DON XAVIER N.D CHLAMYDIAE

MORPHOLOGY Obligate intracellular parasites of humans, animals & birds in Squamous epithelial cells & Macrophages. Resemble bacteria except it cannot multiply outside living cells/ tissues (like viruses).But have both DNA & RNA, Replicate by binary fission. Do not have Peptidoglycan cell walls Cannot synthesize ATP – depends on host cell for energy & nutrient sources due to the absence of ETC. Hence, called Energy Parasites. 4 species in the Genus Chlamydia – C. trachomatis, C. pneumoniae, affects humans C. psittaci and C. pecorum affects ruminants All are non-motile, gram negative.

C.trachomatis : eye & genital infections, infant pneumonia, and LGV (Lymphogranuloma Venereum) in adults.They form compact inclusions with Glycogen matrix. C.pneumoniae : different types of respiratory infections exclusively to humans. C.psittaci : psittacosis in man, ornithosis in birds.

Chlamydiae occur in 2 forms : Elementary body – extracellular, infective form,Spherical in shape having cell wall similar to gram –ve bacteria. Reticulate body(Initial Body) – intracellular, growing & replicative form Chlamydial microcolony within the host cell is called Inclusion body. Mature inclusion body contains 100 - 500 elementary bodies During growth Chlamydial specific LPS accumulate in cell surface that is highly Inflammatory, Immunological and main factor of pathogenesis

Spheroplast like transformation EB-RB Nucleus pushed to periphery & EB exocytosed Binary Fission, Host cell growth arrested Inclusion body with RB & Developing EB

Three major Ags Genus specific Ag – heat stable, common to all chlamydiae, a lipopolysaccharide resembling LPS of GNB. Present in all stages. Species specific protein Ags – present at the envelope surface, help in classifying chlamydia into species Ag for Intraspecies typing – found only in some members of a species, located on major OMP (MOMP), demonstrated by micro- IF. Classifies species into serovars/ serotypes C. trachomatis – 2 biovars: TRIC & LGV TRIC – Trachoma, Inclusion conjunctivitis - divided into 12 serovars LGV – Lymphogranuloma venereum – 3 serovars

4 approaches available: LAB DIAGNOSIS 4 approaches available: Microscopic demonstration of inclusion or elementary bodies Isolation of chlamydia Demonstration of chlamydial Ag Demonstration of Abs or hypersensitivity Gram negative but stained better by Giemsa, Castaneda or Machiavello stains. Giemsa Stain: Elementary body & the Reticulate body stains blue in cytoplasm Lugol’s iodine: rapid & simple screening method for ocular infections, stains glycogen matrix of C. trachomatis Immunoflurescence staining: more sensitive & specific, by using monoclonal Abs. Identifies inclusion bodies as well as extracellular elementary bodies. Used for ocular, cervical or urethral specimens.

LYMPHOGRANULOMA VENEREUM Demonstration of characteristic inclusion bodies (Halberstaedter Prowazek or HP bodies) in conjunctival scrapings by Giemsa in case of trachoma. LYMPHOGRANULOMA VENEREUM Most commonly caused by L2 type Site – regional lymph nodes Incubation period – 3 days to 5 wks 1° lesion – small painless papulovesicular lesion on external genitalia 2° stage – after 2 wks, lymphatic spread to draining LNs (men – inguinal, women – intrapelvic & pararectal) Nodes enlarge, suppurate, become adherent to the skin & break down to form discharging sinuses. Metastatic complications – may occur, involves joints, eyes & meninges 3° stage – chronic, lasts for several years; scarring & lymphatic blockage Late sequelae more distressing in women – rectal strictures, elephantiasis of vulva