Chlamydiaceae family Lecture 26 Flashcards
Chlamydiaceae family
two genera: chlamydia (C. Trachomatis) and chlamydophilia (c. pneumoniae, and C. psittaci)
obligate intracellular pathogens
originally considered viruses due to small size
reclassified as bacteria. Possess inner and outer membranes similar to gram negative bacteria (but lack peptidoglycan layer). Contain both DNA and RNA. Possess prokaryotic ribosomes. Synthesize own proteins, nucleic acids, and lipids. Susceptible to antibacterial antibiotics.
Chlamydia: development cycle
exist in two forms. IN active infectious form (elementary bodies) and metabolically active non-infectious forms (reticulate bodies)
- EBs infect host cell and convert to RBs.
- RBs replicate using host cell’s ATP for energy and form inclusion (phagosome with replicating RBs)
- Reticulate bodies reorganize into EBs
- EB’s released by reverse endocytosis
Chlamydia trachomatis
Divided into two biovars: trachoma and LGV
major outer membrane protein (MOMP) important structural component
variable regions in gene encoding momp results in 18 serologic variants or serovars
trachoma: serovars A, B, Ba, C
Urogenital tract disease: serovars D-K
Lymphogranuloma venerum: Li, L2, L2a, L2b, L3
pathogenesis and immunity: chlamydia trachomatis
limited range of cells that can infect
receptors for EBs restricted to nonciliated columnar, cuboidal and transitional epithelial cells
Found on mucous membranes of urethra, endocervix, endometrium, falopian tubes, anorectum, respiratory tract, conjunctivae
LGV serovars more invasive due to replication within mononuclear phagocytes
Pathogenesis and immunity: chlamydia trachomatis 2 Chlamydia
Clinical manifestation caused by: direct destruction of cells during replication. Proinflammatory cytokine response they stimulate
entry via minute abrasions or lacerations
severe inflammatory response with neutrophils, lymphocytes, and plasma cells
LGV serovars form lesions in lymph nodes with resulting granuloma formation
infection does not result in immunity
reinfection results in vigorous inflammatory response and tissue damage
results in scarring (ocular and UG), blindness, sterility and sexual dysfunction
Epidemiology: trachoma Chlamydia
leading cause of preventable blindness worldwide
WHO estimates: 6 million blind due to trachoma. 150 million in need of treatment.
endemic in NOrth and sub-Sahara Africa, Middle east, Asia, and South America
Infections predominantly in chidlren and are chief reservoir for endemic disease
trasmitted eye to eye via droplet, hand, clothing, and eye seeking flies
Epidemiology: Urogenital disease Chlamydia
Most common bacterial STI in US
2006 reported 1 million infections
underestimate many patiients do not seek medical care, asymptomatic disease
estimated 2.8 million new infections each year in the US
50 million new infections each year worldwide.
Epidemiology: LGV Chlamydia
occurs only sporadically in US.
Highly prevalent in Africa, Asia, and South America
Seen more frequently in men (women with more asymptomatic disease)
recent outbreaks reported in Europe and NOrth America in MSM
HIV coinfection common
Clinical diseases: Trachoma Chlamydia
Two phases of infection
Active Trachoma: initial infetion causes mild self limited follicular conjunctivitis. Characeristic follice on superior tarsal conjunctiva. Often Asymptomatic.
Cicatricial disease: Severity and duration of active trachoma predicts progression to cicatricial disease. Repeated episodes infection -> conjunctiva inflammation and eyelid scarring. Scarring leads to corneal abrasion and scarring and blindness.
Trachoma Chlamydia
WHO grade TF (trachomatous inflammation, folicular). To make a diagnosis of WHO grade TF, five or more white or yellow follicles > 0.5 mm must be visualized on the upper tarsal conjunctiva
Herbert’s pits are shallow pits in the cornea that form as a result of follicle rupture. They are pathogenomonic for trachoma but are not assessed in the current grading scheme.
Trachoma 2 Chlmydia
- Trichiasis occurs when eyelid conjunctiva scar tissue contracts, distorting the lid margin and causing the eylashes to rub on the cornea.
- Pannus is the growth of vascular tissue over the cornea as a result of edema and ulceration due to eyelash abrasion on the cornea
- evidence of corneal opacity blurring part of the pupil margin.
Clinical disease: Urogenital disease in Women Chlamydia
Asymptomatic disease common in women (up to 80%)
clinical manifestations in women include bartholinitis, cervicitis, endometritis, perihepatitis, salpingitis, and urethrtis
cervicitis most common presentation in women
mucopurulent discharge, friable cervix, and cervica edema see
urethritis often accompanies cervicitis and presents with UTI like symptoms
Tishugh-curtis syndrome: perihepatitis with inflammation of liver capsule
if untreated may develop PID
Chlamydia Cervicitis
mucopurulent discharge is visible coming from the OS in a patient with chlamydia cervicitis. The cervix is erythematous and friable.
Clinical diseases: Urogenitcal disease in Men Chlamydia
Most infections 75% in men symptomatic.
urethral discharge and/or dysuria
Causes 35-50% of cases of NGU (non gonococcal urethritis)
Incubation period longer than N. Gonorrhoeae so consider diagnosis in patients treated for GC who present with new symptoms
Clinical disease: Oculogentical syndromes Chlamydia
Newborn inclusion conjunctivits: acquired during passage of infant through infected birth canal. Develops in 25% of infants whose mothers have active genital infections. After incubation of 5-12 days develop swollen eyelids, hyperemia and purulent discharge
Adult inclusion conjunctivitis: Afflicts 18-20 year olds. Genital infection precedes eye involvement. Transmitted via autoinoculation or oral genital contact. Mucopurulent discharge, keratitis, corneal infiltrates and scarring.
