Chlamydia trachomatis is an obligate intracellular bacterium with a unique biphasic life cycle alternating between the infectious but metabolically inactive elementary body (EB) and non-infectious but metabolically active reticulate body (RB). It has developed several virulence factors that allow it to evade the host immune system, including a cryptic plasmid, type III secretion system, and the ability to enter a persistent dormant state. C. trachomatis causes a variety of diseases in humans by targeting mucosal surfaces and remains an important global public health issue.

1. Mays Yousuf Ismail ©
Chlamydia trachomatis:
Structure, Life cycle &
Virulence factors
Al-Quds University
Nov 2012 Jerusalem- Palestine

2. It’s Challenging !!
PID:4-5 POVERTY
US$10
Million/year
billion/year
> 500
>6 Million
%90 pop.
Million @
ECONOMY LIMITEDPOVERTY TO
ACCSESS
are Blind
infected
high risk
WATER
PERSONAL HYGIENE

3. Throat infection
Trachoma
Cervicitis

4. What we already know
about Chlamydia
trachomatis !!
Aerobic, obligate intracellular
parasite of eukaryotic cells

5. Questions raised from this
cryptic fact!!
1. Why does it live only intracellularly?
2. Is it really a bacteria? Or a virus?
3. What are its morphology? And its Metabolism
pathways?
4. How does it cause disease?
5. What are its weak points?
6. Can we prevent its infection? Can we make a
vaccine?

6. What makes Chlamydia trachomatis
UNIQUE; What makes it CLEVER !!
Scientists discovered that Chlamydia
trachomatis has a biphasic life cycle
Infectious Non-infectious,
extracellular intracellular
elementary bodies reticulate bodies

7. Chlamydia trachomatis biphasic life cycle
3 hrs 7-21
days
30 – 72 hrs
20 hrs

8. But what makes EB infectious??
why isn’t it found intracellularly?
and What makes RB survive intracellularly?
why isn’t it found extracellularly?

9. Hmmmm.. Let’s see …!!
Elementary Body Reticulate Body
Extracellular form Intra-cytoplasmatic form
Infectious particle, released Non-infectious particle, never
when infected cells rupture. released.
With iodine stain, appears as
Analogous to a spore
cellular inclusions
0.25 to 0.3 μm in diameter 0.6 μm in diameter.
No rigid cell wall; still,
Presence of rigid cell wall
membrane-bound
Preserves genome, plasmids,
RNA polymerase, All structures are retained
and ribosomes.
Replication by binary fission,
No Replication
rate of 2-3 hrs per generation
Metabolically inactive Metabolically active
Can induce Exo-, and Endo- Can’t induce Exo-, and Endo-
cytosis cytosis

10. So, now we know we’re not dealing with
only one Bacterium it’s
TWO in ONE !!
And this maybe makes it easier ?!

11. **The fact that the Elementary body is found extracellularly, and
has a cell wall.
** Chlamydia has a unique cell wall; outer LPS membrane but NO
peptidoglycan.
Made it possible to use Gram Stain to figure out the bacteria’s
Morphology !!
Chlamydia trachomatis is a Gram-negative coccobacilli bacteria.
**The fact that the Reticulate body is found intracellularly as
inclusions.
Made it possible to use Giemsa to detect it intracellularly !!
Chlamydia trachomatis is as small or smaller than many viruses;
0.25 to 1.5 μm.

13. Why does it live only
intracellularly?

14. Although Chlamydia trachomatis has a Glycolytic pathway,
a linked tricarboxylic acid cycle and an electron
transport system to produce energy, also Glycogen
synthesis pathway.
Still, it’s an Energy Parasite;
i.e. can’t synthesize sufficient ATP and is host-dependent.
(EB  RB)

15. What makes a bacteria this clever to live
inside a cell?
Will this protect it from the immune
system?

16. Those who wanna compete should work
harder !!
Polymorphic membrane
Chlamydial Anomaly
transporter
unique
cell
wall
cryptic
genome
plasmid
Compete
host for LPS
lipids Chlamydia
Type III secretion trachomatis Sialic acid of mucous
apparatus membranes
Pathogenicity 15
%75 Adhesion
Islands
serotypes
sub- Antigenic
clinical variation

17. Virulence Factors
1. Chlamydia has a unique cell wall; outer LPS membrane but NO peptidoglycan.
It contains Cystine-rich proteins functionally equivalent to peptidoglycan. This
inhibits phagolysosome fusion.
2. Chlamydia genome encodes for peptidoglycan biosynthesis enzymes but PGs
aren’t synthesized; Hence, resistance to beta-lactam drugs. Chlamydial
anomaly.
3. LPS that causes septic shock.
4. Adhesion to sialic acid receptors on mucous membranes; presence at sites
inaccessible to phagocytes, T-cells & B-cells.
5. Antigenic variation resulting in15 known serotypes.
6. 75% of the infections are sub-clinical still infectious though.
7. Pathogenicity Islands coding for needle-like projection type III secretion
apparatus that inject proteins directly from the bacteria into the cell cytoplasm
and avoid lysosomes.
8. Chlamydia-infested vacuole divert lipids to itself rather than to another
compartment of the host cell.
9. Proteins and regulatory factors produced by the cryptic plasmid. Polymorphic
outer membrane auto-transporter family of proteins, the putative large
cytotoxin, and stress response proteins.

18. Scientists: What if the immune system
attacks?
Chlamydia trachomatis: I’ll get dormant !!
This raised the concept of :
Chlamydial persistence

19. What we know about Chlamydial
persistence
• Long-term association between Chlamydia and host
cell in which it’s viable but culture-negative state.(are
detectable but show no growth)
• In vitro persistence show altered growth characteristics;
enlarged, and pleomorphic RBs that neither undergo
binary fission, nor differentiate back to EBs, but still
continue to replicate their chromosomes.
• Due to failure of secondary differentiation from RB to
EB due to gene down regulation.
• Induced by penicillin treatment, amino acid
starvation, iron deficiency, IFN-γ exposure, monocyte
infection, phage infection, continuous culture and
altered levels of sex hormones.
• Lasts in vitro until removal of the exogenous stressor.

20. Aren’t there any gaps ??
1. Penicillin arrests Bacterial Cytokinesis
2. Tetracycline, Erythromycin block Protein Synthesis
3. Although there’s no immunogenic surface proteins;
still, LPS can be used, but they are weak !! (vaccine).

21. Be Aware !!
Chlamydia trachomatis is present as
asymptomatic state within specific hosts providing a
natural reservoir.

22. ECOLOGY

23. References
1.http://en.wikipedia.org/wiki/Chlamydia_(bacterium)
2.http://www.ncbi.nlm.nih.gov/pubmed/10411734
3.http://microbewiki.kenyon.edu/index.php/Chlamydia_trachomatis
4. http://www.biomedcentral.com/1471-2180/11/150
5.http://www.sunysccc.edu/academic/mst/microbes/32ctrac.htm
6.http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0007
723
7.http://web.uconn.edu/mcbstaff/graf/Student%20presentations/Chlamydia/Chla
mydia%20trachomatis.html
8.http://www.tjclarkdirect.com/bacterial_diseases/chlamydia_trachomatis.htm
9. http://www.austincc.edu/microbio/2421a/ct.htm
10. http://www.ncbi.nlm.nih.gov/pubmed/20470049
11. http://jid.oxfordjournals.org/content/201/Supplement_2/S126.full
12. http://www.hindawi.com/journals/idog/2011/525182/fig2/