**5. The causative organism Chlamydia trachomatis**

#### **5.1. Taxanomy**

Chlamydial organisms were historically referred to as Bedsonia or Miyagawanella and were initially thought to be protozoa. Because of their small size and the problems encountered with propagation, they were subsequently thought to be viruses. In the 1960s they were clas‐ sified as bacteria because *Chlamydia* express proteins (e.g., lipopolysaccharides) that are functionally analogous to other bacteria, divide by binary fission, are inhibited by antibacte‐ rial drugs, contain ribosomes, and are structurally and morphologically similar to gram-neg‐ ative bacteria. However, Chlamydia are only distantly related to other eubacterial orders based on phylogenies of ribosomal ribonucleic acid (rRNA) gene sequences. Chlamydiae comprise their own order, Chlamydiales; a single family, Chlamydiaceae; and one genus, *Chlamydia.* The genus *Chlamydia* is comprised of four known species: *C. trachomatis, C. psitta‐ ci, C. pneumoniae,* and *Chlamydia pecorum.*

Chlamydia trachomatis is made up of three biologic variants or biovars: trachoma, lym‐ phogranuloma venereum (LGV), and the rodent biovar that includes the mouse pneumoni‐ tis (MoPn) and hamster strains. There is 87% to 99% deoxyribonucleic acid (DNA) homology among the human strains and biovars of *C. trachomatis* but only 30% homology for the rodent strains.

With the exception of the rodent strains, C. trachomatis is currently known to infect only hu‐ mans. The infections in humans include the conjunctiva and lower and upper genital tracts, including the rectum and lymphatics that drain the perineum. These infections are caused by the 19 currently recognized serologic variants or serovars (defined by monoclonal and polyclonal antibodies that react to epitopes on the major outer membrane protein MOMP of C. trachomatis.) of the trachoma and LGV biovars.

**2.** TI: Trachomatous inflammation-intense is diagnosed when pronounced inflammatory thickening of the upper tarsal conjunctiva obscures more than half of the normal deep

**3.** TS: Trachomatous scarring is diagnosed by the presence of scarring in the tarsal con‐ junctiva. These scars are easily visible as white, bands or sheets (fibrosis) in the tarsal

**4.** TT: Trachomatous trichiasis is labeled when at least one eyelash rubs the eyeball. Evi‐ dence of recent removal of intured eyelashes should also be graded as trachomatous tri‐

**5.** CO: Corneal opacity is labeled when easily visible corneal opacity is present over the pupil. This sign refers to corneal scarring that is so dense that at least part of pupil mar‐ gin is blurred when seen through the opacity. The definition is intended to detect cor‐

Chlamydial organisms were historically referred to as Bedsonia or Miyagawanella and were initially thought to be protozoa. Because of their small size and the problems encountered with propagation, they were subsequently thought to be viruses. In the 1960s they were clas‐ sified as bacteria because *Chlamydia* express proteins (e.g., lipopolysaccharides) that are functionally analogous to other bacteria, divide by binary fission, are inhibited by antibacte‐ rial drugs, contain ribosomes, and are structurally and morphologically similar to gram-neg‐ ative bacteria. However, Chlamydia are only distantly related to other eubacterial orders based on phylogenies of ribosomal ribonucleic acid (rRNA) gene sequences. Chlamydiae comprise their own order, Chlamydiales; a single family, Chlamydiaceae; and one genus, *Chlamydia.* The genus *Chlamydia* is comprised of four known species: *C. trachomatis, C. psitta‐*

Chlamydia trachomatis is made up of three biologic variants or biovars: trachoma, lym‐ phogranuloma venereum (LGV), and the rodent biovar that includes the mouse pneumoni‐ tis (MoPn) and hamster strains. There is 87% to 99% deoxyribonucleic acid (DNA) homology among the human strains and biovars of *C. trachomatis* but only 30% homology

With the exception of the rodent strains, C. trachomatis is currently known to infect only hu‐ mans. The infections in humans include the conjunctiva and lower and upper genital tracts, including the rectum and lymphatics that drain the perineum. These infections are caused by the 19 currently recognized serologic variants or serovars (defined by monoclonal and polyclonal antibodies that react to epitopes on the major outer membrane protein MOMP of

neal opacities that cause significant visual impairment (less than 6/18).

