiation
of the growth cycle.
Ribosomes and ribosomal subunits are present in the elementary bodies. Throu
ghout the developmental cycle, the DNA genome, proteins, and ribosomes are r
etained in the membrane-bound reticulate body.
17/9/7
microbiology 8-year
5
Developmental cycle
EBs attach to the microvilli of susceptive cells.
Penetration into the host cell via endocytosis or pinocytosis and for
ming phagosomes
Fusion of lysomes with the EB-containing phagosome are inhibited
EBs reorganize into the metabolically active RBs.
RBs synthesize their own DNA, RNA and protein but lack the necess
ary metabolic pathways to produce high-energy phosphate compou
nds.
Energy parasites.
RBs replicate by binary fission and inclusion forms.
RBs begin reorganizing into EBs.
Cell ruptures and releasesthe infective Ebs.
The developmental cycle takes 24 ～ 48 hours.
17/9/7
microbiology 8-year
6
Developmental cycle
17/9/7
microbiology 8-year
7
Staining properties
EBs stain purple with Giemsa stain—in contrast to the blue
of host cell cytoplasm.
RBs stain blue with Giemsa stain.
The Gram reaction of chlamydiae is negative or variable and
is not useful in identification.
Inclusions stain brightly by immunofluorescence ,with group-
specific,species-specific, or serovar-specific antibodies.
17/9/7
microbiology 8-year
8
Antigens
Group(fenus)-specific antigens:
– heat-stable LPS as an immunodominant component.
– Antibody to these antigens can be detected by CF an
d immunofluorescence
Species-specific or serovar-specific antigens
– Antigens are mainly outer membrane proteins(MOM
P).
– Specific antigens can best be detected by immunoflu
orescence,particularly using monoclonal antibodies.
17/9/7
microbiology 8-year
9
Growth and metabolism
Unable to synthesize ATP and depend on the host cell for energy requirement
s.
Grow in cultures of a variety of eukaryotic cell lines
– McCoy cells are used to isolate chlamydiae
– C pneumoniae grows better in HL or Hep-2 cells.
– All types of chlamydiae proliferate in embryonated eggs,particularly in th
e yolk sac.
The replication of chlamydiae can be inhibited by many antibacterial drugs.
– Cell wall inhibitors (penicillins) result in the production of morphologicall
y defective forms but are not effective in clinical diseases.
– Inhibitors of protein synthesis (tetracyclines,erythromycins)are effective
in most clinical infections.
– C trachomatis strains synthesize folates and are susceptible to inhibition
by sulfonamides.
17/9/7
microbiology 8-year
10
Classification
C trachomatis
– Biovar trachoma
– Biovar lymphogranuloma venereum
– Biovar mouse
C pneumoniae
C psittaci
C pecorum 兽类衣原体
17/9/7
microbiology 8-year
11
Transmission
17/9/7
microbiology 8-year
12
Pathogenicity
transmission
Who is at risk
Virulence factor
Clinical syndromes
Epidemiology
immunity
17/9/7
microbiology 8-year
13
Transmission
C. trachomatis
– Sexually transmitted;most frequent bacterial pathogen in
united states.
– Infected patients , who may be asymptomatic.
– Inoculation through break in skin or membranes.
– Passage to new born at birth.
– Trachoma spread to eye by means of contaminated hand,d
roplets,clothing, and flies.
17/9/7
microbiology 8-year
14
Transmission
C. pneumoniae
– Person-to-person spread by inhalation of infecti
ous aerosols.
– No animal reservoir
C. psittaci
– Infection acquired by contact with infected bir
d or animal(may appear healthy).
– Person-to-person infection very uncommon.
17/9/7
microbiology 8-year
15
Who is at risk?
C. trachomatis
– People with multiple sexual partners.
– Homosexuals,who are more at risk for LGV.
– Newborns born of infected mothers.
– Reiter’s syndrome: young white men.
– Trachoma:children,particularly those in crow
ded living conditions where sanitation and hygi
ene are poor.
17/9/7
microbiology 8-year
16
Who is at risk?
C. pneumoniae
– High prevalence of infections throughout life;m
ost infections asymptomatic.
– Diease most common in adults.
C. psittaci
– Disease most common in adults.
– Occupations at increased risk include veterinari
ans,zookeepers,pet shop workers,and employee
s in poultry processing plants
17/9/7
microbiology 8-year
17
Virulence factors
C. trachomatis
– Intracellular replication,
– prevention of phagolysosomal 吞噬溶酶体 fusi
on,
– survival of infectious EBs as a result of cross-li
nkage of membrane proteins.