**5. The causative organism Chlamydia trachomatis**

*ci, C. pneumoniae,* and *Chlamydia pecorum.*

C. trachomatis.) of the trachoma and LGV biovars.

for the rodent strains.

tarsal vessels.

234 Common Eye Infections

conjunctiva.

chiasis.

**5.1. Taxanomy**

**Figure 1.** Top left: **Trachomatous Inflammation - Follicular** Presence of follicles on the flat surface of the upper tar‐ salconjunctiva.Top right: **Trachomatous Inflammation - Intense** With enlarged vascular papillae marked inflamma‐ tory thickening of the upper tarsal conjunctiva obscures the deep conjunctival vessels. Middle left: Trachomatous Scarring The scar (white/yellow) lines form a 'network' of fibrous scarring in the tarsal conjunctiva.Middle right: **Tra‐ chomatous Trichiasis** There is evidence of one or more eyelashes rubbing on the eyeball.Bbottom: **Corneal Opacity** The patient has significantly reduced vision due to corneal scarring.

Serotyping has distinguished these serovars into different serogroups or classes: B class (serovars B, Ba, D, Da, E, L2, and L2a), intermediate class (serovars F and G), and C class (serovars A, C, H, I, Ia, J, Ja, K, Ka, L1, and L3). Serovars A through K and Ba, Da, Ia, Ja, and Ka were previously referred to as trachoma-inclusion conjunctivitis (TRIC) strains. Trachoma is primarily caused by serovars A, B, Ba, and C, whereas adult and neonatal inclusion conjunctivitis are caused by serovars B or Ba, D through K, Da, Ia, Ja, Ka, L1, L2, L2a, and L3, which are the sexually transmitted strains of the organism. The LGV serovars tend to cause more severe disease and can invade regional lymphatics, whereas the non-LGV serovars are currently known to infect epithelial cells at ocular, respiratory, rectal, and genital mucosal surfaces.

Serotyping has been the most widely accepted technique for classifying C. trachomatis or‐ ganisms. However, within the last decade, a new technique has been developed based on sequencing of ompA and is referred to as ompA genotyping. (ompA was previously called omp1, but the nomenclature has changed to be consistent with that of other bacteria.) This latter technique has been and continues to be invaluable for evaluating the molecular epi‐ demiology, disease pathogenesis, and transmission dynamics of chlamydiae for STD and trachoma populations.

#### **5.2. Chlamydia trachomatis development cycle**

Chlamydia trachomatis are obligate intracellular parasites that are unable to synthesize their own energy (ATP) and are completely dependent on their host for energy. It has a unique biphasic developmental cycle not found in any other bacteria. There is the ele‐ mentary body (EB) is the infectious form (spore-like particle) that posses a rigid outer membrane that bind to receptors on host cells and initiate infection. and the reticulate body (RB), which is the metabolically active form. Once the EB comes in contact with susceptible epithelial cells, it attaches by divalent cations and polycations, using heparin sulfate as a bridge between receptors on the EB and the cell surface. The EB is taken up into a phagosome by receptor-mediated endocytosis. There is ineffectual lysosomal fu‐ sion with the endophagosome because of their rigid outer membrane, and hence intracel‐ lular survival is insured.

A vacuole encloses the elementary body and the bacterium is now a reticulate body. Reticu‐ late bodies obtain their energy by sending forth "straw-like" structures into the host cell cy‐ toplasm. It can then replicate itself through binary fission. After division, the reticulate body becomes the elementary body. Anywhere from 100 to 1000 EBs can be produced per infected cell. In many cases, the cell ruptures and dies releasing the infectious progeny, but the cell can also extrude the inclusion body by a process of exocytosis and is released trough reverse endocytosis