17/9/7
microbiology 8-year
18
Virulence factors
C. pneumoniae
– Intracellular replication;
– prevention of phagolysosome 吞噬溶酶体 fusi
on;
– ability to infect and destroy ciliated epithelial c
ells of respiratory tract,smooth muscle cells,end
othelial cells,and macrophages;
– extracellular survival of infectious EBs.
17/9/7
microbiology 8-year
19
Virulence factors
C. psittaci
– Intracellular parasite,
– prevention of phagolysosomal fusion,
– survival of infectious EBs as result of cross-link
age of membrane proteins.
17/9/7
microbiology 8-year
20
Clinical syndromes
C. trachomatis
– Trachoma
– Adult inclusion conjunctivitis
– Neonatal conjunctivitis
– Infant pneumonia
– Ocular lymphogranuloma
venereum
– Urogenital infections
– Reiter’s syndrome
– Lymphogranuloma venereum
17/9/7
microbiology 8-year
21
Clinical syndromes
C. pneumoniae
– Bronchitis
– Pneumonia
– Sinusitis 鼻窦炎
– Pharyngitis
– atherosclerosis 动脉粥样硬化
17/9/7
microbiology 8-year
22
Clinical syndromes
C. psittaci
– psittacosis
17/9/7
microbiology 8-year
23
Epidemiology
Trachoma
– Trachoma is still prevalent in Africa and Asia, and sporadic cases o
ccur all over the world.
– The disease flourishes in hot, dry areas where there is a shortage of
water and where standards of hygiene are low.
– The agent is spread to the eyes by flies, dirty towels, fingers, or co
smetic eye pencils.
– The initial infection usually occurs in childhood, and the active dis
ease eventually appears (mostly by 10 to 15 years of age). Tracho
ma may leave a residuum of permanent lesions that can lead to bli
ndness.
– Chlamydia trachomatis also resides in the genital tract, cervix, and
urethra of adults, and genital infection is spread sexually.
17/9/7
microbiology 8-year
24
Epidemiology
Lymphogranuloma venereum
– Lymphogranuloma venereum persists in the genital tract of infecte
d persons.
– LGV is a chronic sexually transmitted disease caused by serotype
L1,L2,and L3.
– Because C trachomatis is able to infect both the eyes and the urog
enital tract, antitrachoma campaigns involving only ocular treatme
nts are futile.
– It occurs sporadically in North America ,Australia ,and Europe but
is highly prevalent in Africa, Asia and South America.
– Male homosexuals are the major reservoir of disease.
– Acute LGV is seen more frequently in men,primarily because sym
ptomatic infection is less common in women.
17/9/7
microbiology 8-year
25
Epidemiology
Chlamydia pneumoniae
– Chlamydia pneumoniae spreads in human populations
by respiratory tract infections.
– It is the agent of atypical pneumonia in hospitalized pat
ients as well as in young individuals with an acute respi
ratory disease.
– It has caused epidemics in Scandinavia.
– Studies of the prevalence of antibodies to C pneumonia
e in humans around the world showed that it also prevai
ls in Japan, Panama, and North America.
17/9/7
microbiology 8-year
26
Epidemiology
Chlamydia psittaci
– the cause of psittacosis in birds and occasionall
y in humans,
– it is carried by wild and domestic birds, includi
ng poultry.
– The severity of psittacosis in humans has been
considerably reduced by the susceptibility of C
psittaci to antibiotics.
17/9/7
microbiology 8-year
27
Immunity
C. trachomatis
– Untreated infections tend to be chronic with per
sistence of the agent for many years.
– Little is known about active immunity.
– The coexistence of latent infection,antibodies,a
nd cell-mediated reactions is typical of many ch
lamydial infections.
17/9/7
microbiology 8-year
28
Immunity
C. pneumoniae
– Little is known about active or potentially prote
ctive immunity.
– Prolonged infections can occur with C. pneumo
niae, and asymptomatic carriage may be comm
on.
17/9/7
microbiology 8-year
29
Immunity
C. psittacosis
– Immunity in animals and humans is incomplete.
– A carrier state in humans can persist for 10
years after recovery.
– During this period, the agent may continue to
be excreted in the sputum.
– Live or inactivated vaccines induce only partial
resistance in animals.
– They have not been used in humans.
17/9/7
microbiology 8-year
30
Diagnosis
Most diseases caused by the chlamydiae are
diagnosed on the basis of their clinical ma
nifestations.
Eye damage caused by C trachomatis is typ
ical, as are the vesicles in the infected uroge
nital tract.
Diagnosis of pneumonitis requires laborator
y testing
17/9/7
microbiology 8-year
31
Diagnosis
Chlamydia trachomatis can be identified microscopically i
n scrapings from the eyes or the urogenital tract. Inclusion
bodies in scraped tissue cells are identified by iodine staini
ng of glycogen present in the cytoplasmic vacuoles in infe
cted cells.
To isolate the agent, cell homogenates that contain the chla
mydial elementary bodies are centrifuged onto the cultured
cells (e.g., irradiated McCoy cells).
After incubation, typical cytoplasmic inclusions are seen in
the cells stained with Giemsa stain or iodine.
17/9/7
microbiology 8-year
32
Diagnosis
Staining with iodine can distinguish between inclusion bod
ies of C trachomatis and C psittaci, as only the former cont
ain glycogen.
Each chlamydial agent can also be identified by using spe
cific immunofluorescent antibodies prepared against either
C trachomatis or C psittaci.
Homogenates or exudates of infected tissues also have bee
n used to isolate the agent in the yolk sac of embryonated e
ggs.
17/9/7
microbiology 8-year
33
Diagnosis
Sera and tears from infected humans are use
d to detect anti-Chlamydia antibodies by the
complement fixation or microimmunofluore
scence tests.
The latter is useful for identifying specific s
erotypes of C trachomatis.
Fluorescent monoclonal antibodies are used
to stain C trachomatis elementary bodies in
urethral and cervical exudates.
17/9/7
microbiology 8-year
34
Diagnosis
It is possible to diagnose C trachomatis in tissue biopsy sp
ecimens by in situ DNA hybridization with cloned C trach
omatis DNA probes.
DNA from C trachomatis isolates can be examined by rest
riction endonuclease analysis.
The DNA cleavage pattern of C trachomatis isolates differ
s greatly from that of DNA from C psittaci isolates.
DNAs of the agents of trachoma and lymphogranuloma ve
nereum differ in their cleavage patterns, and this allows ide
ntification of the biovars
17/9/7
microbiology 8-year
35
Diagnosis
Chlamydia pneumoniae DNA has 10 percent homology
with C trachomatis or C psittaci;
C pneumoniae isolates have 100 percent homology. Chl
amydia pneumoniae isolates can be diagnosed by hybrid
ization with a specific DNA probe that does not hybridi
ze to other chlamydiae.
Two additional serologic tests are in use:
the microimmunofluorescence test with C pneumoniaespecific elementary body antigen, and the complement f
ixation test, which measures Chlamydia antibodies.
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Prevention and control
C. trachomatis
– It is difficult to prevent C. trachomatis infection
s because the population with endemic disease f
requently has limited access to medical care.
– It is difficult to eradicate the disease within a po
pulation and to prevent reinfections.
– Chlamydia conjunctivitis and genital infections
are prevented through the use of safe sexual pra
ctices and the prompt treatment of symptomatic
patients and their sexual partners.
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Prevention and control
C. pneumoniae
– Treatment is with tetracycline or erythromycin.
– Failures are common.
– Retreament maybe required.
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Prevention and control
C. psittaci
– Tetracycline or erythromycin is used for treatm
ent.
– Infections should be controlled in domestic and
imported pet birds using chlortetracycline.
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Treatment
C. trachomatis
– Ocular,genital & respiratory infections
– In endemic areas,sulfonamides,erythromycins,and tetracyclines have b
een used to suppress chlamydiae and bacteria that cause eye infections.
– Genital infections & inclusion conjunctivitis
– It is essential that chlamydial infections be treated simultaneously in bo
th sex partners and in offspring to prevent reinfection.
– tetracyclines are commonly used in non pregnant in fected females.
– Erythromycin is given to pregnant women.
– LGV
– The sulfonamides and tetracyclines have been used with food results es
pecially in the early stages.
– Little is known about active immunity.
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Treatment
C. pneumoniae
– It is susceptible to the macrolides and tetracyclines and
to some fluoroquinolones.
– Treatment with doxycycline, azithromycin,or clarithro
mycin appears to benefit patients with the infection.
– The symptoms may continue after routine courses of th
erapy with erythromycin,doxycyclinbe, or tetracycline.
– These drugs should be given for 10- to 14-day courses.
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Treatment
C. psittacosis
– tetracyclines. Are the drugs of choice and shoul
d be continued for 10 days.
– It may not free the patient from the agent.
– Intensive antiviotic treament may also delay the
normal course of antibody development.
– Strains may become drug-resistant.
– With antibiotic therapy the mortality rate is 2﹪
or less.
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